Death of a 22-year old

A man in London has died of alcohol-induced liver failure at the age of 22. You may have seen reports of it in the news. Gary Reinbach died less than 48 hours after his mother had highlighted her son's plight at the weekend. Already some people are using it as a stick to beat the Obama health plan. This is what happens, they say, when the government gets involved in healthcare. This begs the question as to whether or not the government is already involved in the US health care – it is of course heavily involved, spending more on health as a proportion of GDP than the British government spends on the NHS.

However, in this case, no-one in government was remotely involved; these were clinical decisions made by the doctors involved, based on agreed guidelines within the medical profession.

More than 8,000 Britons are awaiting an organ transplant, 259 of whom require livers. More than 400 people died on the waiting list last year. There is undoubtedly a shortage of liver donors. Why? Partly because there are fewer people dying in road accidents, but also because since the outrageous fuss made by the Press some years ago over the Alder Hey scandal of retained organs (see my previous article on Morbid Anatomy), relatives are more reluctant to offer up parts of their dead and dying kin for transplant. In Spain, where consent for organ donation is presumed, they do it better.

So criticism of the government for not introducing a more transplant-favorable regime might be in order, but since supply of livers does not meet the demand there has to be rationing. How should they be rationed? It could be by price. Only rich people get transplants? Not acceptable in the UK; I don’t know about the US. At the moment it is by utility. Those with the greatest need who can make the best use of a transplant should be first in line. On the whole alcoholics are not good candidates for transplants. All they do is ruin the new liver with alcohol. Of course, some are redeemable, but alcoholics are notorious liars. Therefore doctors have introduced a test to see whether they are suitable recipients. Can they stay clean for 6 months out of hospital? If they can they are put on the list for a liver. For the truth is that if someone gets a liver transplant, someone else on the waiting list won’t and will die of their disease. A famous case involved the footballer George Best. He was perhaps the best footballer of his generation, but success went to his head and he drank himself into liver failure. He passed the test of being clean for six months and got his transplant. But having received his new organ he proceeded to ruin it with alcoholic binges. You can see why doctors don’t trust alcoholics.

Moralists might declare that if the disease is self inflicted they should be at the end of the line. We don’t make those judgments in the UK. The list is made up according to who would be likely to benefit.

Poor Gary Reinbach never stood a chance. He started drinking at the age of 11 when his parents’ marriage broke up and by 13 he was binge drinking. The roots of his troubles lie with a lax attitude to family break up and an even laxer attitude to under age drinking.

Binge drinking among young people has led to a sharp rise in deaths from cirrhosis of the liver in the 25-34 age group and hospital admissions among young people have been increasing. In 2007-8 the London Ambulance Service NHS Trust dealt with 8,126 alcohol-related calls for 11 to 21-year-olds, a 27% increase on 2004-5.
The regulation of alcoholic drinks has been heavily influenced by the Portman Institute, a front organization for the alcohol manufacturers. The government is highly reliant on taxes on alcohol. They ignore recommendations from the Chief Medical Officer. This is where I hold them culpable. If the same strict policing of alcohol availability were available in the UK as is present in the USA or better still in Canada, problems like that of Gary Reinbach would not exist.

More health news

I am now into day 5 of the eighth course. This time we have omitted the oxaliplatin because the peripheral neuropathy was getting to a level that long term loss of sensation was becoming likely.

Surprisingly, the new regime has not been easier to bear. On day 3 I was very ill with extreme fatigues and an unsound abdomen with a lot of bloating and funny noises. I am a bit better this morning, but I have noticed that far from improving, the numbness has started to migrate up the outside of my legs. I am also suffering from autonomic neuropathy, with a very labile blood pressure and postural hypotension. Oxaliplatin neuropathy is cumulative and continues to deteriorate for some time after the drug is stopped.

I am concerned that not enough thought is given to side effects of chemotherapy. The clinical trials do address side effects,but only in the round. They will report grade 4 neutropenia occurred in 5%, grade 4 diarrhea in 9%, grade 3 rash in 13% and think that this is acceptable, without thinking what it was like for the patient to suffer these side effects. Sure enough, no-one died of the toxicity, but it may well have been torture for the patient. We almost need a palliative care team plugged into relieving the side effects of chemotherapy.

One of the problems is that we are all different. Doses of cytotoxic drugs are based on what the average Johnnie can stand. Drugs are detoxified by a variety of enzymes, and we not only have polymorphisms of these enzymes which alter their effectiveness, the enzymes are inducible by exposure to toxic agents. Heavy smokers and drinkers, for example, are likely to be able to detoxify their drugs more easily, while those like myself who do not smoke and drink alcohol only very occasionally, may nor metabolise the drugs very well at all. This will mean that for a given dose I will suffer more side effects, but also more beneficial effects.

We should not be surprised then that Oncologists have to titrate the dose intensity to suit the patient, nor think of patients who can't stay the course as wimps.

In my case I think one of the problems making this course so severe is that the anti-emetics that I had for oxaliplatin have been withdrawn as unnecessary for 5-FU. But one of those anti-emetics was dexamethasone, which has other effects in combating fatigue. I am presuming that future courses will also exclude oxaliplatin, in which case I will take a short course of steroids to cover the first few days.

New hymn

Some time ago I wrote a hymn about the Second Coming. It was written for a particular service and as it stood would not find a more general use. I have now written a new first verse and chorus. The tune is "These are the days of Elijah".

Christ is the king of creation
Fallen the world he has made
Soon he’ll return to release our shackles
The ransom is already paid.
Caught in a web of corruption
Stunted and stifled by sin
Jesus the victor has promised to save us
The rescue is ripe to begin

The trumpet sounds;
Listen to the shout!
Heaven opens wide;
Hear the angels sing!
All shall rise!
It’s the voice of victory
Raise your lamps to light
The coming King!

See how the sick need a doctor!
The children are dying for bread;
The Devil delights in his bombs and hatred
As panic and terror are spread.
The Church still debates its tradition,
Recalling the days that are dead,
When into the tumult there strides the Bridegroom
Demanding His Bride to be wed.

The trumpet sounds;
Listen to the shout!
Heaven opens wide;
Hear the angels sing!
All shall rise!
It’s the voice of victory
Raise your lamps to light
The coming King!


See how the world needs a Saviour!
The children are shrivelled and bored;
And mothers despair for their sons and daughters
As claims of the Christ are ignored.
But these are the days of new wineskins;
We watch as new wine is outpoured,
And see in the stretching out hands of Jesus
The joy of the world is restored.

The trumpet sounds;
Listen to the shout!
Heaven opens wide;
Hear the angels sing!
All shall rise!
It’s the voice of victory
Raise your lamps to light
The coming King

Physiology

Apart from anatomy, new medical students study physiology, which included biochemistry in my day. I must say I was looking forward to this. At school I had been excited by the descriptions of DNA and protein chemistry in Scientific American. Was I disappointed! In the whole course DNA was not mentioned once. The Professor had qualified in 1923 and had been appointed in 1936. His knowledge was all pre-war and he was also a boring lecturer. Not as boring as some of his underlings who simply read out the relevant chapter of Bell, Davidson and Scarborough, the textbook we were using.

The practicals were designed like the anatomy practicals to coarsen our sensibilities. As I remember they consisted mainly of mutilating small animals. Our behaviour to frogs would nowadays have us petrol bombed by the Animal Liberation Front. It was necessary to stun the animal first. To do this one picked up the frog by its hind legs and swung it to give it a hefty clunk on the edge of the laboratory bench. Then using scissors one cut its head off leaving the lower jaw intact. The next operation was to 'pith' the frog by inserting a metal probe down its spinal cord and pulping it. This was such an unpleasant task that the girls got the boys to do it for them. After that it was necessary to remove a hind leg from the corpse whose heart was still beating. The leg had the femoral nerve attached for this was the purpose of the experiment. We were to show that passing an electric current down the nerve would make the frog's thigh muscle twitch. The electric current was generated by two pieces of wire wrapped round each other, one made of copper and one of zinc. This was an experiment first performed by Galvani (of galvanic current and galvanized buckets fame) in the eighteenth century. The twitching was recorded on a smoked drum.

Smoking drums took more of our time than smoking weed did of a subsequent generation. It was done within a fume cabinet using a Bunsen burner to which was attached a device that produced an evil and oily black plume. The paper covered drum was then placed in the smoke until it was fully blackened. The drum was then attached to a contraption that rotated it. A metal arm moved with every twitch of the frog’s muscle and traced a white line on the blackened paper. The paper was then removed and dunked in varnish to make the tracing permanent.

In our second year we moved from the old Victorian buildings into spankingly modern medical school. We hurried to see the new Physiology lab. Would there be new equipment, perhaps to do experiments with DNA? Of course not. What we saw were row upon row of new fume cabinets, each containing brand new, brass Bunsens to smoke a new generation of drums.

I pass over what we were supposed to do to rats and rabbits but it left me with a distaste for animal experiments. I recognize their necessity and in fact late in my career I became a Council member of the Research Defence Society and made a TV film defending animal experiments. But this was after the RDS had instituted its policy of reducing the number of animal experiments, replacing them with other techniques where possible and refining the way that animals are kept and experimented on so that suffering is kept to a minimum.

I had little personal experience of experimenting on animals myself – I kept a couple of goats and six rabbits that I vaccinated with a harmless vaccine that I had received myself and took blood samples from them (in a way that I had myself been bled). The animals were kept in luxurious conditions that were better than how some of my patients lived. From the days in the 1960s when animal experiments were often unnecessary and crudely performed, there has been a great improvement in animal husbandry and much better designed and humane experiments. Some people won’t listen. I found a great reluctance among scientists to be interviewed for my film, for fear of animal liberation terrorists, and I was advised by then police always to look under my car for bombs before setting out for work in the morning.

Biochemistry was a small part of physiology. We were lectured on the Kreb’s cycle and the glycolytic pathway and had practicals on measuring glucose and urea by simple chemical tests. The macro-equipment that we used made the equipment we had in school look like something out of the Space Age. We were taught by a plump, balding and bespectacled old gentleman and a lady who flirted with the young men. She was certainly over-40, but dressed to look 16. She wore bright red lipstick which always migrated to her teeth and consequently she was known as Dracula’s daughter.

Nobody liked physiology and we took to turning up at five past nine in the morning. The Lecture Theatre’s doors were locked ant nine.

Dave, my dissecting partner, wrote a song for the Christmas Smoker about Anatomy and Physiology. I can’t remember all the words but it was to the tune of Camp Granada (which some of my older readers may remember)

It began:

Hello Mother, Hello Father,
Here I am at my cadaver.

A later verse went something like this:

All around us dogs are dying
Frogs and cats we’re crucifying
It’s not science makes us willing
The truth is that we quite enjoy the killing

The chorus was something like this:

We have sins
Beer, gin and women,
Cigarettes,
The placing of bets.
Can’t you see
Though medicine is our bent
We… want…to…stay…stu…dents.

As I said, Dave left medicine after the fifth term. I often wonder what became of him. I’ve never seen his name in the credits of TV comedy shows.

New health update

I saw the oncologist yesterday. He felt that the peripheral neuropathy was getting so bad that we should drop the oxaloplatin for the moment, so my treatment tomorrow (course 8) will consist of 5-FU and folinic acid. Otherwise he was pleased with my progress and ordered another scan for after course 9. Next week the colorectal multi-disciplinary team will discuss my case with a view to thinking about a second look laparotomy to see if the primary around the ileo-cecal junction is now operable.

MBL v CLL

I have beavering away at the chapter I promised to write and have completed this section on monoclonal B-cell lymphocytosis. The references are not yet complete but if anyone particularly needs them, they will be ready in a day or two, so ask.

Monoclonal B-cell lymphocytosis

Having defined CLL as a lymphocytosis with a characteristic immunophenotype it became clear to CLL specialists that early stage CLL was apparently getting commoner. In fact, apparent fluctuations in the incidence of CLL have been occurring for a long time. In the nineteen fifties and sixties several studies reported incidences in excess of 6 per 100,000 [5]. This was in the days before immunophenotyping when any lymphocytosis over 10 x 10^9 per microlitre of relatively appropriate morphology was designated CLL. From our own experience we can be sure that we misdiagnosed many patients during this period and in our work as a reference center we have recognized that these types of mistakes were not rare. Immunophenotyping has excluded the majority of interlopers and as a result the perceived incidence of CLL fell between the nineteen seventies and nineteen nineties. Sgambati et al [6] reporting on statistics from the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) Program described a fall in incidence rates for CLL for white males from 4.2 per 100,000 to 3.2 per 100,000 between 1973 and 1976 while the rate for white females fell from 3.8 to 2.6 over the same period. The rates for those of African-American, Hispanic or Asian origin were much lower.

Exactly how many cases of CLL are collected depends on how assiduous is the collection. Simply relying on death certificates or hospital admissions will miss all those early stage patients that never progress and never require treatment. Between 1984 and 1988 Cartwright et al [7] enlisted the help of hematologists performing blood tests for one third of the population of England and Wales to register every new diagnosis of CLL. The annual incidence was 5.54 per 100,000 with a male to female ratio of 1.95. There was no temporal variation, but a threefold difference between districts. Racial differences could not explain the discrepancies, though districts where the disease was commoner tended to have more old people. What was noticeable was that the disease was apparently commoner where the hematologists took a special interest in the disease, suggesting that such specialists would be more likely to make the diagnosis with relatively low lymphocyte counts that less obsessed doctors might pass as normal.

Guidelines for the diagnosis of CLL were published in 1988 by a National Cancer Institute Working Group (NCI-WG) [8] and in 1989 by the International Workshop on CLL (IWCLL) [9]. The former required a lymphocytosis of >5 x 10^9/L but the latter a lymphocytosis of >10 x 10^9/L. This confusion was removed by the 1996 guidelines published by the NCI-WG [10] which settled on a lymphocytosis of >5 x 10^9/L but has been further complicated by the 2008 guidelines published by the IWCLL [11] which raise the threshold to a B-cell lymphocytosis (rather than a total lymphocytosis) of >5 x 10^9/L.

In 2002 Rawstron et al [12], using four-color flow cytometry of the dregs of blood samples taken for other reasons, discovered that 3.5% of the population over the age of 40 harbors a population of cells immunophenotypically similar to those of CLL and this has been confirmed by others, who emphasize that marginal zone lymphoma also exists in this pre-clinical form [13]. The prevalence of such cells rises with age, to 7.7% of people in their seventies. Recently the group from Salamanca, Spain, using a more highly sensitive multicolor flow technique have suggested that as many as 12% of the population over the age of 40 have a small population of CLL-like cells in heir blood [14].

An International Working Group [15] has designated this condition as Monoclonal B-cell Lymphocytosis (MBL) and laid down diagnostic criteria (Table 1). Of course, this new entity did not suddenly appear in 2002, and the International Group also reported on previous sightings of the condition under such names as ‘smoldering CLL’ and ‘benign monoclonal B-lymphocytosis’.

Rawstron et al [16 NEJM 2008] have reported on the relationship between MBL and CLL. Among subjects with a normal blood count, the prevalence of MBL was 78 in 1520 or 5.1%. Because the samples were taken from anonymous subjects no follow-up was possible. In such patients the B-lymphocyte count could be as low as 0.015 x 10^9/L and none were higher than 1.2 x 10^9/L (normal range: 0.025-0.49 X 10^9/L). Another cohort, who did have a lymphocytosis (lymphocyte count >4.0 x 10^9/L) could be followed up. Of 2228 such individuals, 309 had MBL (13.9%) and 185 of these had sequential monitoring for between 0.2 and 11.8 years (median 6.7). While in most cases the lymphocytosis was stable or regressive, in 51 subjects (28%) there was progressive lymphocytosis; in 31 to a lymphocyte count of >30 x 10^9/L. Among the 51, other features of progressive CLL, predominantly lymphadenopathy, developed in 28 (55%) while 13 (25%) required chemotherapy a median of four years after the initial diagnosis. The estimated rate of progression to CLL requiring treatment of MBL with lymphocytosis was 1.1% per year; about the same rate at which monoclonal gammopathy of undetermined significance (MGUS) transforms to myeloma.

The only factor among those examined that predicted progression was the absolute B-lymphocyte count. Those with B-lymphocyte counts below 1.9 x 10^9/L seldom progressed, while of those with a B-lymphocyte count of greater than 4 x 10^9/L, more than half had progressed at 10 years follow-up. There were 62 deaths among the 185 who were followed up; the majority had died from an unrelated cause, but 13 had had progressive CLL, although CLL was mentioned on the death certificate of only four.

Although MBL only seldom transforms to CLL, almost all cases of CLL were once MBL. Taking advantage of the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, Landgren et al [17] were able to identify among 77,469 healthy adults 129 subjects who eventually developed. Of these, 45 had available pre-diagnostic cryopreserved whole blood. Using flow cytometry and molecular techniques they were able to identify an MBL clone in 44 of the specimens.

The new definition of CLL and its relationship to MBL will change clinical practice. One of the consequences would be a demand to monitor cases of MBL with flow cytometry to check on B-cell numbers. Shanafelt et al [18] have addressed this problem by re-evaluating 459 Rai stage 0 patients in view of the new guidelines. They found that 190 patients would be reclassified as MBL. By studying the likelihood of progression they determined that a threshold B-cell count of 11 x 10^9/L was necessary for the condition to progress to clinically significant CLL. This equates to an absolute lymphocyte count of 20 x 10^9/L. The fascinating corollary is that CLL should not be diagnosed until the absolute lymphocyte count consistently exceeds 20 x 10^9/L. This would obviate the need for expensive flow cytometry measurements for follow-up patients. For those more conservatively minded, their study found that the current CLL definition threshold of a B-cell count of 5 x 10^9/L equates to an absolute lymphocyte count of 11 x 10^9/L. So much for progress over the past 35 years.

Living anatomy

As opposed to morbid anatomy. I remember well that first evening when I gained access to the dissecting room. It was in a gloomy Victorian building, constructed like a Gothic church. The only light was admitted through the high windows and was that of an orange, sodium streetlight. That October evening in 1962 is etched in my memory. The dissecting room was large with ten lead-topped tables arranged in two rows of five. On each was a body laid and covered with a green cloth so that all you could see was the body's shape - far more frightening than the body itself.

The smell, sweet and sickly, was a mixture of formalin and chalk dust. I'm not sure what scared me, but I was glad to be out of there having ascertained that I would be assigned table number 4 along with Roger, Adrian and Dave.

The next morning was altogether different. The lights were full on and there was an air of jollity, mainly engendered by those students who had done 1st MB, a sort of resits for failed A levels taken at the University instead of school. These, with their year's experience of University life, were the early leaders. We didn't realize at the time that they were the rich but dim kids whose parents could pay the extra cost of resitting their exams at University rather than school. It is easy to be cowed by confidence.

Looking back it is hard not to feel that the medical course was designed to coarsen our sensitivities. We were naive schoolboys (and girls) who needed to be toughened up. Perhaps that was a true perspective; I have since seen several young female residents and one male who found the rough and tumble of medical life too pungent to be tolerated. Interestingly, they have all been Christians. Are Christian doctors such delicate flowers that life and death in the raw are too unpalatable?

We began our dissection in the armpit. I had no idea that smelly armpits hid such a nexus of nerves. We called our body (or cadaver, to give it its professional name) Ernest (because we were always working in dead earnest). For six weeks I had a recurring nightmare. Ernest would be lying there with his great hook nose. As I stuck my scalpel in his armpit he suddenly raise himself up from the table laughing ans said, "Stop tickling!"

Each week we dissected something different or at least Roger and Adrian did - they were keen as mustard on the whole business - while Dave and I nipped down to the Refectory for coffee and to try writing something for the Christmas party. I wonder what became of my earnest colleagues. Last I heard of Dave he was driving a soda-pop delivery truck, having failed his 2nd MB twice. Roger only failed once and became a GP. I did hear that he had some trouble with the GMC; something to do with drugs and prostitutes, I believe. I think Adrian ended up in the Solomon Islands. Every week we had a viva-voce examination with one of the Demonstrators. The Demonstrators were trainee surgeons who were taking time out to learn some serious anatomy. Surgeons are among the few doctors who really need to know anatomy; for the rest of us it is an exercise in rote learning designed to keep us off the streets. The degree of detail is seldom any use to us during clinical practice. We generally managed to pass the vivas, even though Dave's usual answer was, "I think I have a mental block on that one."

On one occasion we all failed miserably. The viva was on the larynx and we had drawn a demonstrator who was a trainee anesthesiologist rather than a surgeon. Crico-aretinoid muscles were a mystery to me and still are.

Apart from cutting up dead bodies we also had a series of demonstrations of living anatomy. This meant we had to examine our own bodies. For some this had immense attraction as there were girls in the group. In fact there were 12 women out of 60 students. Since we were to be divided into groups of 8, it looked as if at least one group would be mixed. Alas for some the men were separated into 6 groups of eight and the women into 2 groups of six. One coarsened wag posted a poem about it on the anatomy notice board. I think I can remember it:

O living anatomy
Thou dost seem flat to me
Since they did segregate
The sexes into groups of eight
Or so.
O blow!
The shame and degradation
Never to have seen
An hemispherical elevation
Or touched one e'en.
Perhaps it would be best
To entertain our guests
With poetic tales of roses on twin crests,
Or accept the bland
A modified sebaceous gland
Divided by some fibrous strands,
Lest the shock should dull the mind
When in the course of time we find
That as we watch the garments fall
It wasn't really worth it after all.

The culprit was summoned to see Professor Yoffey the head of the Department of Anatomy, and then sent away to return wearing his blackstuff gown. He was given a final warning pending rustication.

Yoffey had more to worry about. Dick Smith, one of the students whose father was a GP, desperately did not want to be a doctor. Instead of dissecting bodies he used to drive in his little Standard Eight to Weston-Super-Mare and from there send Yoffey a postcard saying, "Wish you were here!"

Yoffey was interested in the lymphocyte, which he was convinced turned into red blood cells as it matured. After he retired he emigrated to Israel and became a Professor there. Years later I met his granddaughter who also happened to be related to Victor Hoffbrand, the Professor of Hematology at the Royal Free Medical School. She had written a play about the Song of Deborah and was astonished that anybody else had ever heard of it.

Dick Smith left Medical School and became an Army officer. I met him years later. He still had the old Standard Eight. In the trunk he had a case of smuggled gin, which he tried to flog me.

The myth of more

Do you want to know the secret of contentment? It's hard to be content in an economic downturn. Still harder if you have cancer. Is it knowing you've done your best? Is it in providing for your family? Is it becoming a household name? Is it making enough money that you never have to work again?

I heard a story of a fisherman basking in the afternoon sun, enjoying the warmth and resting contentedly as the evening drew on. He was approached by a young man who asked why he was not out fishing. He replied that he'd been out this morning and had a good catch, sold his produce at the market and now he was relaxing.

"I can see you need someone like me in your business," said the young man, "if you'd gone out this afternoon you could have doubled your profits. Before long, if you kept up the practice of going out twice a day, you could have expanded your business, bought a second boat, then a third and so on. You could have employed other fishermen and eventually you would have made so much money you would never have to work again."

"And what would I have done then?"

"You could sit in the sun and enjoy God's beautiful creation."

"And what do you think I am doing now?"

The myth of more tells us that there is always something better round the corner. A better address, a better car, a more glamorous wife, smarter gadgets; the grass is always greener. In truth, such an attitude leads to discontent.

In Philippians chapter 4 Paul tells us the secret of contentment. "I have learned to be content whatever the circumstances," he says(v 11). "I have learned the secret of being content in any and every situation, whether well fed or hungry, whether living in plenty or in want." (v12)

What is that secret? "I can do everything through him who gives me strength." (v13)

Relying on God is seen as a weakness in this world. It's OK for those who need a crutch, but I can stand on my own two feet. No, actually, you can't. I have seen so many who thought they could, brought low. Beware of the media; they will only build you up to knock you down. Every political career ends in failure, said one very wise man. Obama beware! Look at the ignominy of your predecessors. Bush was caricatured as a monkey, Clinton as a lecher, Bush senior as a time server, Reagan as senile, Carter as naive, Ford as an idiot, Nixon as a crook, Johnson as a warmonger, Kennedy as a womaniser. In the UK Brown is seen as incompetent, Blair as a liar, Major as a no-hoper, Thatcher as bully, Callaghan as worse than useless, Wilson as a crook, Heath as a humorless robot, Douglas-Home as a simpleton, Macmillan as an old dodderer, Eden as a self-serving snob. Only Churchill maintains his reputation, despite his drunkenness, bad judgement and betrayal of his party. Still Churchill was himself a journalist, so perhaps he was immune to criticism.

I have before commented on the hollowness of fame on this blog, but still it is the ambition of young people to be famous. How I wish that young people aimed for Godliness.

In today's paper is a story about Kaka the Brazilian soccer player who has just been transferred to Real Madrid for a huge sum. When he scores a goal Kaka is given to pulling up his shirt to reveal a message on his T-shirt that says, "I belong to Jesus." FIFA has objected to this show of religion. Apparently, too many South American footballers have been making too much of a show of their faith. The majority of those accused are Pentecostals who have abandoned Roman Catholicism. I always warm to them. Why should these young men not display their trust in the Lord? If only more young people would. And old people.

To trust in God is a sign of strength, not weakness.

Paul goes on in the letter to extol generosity. The Philippian church, probably the first European church, had been one of Paul's most faithful supporters. What an example to us! How many years are you away from relying on your income? How much do you have saved against a rainy day? It may be fine in your home, but there is plenty of rain outside. Obama, rightly told African leaders in Ghana that they must take the blame for the poverty in Africa. Corrupt government is rife and most aid is subject to a large surcharge that goes straight into Swiss bank accounts of crooked leaders. That doesn't negate the poverty in Africa. The only hope for Africa is a change of heart of its people. But that can only come if we in the West show winsome ways.

At the G7 meeting in Italy last week the great powers admitted to falling short of the Gleneagles commitment to the third world by $15 billion. We know that politicians are not to be trusted, but for Christians generosity with their time, their service and with their pocket-book should be a watchword.

For why? Because Jesus himself told us, "Do not store up for yourselves treasures on earth, where moth and rust destroy, and where thieves break in and steal. But store up for yourselves treasures in heaven, where moth and rust do not destroy, and thieves do not break in and steal. For where your treasure is, there your heart will be also." (Matthew 6:19-21)

Where is your treasure? Where is your heart?

Morbid Anatomy

I used to wear a hat in those days. Actually, I owned two; one was an oversized Homberg that my father had given me and the other was a 'Robin Hood' with a feather in the hatband, which I bought from Dunns the hatmaker. In 1963 most people wore hats. As a medical student I had been heavily influenced by the Richard Gordon books, 'Doctor in the House', and 'Doctor at Large'. My ambition was to take part in Rag Week, when the students got up to all sorts of pranks. I had been early disappointed by the fact that the medical course ran on facts from the 1930s, and all the recent science that I had done at school like DNA and molecular pathways hadn't penetrated the University. I did not take my studies seriously since there was no chance of being sent own at the end of the first year. I did enough to survive and treated the first year exams as a joke.

This was the year that General DeGaulle rejected Harold Macmillan's application to join the Common Market (as it was then called). We constructed a papier mache caricature of General DeGaulle with a caterpillar's body and called it 'de gall stones bug'. The nights before the Rag Parade we camped out guarding the effigy against the Engineers who had sworn to destroy our float. The Spring of 1963 was one of the coldest on record. It snowed heavily at Easter. The swimming costumed Rag Queen shivered as snowflakes landed on her bare flesh during the Rag parade. We won second prize, first going to the veterinary students who made a giant elephant which contained half a ton of rhinoceros dung that was shoveled out over the watching crowd at discrete intervals. Student humor!

Anyway, in the middle of this I attended a lecture in pathology. We were supposed to spend two hours the first half listening to a talk with slides on a particular pathological topic and then an hour looking down the microscope trying to identify what we had been lectured about. As soon as the lights went out I fell into a deep sleep. When the time came for us to troop out into the microscopy room, the other students left me there fast asleep. Eventually, a lecturer came in to wake me and I had to go and apologize to the Professor. For my pains I was invited to Sunday tea at his house. I didn't realize it at the time, but this involved an afternoon's back-breaking gardening!

I was reminded of this because my wife used the term 'morbid anatomy'. This is a phrase that has gone out of fashion. It used to be the term used to describe that branch of Pathology that did autopsies and looked at dead tissues to find out why someone died. Nowadays they call themselves 'histopathologists' and they mainly deal with the living. The autopsy has died. As a student I was a frequent attender at the mortuary. Every lunchtime there was an autopsy demonstration when three of four bodies that had been dissected that morning were displayed to students. We learned to recognize sago spleens and nutmeg livers. In my last year in practice the pathologist only conducted 11 autopsies in the hospital mortuary. In part this was due to the reluctance of relatives to allow post mortem examinations, but mostly it is a result of CT scans and MRIs. Hardly anyone dies undiagnosed now.

Out in the community people drop dead, but usually their family doctor knows that they had high blood pressure or a dicky heart and they are written up as 'stroke' or 'coronary' and a death certificate issued. People forget that an autopsy would often reveal several other diseases that the person was suffering from.

The reluctance of relatives to consent to autopsy stems from the Dutch Professor of Pathology at Liverpool who kept a collection of children's heats in formalin-filled pots in his office. He said that he needed them as 'research' though research on what no-one knew. More likely they were trophies.

Bereaved parents were outraged that little Betty's heart wasn't buried with them. (Shades of Michael Jackson's brain). This led to Draconian legislation that effectively barred any part of an autopsied body being retained. Distressed relatives were even asking for the paraffin block containing Junior's appendix, removed years before, so that they could exhume the coffin and bury it with the whole body in a new funeral service. Bizarre!

The legislation even extended to the dregs of blood tests, which would otherwise be tipped down the drain. The research on IgVH genes for which I made my name would have been impossible under the new legislation. there was even talk that hairdressers would have to return cut hair to the individual. Such 'reductio ad absurdo' softened the legislation.

Today histopathologists mainly work on the living. Most of their specimens come from biopsies not autopsies. The take part in many 'multi discipline team' meetings where they explain what the biopsies show and why it is important. Their role is vital.

When I was appointed at a Consultant Pathologist I was asked on what day did I want to do my autopsies. This was a perk, since autopsied requested by the coroner attracted a substantial fee. I replied that I had never done an autopsy in my life and I didn't intend to start then. I was one of the first to see hematology as a clinical discipline. I intended to treat patients with blood diseases who at that time were being mistreated by general physicians. But I also intended to build a laboratory where treatment was based on science not tradition. It took me a long time to get what I wanted, but on February 1st 1974 I made a start.

Codex

The Codex Sinaiticus has been virtually reassembled and made available on line to those who can read Hellenistic Greek. It has been an occasion for atheists to disparage the Bible and talk about discrepancies.

Actually there is only one major point of issue between early manuscripts, and that is whether or not to include the story of the woman taken in adultery at the end of John chapter 8. (Though I suppose there are some who believe that the strange ending to Mark 16 was not a late addition.) The John story should be included, I believe, since it is more likely to have been removed by prudes than inserted by liberals. In any case there is another instance of Jesus being forgiving to promiscuous women; the Samaritan woman at the well.

I have a book on my shelf entitled 'Alleged discrepancies in the Bible' which goes to great length to explain and refute every alleged discrepancy. I believe that most are due to failure to appreciate literary form.

Any story can be told in many ways. I once wrote anonymous leaders for both the BMJ and the Lancet in the same week on the same topic, but wrote them in their respective house styles that were so different that nobody suspected that they were by the same author. In Japan a story might be told according to the tradition of tyhe Noh play; in Russia the story might be told by dance according to classical ballet. Falstaff can be a character in Shakespeare's plays (Henry IV parts I and II, Henry V and Merry Wives of Windsor) or a character in Verdi's opera. In each case his story is told differently. We are used to reading novels, where action usually follows sequentially in a fairly naturalistic way, but the novel as a literary form is only about 400 years old. And some novels are not in this form at all. Ulysses by James Joyce certainly isn't. When we watch a movie we often assume it to be naturalistic, but listen, there is usually no music playing in real life action. Homer and Virgil wrote they stories as poetry; Sophocles wrote drama where the actors covered their faces with sad or happy masks. The same story may be told in several literary genres. Science fiction, chick lit, western, cops and robbers, period drama or impressionist modern novel may all be telling the same story of love and betrayal or greed and rebellion.

We should not assume when reading the gospels that they should flow sequentially like a novel or a biography, on the contrary they were polemics, designed to convince their readers or hearers that Jesus Christ was the Messiah. Form was dependent on the message. Matthew's gospel is replete with Old Testament references, designed to stress how Jesus fulfilled the prophecies about the coming Messiah; Mark on the other hand almost certainly is dependent on Peter's recollections and reflects his experience of accepting and preaching to the Gentiles. Time and again we see teh Jews-to-Gentiles transition. It is the structure that dictates the sequence of stories, not the time line.

Sleeping Jesus

In Mark chapter 4 we meet a Jesus who seems not to care. There he is sleeping on a pillow at the bottom of the boat while the squall rages and the water is coming in. These disciples were not landlubbers. They were seasoned fishermen, well aware of the way a storm could get up on Galilee. They were really afraid; they feared for their lives. And it was Jesus's idea to cross the lake. Another fine mess you've got us into, they might well have said.

Yet here was Jesus sleeping. Of course he'd had a busy day. What with healing and preaching, and casting out demons, he's every right to be tired. But didn't he care that they were perishing?

Sometimes we worry that Jesus has abandoned us. We get into all sorts of trouble and when we cry out and nobody comes. I remember as a small child I used to get earache at night. I would scream in pain and every time my mother would come to me and sleep in my bed to comfort me. Why should Jesus abandon them? But, of course, he had not left them. He was still there in the stern, sleeping. They could see the Savior; our problem is that we can't. We must rely on His promises, "I will never leave you or forsake you." "All that the Father has given me shall come to me and no man can snatch them from my hand."

The problem of the disciples was not that they could not see Jesus, but they didn't realise who he is.

This may seem a bit surprising. They had already seen many healed including a leper and a demon-possessed man. He had claimed to be able to forgive sins and proved it by healing a paralytic. But all this had happened to somebody else. for the first time their own lives were threatened.

It's amazing what a difference this makes. I have seen hundreds of patients with cancer. Having cancer myself put me in a totally different position. I used to have all sorts of doubting questions - How could prayer work? Do miracles still happen? How to reconcile Man's responsibility with God's Sovereignty? - Now I know that the secret thing of God are God's to know, not mine. Job was tormented greatly by his family's demise and his loss of his wealth, but only when his body was touched by Satan was he brought low enough for God to really reach him.

Jesus had not been sleeping to put the disciples in danger. His purpose was to demonstrate to the disciples who he really was. They were slow to learn, but in stilling the storm with a single word he revealed himself "He stilled the storm to a whisper; the waves of the sea were hushed" (Psalm 107:29). "You rule over the surging sea; when the waves mount up you still them" (Psalm 89:9). Who is it who controls the Sea? It is Yahweh the Creator God. When the disciples ask the question, "Who is this, even the wind and waves obey him?" they know the answer. Jesus is the Creator God.

God's purpose is not our comfort but our holiness. For this we need to submit to him, accept the gift of salvation, and follow him. Through our changing circumstances he cajoles us into acceptance. Is he there? Is he sleeping? Doesn't he care? He's there, he cares, and he's wide awake; but he knows what's best for us and he leads us into it.

Wimbledon

Gary Lineker once said that the best way to watch Wimbledon was on teletext. He was speaking about the soccer club AFC Wimbledon, home of mute movie star, Vinnie Jones. But he could have been talking about tennis. I mean Veneria versus Senus - who cares?

But nice to see the Lions give South Africa a stuffing. Notice how many South Africans play for the Cheetahs?

Hope

Seventh course completed, now for the side effects. Actually I have weathered this course much better. The dose of oxaloplatin has been reduced and I am back taking the steroids, but I think the greatest improvement has been in my psyche. Simply by seeing the improvement in the CT and entertaining to prospect of a curative resection of the primary after the chemotherapy is completed, I have rediscovered some hope.

Spiritual hope is something I have always had, of course. Hope in a Biblical sense is not just a benign expectation, but a certainty achieved by believing the promises of God, but earthly hope is a lot more chancy. Andy Murray hoped to win Wimbledon but there was no certainty in that hope. Perhaps next year...

As an oncologist, I always believed in leaving patients with some hope. Survival curves always have a long tail and though it may be a long thin one like a laboratory rat's someone has to ride that tail and it may be you.

Anyway something has raised my spirits. Thanks for all those who have been praying.

Deserving rich; deserving poor.

John Denham, one of the few members of the British Labor cabinet from the south of England made an interesting speech yesterday. It is well known that the Labor party is only in power because Scotland is massively over-represented in Parliament and that their ranks are packed with representatives of deserted inner cities with low voter numbers (apart from the vote rigging by mainly Muslim tribe leaders in northern cities who commandeer the postal votes of non-English speaking recent immigrants and give them to Labor).

The substance of the speech was inequality. Labor has made a big thing about level playing fields in employment, social benefits, housing and so on. Hutton's point is really about the deserving poor as opposed to the undeserving poor and more to the point, the deserving rich as contrasted with the undeserving rich.

It is easy to pick out poor people who deserve to be helped: those born with physical handicaps, those struck down with life-threatening diseases, those whose ethnicity exposes them to prejudice (though as prejudice has massively diminished this is a dwindling number that should not include most black and Asian people, and certainly not the East Asians who do very well for themselves), and a few other individual cases not easily categorised.

It is possible to get rich by hard work. Enterprising entrepreneurs who take risks with their own money should be rewarded. Nobody even minds the odd Lottery winner. However, most people who are very rich have bent a few rules on the way up and many are consummate criminals. At the moment the public's ire is directed at bankers who have gambled knowing that if they win they will reap ridiculous rewards but if they lose the public purse will bail them out, and members of parliament who have gamed the system to enjoy rewards that were never intended and particularly those who represent members of the public who are living on minimum wages. But others will be caught in their sights before the recession ends. Executives who work for the publicly funded BBC will be next.

When my son was redecorating his house in Oxford prior to selling it, he was up a ladder and unseen by his neighbors sunning themselves in their garden. They were two young women. The fact that they were both black is probably irrelevant; there are just as many white tarts in the Blackbird Leys estate. One was obviously impressed by the quality of housing, "How did you manage to get yourself a nice house like this when you're on the dole?"

"That's simple," replied the other one with a toddler on her lap, "Just get yourself a kid and council will find you one."

When my son's house was burgled during his absence, when the police finally arrived they found evidence that the burglar had entered and exited the property via next door's fence. On knocking on his neighbor's door they immediately recognized the occupant, found drug paraphernalia, and enquire about her well long term associate, who had a record for burglary.

To my mind most burglars and drug addicts and benefit cheats are not the deserving poor. Labor promised to follow Bill Clinton's Workfare policies, but too many of their grassroots supporters objected.

Just how common is CLL?

Just exactly how common is CLL?

Most articles about CLL begin with the sentence, “CLL is the commonest type of leukaemia in the Western world.” However, the apparent incidence of CLL has fluctuated widely over the years. In Hansen’s magnum opus [1] published in 1973 and based on 189 cases of CLL followed for a long time, he reports on previous studies that found an incidence of 5.5 per 100,000 in 1949, 6.6 per 100,000 over the period 1943-52, and 6.4 per 100,000 between 1958 and 1961. In 1964 a Danish study found an incidence of 7.8 per 100,000.

This was in the days before immunophenotyping when any lymphocytosis over 10,000 per microlitre of relatively appropriate morphology was designated CLL. In a retrospective examination of patients previously diagnosed in our own unit we have identified patients misdiagnosed as CLL who in fact had splenic marginal zone lymphoma, mantle cell lymphoma, follicular lymphoma, small cell Sezary syndrome and T-cell prolymphocytic leukaemia. In our work as a reference center we have recognised that these types of mistakes were not rare. Immunophenotyping has excluded the majority of interlopers and as a result the perceived incidence of CLL fell between the nineteen seventies and nineteen nineties. Sgambati et al [2] reporting on statistics from the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) Program described a fall in incidence rates for CLL for white males from 4.2 per 100,000 to 3.2 per 100,000 between 1973 and 1976 while the rate for white females fell from 3.8 to 2.6 over the same period. The rates for those of African-American, Hispanic or Asian origin were much lower.

Exactly how many cases of CLL are collected depends on how assiduous is the collection. Simply relying on death certificates or hospital admissions will miss all those early stage patients that never progress and never require treatment. Between 1984 and 1988 Cartwright et al [3] enlisted the help of hematologists performing blood tests for one third of the population of England and Wales to register every new diagnosis of CLL. The annual incidence was 5.54 per 100,000 with a male to female ratio of 1.95. There was no temporal variation, but a threefold difference between districts. Racial differences could not explain the discrepancies, though districts where the disease was commoner tended to have more old people. What was noticeable was that the disease was apparently commoner where the hematologists took a special interest in the disease, suggesting that such specialists would be more likely to make the diagnosis with a relatively low lymphocyte count that less obsessed doctors might pass as normal.

Guidelines for the diagnosis of CLL were published in 1988 by a National Cancer Institute Working Group (NCI-WG) [4] and in 1989 by the International Workshop on CLL (IWCLL) [5]. The former required a lymphocytosis of >5 x 109/L but the latter a lymphocytosis of >10 x 109/L. This confusion was removed by the 1996 guidelines published by the NCI-WG [6] which settled on a lymphocytosis of >5 x 109/L but has been further complicated by the 2008 guidelines published by the IWCLL [7] which raise the threshold to a B-cell lymphocytosis of >5 x 109/L.
In 2002 Rawstron et al [8] discovered that 3.5% of the population over the age of 40 harbors a population of cells immunophenotypically similar to those of CLL. More sensitive techniques suggest that this percentage might be as high as 12% [9]. This new entity, monoclonal B-cell lymphocytosis (MBL), seems to precede most new cases of CLL [10], but clearly most cases never progress to become CLL. Since individuals with MBL may have up to 5 x 109/L B lymphocytes, the new threshold for CLL was absolutely essential to distinguish between them.

In this issue of Leukemia Research, Seftel et al [11] have analyzed the effect that diagnosis by immunophenotyping has had on the incidence of CLL according to the 1996 criteria. The SEER figures for the period 1993-2004 give a combined incidence of CLL and small lymphocytic lymphoma (SLL) of 5.13 per 100,000 [12]. SLL is essentially the same disease as CLL in which the lymphoid expansion is confined to lymph nodes and not present in the blood. It differs from MBL in having definite lymph node enlargement. For the period 1996-2005 the Public Health Agency of Canada, using data from provincial cancer registries reported an incidence of 5.9/100,000 [13]. Seftel et al assembled the data from the provincial cancer registry at CancerCare Manitoba and supplemented these with flow cytometry reports from the two tertiary referral centers in Winnipeg. In both cases the data covered the period from January 1st 1998 to December 31st 2003.

The results of their study demonstrated the fragility of data from cancer registries. Although they assembled 813 patients, 14.5% had to be excluded for administrative reasons, mainly because the diagnosis had been made before the study period. This is a common problem, because diagnosis by a haematologist is very likely to predate a patient being brought to the attention of a cancer registry. A further 9.7% were excluded because of a wrong diagnosis, most commonly marginal zone lymphoma. Despite these exclusions the apparent incidence of CLL has risen. Over the study period as flow cytometry was more regularly used, the annual incidence went from 6.73/100,000 in 1998 to 9.40/100,000 in 2003. It was this apparent increase in early stage CLL that prompted Hoffbrand and Hamblin in 2007 to warn that patients were having the label ‘leukemia’ attached to them when they might realistically expect and normal and healthy lifespan [14].

The new 2008 guidelines for the diagnosis of CLL will have the effect of reducing the incidence since a B-cell lymphocytosis of 5x109/L roughly equates to a lymphocytosis of 11x109/L [15]; back to where we were in 1973. The new guidelines has been criticised on the grounds that there would be unintended consequences of cost and access, and that there was no established clinical relevance of making the change [16]. Furthermore, follow-up monitoring of patients with MBL would be more expensive since it would now have to include flow cytometry [16]. However, these criticisms have been rebuffed by the IWCLL working group although they admit that more work needs to be done at the MBL/CLL interface [17].

The true incidence of CLL remains a mystery. We shall have to await studies using the 2008 diagnostic criteria.

Good news!

Today I went for my pre-chemo appointment and got the result of my scan. The previous scan showed an area around the ileocecal valve that was the presumed primary that was 3.2 cm in diameter and some thickening of the mesentery. In the scan of 10 days ago (taken during the 6th infusion) this ileocecal area was 2.0 cm in diameter and there were no other abnormalities on the scan. If we think of the original lesion as a sphere, it would have had a volume of 12.8 cubic cms. The volume of the current lesion is 3.14 cubic cms. In other words we are talking of three quarters of the volume of the cancer gone after less than half the treatment. It holds out the possibility of curative surgery when the chemo is finished
, though this is not to be relied on.

In other words, good news.

Anemia in cancer patients

Why have a blood transfusion? Is it a] to raise your hemoglobin? b] to improve your color? c] to improve the oxygen carrying capacity of your blood?

The answer, of course, is c] but while it will do both a] and b] it won't do c] immediately. Oxygen is carried by hemoglobin and is released to the tissues where it is needed. It is helped to do this by a chemical called 2,3,DPG. In order to release oxygen, its place on the hemoglobin molecule must be taken by this chemical. 2,3,DPG is manufactured by all cells from the burning of glucose (the process is known as glycolysis and the biochemical pathway is known as the Emden-Myerhoff pathway. The particular trick of producing 2,3,DPG is known as the Rapaport-Leubering Shuttle). If a cell is not metabolising glucose then it won't make any 2,3,DPG, and this is what happens when blood is stored in a fridge. So when you receive blood from the blood bank it has very little 2,3,DPG and therefore the hemoglobin molecules cling on to their oxygen. That's why someone who has been transfused gets no immediate benefit from it; it can't release its oxygen to the tissues until it regenerates 2,3,DPG, which takes a couple of days.

This is one of the reasons that patients are dissatisfied with blood transfusion. That and the risk of transmitting viruses, or prions, or making their cancer worse by suppressing their immunity. In fact blood transfusion is very safe. Blood is screened for HIV, hepatitis B and C and a host of other possible infections. It cannot be screened for prions, but the risk of developing new variant CJD from transfusion is vanishingly small. The greatest risk of a transfusion is that some idiot will give you the wrong blood.

The alternative is EPO. Lots of cancer patients have been given it, but the unfortunate fact is that it shortens life. A recent meta-analysis published in the Lancet looked at 53 separate trials involving 13,933 patients. Although the effect was not great (a hazard ration of 1.06) it was statistically significant. Partly this effect is because EPO may raise the hemoglobin too much and the thrombotic complications of polycythemia come into play, but also there is the worrying fact that EPO is a growth factor for some tumors.

With so much to worry about we need to look at anemia again. In some cases the problem can be sorted with iron therapy. (Oral iron is best; there is no evidence that intravenous or intramuscular iron is more likely have a response or have a quicker response.) But we need to be able to recognise iron deficiency (which is almost always caused by bleeding). The easiest way is to look at the mean cell volume on the blood count. If this is below 80 fl then iron deficiency is the most likely diagnosis. Thalassemia trait can cause a low MCV and this is an important catch for people of Mediterranean background, but the only other cause of a low MCV is the anemia of chronic disorders (ACD).

I have bee surprised recently by how little even hematologists know about ACD. They seem to be unaware that it can cause a low MCV. I can only think that they have never looked at the blood counts of patients with rheumatoid arthritis, ulcerative colitis and Crohn's disease, let alone people with chronic infections or disseminated cancer. The serum iron in ACD can be as low as it is in iron deficiency, as can the MCV. The difference is that the iron binding capacity or the blood (or the serum transferrin) is raised in iron deficiency and lowered in ACD. Serum ferritin is low in iron deficiency and raised in ACD.

What happens in ACD is that the macrophages are over active and snaffle all the iron in the body and won't release it to the newly formed red blood cells. We now know that a chemical called hepcidin, a small peptide produced by the liver that inhibits both iron absorption and release of iron from the macrophages. Patients with excess hepcidin will not respond to more iron, whether oral or intravenous, nor to EPO. Only blood transfusion will raise the hemoglobin.

High hepcidin levels are found in association with high sed rates, high CRPs, high IL-6 levels and other indicators of inflammation.

Rules lure

Thirty-five years ago at the beginning of my consultant career I wrote a ‘Personal View’ for the BMJ. At the time I was frustrated by the inappropriateness of the hurdles I had to scamper over to achieve that status, but full of hope for the future and anticipating the exciting developments that the application of science to medicine would bring. Now that I have retired and become a patient, how does the NHS look?

In many ways there has been a great improvement. The plant that I am being treated in is far superior to the make-do-and-mend Victorian buildings that I practised in at the start of my career. There are many more consultants; for much of my career I had three consultant physician and three consultant surgeon colleagues – now there are more than thirty of each at our District General Hospital (DGH). The imaging departments have been revolutionised, so much so that autopsies have become almost a thing of the past – nobody seems to die undiagnosed – and the exploratory laparotomy is as archaic as the tuberculosis sanatorium.

There has been an enormous increase in regulation, much of it necessary, I am sure. I can think of colleagues who ‘paddled their own canoes’ in the hospital environment, not really caring how it affected their colleagues, who were powerless to influence what they did. The introduction of managers who really managed made a difference. On the other hand many of the innovations that I was able to introduce and the advances that I effected would probably have been impossible under the current regime. They would have been judged inappropriate in a DGH. The time and energy involved in bringing research enterprises to the clinic is certainly excessive now.

Junior doctors are much more junior now and hardly seem to work for any hours. As a Senior Registrar I expected to know everything about every patient under my care, even down to the minutest detail about how long an infusion lasted, what side effects were suffered, and whether the neutrophils were granulated or not. It seems that today that degree of surveillance has been delegated to the nurses and laboratory scientists while the more junior registrars are away on diversity training or maternity leave.

Of course, nurses are not the nurses I knew when I started out. No more ‘mopping fevered brows’ but they really are excellent at running wards. They form a smooth cadre of carers with the Health Care Assistants, and my experience as an in-patient was that things got done on time according to well-designed protocols.

Ah protocols! When I ran a laboratory we had to introduce standard operating procedures (SOP) which ensured that every blood test was done in exactly the same way so that no random variation crept in. There was even an SOP for answering the telephone. (“Good morning, how may I help you?”) I can see that as you deskill the hospital it is necessary to introduce rigid protocols and deskilling has become necessary with shorter working hours, more training and the really bright people being seconded to very complicated tasks, but has that rigidity gone too far?

I give you three examples. In the first the rigid rule was ‘no more than four doses of paracetamol (acetaminophen) in 24 hours’. The patient in question had his post-operative pain well controlled by paracetamol 1 gram four hourly. When he awoke at four am and asked for more paracetamol he was denied because only 23 hours had passed. He could either wait for an hour or have a morphine injection. Now I know paracetamol can be lethal. The fatal dose is around 150 mg/kg. For an 80 kg man (for such he was) that makes the potential lethal dose 12 grams if given over an hour. Even in a man with alcohol problems (which he did not have) there is no way that 5 grams in 24 hours could be harmful. Besides, there is a very effective antidote. Because morphine made him sick (and he was not boarded for an anti-emetic) this patient elected to suffer in silence for an hour.

The second rigid rule was ‘no-one but a doctor is allowed to prescribe intravenous fluids’. In this case it was clearly the junior doctor’s duty to write up the intravenous fluids for the next 24 hours. But guess what, she was too busy. As a recent graduate she found getting through her day’s tasks onerous and she went off duty at 5pm (something that is compulsory these days unless you want a black mark). The ‘hospital at night’ team doesn’t really work unless funded at extravagant levels. Despite being rung on numerous occasions, the F2 (an NHS term for a resident doctor in his second year after qualifying) on duty never turned up on the ward to write up the fluids until 2am. The drip had stopped at midnight and no attempt had been made by the nursing staff to keep the drip open. Why should they? No further intravenous fluids had been prescribed. It took seven attempts from three different doctors and a nursing sister to resite the intravenous cannula. In the past the nurses would have accepted a telephoned instruction or even kept the same fluid regime running or at the very least kept the drip open with slowly running dextrose saline. Now they dare not.

The third rigid rule was ‘blood must not be transfused to patients who are pyrexial’. On this occasion the patient had had major hip surgery and dropped his haemoglobin from 140 g/L to 70 g/L. Blood was prescribed but before it could be given his temperature was noted to be 37.4 degrees C. Obviously blood could not be given! No matter that his pyrexia was almost certainly caused by the presence of several litres of altered blood in his thigh. Never mind someone had some ingenuity. They took the patient to an open window, divested him of his pyjama jacket and played an electric fan on him. When his temperature fell by the requisite 0.4 degrees C they transfused the blood and no, he didn’t catch pneumonia. As an aside, I recently came across a medico-legal case where in a similar situation a haemoglobin of 50 g/L was left untransfused because of a pyrexia. The poor woman became blind from her anaemia and it cost the hospital a lot of money in damages.

These three cases have this in common; in obeying the ‘rules’ nobody was available to think what the rules were there for. Such rules do not have the authority of the Law of the Medes and Persians; they are more like guidelines. They should be a spur to thinking and asking questions. But perhaps the NHS no longer employs thinkers.

More NICEties

Sorry to have been silent for so long. The chemotherapy wipes me out for a few days, but today I am on the mend. I have been gradually working through a number of articles in WORD and they will be posed over the next few days.

I understand that NICE have agreed that Revlimid should be paid for for the treatment of Myeloma, even though the cost per QALY is £43,000 (around $70,000). This is good news for CLL patients, though we wait to see how the economics will play out for CLL.

The myeloma people tell me that it has been quite difficult to recruit for the myeloma trials with the greatest difficulty coming from the West Midlands around Birmingham. So I was not surprised to hear a radio comment from Birmingham expressing dismay at the NICE decision. The speaker apparently believed that the money could be better spent of statins for everybody over 50 to prevent heart attacks and strokes. He is probably right in that the cost of statins is extremely low - around £7 ($11) a month. But he is wrong on several counts.

First, the NHS is basically a state funded insurance system. It exists on the premise that what you can't do for yourself the community will do for you. Few of us could find a quarter of a million for marrow transplant, but as a community, that transplant will cost us 0.4 pence each. We can afford a lot of those. In belonging to a society we agree to spend a few pennies each on a wide variety of enterprises - roads to travel on, schools to educate our children, an army and police force to protect us, and public health measures to prevent epidemics. Different societies differ by how much of this community support is provided privately and how much by the state, but in all societies individuals have to rely on the whole. I doubt that many would be happy about the military or the police force being provided by industrial companies, but in some lawless communities that may be the best option.

There is also a decision to be taken on thresholds. How much does the individual want to buy from the community for each of these services? Private refuse collection versus personal visits to landfill sites? Home schooling versus inner city schools? A Montana campsite and an AK47 versus New York's Finest? In the UK we have opted for more state provision of services than in the US, but less than in Sweden or Denmark. Where the threshold lies does not affect the principle of the social contract; it is there to insure the weakest against the highest costs. It therefore makes no sense for the NHS to pay $11 a month for a pill to protect citizens against heart attacks when if that is what they want to do they could easily afford to pay for it themselves. On the other hand treatment of myeloma with Revlimid is beyond the reach of most people unless the rest of the community join in.

There is a second reason why the NHS paying for statins is wrong, and it goes to the whole basis of insurance. When the NHS was first introduced it provided free hot water bottles. Now 1947 was a very cold winter and there was no central heating in the UK then. There might well be good public health reasons for providing everyone with a hot water bottle, but why should people not buy their own? In fact, even Nye Bevan saw the silliness of this and it was stopped.

When I insure my car or my house, I elect to accept an excess. This means that the first £100 or £200 of the claim I pay myself. Naturally, I don't make small claims. Although, I get benefit from paracetamol (acetaminophen) when I am receiving chemotherapy, I would not dream of asking for a free prescription for it. At less than a dime a day a think I can afford it. Those who volunteer to have an excess get lower premiums - there are not so many claims therefore they pay less.

The third reason that the NHS should not pay for statins is that strokes and heart attacks are largely self-inflicted wounds. What is the point of spending $11 a month when the customer is spending more than that on cigarettes and fatty foods to counteract their effect?

The final point I want to make is about personal freedom. People who have opted for cigarettes and whisky rather than statins have already taken a decision about their health. Bib Brother has no right to gainsay it. By all means educate people into making good restrictions; even prevent manufacturers from influencing people with biased propaganda (as cigarette advertising was banned), but when someone says they would rather enjoy a particular lifestyle than possibly prolong their time in an old people’s home, they must be listened to.

The nanny State can intrude too much. It starts by offering help and ends up being compulsory.

Titles and letters after your name

The dose reduction of oxaliplatin has left me less befuddled this time and perhaps the cold-induced parasthesiae are less. I have gone back to the steroids this time with heavy doses of lanzoprazole to avoid the indigestion. This means that I wake at 3am and start to compose a blog. This time I started thinking about titles.

In America President Clinton is still called President even though he is no longer the President. Senator is a prized title and I suppose there are many others. Every country has its own traditions. In Germany the wife of a University Professor who has a medical degree and a PhD is formally called "Frau Professor Doctor Doctor Schmidt". In America even a schoolteacher is known as Professor and most medical academics prefer to be called Doctor except in Europe where Professor is the more revered title.

Medical degrees is the UK are officially Bachelor of Medicine and Bachelor of Surgery (some Universities also add Master of Midwifery) yet everyone is called Doctor. In most other countries the qualifying degree is MD, though in some countries it is simply a license to practise. In the UK many people with a PhD do not call themselves Doctor for fear of being asked to officiate at an emergency. I notice that theologians like to call themselves the Reverend Doctor but musicians prefer Maestro to Dr. In the UK physicians look more to post-graduate diplomas to define their status. Thus MRCP or FRCS are more coveted than than MD or MB,BS. There used to be a qualifying degree called Licentiate of the College of Physicians and Membership of the College of Surgeons (LRCP, MRCS) which those who couldn't pass their University finals took, and for the really hopeless there was the Licentiate of the Society of Apothecaries of Cork which was parodied in the movie 'Doctor at Large' where dear old Cyril Cusack examines Donald Sinden in a ride on a pony and trap and the most difficult question is "What can you tell me about urea?" and Sinden's reply is "Do you mean the thing you hear with of the chemical substance?".

It used to be that when you passed the Diploma exams (which are rather like the Boards exams in the US) you were a Member for a few years and then were automatically promoted to a Fellow when they increased your annual subscription. That's why I have FRCP and FRCPath after my name. To become a hematologist in the UK you have to be doubly qualified in Pathology and Internal Medicine. Oxford and Southampton degrees are a bit different to everybody else's. Instead of having MDs and PhDs they have DMs and DPhils. Which is why my letters are DM (though I often write MD to avoid confusion). In the UK the MD is a research degree like a PhD (though it is usually on a clinical subject rather than a laboratory one. It can be awarded for a period of study in a time out from training or as a result of published works on a particular subject as mine was - 13 years of studying CLL.

Of course all these letters after someone's name can be very confusing. I remember being with Reg Clift in a line for refreshments at a meeting. Together with Don Thomas he pioneered the development of bone marrow transplantation in Seattle. Someone came up to Reg and asked what the letters FIMLS after his name meant. Reg wasn't a doctor (though he practised like one). Before Reg could answer, the then Editor of the Lancet who was an Immunologist piped up, "It stands for Fellow of the Institute of Medical-Laboratory Scientists. I've got twenty of those working for me back in England." To which Reg responded, "That's a coincidence, I've got 20 MDs working for me."

Not all letters after the name are what they seem. FRSM simply means that you belong to an expensive Gentleman's Club in central London. It does have a superb Library and a wonderful restaurant as well as cheap lodging so it is worth the annual subscription, but FRSH is a simply a vanity purchase to fool the customers. Buying letters after your name is a common practise; Oxford and Cambridge BAs can upgrade their degrees to MAs after a year for only 10 quid. In the past the only MD degrees awarded were to Oxford and Cambridge graduates who had to take examinations in Latin, Greek and Physic. Edward Jenner, one of the greatest physicians ever, (he invented smallpox vaccination) trained as an apprentice surgeon and qualified as an Apothecary. He couldn't get an MD because he had no Latin or Greek, for the same reason he could not become a member of the Royal College of Physicians. Eventually he bought an MD from Glasgow University for £100; even then the Scots were canny with money. It should be remembered that at the time Jenner was already a Fellow of the Royal Society (the highest Scientific Accolade), not for smallpox, but for discovering how the fledgling cuckoo removed the other eggs and birds from the nest.

Not many medics make FRS and to compensate for that a few years ago a few senior academic doctors set up a new Society, the Academy of Medical Scientists. Leading medical academics were invited to become FMedSci. They guard their doors assiduously against anyone who has not achieved very much yet.

Nowadays it seems that everyone wants to be called Doctor; Dentists, back manipulators, acupuncturists, and even podiatrists. In Russia doctors are called "vrach" I believe, which being translated means "leech". Surgeons in the UK are offended by being called Doctor. Once they have their FRCS they insist on being called Mister. This dates from their origin as barber-surgeons (like Sweeney Todd).

In the church there are many titles, as I illustrated in a previous blog. But it is Bishops I want to attack. The Greek word 'episcopos' which is translated 'bishop' literally means overseer and it is used interchangeably in the New Testament with 'presbutos' which is often translated as 'priest' but actually means 'elder'. The NT only recognises two clerical offices in the church: elder and deacon (which could also be translated as 'minister' or 'servant'. The problem arose when bishops got too big for their mitres ans started assuming and authoritative power. The Bible assumes a plurality of elders in a local church, all of whom should be apt to teach (a quality missing from the list of requirements for deacons). Some elders (but not all) are to be set aside for the preaching of the word and the elders as a whole are to be given the governance of the church, but the NT specifically warns against getting involved in the affairs of the world. It is therefore a nonsense that certain Bishops are guaranteed seats in the British House of Lords, that hangover from feudal times.

Permit this small digression. I watched the Trooping of the Color last week on the Queen's birthday. It was a colorful pageant with clever marching and martial music. I would not want to see it lost, but all the various ranks: knights, baronets, marquises, viscounts, barons, earls and dukes seem to be an affectation too far. The House of Lords as a chamber for refining and modifying legislation seems a sensible organisation, though it is largely a resting place for retired politicians, many of whom remain the crooks they were in the House of Commons.

Anyway, back to Bishops. They quickly became secular authorities in the Roman Catholic Church. Bishop Odo fought with William the Conqueror. Others in England became Lord Chancellors of effectively Prime Ministers. Even in the Church Bishops sought to lord it over people, specifically against the instructions given in the New Testament.

The Quakers have it right, I think. Everyone there is plain John Smith or Jane Baker. If a qualifier is needed it could be Jane Baker, secretary, or John Smith, businessman. I would be happy to be Terry Hamblin, with the physician only added if someone needed one.

Recent Reading

I had my sixth course today with a 25% dose reduction of the oxaliplatin. I already have the cold induced pins and needles, but let's wait and see if the dose reduction does reduce the side effects. Tomorrow I have a CT scan to assess response.

What have I been doing recently? Mostly reading. The books that I have completed in the past couple of weeks since finishing the new Lee Child are three thrillers: "Drop Shot" by Harlen Coben - with much borrowing from Hitchcock's "Strangers on a Train" - "A Good Day to Die" by Simon Kernick and "The Last Watchman" by Robert Crais. I have also read Bernard Cornwell's "Sharpe's Story" a make weight done for charity and I have re-read CS Lewis's "Out of the Silent Planet". I last read that about 50 years ago and could remember very little of it. I read it in conjunction with "Planet Narnia" which I am working my way through. The first of the Science fiction trilogy is about Mars which looms large in the Lewis pantheon. "Prince Caspian" in my next book and also comes under the Martian influence. "War of the Worlds" by HG Wells expressly states the link between Mars and war and Lewis is an interesting Christian writer who clearly feels that pacifism is wrong. He famously wrote a piece entitled, "Why I am not a pacifist".

If I felt fitter I would write at length about this subject, but I will finish with a quote from the Cornwell book and invite my readers to comment on the question of Christianity and pacifism. "A soldier fights battles for those who cannot fight for themselves."

Lines written on John chapter 1

After this morning's sermon by Bev Savage I felt well enough and compelled to write this sonnet.

But Jesus was not Jesus then, no more
The Virgin Mary’s son; He was the Word,
With God, the Three in One, in rapt rapport
Held fast by love. The Holy Three conferred
And made the sky, the earth, the sea; His hand
In each creative act. The Spirit soared
Above the seas before that great command,
“Let there be light!” He was the Light; adored
By angels. Darkness could not comprehend.
Then there was life, of countless, teeming kind.
In Him was life and His that life to lend;
The light of men; for Man he had designed
To hold His image and while thus constrained
To free from bondage those whom sin had stained.

Better today

Thanks to those who have been praying. I definitely feel better today. My appetite has returned and for the first time in a month we were able to go out for a walk. If you had any doubt that I was under spiritual attack, doubt no more. I have even begun writing a poem based on Bev Savage's sermon this morning.

Job's Variant

I'm not sure whether I have told this story before, but when I was in charge of blood transfusion transfusion at my old hospital (which lasted for 29 years), there were just two occasions when we managed to give a patient the wrong blood. On both occasions we gave a Group O patient Group A blood. The first time was in August. The orthopedic ward was closing for the summer, so patients having hip surgery returned from the operating theater to the general surgery ward for recovery. Two patients returned at the same time, and the ward sister instructed a nurse to set up a unit of blood on Mr A. The nurse confused Mr A with Mr B, failed to carry out the usual check, did not involve another nurse as she should and gave Mr A's blood to Mr B. Mr B had a severe transfusion reaction, went into kidney failure, but, fortunately, made a complete recovery.

On the second occasion, five years later, the mistake was made by a laboratory technician cross matching the blood at night. Here, he picked up a tube of blood to cross match and found some compatible blood. It was only after he had issued the blood to the ward that he realized that the tube of blood he had matched against had not come from Mr X, but from Mr Y. Realizing his mistake he rushed over to the ward and snatched the drip out of the patient's arm. Only 20 mls had been transfused and the patient suffered no ill effects. The astonishing thing was that Mr B and Mr X were the same person. The only patient we had ever inflicted the wrong blood on in nearly 30 years and we did it to him twice!

Murphy's Law states that if anything can go wrong it will go wrong. When I first wrote about this remarkable coincidence, I coined the term 'Job's variant' of Murphy's Law; not only would everything go wrong that could go wrong, it would all go wrong at the very same time. If you read the book of Job, you will realize what I mean.

As I look back at the past 5 years I consider myself a victim of Job's variant. Many of my readers won't understand this, but those who know me best will realize that the cancer and its problems have just be the culmination of bad things happening to this family. If you understand what was at the back of Job's calamities you might begin to wonder if the same thing is not at the back of mine.

CS Lewis in the 'Screwtape Letters' tells us that the Devil welcomes both the materialist and the magician. He tells us that the two mistakes mankind makes about the Devil are to take an inordinate interest in him and to believe that he doesn't exist.

In "Tramp for the Lord", by Corrie Ten Boom she tells of a visit to Poland while it was still behind the Iron Curtain. Despite sleeping for a full eight hours she always awoke exhausted and weak. It wasn't that she had picked up an infection or was being poisoned by pollution. A local Pastor explained their predicament, "Your tiredness is nothing less than an attack of the devil. He does not like your work here in Poland, for the Antichrist is busy here, arranging his army." He then prayed over them, rebuking Satan. Thereafter the tiredness left them. Corrie Ten Boom further testified that they had felt the same tiredness on other speaking tours, even in some American cities, but on rebuking the devil in Jesus's name, the tiredness always left them.

How should we view this testimony? For those who do not know her, Corrie Ten Boom was a Dutch lady who was famous for hiding Jews from the Nazis in World War II. She was herself arrested and sent to the Ravensbruk concentration camp where her sister died. After the war she toured the world preaching a gospel of love and forgiveness, even on one occasion being confronted by one of her camp guards and being challenged to forgive him. She was not a fatuous, air-head Christian, but one who had really suffered for her faith. But she came from an old school Christianity (she was 50 when the war began); was her experience merely psychological?

The Bible tells us that our struggle is not against flesh and blood, but against the rulers, against the authorities, against the powers of this dark world and against the spiritual forces of evil in the heavenly realms. (Ephesians 6:12)

Why should I be attacked? The only prominent thing I can do now is witness through this blog. Many have told me how it has strengthened their faith. Satan, I am not going to stop writing this blog no matter what you throw against me. Reader, praying friend, if you want to know what to pray for, please pray against the evil one.

In the Book of Revelation we read of how Satan was brought down. "They overcame him by the blood of the Lamb and by the word of their testimony; they did not love their lives so much as to shrink from death." (Ch 12:11)

health update

Today has been a better day. I have felt well enough to cut the smaller of our lawns. I managed to get the date of my CT scan wrong. It is next Thursday, not today. My blood count was normal today - no sign of the heparin lowering my platelets.

More of the CLL Chapter

I have been gradually improving since the weekend and I have put some work in on the chapter that is due next month.

Diagnosis
The diagnosis of CLL is superficially very easy. For most patients the only abnormality is in the blood count, which shows a lymphocytosis comprising small round cells consisting of mainly nucleus with very little cytoplasm. The nuclear chromatin is coarsely condensed and nucleoli are not usually visible. Cytoplasm appears as a pale blue rim in Romanowsky stained blood films. Characteristically there are cells present on the blood film that appear to have burst or disintegrated; these are known as ‘smudge’, ‘smear’ or ‘basket’ cells. An admixture of larger cells is usually seen. Typically, prolymphocytes are present with larger nuclei with less condensed chromatin and a single prominent nucleolus. The nucleus is often eccentric set in rather more abundant pale cytoplasm.

Very rarely cells with a nuclear cleft are seen leading to confusion with follicular lymphoma. The term ‘atypical CLL’ has been applied to cases of CLL where the number of prolymphocytes exceeds 10% or where the total of atypical cells including prolymphocytes, clefted cells and plasmacytoid cells exceeds 15%. Although it is a commonly used term it has no basis as a different disease entity and the term is just as often used to describe cases of CLL with atypical cell markers. Atypical cell morphology is often associated with the presence of certain chromosomal abnormalities, particularly trisomy 12.

The definitive diagnosis of CLL relies not on the cellular morphology, but on the immunophenotype. The cells are monoclonal. Clonality is assumed by the finding of a single immunoglobulin light chain type (either kappa or lambda) on the surface of the CLL cells, but the quantity of surface immunoglobulin is only about 10% of that on normal B cells. The cells are typically positive for CD5, CD19 and CD23 and negative for FMC7 and surface CD22. The immunoglobulin associated molecule CD79b is only weakly positive. The Matutes score utilizes these markers to differentiate CLL from other lymphoid tumors. In its latest guise it allocates one point each for positive staining for CD5 and CD23, one point for negative staining with FMC7 and one point each for weak or negative staining for surface Ig and either CD79b or CD22. Most cases of CLL have scores or 4 or 5; those scoring 3 often have ‘atypical’ CLL and those scoring 0-2 have other lymphoid tumors.

The monoclonal antibody FMC7 detects and epitope of CD20 which is obscured by changes in membrane cholesterol metabolism. CD20 is also only relatively weakly expressed on CLL cells compared to other B cells. There are other antigens that are differentially expressed on CLL cells, including CD43, CD11c, CD25, and very low levels of CD45, but these markers are of less value in distinguishing CLL from other B cells malignancies than those used in the Matutes score. Flow cytometric examination of CLL cells usually includes CD20 and CD52 in the examining panel since antibodies to these antigens are part of the therapeutic armory.

Clinical features
Apart from the lymphocytosis, patients may have accumulations of lymphocytes elsewhere. Peripheral lymphadenopathy in cervical, axillary and inguinal regions must be looked for since lymph node enlargement in these areas form the basis of the clinical staging systems as do enlargement of the spleen and liver. More comprehensive lymphadenopathy may be detected by imaging techniques such as abdominal ultrasound (US) and computerized tomography (CT), but these techniques play no part in clinical staging. It should be emphasized that there is usually no place for CT scanning in the initial examination of most patients with CLL and staging based on CT findings can lead to serious mistreatment of patients.

The other area of lymphocytic infiltration that is clinically important is the bone marrow. This is assessed by measurement of the haemoglobin and platelet count and there is usually no need for bone marrow examination in the initial assessment of patients with CLL. Of course, there are other reasons than bone marrow infiltration for anemia and thrombocytopenia in CLL, such as autoimmunity, iron deficiency and hypersplenism. It is important to exclude these when clinical staging is assessed.

Two forms of clinical staging are currently used; Rai staging in America and Binet staging in Europe. Details of these systems are given in Table 1. Although they differ in detail they both in effect measure tumor mass, and neither measures the pace of disease. Both have prognostic value and both suffer from the same defects (such as using the same threshold haemoglobin value for males and females). Both have stood the test of time and both remain valuable despite the appearance

DVT confirmed

Today I had an ultrasound scan on my leg which confirmed the presence of a DVT in my lower thigh. This means three months of low molecular weight heparin by injection every day. I am awake at last on day 7 of this course. Let's hope for good news after my CT scan

DVT

The past couple of days have been the worst so far. The peripheral neuropathy has been more severe and I have spent most of the time asleep, unable to rouse myself for anything. I also seem to have developed a deep venous thrombosis, with calf pain. They have started me on clexane.

I really don't think I could take another course of chemotherapy at this dose.

Why so joyless?

Michael Otts preached a sermon on this passage last Sunday and my essay here is highly derivative of his sermon (which you can hear here.) I have also been reading Planet Narnia by Michael Ward which is also a source of what I have to say.

The first five verses of John chapter 17 gives us a close contact with the Lord Jesus Christ, for they tell us what he prays for himself. They also illuminate the meanings of “Christian” words or phrases that may astonish us.

The first word is “authority” (v2). This is a word much devalued by recent events. We complain about an authoritarian government. We look at British MPs and jeer at their assumed authority. Our leaders in almost every profession have become figures of fun. George Bush became a laughing stock, military leaders were undone by the scandals in Iraqi prisons, scientists are derided as they will say anything in order to get research grants, bankers have misled us and trousered huge bonuses in payment for failure, industrial giants have collapsed, the Roman Catholic church is mired by allegations of child abuse, doctors have been besmirched by the activities of Harold Shipman and others. Islamic leaders are seen as terrorists and murderers. Teachers are unable to control classrooms, the police are corrupt or racists and the list goes on.

A recent poll in Britain concluded that the majority of respondents thought that politicians were in it to feather their own nests rather than serve their constituents. For some reason they would rather be governed by celebrities, actors or pop-singers. Authority is seen to be something to be avoided, though the reputation of those who seek “freedom” for authority was hardly enhanced by the arrest of the man alleged to be the murderer of the abortion doctor last week.

Jesus gives a new meaning to authority. Authority was given to Jesus so that he might give eternal life to those that were given him.

Authority is about giving not taking. Even the best governments take from us in the form of taxes. Here is an authority that is about giving.

The second phrase is “eternal life”. “Pie in the sky when you die” say the sceptics. And we have to admit that we think of eternal life as something that begins when we die, but Jesus defines it differently. “This is eternal life: that they may know you, the only true God, and Jesus Christ, whom you have sent.” (v3) Eternal life is about relationships. The word “know” implies the most intimate relationship possible. Jesus came that we might know God intensively. Forever. Beginning now. God the Holy Spirit indwells every believer. How many of us make ourselves aware of his presence. I don’t mean in a theatrical way, waving our arms about, speaking in a language that no-one understands, but being conscious that ever word you say and every action you take is observed by him, that every thought you have is available to him, and that if you learn to listen to him he will prompt your thoughts and actions according to God’s will. Take time to be silent and listen to him and get your mind right by reading his word regularly. You can be sure that it is his words you are listening to by checking against what he has already said.

The third word is “glory”. Again glory is something that means less today than once it did. Newspaper headlines ascribe glory to football teams, dancers on TV, and Oscar winners. Once it attended empires, now a pub cricket team has it for winning a 20-over knockabout. How glory has been devalued. Yet it was once an attribute of magnificence, demanding awe and worship. Fanfares and parades, processions with elephants strung with jewels and gold, soldiers and slaves, dancing girls and jugglers, drums and trumpets; Hollywood had it down to a ‘T’.

Yet Jesus had it differently: “I have brought you glory on earth by completing the work you gave me to do. And now, Father, glorify me in your presence with the glory I had with you before the world began.” (vv 4-5).

What was the work that Jesus had come to do? Why, to redeem sinners. But this task had not been completed when the prayer was prayed. Nevertheless, Jesus was resolute that it would be so. He had set his face towards the cross and would not be diverted even when passionately considering all the options in Gethsemane. The task given was to bring all those who were given to him to eternal life (v2); this would be done and this was the key to glory. We talk about the glory of the cross, but if the cross was all their was, it would not be glory. The Resurrection is the affirmation that the cross was effective and Pentecost is the demonstration of its effectiveness.

Glorious though the cross was, I sometimes think we get stuck there. Surely we should preach Jesus Christ and him crucified, but that is the key to an eternal life of knowing God, not an end in itself. We should never forget the debt we owe, but we should not forget to ‘pick up our winnings’. Some Christians seem to want to leave them on the table and play the game over and over again. Our sins have been wiped away. Not only forgiven but forgotten. If we brought them up at the Judgement Seat they would be answered with, “When was that then, we have no record of that here?” Of course we have to keep short records with God and be ready to confess the sins of the day in the sure knowledge that “If we confess our sins, He is faithful and just to forgive us our sins and to cleanse us from all unrighteousness.”

The chief end of Man is to love God and enjoy Him forever. It’s the ‘enjoy him forever’ that we are missing out on. Miserable Christians everywhere, start smiling. Laugh! Enjoy yourself!

CS Lewis was a student of medieval and renaissance literature. Their model of the Universe was one guided by the planets, with seven spheres of influence. A recent book by Michael Ward “Planet Narnia” describes how each of the Narnia books is concerned with the atmosphere engendered by each of the seven planets (not our planets, but theirs – the sun, the moon, Mercury, Venus, Mars, Jupiter and Saturn.) The first in the series “The lion, the witch and the wardrobe” is assigned to Jupiter (or Jove) and Aslan is a Jovial character, kingly yet full of joy and mirth.

I have always enjoyed the poetry of John Donne and the War Poets, Wilfred Owen and Siegfried Sassoon. Lewis calls them writers about death under Saturnine influence. To quote Narnia, “It’s always winter and never Christmas.” Lewis was also a subaltern at the Western Front. He saw equally terrible things, but after a period of grief he saw it as time to move on. Poets have seldom been good at glory in the way that musicians or architects and painters have. Francis Schaeffer was convinced that we should enjoy these glorifications of Christ as their makers intended. He was no iconoclast. Puritans and Hypercalvinists have despised such attempts as idolatry, and of course they can be used as such, but as aids to worship I see no sin. Certainly, I could stand never singing “Shine Jesus Shine” again for the chance of standing in the nave of Salisbury Cathedral or forfeit another chorus of Celebration for the chance of taking part in Handel’s Messiah at Huddersfield Town Hall. The are joys to be had in the Christian life and we must not despise them.

CLL: Introduction

Sorry to have been silent for so long. Two things: the side effects lasted longer this time than usual; that in itself would not have stopped me blogging, but I have also swapped my computer system. That has meant that I did not have enough 'oomph' to set it up with an internet connection. Today, feeling better, and with the help of my son, I have been able to set up a wi-fi connexion.

Anyway I have been able to do some work on the CLL chapter that I have to produce. Here is the introduction:



Most people begin their article on chronic lymphocytic leukemia (CLL) with the words “CLL is the commonest leukemia in the Western world”. It may or not be true, but with recent changes in the definition of the disease we can no longer be sure. Not only that, but the general impression that CLL is getting commoner and more benign may simply be an accident of disease discovery, with more alert physicians recognizing a disease that may or may not be there.

A new heterogeneity in CLL was discovered a decade ago and this has provided a key to opening up the complex pathophysiology of the condition and coincidentally has important prognostic value. In addition, a range of new treatments has become available during this time as well as the means of detecting minimal residual disease. As a result we now have to look at CLL differently. For some patients this will mean that we may never treat their leukaemia, but may still have to manage late complications; for others we will hold out the prospect of cure, though this will not be without hazard; for yet others there will be a sequence of treatments and remissions with the physician balancing benefit and harm with the aim of producing the longest possible, good quality life.