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Dr Morgan is absolutely right about 'imaginary' conditions, there are a
number of examples in obstetrics in particular.
Greta Beresford and I have recently returned from Azerbaijan, and were
most encouraged by enthusiastic, knowledgeable seminar participants, many
most willing to take on board the principles of evidence-based medicine
Bond and Beresford's helpful article makes many important points about
health care in the former Soviet Union. One thing they don't mention
however is that the long years of isolation from 'Western' science have
resulted in the development of disease concepts that have no definitive
scientific/pathological validity, some of which involve large numbers of
the population and have concomitant social and e...
Bond and Beresford's helpful article makes many important points about
health care in the former Soviet Union. One thing they don't mention
however is that the long years of isolation from 'Western' science have
resulted in the development of disease concepts that have no definitive
scientific/pathological validity, some of which involve large numbers of
the population and have concomitant social and economic allowances
attached to them.
In one former Soviet Republic, where I worked intermittently for many
years, for example, a condition translated as 'benign intracranial
hypertension' afflicted up to a third of children, was considered to be a
cause of fits, failure to thrive, irritability, developmental delay and
numerous other problems, and if it persisted into adolescence could be
officially certified as a means of avoiding national service. Diagnosis
could be confirmed by serial CT scanning of the cerebral ventricles
(supposedly showing miniscule dilatation), and treatment was massaging the
base of the skull (what we would call cranial osteopathy).
It was initially shocking to find such a large scale investment of medical
and socio-economic resource in a condition that 'isn't real' from our
perspective, but as the authors helpfully point out it is salutory to be
reminded of the non-scientifically based ideas and practices that have
evolved in the supposedly enlightened West, and one of the important
learning points from working in former Soviet Republics is to reflect
critically on our own disease concepts.
I read with interest this case of ischaemic hepatitis mimicking intestinal
ischemia by Powell et al.[1]
This patient who presented with upper GI bleeding
for three days, was in hypovolemic shock as initial examination revealed
tachycardia, tachypnoea, hypotension and severe anaemia. This was certainly
due to an upper GI bleed from the acute duodenal ulcer found on endoscopy. The
shock...
I read with interest this case of ischaemic hepatitis mimicking intestinal
ischemia by Powell et al.[1]
This patient who presented with upper GI bleeding
for three days, was in hypovolemic shock as initial examination revealed
tachycardia, tachypnoea, hypotension and severe anaemia. This was certainly
due to an upper GI bleed from the acute duodenal ulcer found on endoscopy. The
shock was sufficient to cause lactic acidosis. Melaena can be easily
explained by upper GI bleeding . This shock state by itself is sufficient to
cause non-occlusive mesenteric ischaemia (NOMI) due to intestinal
vasoconstriction and ischaemic hepatitis that can explain the acute abdominal
signs and typical course of liver enzymes. While the course of NOMI may be
self-limited as in this case, elderly and diabetic patients, as well as
those developing ischaemia following aortic surgery or hypotension,
continue to have a poor prognosis.[2] So my impression on reading this
case was acute hypovolemic shock due to an upper GI bleed secondary to acute
duodenal ulcer causing lactic acidosis, non-occlusive mesenteric ischaemia
and ischaemic hepatitis. I do not understand why the authors have put the
entire presentation as a case of ischaemic hepatitis presenting as an acute
abdomen when in fact the patient presented with an upper GI bleed and went on
to develop the obvious sequelae of NOMI and ischaemic hepatitis. In fact
it is important to recognise NOMI in shock states because in cases not
responding to restoring intravascular volume and haemodynamic stability,
angiographic papaverine infusion into superior mesenteric artery or
peripheral infusion of glucagons can be tried.[3] Operative therapy is
reserved for resection of necrotic bowel.[3]
References
(1) L Powell, S Tesfaye, R Ackroyd, and D S Sanders. Surgical presentation of ischaemic hepatitis. Postgrad Med J 2003; 79: 350-351.
(2) Longo WE, Ballantyne GH, Gusberg RJ. Ischemic colitis: patterns and
prognosis. Dis Colon Rectum. 1992 Aug; 35(8): 726-30.
(3) Mulholland MW, Sweeney JF. Approach to the patient with acute abdomen.
In: Yamada T, ed 4. Gastroenterology vol 1. Philadelphia: Lippincott
Williams and Wilkins, 2003; pp 823-824
In their article, Tanner and Culling describe the
risk of cardiomyopathy in clozapine treatment.[1]
Kilian et al.[2] reported about 15 patients with myocarditis and
cardiomyopathy out of 8000 patients treated with clozapine (0.178%) in
Australia. In the European Drug Safety Program (AMSP) in Germany,Austria
, and Switzerland,3 cases of myocarditis among 10,263 monitored patients
with clozapine therapy...
In their article, Tanner and Culling describe the
risk of cardiomyopathy in clozapine treatment.[1]
Kilian et al.[2] reported about 15 patients with myocarditis and
cardiomyopathy out of 8000 patients treated with clozapine (0.178%) in
Australia. In the European Drug Safety Program (AMSP) in Germany,Austria
, and Switzerland,3 cases of myocarditis among 10,263 monitored patients
with clozapine therapy were observed (0.029%). In all these cases young
male patients with schizophrenia in good cardiovascular condition were
affected. Symptoms started 13 to 20 days after clozapine initiation (e.g.
clinical signs, elevated creatine kinase, characteristic ECG findings.) For
ethical reasons cardiac biopsy was not possible in
these patients.[3] In unexplained hyperthermia and perhaps in the first 4
to 6 weeks after starting the treatment with clozapine ECG monitoring
would be perhaps recommended.
References
(1) Tanner MA and Culling W. Clozapine associated dilated cardiomyopathy. Postgrad Med J 2003; 79: 412-413.
(2) Kilian,JG et al. Myocarditis and cardiomyopathy associated wih
clozapine.Lancet 1999;354:1841-1845.
(3) Degner D et al. Myocarditis associated with clozapine treatment Aust N
Z J Psychiatry 2000;34:880.
We read this lucid and comprehensive article by Professor Pirmohamed.[1] However, the article does not take into the account the realities
prevalent in developing world. Moreover, it is not applicable even in
developed nations, where the active ingredients of the forumulations used
by patients are unknown.[2]
According to World Health Organization over 80%
of the people in less developed nations like...
We read this lucid and comprehensive article by Professor Pirmohamed.[1] However, the article does not take into the account the realities
prevalent in developing world. Moreover, it is not applicable even in
developed nations, where the active ingredients of the forumulations used
by patients are unknown.[2]
According to World Health Organization over 80%
of the people in less developed nations like India are dependent upon
herbal drugs for their health care.[3,4] Quackery is rampant here; and use
of herbs in all their forms (even raw herbs) is the usual norm. Over 100
different pathies are practiced and practitioners of alternative systems of
medicine easily outnumber the qualified medical doctors. Even the trained
doctors of alternative medicine use modern drugs and use them
indiscriminately with herbal drugs. Though Indian laws forbid use of
herbal medicines by doctors trained in allopathy; a large number of
general practitioners prescribe them to their patients with or without
herbal drugs. Patients’ belief in this system of medicine is age old and
profound. They not only take the drugs concomitantly with allopathic
drugs; but they even continue to do so, while being in hospitals for the
treatment of ailments like slipped disc and other surgical problems3.
While ‘always ask your patient about herbal medicines’, seems to be a
workable solution; where the active ingredients are known, it has limited
utility when preparations are anonymous. Taking herbal drugs for all sorts
of ailments is normal in less developed nations, and the worse is that
clinicians can never ascertain, what the patient has taken because;
preparations given are unlabelled. This is because they are given in form
of ‘pudia’ (local Hindi equivalent of ‘drug packing’ upon which, nothing
is written). So what information can a clinician possibly get when he does
not know what does the preparation contain?
If on history physician finds patients taking them, they may
discourage them gently from consuming them especially for serious
illnesses, on a long-term basis; as the evidence for the same is scant or
unavailable.[5] If patients seem adamant, they can only be encouraged to try
them for minor and self-limiting illnesses. Due to universality of their
use in less developed countries; patients should be presumed to have taken
or taking them currently until proven otherwise. This is especially true
for chronic long-term problems like bronchial asthma, arthritis, cancers
etc. Although, recent publication of a draft directive1 is a welcome step
and if this sector is properly regulated; no doubt the quality of
medicines would improve. In less developed nations, one workable solution
seems to be preparation of a standardized reference or indexing system of
herbal remedies by registered practitioners of alternative systems of
medicine. By this, modern doctors can know what the patients are taking and
what are their therapeutic effects or adverse effects. This should be done
regardless of the fact whether the remedies have undergone randomized
controlled clinical
trials. However, the final solution rests with standardization of
individual preparations and their formal therapeutic evaluation. Then,
‘always ask your patient about herbal medicines’ can be applied.
References
(1) M Pirmohamed. Herbal medicines. Postgrad Med J 2003;79:489.
(2) Goldman P. Herbal medicines today and the roots of modern pharmacology.
Ann Intern Med 2001;135:594-600.
(3) Kong JM, Goh NK, Chia LS, Chia TF. Recent advances in traditional plant
drugs and orchids. Acta Pharmacol Sin 2003;24:7-21.
(4) Dhikav V, Singh S, Gupta LC. Use of the alternative medicines by the
patients in a governmental hospital. Ind Med Gazette (accepted for
publication).
(5) Ernst E. The risk-benefit profile of commonly used herbal therapies:
Ginkgo, St John's Wort, Ginseng, Echinacea, Saw Palmetto, and Kava. Ann Intern Med 2002;136:42-53.
Painful muscle cramps occuring in long-term hemodialysis (HD)
patients most often involve the lower extremities typically the
gastrocnemius and the small muscles of foot and interefere with free and
effective voluntry activity. They represent an extremely common and
annoying problem associated with HD treatment. The HD associated muscle
cramps have been estimated to occur in about 20% of the HD sessions....
Painful muscle cramps occuring in long-term hemodialysis (HD)
patients most often involve the lower extremities typically the
gastrocnemius and the small muscles of foot and interefere with free and
effective voluntry activity. They represent an extremely common and
annoying problem associated with HD treatment. The HD associated muscle
cramps have been estimated to occur in about 20% of the HD sessions.[1]
Benna et al in their study of 14000 HD treatments reported a cumulative
incidence of cramps of 86%, on 103 patients of chronic renal failure.[2]
Muscle cramps have been found to be frequently associated with
ultrafiltration of large volumes of fluids resulting into a state of
relative hypovolumia due to the discrepancy between the rate of
ultrafiltration and vascular refilling during HD.The observations that
hypotension may herald or accompany muscle cramps and that the muscle
cramps can be relieved by isotonic volume expansion with saline or albumin
solutions- support the role of plasma volume depletion.[3] Progressive
hypoosmolality during HD increases the passive transport of water
intracellularly, further contracting the plasma volume beyond the
reduction cause by ultrafiltration. Hypotonicity enhances the tension and
the mechanical activity in an isolated muscle and thus may precipitate
muscle cramps by the reduction in myoadenylate deaminase levels
intracellularly.[4] Postdialytic alkalimia has been associated with a
reduction in red blood cell levels of 2,3 di-phosphoglycerate. This
alteration in acid-base status could produce tissue hypoxia resulting in
muscle cramps.[1]
In addition, patients undergoing HD treatment have been reported to
have a secondary form of carnitine deficiency. Several factors such as
significant dialytic losses, decreased endogenous production and the
undernutrition due to dietary restriction lead to the secondary form of
carnitine deficiency among long-term HD patients.[5] Carnitine is a
naturally occuring aminoacid that is also synthesized mainly in the liver,
brain and kidneys while meat and dairy products are rich dietary sources.
Carnitine facilitates the entry of fatty acids into the mitochondria for
the production of energy (ATPs).[6]
During the last decade, there had been a greater interest in the treatment
of dialysis-leg cramps through L- carnitine supplementation. A reduction
in the intradialytic muscle cramps and asthenia in patients recieving L-
carnitine, has been reported by several researchers [7-10]. Variable
supplemental doses (5-100 mg/kg) of L-carnitine have been administered
either intravenously-at the end of each dialysis session, orally- just
prior to HD session or via addition to the dialyzate. Bellingheri et al in
their double blind cross-over trial evaluating the the effect of 60 days
of L-carnitine oral therapy (2 g/day) on a group of 14 uremic patients on
intermittent HD- reported the simultaneous increase in the levels of
metabolite in the blood and the muscles with the significant reductions in
the incidence of asthenis and muscle cramps in the treatment group.[10]
Likewise, in a double blind placebo controlled randomized multicenter
clinical trial conducted by Ahmad et al. on 82 long-term HD patients who
were given either carnitine (n=38) or placebo (n=44)- intra dialytic
hypotension, asthenia, excercise tolerance and muscle cramps were found to
be significantly reduced in carnitine treated group.[8]However, the
optimal dose, duration of treatment and the best route of administration
is not yet known; the cost of treatment as well, is a limiting factor for
the routine L-carnitine supplementation in the patients having dialysis
leg cramps. Nonetheless the most economical and practical way suggested
is, possibly either the oral ingerstion of 660-990 mg/day or 2-3 grams
just prior to the begining of the hemodialysis session.[11]
References
(1) Hakim RM, Lazarus JM. Complications during Hemodialysis. In:
Clinical Dialysis, AR Nissensen, RN Fine, DE Gentle ( eds,). Norwalk, CT :
Appleton–Centry-Crofts, 1984, pp 192-195.
(3) Blagg CR. Acute complications associated with hemodialysis. In :
Replacement of Renal Function by Dialysis, JF Maher (Ed.)Dordrecht, The
Neatherlands: Kluwer Academic Publishers, 1989, pp 762-763.
(4) Adams RD, Victor M. Principles of Neurology. Mc-Graw-Hill
Information Services Co, 1989.
(5) Rodriguez-Segade S, Alonso de la Pena C, Paz JM, et al. Carnitine
deficiency in hemodialyzed patients. Clin Chim Acta 1986, 159: 249-256.
(6) Bahl JJ, Bressler R. The pharmacology of carnitine. Am Rev Pharmcol
Toxicol 1987;27: 257-277.
(7) Golper TA, Ahmad S. L-Carnitine administration to hemodialysis
patients: Has its time come? Semin Dial 1992;5: 94-98.
Your correspondent (Sudhir Kumar 5 June 2003) makes some constructive
comments.[1] Our study group represented a normal range of patients with
vitamin B12 deficiency in a UK inner city general practice. Previous
studies [2,3] satisfied us that we could treat this group with mixed
aetiologies for their vitamin B12 deficiency in the same way using oral
vitamin B12 1000mg tablets as replacement therapy....
Your correspondent (Sudhir Kumar 5 June 2003) makes some constructive
comments.[1] Our study group represented a normal range of patients with
vitamin B12 deficiency in a UK inner city general practice. Previous
studies [2,3] satisfied us that we could treat this group with mixed
aetiologies for their vitamin B12 deficiency in the same way using oral
vitamin B12 1000mg tablets as replacement therapy.
The ten excluded patients were representative of the group as a whole
(2/10 intrinsic factor positive, 1/10 gastrointestinal surgery related,
7/10 intrinsic factor negative compared with 10/50, 9/50 and 31/50
respectively) and this does not affect interpretation of the results.
To reflect the long periods of time that vitamin B12 is stored in the
liver, patients did not enter the oral arm of the study until their serum
levels had fallen to the lower 25th centile (418pg/ml) in all cases. With
respect to follow up, we now have unpublished data for a further 12 month
period which confirms the effectiveness of the oral vitamin B12 - no
patients required transfer back to injection treatment and maintained
levels above the lower 25th centile.
The issue of compliance is always a matter for concern. It is our
experience as general practitioners that patients on long term therapy
always require close monitoring and it is the responsibility of both the
patient and the doctor to ensure compliance. Such monitoring is
successfully carried out in patients on thyroid replacement therapy and
treatment for vitamin B12 deficiency is no different in this respect.
Patients need recall and active intervention to maintain injection
therapies as they do for oral treatments. Where an individual is non
compliant with oral medication, then it is easy to revert to injection
therapy but with continued recall and monitoring.
We agree that any savings from an oral preparation of vitamin B12
will relate to the cost of the tablets – the 1000 mcg preparation is not
currently licensed in the UK. However, such preparations are easily
available from the US by post with costs of about US$ 39.95 for 500
tablets. It is highly likely that our costing analysis [4] will effect
savings in NHS staff costs.
The place of oral B12 therapy in the UK has yet to be decided and it
is important to stimulate debate as to its role. This study showed that
patients prefer an oral to an injection treatment and we should reflect
that in our management. The knowledge that we have an effective and safe
preparation to use as replacement therapy for vitamin B12 deficiency
surely means that we must offer our patients the choice.
References
(1) Kumar S. Is oral vitamin B12 a prefect replacement for its parenteral form in all clinical situations? [electronic response to Nyholm E et al. Oral vitamin B12 can change our practice] postgradmedj.com 2003 http://pmj.bmjjournals.com/cgi/eletters/79/930/218#38
(2) Berlin H, Berlin R, Brante G. Oral treatment of pernicious anaemia
with high doses of vitamin B12 without intrinsic factor. Acta Med Scand
1968; 184:247-258.
(3) Kuzminski AM, Del Giacco EJ, Allen RH, Stabler SP, Lindenbaum J.
Effective treatment of cobalamin deficiency with oral cobalamin. Blood 1998;92:1191-98.
(4) Nyholm E. Oral or parenteral therapy for B12 deficiency.
Correspondence Lancet 1999;353:411.
I read with interest the recent article by Nyholm E et al.[1] It is
indeed an exciting prospect to be able to safely and effectively switch
over from the traditional parenteral form of vitamin B12 to the oral form.
However, I would like to make certain observations.
The group of patients included in this study is highly heterogeneous
with majority of them (almost two-thirds) being neg...
I read with interest the recent article by Nyholm E et al.[1] It is
indeed an exciting prospect to be able to safely and effectively switch
over from the traditional parenteral form of vitamin B12 to the oral form.
However, I would like to make certain observations.
The group of patients included in this study is highly heterogeneous
with majority of them (almost two-thirds) being negative of intrinsic
factor antibody. The group of prime interest to us- intrinsic-factor
antibody positive and post-gastrointestinal surgery- had only 19 patients.
It is well known that vitamin B 12 absorption is grossly reduced in the
two groups of patients mentioned above.[2] Hence, the results obtained in
this study may not be applicable uniformly to the whole group.
Secondly, ten patients were excluded from the final analysis. It is
not clear whether they were intrinsic factor antibody-positive or
negative. If they belonged to the antibody-positive group, it could make a
major difference in the interpretation of results of this study.
All patients received a parenteral dose at the beginning of the
study. We know that vitamin B12 can be stored in the liver for a prolonged
period of time and hence finding a normal serum vitamin B12 level at
variable periods of follow up may be due to the initial injection rather
than the subsequent oral tablets. Also, the follow up of the patients has
not been long enough in this study. No patients were followed up for two
years and only 11 were followed up for 18 months. It would have been
interesting to see if the serum vitamin B12 levels declined with longer
periods of follow up.
A concern has been raised earlier regarding the problem of drug
compliance [3] with the oral preparation, as it needs to be taken on a
daily basis for longer periods including for a lifetime. Compliance with
long-term medications is generally poorer and it may be more of a problem
in B12-deficient patients with cognitive deficits.
Authors talk about saving money with oral treatment. However, money
saved on the injection procedure may be offset by the total cost of
tablets. Tablets need to be taken daily as compared to injections that
need to be taken monthly or even less frequently. The cost with oral
therapy may go even higher if there is a need to check serum B12 levels
periodically. There is no such need after starting parenteral B12 therapy.
Oral B12 therapy may take longer to replenish the body stores and
hence, it may not be suitable for sicker patients with severe anaemia or
neuropsychiatric deficits.
Lastly, authors have not discussed other routes of administration of
vitamin B12 such as intranasal route. 500 micrograms intranasal vitamin
B12 weekly has been found to be an easy and effective alternative to
parenteral therapy, which can be administered by the patient also.[4]
In conclusion, based on the data presented, oral vitamin B12 therapy
can not be recommended for all cases of B12 deficiency, though it may be
an effective option in a selected group of vitamin B12-deficient patients.
References
(1) Nyholm E, Turpin P, Swain D, et al. Oral vitamin B 12 can change
our practice. Postgrad Med J 2003;79:218-9.
(2) Dharmarajan TS, Norkus EP. Approaches to vitamin B12 deficiency.
Early treatment may prevent devastating complications. Postgrad Med 2001;110:99-105.
(3) Elia M. Oral or parenteral therapy for B 12 deficiency. Lancet 1998;352: 1721-2.
(4) Swain R. An update of vitamin B 12 metabolism and deficiency
states. J Fam Pract 1995;41:595-600.
The differential diagnosis of JME should have mentioned specifically
Sub-acute Scerosing Pan Encephalitis (SSPE), although progressive
myoclonic epilepsies have been mentioned. SSPE occurs in India as measles
still occurs and the age for first symptom of SSPE is similar to that of
JME. SSPE carries a poor prognosis but JME responds to sodium valproate.
The differential diagnosis of JME should have mentioned specifically
Sub-acute Scerosing Pan Encephalitis (SSPE), although progressive
myoclonic epilepsies have been mentioned. SSPE occurs in India as measles
still occurs and the age for first symptom of SSPE is similar to that of
JME. SSPE carries a poor prognosis but JME responds to sodium valproate.
The diagnosis of SSPE is based in clinical settings in India on EEG,
myoclonus, early dementia and past history of measles, which may be
elicited as measles was common but may not be aetiological factor in a
patient of JME.
We fear if a patient of JME is misdiagnosed as SSPE then upon hearing
a poor prognosis the parents may not return for follow-up or discontinue
(whatever) medications given.
Thank you very much for an excellent review of thalidomide. It really
made an interesting reading.
I would like to describe a case of thalidomide-induced peripheral
neuropathy that I came across. A 58-year old man was diagnosed to have
multiple myeloma three years ago and was treated with a combination of
melphalan and steroids. He responded well to that treatment protocol. He
presented eigh...
Thank you very much for an excellent review of thalidomide. It really
made an interesting reading.
I would like to describe a case of thalidomide-induced peripheral
neuropathy that I came across. A 58-year old man was diagnosed to have
multiple myeloma three years ago and was treated with a combination of
melphalan and steroids. He responded well to that treatment protocol. He
presented eight months ago with features of a myeloma relapse. He was
started on thalidomide. While on thalidomide, he developed numbness of
feet and hands associated with paresthesias. He also had weakness of his
lower limbs. Clinical examination revealed a glove and stocking
distribution of sensory impairment. Deep tendon reflexes were sluggish.
Nerve conduction studies showed features of axonal length-dependent
sensori more than motor neuropathy. He was investigated for possible
causes of neuropathy including diabetes mellitus, Hansen's disease,
vasculitis and paraneoplastic aetiology. All investigations were normal. A
possible diagnosis of thalidomide-induced peripheral neuropathy was made.
Thalidomide could not be stopped as his myeloma would have worsened.
Therefore, the dose of thalidomide was reduced. Within a week, the patient
noted an improvement in his symptoms with disappearance of paresthesias.
At three-month follow up, he was asymptomatic with normal power and
sensations. His myeloma was also in remission.
This report thus highlights that thalidomide-induced peripheral
neuropathy is reversible with no residual deficits. Similar results were
observed in two patients in an earlier report, though the severity of
neuropathy was mild.[1]
Previous reports have found the neuropathy to be related to the
initial thalidomide dose, with negligible risks at doses below 25 mg per
day.[2,3] Older age has also been found to be a risk factor for this
condition.[3]
References
(1) Gupta A, Cohen BH, Ruggieri P, Packer RJ, Phillips PC. Phase I
study of thalidomide for the treatment of plexiform neurofibroma in
neurofibromatosis 1. Neurology 2003; 60(1):130-2.
(2) Bastuji-Garin S, Ochonisky S, Bouche P, Gherardi RK, Duguet C,
Djerradine Z, Poli F, Revuz J; Thalidomide Neuropathy Study
Group.Incidence and risk factors for thalidomide neuropathy: a prospective
study of 135 dermatologic patients. J Invest Dermatol 2002;119(5):1020
-6.
(3) Molloy FM, Floeter MK, Syed NA, Sandbrink F, Culcea E, Steinberg
SM, Dahut W, Pluda J, Kruger EA, Reed E, Figg WD.Thalidomide neuropathy in
patients treated for metastatic prostate cancer. Muscle Nerve 2001;24(8):1050-7.
Dear Editor
Dr Morgan is absolutely right about 'imaginary' conditions, there are a number of examples in obstetrics in particular.
Greta Beresford and I have recently returned from Azerbaijan, and were most encouraged by enthusiastic, knowledgeable seminar participants, many most willing to take on board the principles of evidence-based medicine
Andrew Bond
Dear Editor
Bond and Beresford's helpful article makes many important points about health care in the former Soviet Union. One thing they don't mention however is that the long years of isolation from 'Western' science have resulted in the development of disease concepts that have no definitive scientific/pathological validity, some of which involve large numbers of the population and have concomitant social and e...
Dear Editor
I read with interest this case of ischaemic hepatitis mimicking intestinal ischemia by Powell et al.[1]
This patient who presented with upper GI bleeding for three days, was in hypovolemic shock as initial examination revealed tachycardia, tachypnoea, hypotension and severe anaemia. This was certainly due to an upper GI bleed from the acute duodenal ulcer found on endoscopy. The shock...
Dear Editor
In their article, Tanner and Culling describe the risk of cardiomyopathy in clozapine treatment.[1] Kilian et al.[2] reported about 15 patients with myocarditis and cardiomyopathy out of 8000 patients treated with clozapine (0.178%) in Australia. In the European Drug Safety Program (AMSP) in Germany,Austria , and Switzerland,3 cases of myocarditis among 10,263 monitored patients with clozapine therapy...
Dear Editor
We read this lucid and comprehensive article by Professor Pirmohamed.[1] However, the article does not take into the account the realities prevalent in developing world. Moreover, it is not applicable even in developed nations, where the active ingredients of the forumulations used by patients are unknown.[2]
According to World Health Organization over 80% of the people in less developed nations like...
Dear Editor
Painful muscle cramps occuring in long-term hemodialysis (HD) patients most often involve the lower extremities typically the gastrocnemius and the small muscles of foot and interefere with free and effective voluntry activity. They represent an extremely common and annoying problem associated with HD treatment. The HD associated muscle cramps have been estimated to occur in about 20% of the HD sessions....
Dear Editor
Your correspondent (Sudhir Kumar 5 June 2003) makes some constructive comments.[1] Our study group represented a normal range of patients with vitamin B12 deficiency in a UK inner city general practice. Previous studies [2,3] satisfied us that we could treat this group with mixed aetiologies for their vitamin B12 deficiency in the same way using oral vitamin B12 1000mg tablets as replacement therapy....
Dear Editor
I read with interest the recent article by Nyholm E et al.[1] It is indeed an exciting prospect to be able to safely and effectively switch over from the traditional parenteral form of vitamin B12 to the oral form. However, I would like to make certain observations.
The group of patients included in this study is highly heterogeneous with majority of them (almost two-thirds) being neg...
Dear Editor
The differential diagnosis of JME should have mentioned specifically Sub-acute Scerosing Pan Encephalitis (SSPE), although progressive myoclonic epilepsies have been mentioned. SSPE occurs in India as measles still occurs and the age for first symptom of SSPE is similar to that of JME. SSPE carries a poor prognosis but JME responds to sodium valproate.
The diagnosis of SSPE is based in clin...
Dear Editor
Thank you very much for an excellent review of thalidomide. It really made an interesting reading.
I would like to describe a case of thalidomide-induced peripheral neuropathy that I came across. A 58-year old man was diagnosed to have multiple myeloma three years ago and was treated with a combination of melphalan and steroids. He responded well to that treatment protocol. He presented eigh...
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