DRASTIC CURES FOR OBESITY

DRASTIC CURES FOR OBESITY

52 stream represents a physiological ideal, which in the long term may be departed from with peril. Our studies on elderly Bantu (over 60 years) in t...

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52 stream represents a physiological ideal, which in the long term may be departed from with peril. Our studies on

elderly Bantu (over 60 years) in that region, although incomplete, reveal far lower prevalences of glycosuria, abnormal glucose tolerance, and electrocardiographic evidence of myocardial infarction than have been reported for elderly Caucasians. Full details will be published elsewhere. These studies are being supported by a research grant from the South African Sugar Association. M.R.C. Human Biochemistry Research Unit, South African Institute for Medical Research, Johannesburg, South Africa.

ALEXANDER R. P. WALKER B. F. WALKER B. D. RICHARDSON.

on the occasion when incidental liver biopsy was done this too was normal. What is essential is a close relationship between the surgeon, well versed in these operations and willing to do a thorough follow-up, and the well-selected cooperative patient. I therefore believe that these procedures should not be undertaken by the occasional operator who is unable to dedicate a good part of his time to the management of these

tion, and

patients. As to your rhetorics concerning why surgeons should perform such operations, I do not see the analogy between your hyperbole of cutting off a smoker’s hand for smoking and this operation for obesity. To understand my objection you would have to have the experience of personal contact over the years with these patients, the majority of whom are grateful. True, there are complaints of abdominal discomgas, and occasional bouts of diarrhaea, rectal and the unpleasantness of certain medications; problems, but so far only one patient has asked me to reconnect her (she was having marital difficulties, allegedly due to her foul-smelling stools). Two years after reconnection her liver was normal. In conclusion, this operation is no panacea, but serves a useful purpose in most cases so long as patients are properly selected and followed up. Therefore, your wholesale condemnation of it, based mostly on isolated warnings of its complications, is not warranted, in my opinion.

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DRASTIC CURES FOR OBESITY SIR,-In your editorial on this subject (May 23, p. 1094) you say that jejuno-ileal shunts must join the list of dangerous cures for obesity. This judgment was primarily based on a report by Drenick et al.,I who demonstrated marked fatty degeneration of the liver in all of three patients who had a bypass procedure, in contrast to a larger number of medically treated subjects whose liver-biopsy specimens showed improvement of the fatty metamorphosis after weight reduction. Drenick’s article does not, however, state whether these three surgically treated patients were reported because of their liver complications or whether they comprised the whole surgically treated group. The distinction is important, since, in a larger series of intestinalbypass patients, this complication, which requires prompt reconnection for survival, approximates 3%. In a series of sixty cases operated on by me in the past eight years-all now postoperative at least six months-one patient was successfully reconnected because of marked fatty metamorphosis of the liver; and one patient died six months after bypass owing to hepatitic liver necrosis, after being exposed through her husband (who himself almost succumbed) to infectious hepatitis. One other patient, operated on eight years ago, was found to have biliary cirrhosis with moderate fatty metamorphosis at reoperation two years ago for a ventral hernia. This patient had a jejuno-colic shunt (no longer being done), and admitted to moderatelyheavy alcoholic intake. She declined reconnection of the bypass, has curtailed her drinking, and is apparently getting along well. As to the rest of these patients, there is no indication of liver failure clinically or biochemically. Two points are worthy of mention here. Firstly, if severe liver damage ensues, it is likely to occur in the first year or

thereabouts; then

one

year

sixty patients, forty-nine are more postoperative. My second point is in reference

among my

to Drenick’s assertion that the liver-function tests were well within normal limits at a time when liver fatty infiltration was already advanced, and that hence liver-function tests are of no avail. There appears to be a contradiction here, since in one patient he reports a bromsulphthalein test of 9%, and in another one a bilirubin of 1-9 mg.-both apparently abnormal findings-and these could be construed as sufficient warning signals. There is no mention of specific liver-function tests in respect of the third patient. The fact is that liver-function tests can be of some value in watching these patients. However, the point that liver biopsy affords a useful further precaution is well taken.

Similar experience is described with eighty patients by Payne and DeWindwho document two cases in which liver biopsies at later reoperation showed distinct decreases in fatty changes. In my series, at reoperation of 7 patients for other conditions the liver was always normal on inspec1. 2.

Drenick, E., Simmons, F., Murphy, J. F. New Engl. J. Med. 1970, 282, 829. Payne, J. H., DeWind, L. T. Am. J. Surg. 1969, 118, 141.

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STEPHEN KANTOR.

SIDE-EFFECTS OF INSULIN CONTAMINATING COMMERCIAL GLUCAGON SiR,ňThe minute amounts of insulin contaminating commercial glucagon preparations 1,2 are generally regarded as clinically unimportant. However, the following observations show that this is not the case in certain situations. The glucagon-stimulation test, with determination of plasma-insulin, is used in the diagnosis of hyperinsulinism due to insuloma.3,4 In two consecutive patients we found that the first plasma-samples collected after intravenous injection of 1 mg. glucagon contained more than 200 jjLU of insulin per ml., a value suggesting hyperinsulinism. This aroused the suspicion that the insulin content of the glucagon preparations might have contributed to the raised insulin concentrations observed. Radioimmunoassay 5,6 showed that this dose of glucagon contained approximately 100,000 U of insulin (equivalent to 0-4%). According to the manufacturers, this glucagon contains, at most, 0-2% of insulin.’ Before distribution to the extravascular compartments, these amounts of insulin may add more than 50 U to the insulin content of the plasma. Contamination of the blood-samples with glucagon, as by the use of a single indwelling catheter both for injection of glucagon and for collection of blood may also result in false high values. Another effect of contaminating insulin is obvious from the following case-report. A 20-month-old girl with severe hypoglycxmia since birth had been treated with protamine glucagon for 17 months. Before the start of treatment with glucagon, the plasma-insulin response to repeated glucosetolerance tests was normal. At 15 months of age, an intravenous glucose-tolerance test was performed. Radioimmunoassay then showed a constant high plasma-insulin McNaught, M. L. J. Endocr. 1958, 17, 17. Yalow, R. S., Berson, S. A. Proc. Soc. exp. Biol. Med. 1961, 107, 148. Marks, V., Samols, E. J. clin. Path. 1968, 21, 346. Fajans, S. S., Floyd, J. C., Thiffault, C. A., Knopf, R. F., Conn, J. W. in Diabetes. Excerpta med. (int. Congr. Ser. 172); p. 894. Stockholm, 1967. 5. Wide, L., Porath, J. Biochim. biophys. Acta, 1966, 130, 257. 6. Thorell, J. I. Clinica chim. Acta 1968, 22, 579. 7. Hassing, V. (Novo Industri A/S, Copenhagen). Personal com1. 2. 3. 4.

munication.