DANGERS OF CALCIFEROL

DANGERS OF CALCIFEROL

960 routine cross-matching of patient’s serum and donor’s cells performed on a tile may sometimes not show this incompatibility. (5) A transfusion r...

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960 routine cross-matching of patient’s serum and donor’s cells performed on a tile may sometimes not show this

incompatibility. (5) A transfusion

reaction due to high-titre a group-0 blood given to a group-A patient would be unlikely or impossible if the patient’s serum normally contained soluble A factor. This is usually

agglutinin

in

when the saliva contains the A substance, but " secretor " no mention is made whether the patient was a of A substance ; nor was thepresence of this substance in the patient’s serum apparently investigated. This possibility must be eliminated before concluding that the anuria was due to the high-titre ot agglutinin in the donor’splasma. S. SEVITT. Pathological Department, Military Hospital for Head Injuries, Wheatley, Oxon.

the

case

DANGERS OF CALCIFEROL

SIR,-Your leading article of Dec. 14 is timely. We the point of writing to suggest that some restriction should be placed on the sale of calciferol. A sense of harmlessness surrounds the idea of vitamin therapy, but, in fact, the highly concentrated preparations may be most dangerous. We have had some two hundred patients, mostly suffering from lupus vulgaris, under treatment with calciferol over the past twelve months and intend in due course to publish our observations and the results of our investigations. We feel, however, that the incidence of toxic symptoms is so high, and the character of the so serious, that some warning is necessary in symptoms view of the freedom - with which calciferol is being presented to the profession and the public. Symptoms of intolerance arise as often and seriously in adults as in children. A high proportion of these cases present the picture of an abdominal emergency, and the symptoms may deceive the elite. Urgent admission to were on

hospital and operation may follow. In all our cases of intoxication there has been a considerable increase in serum calcium and a raised bloodurea. Though the total calcium may not be raised in those with mild symptoms, the diffusible calcium is invariably raised. Macrae has recently stressed the importance of watching the blood-sedimentation rate. In animals we have found that calciferol severely damages the kidneys. It seems desirable that all patients on calciferol should have written instructions to stop treatment and report immediately should they experience any untoward symptoms, and especially such abdominal symptoms as pain, anorexia, sickness, and extreme constipation. With such precautions, and careful and regular observation and biochemical control, serious harm is not likely to occur.

That calciferol is of importance in the treatment of and that it will play an important part in the control of the problem of lupus is quite certain. That it is of value in other ills is unproven, and it should not be prescribed in high dosage except with proper control. JOHN T. INGRAM J. DAWSON D. E. DOLBY. S. T. ANNING Leeds.

lupus vulgaris

PERFORATED PEPTIC ULCER TREATED WITHOUT OPERATION

SiR,-Mr. Hermon Taylor (Sept. 28) states that the conservative treatment of perforated peptic ulcers has a mortality of 14 %, and that surgical intervention should be reserved for late cases-patients with gastric dilatation from pyloric stenosis-and for those who have ingested a large quantity of fluid just before or after the

perforation. Signs suggesting perforation

are

usually pronounced,

but sometimes, as laparotomy shows, these signs appear without a perforation. At other times the so-called gedeckte (subacute or sealed) perforation, which was first described by the Viennese surgeon, Schnitzler, is found ; here the ulcer is sealed off by adhesions to a neighbouring viscus, either before or immediately after the perforation. The symptoms are less acute, and the peritoneal signs are more or less limited ; in many gas In such cases, may be found under the diaphragm.

if there is

no deterioration in the first few hours, we defer operation until all signs of peritoneal irritation have disappeared. In other cases the perforation is not sealed off by

adhesions ; the opening remains free and uncovered, seen

As

at

laparotomy on late

we

as

cases.

know, the contents of the stomach

are

sterile

by virtue of its hydrochloric acid, so that peritonitis does not develop if the ulcer is closed by adhesions or suture. But if the opening remains, the highly infected contents of the intestines can discharge into the peritoneal cavity by antiperistaltic waves. A surgeon expecting every perforated ulcer to be sealed off by adhesions will be disappointed, especially if he has not the wide experience of Mr. Hermon Taylor ; and failure means the death of the patient. The late results of simple suture of a perforated ulcer are not satisfactory ; in 91 % of these cases a new or recurrent ulcer is found later, so that the patient is exposed to the risk of a second operation or a new perforation. Therefore with

perforations seen after,12-24 hours we partial gastrectomy ; the mortality is 7-2% in the first twelve hours and 12 % in the second, but in many of these late cases peritonitis has already developed. After 24 hours a suture operation only is performed. In all of Mr. Taylor’s cases a, partial gastrectomy would perform

a

have been undertaken. Surgical Clinic, University

of Graz.

A. WINKELBAUER.

MALNUTRITION IN RELEASED PRISONERS-OF-WAR AT SINGAPORE

SiR,-The admirable analysis of malnutrition by Dr. Mitchell and Dr. Black (Dec. 14, p. 855) and similar recent studies make a further advance in the evaluation of the causal relationships of single and multiple deficiency states. Signs of vitamin deficiency have often been noted several weeks after the patient has been on a full nutritious hospital diet with vitamin therapy. Cases 1 and 4 (Mitchell and Black) illustrate this point. Both patients had peripheral neuritis with tingling, numbness, reduced sensibility, and loss of superficial reflexes, with some degree of amblyopia. Both patients were given 6 compound vitamin tablets daily (containing altogether 150 mg. ascorbic acid, 60 mg. nicotinic acid, 6 mg. thiamine, and 6 mg. riboflavin), while case 1 was given in addition 10 mg. of thiamine daily intravenously and case 4 received 50 mg. of thiamine daily intramuscularly. After nine days’ treatment case 1 became suddenly weaker in the legs with gross ataxia of both arms and legs, while case 4 was suddenly unable to walk or write. The authors mention that similar observations were described by Spillane and Scottand also by Clarke and Sneddon.22 During recent years the importance of the interrelationship between various factors of the vitamin-B group has been urged several times, subclinical latent deficiencies becoming manifest after energetic treatment of the obvious deficiency. Pellagrins have been reported as showing signp of beriberi, or what has been described as riboflavin deficiency, after treatment with nicotinic acid 3 4 ; signs of pellagra 5 and of riboflavin deficiency 6 have appeared after treatment with thiamine. Richards7 demonstrated experimentally on rats that excess of thiamine may easily precipitate a masked deficiency of pyridoxine. Mitchell and Black’s case 1 had 10 mg. of thiamine intravenously ; case 4 had 50 mg: intramuscularly. As far as could be ascertained, the cases reported by Spillane8 and by Clarke and Sneddonwere also given generous doses of thiamine, although these writers, especially Spillane, tried to balance the diet of their patients carefully. It is reasonable to submit that in grossly undernourished chronic cases daily intravenous .



1. Spillane, J. P., Scott, G. I. Lancet, 1945, ii, 261. 2. Clarke, C. A., Sneddon, J. B. Proc. R. Soc. Med. 1946, 39, 357. 3. Spies, T. D., Vilter, R. W., Ashe, W. F. J. Amer. med. Ass. 1939, 113, 931. 4. Sydenstricker, V. P., Sebrell, W. H., Cleckley, H. M., Kruse, H. D. Ibid, 1940, 114, 2437. 5. Lehman, J., Nielsen, H. E. Nord. Med. 1939, 1, 289. 6. Leitner, Z. A. Brit. med. J. 1945, i, 609. 7. Richards, M. B. Ibid, p. 433. 8. Spillane, J. D. Proc. R. Soc. Med. 1946, 39, 175.