addition, and so on the tests were read (see figure) and yielded the following results: (1) Dapsone solutions containing 0.3 fLg/ml can be detected

by ELISIT. (2) A positive result for 1 of the Kenyan urine samples may be questionable (well B4). In 2 other samples (C3 and B6) the quantity of dapsone is very low (around 0-3 g/ml. 6 other samples contained not more than 1 fLg/ml (A6, 8, C6, F5-7). The remaining 35 Kenyan urine samples all contained more than 1 fJ-g/ml. (3) 6 h after


single dose of 300 mg dapsone, urine diluted

1/250 was positive.

(4) Positive and negative sera can be clearly distinguished when diluted 1/100. The urine samples were used to compare ELISA inhibition with two conventional spectrophotometric procedures.l.2 Out of 10 samples, negative on one or both spectrophotometric procedures, 9 were positive and 1 equivocal on ELISA inhibition

retrospectively. Criteria have been laid down for such a study in cardiac patients,’ and these would serve as a better basis for the measurement of morbidity than those used by Walesby et al. The literature on surgical nutrition is bedevilled with apocryphal tales, and workers must not perpetuate these by failing to define terms of reference. The paper by Walesby et al. is based on a small number of patients with inadequate information about the statistical methods, and no satisfactory objective evidence to support the statement that "nutritionally depleted patients" undergoing cardiac surgery are "at greater risk from postoperative morbidity". Department of Surgery, University of Newcastle upon Tyne, Royal Victorial Infirmary, Newcastle upon Tyne NE1 4LP


testing. Sera from patients taking dapsone, which would be expected contain 1-3 fLg/mPwere dapsone positive by ELISIT even when diluted a hundredfold. The sensitivity of ELISIT and its simplicity may be of practical value in leprosy-endemic countries with limited laboratory services.



Technical details of the micro-ELIsA (not given here) may be had from H. H. We thank Dr F. van Knapen and his colleagues in the National Institute of Public Health, Bilthoven, Netherlands, for their help, and the Netherlands Leprosy Relief Association for financial sup-


J. E. LANDHEER Department of Tropical Hygiene, Royal Tropical Institute, Amsterdam, Netherlands W.H.O. International Immunology Training and Research Centre, Amsterdam



SIR,-In normal subjects somatostatin significantly inhibits insulin secretion after glucose, glucagon, and tolbutamide stimulation .2 Lorenzi et al. studying four patients with hyperinsulinism (two adenomas, one carcinoma, and another undetermined) found that somatostatin did not inhibit insulin secretion induced by tolbutamide. We have studied a patient with hyperinsulinism due to pancreatic beta-cell hyperplasia. Before pancreatectomy, a tolbutamide (1 g intravenously) stimulation test was done, before Abel, R. M., Fischer, J. E., Mortimer, B. J., Barnett, G. O., Austen, W. G. Archs Surg. 1976, 111, 45. 2. Efendic, S., Luft, R. Claro, A. Acta endocr. 1976, 81, 743. 3. Lorenzi, M., Gerich, J. H., Karam, J. H. and Forsham, P. H. J. clin. Endocr. Metab. 1975, 40, 1121. 1.


SIR,-Mr Walesby and his colleagues (Jan. 14, p. 76) have used two regression equations based on body weight for the calculation of predicted total-body potassium (T.B.K.). Their use of such formulae is open to criticism on two grounds. The formular may give a falsely high value of predicted T.B.K. in the presence of fluid retention which, as Walesby et al. state, is frequently found in the group of patients they studied. Secondly, the formulae are based on data derived from normal adults. There is no evidence that the equations remain valid when used for undernourished patients-indeed one might expect normal homceostatic mechanisms to break down in patients with cardiac failure, the so-called "sick-cell syndrome". The validity of using T.B.K. as a single criterion of undernutrition is also questionable, and Walesby et al. present no other evidence to support their statement that four of their patients were nutritionally depleted or that the remainder were normally nourished. Absence of clinical signs is no guide since these signs, as Walesby et al. state, may be masked by fluid retention. Walesby et al. also fall into the trap of equating duration of hospital stay with morbidity. Delay in discharging a patient may be related to matters completely unconnected with fitness for discharge. Home circumstances, unwilling relatives, or other delays in the hospital or social services may unduly prolong admission, and such incidents are difficult to recognise 1. Bratton, A. C., Marshall, E. K. J. biol. Chem. 1939, 128, 537. 2. Ellard, G. A., Gammon, P. T., Helmy, H. S., Rees, R. J. W. Am. J. trop.

Med. Hyg. 1974, 23, 464. 3. Powell, R. D., De Gowin, R. L., Bennet Eppes, R., McNamara, J. V., Carson, P. E. Int. J. Lepr. 1967, 35, 590.

Time Imn) Insulin and glucose response to tolbutamide stimulation before and after somatostatin infusion. T=Tolbutamide only. ST=Somatostatin-tolbutamide. Tolbutamide give at 10 min, somatostatin

(by infusion) over 0-40 min.

Nutrition and open heart surgery.

281 addition, and so on the tests were read (see figure) and yielded the following results: (1) Dapsone solutions containing 0.3 fLg/ml can be detect...
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