424

above value was taken empirically as a cut-off, the sensitivityof the test was only 57%.’ In the same patients C.E.A. valuesin pleural effusions were, by and large, higher than in plasma.

Surprisingly, all 15 patients with lymphoma or myelomahad C.E.A. concentrations in their pleural effusions < 10 ng/ml;however, &bgr;z-microglobulin concentrations were higher in thesepatients than in all other patients studied.2 Contrary to

reported data,3 we found that orosomucoid concentrations inpleural effusions cannot discriminate between malignant andnon-malignant effusions.

Although no biochemical test differentiates consistentlybetween malignant and non-malignant pleural effusions,measurement of C.E.A. and (32 microglobulin concentrations inthese effusions can help the clinician in this "diagnosticdilemma".4 4

Laboratory of Immunopathology,State University of New York at Buffalo,Buffalo, N.Y. 14203, U.S.A. ADRIAN O. VLADUTIU

COLON CANCER AND BILE-SALT BINDING

SIR,-Dr Cruse and others (June 19, p. 1261) describe thepromotion by bile-salt-binding agents, aluminium hydroxideand cholestyramine, of colonic cancer induced in rats bydimethylhydrazine.

Patients with bile-salt diarrhoea already have an abnormalquantity of bile-salts entering the large bowel. Treatment witha bile-salt-binding agent should be directed at binding onlythose bile-salts entering the colon, and therefore alleviating thediarrhoea. We have shown that treatment with aluminium

hydroxide did not increase the faecal bile-salts in patients withbilesalt diarrhoea as a result of Crohn’s disease or followingtruncal vagotomy and pyloroplasty. 5

Aluminium-containing antacids have been widely used inthe symptomatic treatment of peptic-ulcer disease for overforty years, without any clinical suggestion that they increasethe incidence or alter the prognosis of colonic cancer. How-ever, the animal experimental work of Cruse and others indi-cates the need for a clinical study to determine if an associationexists. The bile acids lithocholate and deoxycholate enhancetumour growth in animals.6 Thus, it is even conceivable thatbile-salt-binding agents may, by their binding action, protectagainst colonic carcinoma rather than promote it.

Department of Surgery,University of Melbourne,Repatriation General Hospital,Heidelberg, 3081 Victoria, Australia AVNI SALI

CLINICAL MEDICAL OFFICERS (CHILD HEALTH)

SiR,&mdash;I was very pleased to see that Dr Tyrrell’s article

(Aug. 5, p. 309) on clinical medical officers brought some oftheir problems into the open and to the attention of a wideraudience. I am surprised but glad that she still has the driveto improve the child-health service from within. When I wasa clinical medical officer, I felt that the problems of the child-health service were not clinical ones but lay more within theprovince of community medicine. It was then, with ill-feelingfrom some of my colleagues and personal feelings of regret,that I deserted my clinics and schools to start training in com-munity medicine; I had found it totally impossible to effect any

1. Vladutiu, A. O., Adler, R. H., Brason, F. W. Am. J. clin. Path. (in the press).2. Vladutiu, A. O. New Engl. J. Med. 1976, 294, 903.3. Diret, M. F., Valdiguie, P. Clinica. chim. Acta, 1977, 77, 219.4. Storey, D. D., Dines, D. E., Coles, D. T. J. Am. med. Ass. 1976, 236, 2186.5. Sali, A., Murray, W. R., MacKay, C. Lancet, 1977, i, 1051.6. Wynder, E. L. J. Am. diet. Ass. 1977, 71, 385.

improvements in the child-health service as a clinical medicalofficer.

I feel that it is the community physician’s task to look at theproblems of coordinating the health services for children in hisdistrict or area, including evaluation of the existing services,strengthening the links between the child-health service andprimary and secondary care, and looking at the educationalneeds of clinical medical officers in relation to the work that

they are doing.We in community medicine are aware of our ambivalent

feelings towards the child-health service: it is there when weneed help but at other times we reject it as not being part ofus.

I feel that the only way for the child-health service to getout of its present difficulties is to strengthen its links with com-munity medicine in the short term and to be able to providea better service for children in the longer term.

Tunbridge Wells Health District,Sherwood Park,Pembury Road,Tunbridge Wells, Kent TN2 3QE

JANET HALLRegistrar in Community Medicine

TRANSMISSION, FROM MAN TO HAMSTER, OFJAKOB-CREUTZFELDT DISEASE WITH CLINICAL

RECOVERY

SIR,-I feel that Professor Manuelidis and colleagues (July1, p. 40) were perhaps wrong to report their case as an exam-ple of Jakob-Creutzfeldt disease in the present state of knowl-edge. In the case they describe the histological changes in thecortical biopsy were not those classically described in Jakob-Creutzfeldt disease and while the histological changes in theinfected hamster were those of that disorder, the distributionof these changes was again not that of Jakob-Creutzfeldt dis-ease. These facts and the patient’s recovery would make itmore correct, I think, to describe the illness as a transmissibledementia with recovery from histological changes in the reci-pient animal resembling those of Jakob-Creutzfeldt disease.Time may well prove it to be a variant of Jakob-Creutzfeldtdisease.

St. James’s Hospital,Leeds LS9 7TF D. W. SUMNER

&bgr;-ADRENOCEPTOR BLOCKERS,PLASMA-POTASSIUM, AND EXERCISE

SIR,-Wang and Clausen’ showed that patients with hyper-kalsemic familial periodic paralysis could be treated with theP2-adrenoceptor agonist salbutamol to avoid hyperkalxmicmuscular weakness and paralysis at rest after exercise. Themechanism of action seems to be a &bgr;2-adrJ.?oceptor-mediatedactivation of the Na+-K+ transport system across muscle-cellmembranes, leading to normalisation of the potassium distri-bution between the intracellular and extracellular fluid.2 Wehave investigated whether or not this (3-adrenoceptor-mediatedeffect on the electrolyte distribution is important in normalpeople.

Oral doses of metoprolol (100 mg) (a &bgr;1-selective blocker3), pro-pranolol (80 mg) (a nonselective p-adrenoceptor blocker3) or placebowere given blind in randomised order to six healthy volunteers at 8.00A.M., 1 h before ergonometer exercise (30 min at a work-load of100-120 W giving a heart rate of about 120 beats/min). They hadeaten a light breakfast at about 7.15 A.M. The subjects rested in therecumbent position for 30 min before and for 60 min after exercise.Blood-samples for potassium analysis were carefully drawn via anintravenous catheter (brachial vein) at the intervals indicated in the

1. Wang, P., Clausen, T. Lancet, 1976, i, 221.2. Clausen, T., Flatman, J. A. J. Physiol. 1977, 270, 383.3. &Aring;blad, B., Carlsson, E., Ek, L. Life Sci. 1973, 12, Part I, 107.