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dence, it seems that either there is no change or the

changes

are

very small and of doubtful clinical im-

port.

proceedings of a recent workshop on vasectomy give a useful account of existing knowledge in this sphere.18 In men followed for 2 years after vasectomy there were no important changes in circulating hormone levels or blood coagulation. The presence of circulating autoimmune antisperm antibodies in a large proportion of vasectomised men and laboratory animals was amply confirmed. For example, PH. RuMKE and H. HELLEMA reported that, of 52 vasectomised men, 77% formed circulating spermagglutinating antibodies, 44% formed sperm-immobilising antibodies, and 23% The

formed antibodies to the sperm nucleus. Other workers likewise reported the development of spermugglutinating antibodies in at least two-thirds of vasectomised men, but sperm-immobilising antibodies were more variable, appearing in one-third to two-thirds. Sperm autoantibody formation usually started during the first year after operation and there was no general tendency for the antibody titres to fall thereafter. Are these antibody reactions at all relevant to function? Their main importance in man may be their possible effect on fertility after reanastomosis operations. However, evidence of disturbed immunity has been found in some laboratory animals. P. BiGAzzi confirmed earlier findingsll that immune complex orchitis can develop in vasectomised rabbits. He also reported that some rabbits show histological changes in their kidneys consistent with early glomerulonephritis associated with immune-complex deposition in the renal glomeruli. K. TUNG observed lesions typical of allergic orchitis in the guineapig, both in vasectomised testes and in the contralateral testis after unilateral vasectomy. T. CLARKSON and N. ALEXANDER have reported that vasectomy increases the severity of dietinduced atherosclerosis in cynomolgus monkeys (Macaca fascicularis).7 They gave a lipid-rich diet to 10 monkeys for six months and then vasectomised 5 monkeys and sham-vasectomised the other 5. The monkeys continued on their high-lipid diet for a further 10 months and were then killed. Atherosclerosis was significantly more extensive in the vasectomised monkeys than in the controls, notably, in the carotid and cerebral arteries, the distal segments of the coronary vessels, and in the abdominal aorta. Antisperm antibodies had developed in all the vasectomised monkeys, complement and immunoglobulins were associated with atherosclerotic plaques in some of the vasectomised monkeys, and CLARKSON and ALEXANDER suggest that 18. Vasectomy: immunologic and pathophysiological effects in animals and man. Edited by I. H. LEPOW, and R. CROZIER. New York. Academic Press 1979.

Pp. 595.

the immunological response to sperm antigens may exacerbate atherosclerosis in the monkey. However, they do advise cautious interpretation: the number of animals was small; normally herbivorous creatures, they were given a diet containing twice as much cholesterol as is consumed by the average North American male; and their plasma cholesterol levels were considerably in excess of those seen in hyperlipidsemic human beings. Extrapolation of findings from laboratory animals to man is always hazardous. Indeed, one of the messages of the workshop is the variation of the immune response to vasectomy both between species and between different strains of the same species. There was no evidence of an immune testicular response to vasectomy in man. Circulating immune complexes related to vasectomy have been sought in man but not found or found only transiently.12 In four prospective clinical studies in the United States a total of 400 men have been followed for 2-3 years but no clinical consequences of vasectomy have been identified.18 M. GOLDACRE and colleagues have used medical record linkage to monitor hospital discharges and deaths in 1760 vasectomised men over an average of 4 years.19 No evidence of excess autoimmune, cardiovascular, or endocrine disease has emerged. Thus, in the short term at least, there is no clinical evidence that vasectomy is harmful in man. However, the possibility of rare or long-term effects cannot yet be ruled out. Large long-term follow-up studies are needed to demonstrate the safety of vasectomy in man or to quantify any serious consequences for comparison with the risks and benefits of other methods of contraception.

BETTER PERINATAL HEALTH ALL

over the world, perinatal mortality rates are under scrutiny. Perinatal mortality is a political today and Governments issue, anxiously check their position in the international league of stillbirths and early neonatal deaths. Well they may, for this is a crucial area of loss and damage. In Britain, interest has been quickened not only by the International Year of the Child but also by the activities of the Children’s Committee and the House of Commons subcommittee on perinatal mortality and morbidity; in newspapers and on television, perinatal mortality rates have been cited as if they directly indicated the quality of perinatal care. In the U.S.A., France, and the developing world interest is hardly less intense. How can we best tackle the matters of perinatal

mortality? The two main approaches are epidemiological and technical. Epidemiologists and statisticians make national and regional comparisons; they study time 19. Goldacre MJ, Clarke JA, Heasman MA, Vessey MP. Follow-up of vasectomy using medical record linkage. Am J Epidemiol 1978; 108: 176-80.

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trends; they rely heavily on perinatal mortality rates. And, after Sir Dugald Baird’s pioneering work in Aberdeen, an increasing number of clinicians have joined them. Britain now has a National Perinatal Epidemiology Unit in Oxford, staffed by epidemiologists to help clinicians. Unfortunately the coarse perinatal mortality rate is but a poor measure of perinatal health. It is greatly influenced by two disparate factors-the background health and nutrition of the mother; and the qual ity of obstetric and paediatric care. We must of course strive to improve the second, but the first commonly has a greater bearing on outcome. We need better perinatal indices to identify the important background influences, which should point the way to effective prevention. As to technical improvements, we now have means to monitor various indices of fetal metabolism, growth, and behaviour during pregnancy and labour. Doubtless all these devices have their place. The danger is that they will be employed unthinkingly on the wrong population, or that the results will be harmfully misinterpreted. Perinatal health, and the exchequer, would benefit if clinicians were more ready to submit new tests to statistical evaluation: at what time are they most valuable and in what population? The British perinatal surveys of 1946, 1958, and 1970 were cross-sectional. At one time it seemed that the 1982 survey might follow a similar plan, but this is now unlikely; expense apart, many people favour other ways of learning about perinatal services. Regional systems are needed; and there must be continuous systematic measurement of perinatal risks. Some countries already have standardised maternity information systems brisk enough to give clinicians an up-to-date picture of their local perinatal affairs. All these themes need drawing together, and this week The Lancet launches a series of linked articles under the heading Better Perinatal Health. Mr Geoffrey Chamberlain (who gave much help with the organisation of the series) and Dr lain Chalmers open with background articles, and in the coming weeks we shall have discussions of the major causes of perinatal ill-health and of the perinatal scene in various countries. As usual we hope that readers will join in, via the correspondence columns. FISH POISONING IN many parts of the world poisonous fish are comand dangerous. The two most frequently reported intoxications are ciguatera, which is essentially tropical, and scombroid poisoning which can happen anywhere. Scombroid fish are dark-meated and migratory; they include mackerel, tuna, bonito, and skipjack, and their flesh has a high content of free histidine which is normally metabolised to ot-ketoglutarate. Many bacteria, particularly Proteus spp., can decarboxylate histidine to histamine and, if fish are contaminated with such organisms, large amounts of amine may accumulate in the flesh.2 Fish are generally toxic when concentrations mon

1 Halstead BW. Poisonous and venomous marine animals of the world:

vol. 1,

Washington, D.C.: U.S. Government Printing Offices, 1967. 2. Taylor SL, Gutherty LS, Leatherwood M, Tillman F, Lieber ER. Histamine production by foodborne bacterial species. J Food Safety 1978; 1: 173-87. Vertebrates.

in the muscle reach about 100 mg per 100 g (normal

Better perinatal health.

1058 dence, it seems that either there is no change or the changes are very small and of doubtful clinical im- port. proceedings of a recent wor...
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