Herpes zoster of the stomach

Herpes zoster of the stomach

953 Letters to the Editor HERPES ZOSTER OF THE STOMACH nerve roots infected by the varicellavirus contain sensory fibres originating in the viscer...

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953

Letters

to

the Editor

HERPES ZOSTER OF THE STOMACH nerve roots infected by the varicellavirus contain sensory fibres originating in the viscera and in the skin, but little has been published on visceral involvement in herpes zoster. Reports include two patients with

SiR,—The posterior

zoster

possible gastric zoster as manifested by gastritis or ulcer,’ a few patients with radiological evidence of colonic zoster,2,3 and a larger group of patients with changes in the anogenital area.4.5 In most cases, the visceral segments affected have corresponded to the dermatomes involved by the skin lesions. The mucosal lesions were not usually examined endoscopically. We have seen a case of probable gastric herpes zoster in a 76-year-old man with skin lesions typical of zoster, affecting the 7th right thoracic dermatome. Before the skin changes appeared, he had had burning epigastric pain, nausea, and vomiting for some days. At gastroscopy a band-shaped mucosal lesion was observed along the greater curvature, consisting of vesicular and streaky bleeding. A repeated endoscopy after one week revealed a normal mucosa. At this time, the patient’s clinical condition as well as his skin lesions had started to improve. Since pain sensations from the stomach are thought to be transmitted to the 7th and 8th thoracic segments, there was a neuroanatomical correlation between the skin and stomach lesions. The correspondence in time between the skin and gastric symptoms and the endoscopy findings support the diagnosis of gastric herpes zoster. Histological examination of biopsy material revealed only low-grade inflammation and intramucosal blood. The biopsy material may not have been representative, or the mucosal changes may not have been fully developed zoster lesions. Abdominal symptoms are not rare in herpes zoster patients, and we expect to see more cases of gastrointestinal involvement in such patients as routine endoscopy becomes more common. Departments of Gastroenterology and Dermatology, Ullevaal Hospital, Oslo, Norway

F. WISLØFF J. BULL-BERG J. MYREN

SCOTTISH HEARTS

SIR,-Your editorial (Oct. 6, p. 726) and the recent Scottish Chief Scientist’s working group report on research into coronary heart-disease6 point up to day’s dilemma/impasse. It may be that Glasgow and West-Central Scotland do have the highest rates in the world. Or perhaps that distinction belongs to South African Whitesas it did, till recently anyhow, to the small towns and villages, the forests and farms, of North Karelia (Finland). What on earth do these three have in common? Plainly there is a great deal we do not know about CHD and the report’ makes intriguing recommendations, mostly for small-scale epidemiological studies. The issue, however, arises: what are we-all of us--doing with the knowledge we already have? Supposing that the research prospers, how much better placed will Government and the Health Departments be, wait1. Wyburn-Mason R. Visceral lesions in herpes

zoster.

Br

Med J 1957;

ing another five or ten years, to make policy on the prevention of coronary heart-disease? Probably little. What we do know, unfortunately, is full of uncertainties, and these uncertainties are unlikely to go away because another research unit is doing good work, much of it along new or different lines. The working group very properly were "unconvinced that the evidence from intervention studies has yet demonstrated that physical activity has a protective effect." However, they do not proceed to name the trials on other behavioural factors that have convinced them. Are there any? The trouble is not lack of technology to conduct the necessary trials, but the difficulty of controlling the everyday behaviour of sufficiently large numbers of ordinary people for a sufficient length of time to give the answers. In view of its provenance it is odd that the group did not discuss this problem which, successive statements demonstrate,8-10 seriously inhibits Government thought and action. (Is this not the sort of problem affecting policy that Rothschild was supposed to be all about?) We have to learn to live with uncertainty and the slow accumulation of knowledge and understanding from every kind of research-and draw the most sensible conclusions we can from the evidence." Like the National Institutes of Health, it looks that "we’ve more or less [to] become adjusted to the fact that we probably will never be able to get the ideal proof that we want ... The weight of the evidence seems to be strong enough so that we can now direct people toward a kind of set of guidelines."12 The consensus of 22 independent committees since 1968, including two BritishP.14is that populations seriously affected by CHD

eat too

much, fat, and in

particular saturated fat; and

they recommend accordingly. The public response is illustrated in these Scottish figures of grams of saturated fatty acids consumed per 1000 kcal:15

There is little doubt that the inertia is due in part to public confusion stemming from the second British report which also recommended some substitution by polyunsaturates. Is it not time to resolve this issue and produce a straightforward message with which the great majority of workers would agree? Who will take the lead? Diet is only part of the answer. Thus we shall soon know whether the latest round of negotiations with the tobacco industry, after 22 years of Government statements against cigarettes, 16 will phase out advertising and sponsorship. As the boom in cycling gets under way ("personal responsibility") the inquiry is opportune-What is the policy of the Health Departments on exercise vis-a-vis Transport, Environment, and the Sports Council? It is noteworthy that the preventive measures currently proposed are all beneficial in themselves. Neither your editorial nor the Scottish report mentions the decline of coronary mortality in the U.S.A., Australia, Canada, and Finland, while our rates have merely stopped ris-

ing. For example:

i:

678-81. 2.

Figiel SJ, Figiel LS. Herpes zoster with ileus simulating intestinal obstruction. Am J Med 1957; 23: 999-1002. 3. Menuck LS, et al. Colonic changes of herpes zoster. AJR 1976; 127: 273-76. 4. Fugelso PD, Reed WB, Newman SB, et al. Herpes zoster of the anogenital area affecting urination and defæcation. Br J Dermatol 1973; 89: 285-88. 5. Jellinek EH, Tulloch WS. Herpes zoster with dysfunction of bladder and anus. Lancet 1976; ii, 1219-22. 6. Scottish Home and Health Department. Research into coronary heartdisease in Scotland. Report to the Chief Scientist by a Working Group.

Edinburgh. 1979. 7. Wyndham CH. Ischæmic heart-disease mortality rates in white South Africans compared with other populations. SA Med J 1978; 54: 595-601.

8. Prevention and health: everybody’s business. London: H.M. Stationery Office, 1976. 9. Prevention and health. London: Stationery Office, 1977. 10. Eating for health. London: H.M. Stationery Office, 1978. 11. Morris JN. Uses of epidemiology, 3rd ed. Edinburgh: Churchill-Livingstone, 1975. 12. Fredrickson DE. Quoted in Science 1979; 204: 1178. 13. Diet and coronary heart-disease. London: H.M. Stationery Office, 1974. 14. Prevention of coronary heart-disease. J Roy Coll Phycns 1976; 10: No 3, 1-63. 15. Household food consumption and expenditure 1972-78. London: H.M. Stationery Office (annual reports). 16. Ministry of Health Circular 7/57, June 27, 1957.