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MALE SUSCEPTIBILITY TO PYRROLIZIDINE ALKALOID POISONING
472 are exposed to sunlight during the following summer, short course of Methoxsalen and ammidin (‘Meladinine’) (two tablets daily taken 2 h before exposure to sunlight or ultraviolet light) will produce normal pigmentation after a few weeks in these patients. Treatment of active lesions by application of clotrimazole (’Canestan’) nightly after a bath for 12-14 days is usually effective, but the greater part of the skin surface, especially the lower limbs, where lesions may be very sparse, must be treated if prompt recurrence is to be avoided. Prophylactically, it would seem wise for those with speckled torsos to carry out this regimen once a week during subsequent visits to their holiday haunts. It would be interesting to see what the current cult of the sauna bath will bring in its train.
patches a
Guy’s Hospital, E.
London SE1 9RT
J. MOYNAHAN
URINARY ANTINUCLEAR FACTORS IN NEPHROTIC SYNDROME is well estaband some other diseases, but little is known about the test in urine except in
SIR The
lished in S.L.E.
L.E.
cell
test
in blood and
marrow
systemic lupus erythematosus (S.L.E.)
patients.
a simple technique, adding the urine of nephrotic patients to a suspension of donor leucocytes, we reproduced the characteristic cellular findings-i.e., L.E. cells, round hxmatoxylin bodies, and erythrocyte phagocytosis. We studied 11’ patients with various renal diseases with or without nephrotic syndrome and 20 healthy controls. Positive cellular tests were recorded (see table) only in patients with nephrotic syndrome regardless of the diagnosis. Urinary cellular tests were as a rule associated with an active glomerular process and an unfavour-
By
POSITIVE CELLULAR TESTS IN NEPHROTIC SYNDROME
VARICOSE VEINS IN DEVELOPING COUNTRIES
SIR,-Mr Hobbs (July 31, p. 259) is to be congratulated on his endeavours to confirm or refute suggestions that the prevalence of varicose veins might relate to bowel behaviour. Such studies are obviously of great value. My colleagues and I have found no constant relationship between frequency of defæcation and weight of stools passed. It would be of interest to know whether the long-standing constipation or diarrhoea which, in Mr Hobbs’ patients, bore no relationship to varicose-vein prevalence was measured in years or decades, since the age incidence of varicose veins suggests that very long exposure to some environmental factors is re-
sponsible. Mr Hobbs "cannot believe that the momentary daily excretory rise of intra-abdominal pressure can be the primary cause of varicose veins in the leg". The following facts must be considered. Abdominal straining does raise intra-abdominal pressures to a much greater extent than do other forms of exercise such as weight lifting.l These pressures which can exceed 200 mm Hg are readily transmitted to the veins of the lower limb when the valves become incompetent.2 They are sustained by the valves while these are competent3 and consequently must have some effect on them. Histological examination of incompetent veins shows widening of the circumference with consequent separation of the valve cusps usually without structural damage to the valves.4 The valves become incompetent sequentially from above downwards.’ In Singapore, trishaw riders who are constantly engaged in active exercise which entails contraction of abdominal muscles have a higher prevalence of varicose veins than do barbers who stand all day. The prevalence of varicose veins has been shown to relate directly to that of diverticular disease which is now widely accepted as resulting from constipating diets.’" These observations are consistent with the hypothesis that abdominal straining is one cause of varicose veins, but they do not prove the case. Where is the evidence that varicosities are related to "degenerative changes in the collagen of the subcutaneous tissue and skin"? I am not suggesting that raised intra-abdominal pressure is the
only
cause
of varicose veins, but it is the only cause sugamenable to preventive
gested that, if substantiated, would be action. Department of Morbid Anatomy, St Thomas’s Hospital Medical School, London SE1 7EH
DENIS P. BURKITT
1. Light, H. G., Routledge, J. A. Surgery, 1964, 56, 747. 2. Adams, J. C. Surg. Gynec. Obstet. 1939, 69, 717. 3. Martin, A., Odling-Smee, W. Lancet, 1976, i, 768. 4. Edwards, J. E., Edwards, E. A. Am. Heart. J. 1940, 19, 338. 5. Folse, R. Surgery, 1970, 68, 974. 6. Rajmohan, N. Singapore med. J. 1968, 9,167. 7. Latto, C., Wilkinson, R. W., Gilmore, O. J. A. Lancet, 1973, i, 1089. 8. Brodribb, A. J. M., Humphreys, D. M. Br. med. J. 1976, i, 424.
able prognosis. patients.
Blood
L.E.
cell
tests were
positive only in s.L,E,
The mechanism of urine-induced cellular tests is, we sug gest, connected with tissue destruction, phagocytosis at an inflammatory focus, and partial disintegration of phagocytes with release of degraded nuclear material, leading to secondary phagocytosis and a localised immune reaction similar to that seen in rheumatoid synovitis. Somehow, as happens in incomplete phagocytosis and raised deoxyribonuclease activity, free antibodies accumulate and are eliminated, together with che motaxic factors, in the urine.
Department of Internal Medicine, 1 Moscow Setchenow, Medical Institute, 119 021 Moscow, U.S.S.R.
E. M. TAREEV LYDIA W. KOZLOWSKAJA LUDMILA R. POLIANZEWA LUDMILA N. KOCHUBEJ
MALE SUSCEPTIBILITY TO PYRROLIZIDINE
ALKALOID POISONING
SIR In your Aug. 7 issue (p. 269) Dr Mohabbat and his colleagues describe an outbreak of hepatic veno-occlusive disease attributed to consumption of seeds of Heliotropiurr. plants. Remarkably, the disorder was almost twice as frequcc’. in males as in females. This unexpected distortion may have been due to some irrelevant influence, but my own interest the susceptibility of males derives from our studies’ which showed that under appropriate conditions male rats were more susceptible than females to monocrotaline, an alkaloid we known to produce lesions similar to those Dr Mohabbat an; his colleagues describe. Case Western Reserve University, Cleveland, Ohio 44106, U.S.A.
1.
OSCAR D. RATNOFF
Ratnoff, O. D., Mirick, G. S. Bull. Johns Hopkins Hosp. 1949, 84, 507
patches a
Guy’s Hospital, E.
London SE1 9RT
J. MOYNAHAN
URINARY ANTINUCLEAR FACTORS IN NEPHROTIC SYNDROME is well estaband some other diseases, but little is known about the test in urine except in
SIR The
lished in S.L.E.
L.E.
cell
test
in blood and
marrow
systemic lupus erythematosus (S.L.E.)
patients.
a simple technique, adding the urine of nephrotic patients to a suspension of donor leucocytes, we reproduced the characteristic cellular findings-i.e., L.E. cells, round hxmatoxylin bodies, and erythrocyte phagocytosis. We studied 11’ patients with various renal diseases with or without nephrotic syndrome and 20 healthy controls. Positive cellular tests were recorded (see table) only in patients with nephrotic syndrome regardless of the diagnosis. Urinary cellular tests were as a rule associated with an active glomerular process and an unfavour-
By
POSITIVE CELLULAR TESTS IN NEPHROTIC SYNDROME
VARICOSE VEINS IN DEVELOPING COUNTRIES
SIR,-Mr Hobbs (July 31, p. 259) is to be congratulated on his endeavours to confirm or refute suggestions that the prevalence of varicose veins might relate to bowel behaviour. Such studies are obviously of great value. My colleagues and I have found no constant relationship between frequency of defæcation and weight of stools passed. It would be of interest to know whether the long-standing constipation or diarrhoea which, in Mr Hobbs’ patients, bore no relationship to varicose-vein prevalence was measured in years or decades, since the age incidence of varicose veins suggests that very long exposure to some environmental factors is re-
sponsible. Mr Hobbs "cannot believe that the momentary daily excretory rise of intra-abdominal pressure can be the primary cause of varicose veins in the leg". The following facts must be considered. Abdominal straining does raise intra-abdominal pressures to a much greater extent than do other forms of exercise such as weight lifting.l These pressures which can exceed 200 mm Hg are readily transmitted to the veins of the lower limb when the valves become incompetent.2 They are sustained by the valves while these are competent3 and consequently must have some effect on them. Histological examination of incompetent veins shows widening of the circumference with consequent separation of the valve cusps usually without structural damage to the valves.4 The valves become incompetent sequentially from above downwards.’ In Singapore, trishaw riders who are constantly engaged in active exercise which entails contraction of abdominal muscles have a higher prevalence of varicose veins than do barbers who stand all day. The prevalence of varicose veins has been shown to relate directly to that of diverticular disease which is now widely accepted as resulting from constipating diets.’" These observations are consistent with the hypothesis that abdominal straining is one cause of varicose veins, but they do not prove the case. Where is the evidence that varicosities are related to "degenerative changes in the collagen of the subcutaneous tissue and skin"? I am not suggesting that raised intra-abdominal pressure is the
only
cause
of varicose veins, but it is the only cause sugamenable to preventive
gested that, if substantiated, would be action. Department of Morbid Anatomy, St Thomas’s Hospital Medical School, London SE1 7EH
DENIS P. BURKITT
1. Light, H. G., Routledge, J. A. Surgery, 1964, 56, 747. 2. Adams, J. C. Surg. Gynec. Obstet. 1939, 69, 717. 3. Martin, A., Odling-Smee, W. Lancet, 1976, i, 768. 4. Edwards, J. E., Edwards, E. A. Am. Heart. J. 1940, 19, 338. 5. Folse, R. Surgery, 1970, 68, 974. 6. Rajmohan, N. Singapore med. J. 1968, 9,167. 7. Latto, C., Wilkinson, R. W., Gilmore, O. J. A. Lancet, 1973, i, 1089. 8. Brodribb, A. J. M., Humphreys, D. M. Br. med. J. 1976, i, 424.
able prognosis. patients.
Blood
L.E.
cell
tests were
positive only in s.L,E,
The mechanism of urine-induced cellular tests is, we sug gest, connected with tissue destruction, phagocytosis at an inflammatory focus, and partial disintegration of phagocytes with release of degraded nuclear material, leading to secondary phagocytosis and a localised immune reaction similar to that seen in rheumatoid synovitis. Somehow, as happens in incomplete phagocytosis and raised deoxyribonuclease activity, free antibodies accumulate and are eliminated, together with che motaxic factors, in the urine.
Department of Internal Medicine, 1 Moscow Setchenow, Medical Institute, 119 021 Moscow, U.S.S.R.
E. M. TAREEV LYDIA W. KOZLOWSKAJA LUDMILA R. POLIANZEWA LUDMILA N. KOCHUBEJ
MALE SUSCEPTIBILITY TO PYRROLIZIDINE
ALKALOID POISONING
SIR In your Aug. 7 issue (p. 269) Dr Mohabbat and his colleagues describe an outbreak of hepatic veno-occlusive disease attributed to consumption of seeds of Heliotropiurr. plants. Remarkably, the disorder was almost twice as frequcc’. in males as in females. This unexpected distortion may have been due to some irrelevant influence, but my own interest the susceptibility of males derives from our studies’ which showed that under appropriate conditions male rats were more susceptible than females to monocrotaline, an alkaloid we known to produce lesions similar to those Dr Mohabbat an; his colleagues describe. Case Western Reserve University, Cleveland, Ohio 44106, U.S.A.
1.
OSCAR D. RATNOFF
Ratnoff, O. D., Mirick, G. S. Bull. Johns Hopkins Hosp. 1949, 84, 507