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HEPATIC ABSCESS ASSOCIATED WITH SCHISTOSOMIASIS
932 CASE 4.-A woman of 34, with a grossly unstable personality, subject to hysterical outbursts of manic intensity. She was instructed to take myanesin elixir (1 oz.) when she or her husband felt that an attack was impending. This has been completely effective. She describes the effect of mephenesin as similar to mild intoxication : she is " knocked out " for a couple of hours, after which her aggressive episode has passed. Her entire personality has changed since her outbursts have been controlled. She has become psychologically accessible, less inhibited, more objective in her outlook, and a happier person. CASE 5.-A man of 52, who had been invalided out of the Army on account of myocardial degeneration and hyperthyroidism, applied unsuccessfully for a pension. Two specialists decided that there was no evidence of the disabilities on account of which he had been discharged from the Forces, but when they identified an anxiety state he became very apprehensive. Anxiety attacks, characterised by trembling, palpitation, giddiness, and fear of collapse, occurred almost daily, and he became unwilling to go out of doors except by car. Myanesin elixir was prescribed, after sedatives had failed to effect any improvement, and the severity of his attacks was immediately reduced. was
,
I should like to express my thanks to the directors and staff of the British Drug Houses for their cooperation in this work. ELLIS STUNGO. London, W.I. DOORMATS FOR OPERATING-THEATRES
SIR,-It has often struck
me that the amount of contamination introduced into the operating-theatre on the soles of nurses’, surgeons’, visitors’, and porters’ feet must be quite considerable, and I venture to suggest that a certain amount of antiseptic cleansing of the soles of shoes and wheels of trolleys could be achieved if a sunken, floor-level, padded mat, soaked in a suitable antiseptic, could be placed at the common entrance to an operating-theatre suite. Anyone passing over this mat would automatically coat the soles of his shoes with a thin layer of antiseptic, in the same way as foot and mouth " traps are situated at certain frontier posts in Europe. BERNARD KAPLAN. Buckhurst Hill, Essex. "
HEPATIC ABSCESS ASSOCIATED WITH SCHISTOSOMIASIS
SIR,-I have only lately had the opportunity of the article on this subject by Dr. Graham and Mr.Orr.l Infestation of the liver by schistosomes has been recognised for a long time. In 1933 Bourguignon, in Elisabethville, showed me some beautiful photomicrographs of adult worms and eggsin the liver. The population around this hospital shows an infestation-rate of 15% with Schistosoma haematobium. This is after a single examination ; repeat examinations would give a considerably higher rate-possibly double. Palpable livers are common, both in small children In almost all children with palpable and in adults. livers schistosome eggs can be found by repeated urinary In adults enlargement of the liver is examinations.
reading
commonly accompanied by enlargement of the spleen and ascites. These cases usually terminate fatally in few years or less. Sometimes the liver has become shrunken and cirrhotic before death ; in such cases schistosome eggs can often not be found in the urine, but cystoscopy often reveals extensive damage of the bladder wall. I conclude that either the worms have the extensive cicatrisation prevents the died orof that the escape eggs. On the other hand, liver abscess from any cause is rare here. I have seen only 2 instances in 120 autopsies and in a, large number of explorations either by operation or puncture. The suggestion by Graham and Orr that in their case the abscess was caused a
1.
Graham, J. G., Orr. J.
L.
Lancet, 1950, i, 714.
by auto-infection of a necrotic area appears to -me very probable. They are to be congratulated on giving us a timely reminder of schistosomiasis as a possible cause of henatomen’alv a.nd hver a.hsf.Mtx. Chibambo Mission
-
PATRICK K. DIXON.
Hospital,
Elisabethville, Belgian Congo.
STRIÆ CUTIS DISTENSÆ
I summarise
SiR,—May controversy ?
some
of the
points arising
out of this
Strise atrophice (I use this term because striae may without any previous stretching of the skin) are an expression of damage to the skin. (2) Sixteen years ago I thought that purple striae atrophiese were characteristic of Cushing’s syndrome due to basophil adenoma.! I abandoned that view because they occur with adrenocortical tumours causing Cushing’s syndrome, and disappear after removal of the tumour (Sdye,2 p. 170). Furthermore, there are typical cases of Cushing’s syndrome with no striae, in spite of rapid increase in weight. Spence demonstrated an example to the endocrine section of the Royal Society of Medicine on Nov. 22. A woman of 47, with a mixed Cushing’s and adrenogenital syndrome due to adrenal cortical carcinoma, had a petechial eruption over her upper chest, neck, and arms, and yet had no strise atrophicae Her excretion of urinary 17-ketosteroids was 42-5 mg. per 24 hours. Only 4 weeks ago I saw a case of the pituitary type without any strise in spite of an increase of a stone in weight within 4-6 weeks at the beginning of the illness. (3) Patients may develop purple striae in association with
(1)
occur
pleural effusion, pulmonary tuberculosis, pneumonia, asthma, dysentery, or tonsillitis; and even without any signs of illness 3-8 (e.g., three cases reported by Hurford and Snelf and one by Parkes Weber 5). In Parkes Weber’s patient they were present from 1934 to 1942, although the girl remained in good health (see Romer ). (4) Cases 10of chronic malnutrition sometimes develop
such striae.9
(5) Overdosage with Cortisone’ or .c.T.x. may produce atrophiese as well as hyperpigmentation, acneiform eruptions, hirsutism, rounded (moon) face, delayed wound strise
and flattening of keloid scars. In the New York conference on A.C.T.H., Sprague 12 stated that the hyperpigmentation resembles that of Addison’s disease. Behrman and Goodman 11 accept Albright’s view that the strise are caused by thinning of the skin due to protein depletion. Selye 10 confirms that the same hyperpigmentation may be found in severe adrenal cortical deficiency ; he says, " if systemic overdosage with cortisone may render the rat skin extremely atrophic and transparent, so do hypophysectomy and adrenalectomy " ; finally, he finds it suggestive to assume some interrelation between the characteristic strise of Cushing’s disease and the cutaneous atrophy which occurs in debilitated individuals, and after overdosage with cortisone or A.c.T.H." (6) Purpura may occur as a result of damage to the capillary endothelium, with or without concomitant alterations in one or more of the factors concerned with bloodcoagulation. It may occur in infectious diseases, after drugs, in cachectic states, in Cushing’s syndrome, after overdosage with cortisone, or from mechanical causes (e.g., in pertussis). (7) Of hyperpigmentation Selye writes, on p. 170 of his textbook 2: " sometimes- there is a melanoderma (in hypercorticoidism) reminiscent of Addison’s disease. This may be either generalised or patchy ; it is not due to secondary destruction of the adrenals since it can appear even in in whom only one adrenal is affected." It is " also noteworthy, though unexplained, that most animal species,
healing,
"
patients
1. Medvei, V. C., Wermer, P. Med. Klin. 1934, 30, 992. 2. Selye, H. Textbook of Endocrinology. Montreal, 1948. 3. Hurford, J. V., Snell, W. E. Tubercle, 1943, 24, 16. 4. Medvei, V. C. Lancet, 1950, i, 1174. 5. Weber, Parkes F. Lancet, 1935, ii, 885 ; Rare Diseases and some Debatable Subjects. London, 1947. 6. Crofts, N. F., Macrae-Gibson, N. K. Lancet, Nov. 18, 1950, p. 595. 7. Romer, C. Ibid, Dec. 16, 1950, p. 825. 8. Kok, D’Almero. Ibid, p. 826. 9. MacLeod, J. M. H. Cited by Hurford and Snell. 10. Selye, H. Physiology and Pathology of Exposure to Stress. Montreal, 1950 ; p. 728. 11. Behrman, H. T., Goodman, J. J. J. Amer. med. Ass. 1950, 144, 218. 12. Sprague, R. G. Proceedings of 1st Clinical A.C.T.H. Conference. New York, 1950 ; p. 384.
,
I should like to express my thanks to the directors and staff of the British Drug Houses for their cooperation in this work. ELLIS STUNGO. London, W.I. DOORMATS FOR OPERATING-THEATRES
SIR,-It has often struck
me that the amount of contamination introduced into the operating-theatre on the soles of nurses’, surgeons’, visitors’, and porters’ feet must be quite considerable, and I venture to suggest that a certain amount of antiseptic cleansing of the soles of shoes and wheels of trolleys could be achieved if a sunken, floor-level, padded mat, soaked in a suitable antiseptic, could be placed at the common entrance to an operating-theatre suite. Anyone passing over this mat would automatically coat the soles of his shoes with a thin layer of antiseptic, in the same way as foot and mouth " traps are situated at certain frontier posts in Europe. BERNARD KAPLAN. Buckhurst Hill, Essex. "
HEPATIC ABSCESS ASSOCIATED WITH SCHISTOSOMIASIS
SIR,-I have only lately had the opportunity of the article on this subject by Dr. Graham and Mr.Orr.l Infestation of the liver by schistosomes has been recognised for a long time. In 1933 Bourguignon, in Elisabethville, showed me some beautiful photomicrographs of adult worms and eggsin the liver. The population around this hospital shows an infestation-rate of 15% with Schistosoma haematobium. This is after a single examination ; repeat examinations would give a considerably higher rate-possibly double. Palpable livers are common, both in small children In almost all children with palpable and in adults. livers schistosome eggs can be found by repeated urinary In adults enlargement of the liver is examinations.
reading
commonly accompanied by enlargement of the spleen and ascites. These cases usually terminate fatally in few years or less. Sometimes the liver has become shrunken and cirrhotic before death ; in such cases schistosome eggs can often not be found in the urine, but cystoscopy often reveals extensive damage of the bladder wall. I conclude that either the worms have the extensive cicatrisation prevents the died orof that the escape eggs. On the other hand, liver abscess from any cause is rare here. I have seen only 2 instances in 120 autopsies and in a, large number of explorations either by operation or puncture. The suggestion by Graham and Orr that in their case the abscess was caused a
1.
Graham, J. G., Orr. J.
L.
Lancet, 1950, i, 714.
by auto-infection of a necrotic area appears to -me very probable. They are to be congratulated on giving us a timely reminder of schistosomiasis as a possible cause of henatomen’alv a.nd hver a.hsf.Mtx. Chibambo Mission
-
PATRICK K. DIXON.
Hospital,
Elisabethville, Belgian Congo.
STRIÆ CUTIS DISTENSÆ
I summarise
SiR,—May controversy ?
some
of the
points arising
out of this
Strise atrophice (I use this term because striae may without any previous stretching of the skin) are an expression of damage to the skin. (2) Sixteen years ago I thought that purple striae atrophiese were characteristic of Cushing’s syndrome due to basophil adenoma.! I abandoned that view because they occur with adrenocortical tumours causing Cushing’s syndrome, and disappear after removal of the tumour (Sdye,2 p. 170). Furthermore, there are typical cases of Cushing’s syndrome with no striae, in spite of rapid increase in weight. Spence demonstrated an example to the endocrine section of the Royal Society of Medicine on Nov. 22. A woman of 47, with a mixed Cushing’s and adrenogenital syndrome due to adrenal cortical carcinoma, had a petechial eruption over her upper chest, neck, and arms, and yet had no strise atrophicae Her excretion of urinary 17-ketosteroids was 42-5 mg. per 24 hours. Only 4 weeks ago I saw a case of the pituitary type without any strise in spite of an increase of a stone in weight within 4-6 weeks at the beginning of the illness. (3) Patients may develop purple striae in association with
(1)
occur
pleural effusion, pulmonary tuberculosis, pneumonia, asthma, dysentery, or tonsillitis; and even without any signs of illness 3-8 (e.g., three cases reported by Hurford and Snelf and one by Parkes Weber 5). In Parkes Weber’s patient they were present from 1934 to 1942, although the girl remained in good health (see Romer ). (4) Cases 10of chronic malnutrition sometimes develop
such striae.9
(5) Overdosage with Cortisone’ or .c.T.x. may produce atrophiese as well as hyperpigmentation, acneiform eruptions, hirsutism, rounded (moon) face, delayed wound strise
and flattening of keloid scars. In the New York conference on A.C.T.H., Sprague 12 stated that the hyperpigmentation resembles that of Addison’s disease. Behrman and Goodman 11 accept Albright’s view that the strise are caused by thinning of the skin due to protein depletion. Selye 10 confirms that the same hyperpigmentation may be found in severe adrenal cortical deficiency ; he says, " if systemic overdosage with cortisone may render the rat skin extremely atrophic and transparent, so do hypophysectomy and adrenalectomy " ; finally, he finds it suggestive to assume some interrelation between the characteristic strise of Cushing’s disease and the cutaneous atrophy which occurs in debilitated individuals, and after overdosage with cortisone or A.c.T.H." (6) Purpura may occur as a result of damage to the capillary endothelium, with or without concomitant alterations in one or more of the factors concerned with bloodcoagulation. It may occur in infectious diseases, after drugs, in cachectic states, in Cushing’s syndrome, after overdosage with cortisone, or from mechanical causes (e.g., in pertussis). (7) Of hyperpigmentation Selye writes, on p. 170 of his textbook 2: " sometimes- there is a melanoderma (in hypercorticoidism) reminiscent of Addison’s disease. This may be either generalised or patchy ; it is not due to secondary destruction of the adrenals since it can appear even in in whom only one adrenal is affected." It is " also noteworthy, though unexplained, that most animal species,
healing,
"
patients
1. Medvei, V. C., Wermer, P. Med. Klin. 1934, 30, 992. 2. Selye, H. Textbook of Endocrinology. Montreal, 1948. 3. Hurford, J. V., Snell, W. E. Tubercle, 1943, 24, 16. 4. Medvei, V. C. Lancet, 1950, i, 1174. 5. Weber, Parkes F. Lancet, 1935, ii, 885 ; Rare Diseases and some Debatable Subjects. London, 1947. 6. Crofts, N. F., Macrae-Gibson, N. K. Lancet, Nov. 18, 1950, p. 595. 7. Romer, C. Ibid, Dec. 16, 1950, p. 825. 8. Kok, D’Almero. Ibid, p. 826. 9. MacLeod, J. M. H. Cited by Hurford and Snell. 10. Selye, H. Physiology and Pathology of Exposure to Stress. Montreal, 1950 ; p. 728. 11. Behrman, H. T., Goodman, J. J. J. Amer. med. Ass. 1950, 144, 218. 12. Sprague, R. G. Proceedings of 1st Clinical A.C.T.H. Conference. New York, 1950 ; p. 384.