- Email: [email protected]
PURGATIVE ABUSE ASSOCIATED WITH REVERSIBLE CACHEXIA, HYPOGAMMAGLOBULINAEMIA, AND FINGER CLUBBING
919
manifestations in those who inherit the gene for familial porphyria cutanea tarda,’, 10,16,18,19 which is inherited as an autosomal dominant characteristic. 2 of our patients came from Spain and the third was of Italian ancestry: these are two countries where familial porphyria cutanea tarda may be 18,19 commoner than in some other parts of Europe. However, further investigations are needed to exclude the possibility that HEP is caused by a new type of uroporphyrinogen decarboxylase defect. A patient who is homozygous for the gene that causes another type of autosomal dominant porphyria, hereditary coproporphyria, has been described.20 As with patient 3, this patient’s fibroblasts had a very low enzyme activity, whereas cells from heterozygotes responded normally to an ALA load .2’ The findings in living cells (fibroblasts) in these patients support the evidence obtained from in-vitro work that the enzymes that metabolise porphyrinogens are normally present in amounts that are far in excess of those needed to maintain haem synthesis.2’ Identification of cases of homozygous porphyria should enable more rapid progress to be made in determining the nature of the mutations in this group of conditions. We thank Mr W. H. Lockwood for much assistance with patient 3; Miss Carol Wyvill, Miss Rose Aston, and Mr C. Bastaricca for technical assistance, and staff of the biochemistry department, Royal Children’s Hospital, Melbourne, for porphyrin analyses. G. H. E. thanks the Medical Research Council for financial support.
Requests for reprints should be addressed to G. H. E., Department of BlOchemIstry, Welsh National School of Medicine, Cardiff CF4
Medical 4XN.
REFERENCES
Moore MR, Goldberg A Enzyme abnormalities in the porphyrias. Lancet 1977, ii: 699-701 2 Brenner DA, Bloomer JR The enzymatic defect in variegate porphyria. N Engl. JMed 1980, 302: 765-68. 3. Czarnecki DB Hepatoerythropoietic porphyria. Arch Dermatol 1980, 116: 307-11 4 Pinol Aguade J, Castells A, Indachochea A, Rodes J. A case of biochemically unclassifiable hepatic porphyria Br J Dermatol 1969; 81: 270-75. 5 Pinol Aguade J, Herrero C, Almeida J, et al. Porphyria hepatoerythrocytaire, une 1 Brodie MJ,
nouvelle forme de porphyrie Ann Dermatol Syphilol 1975, 102: 129-36. Simon N, Berko G, Schneider I. Hepato-erythropoietic porphyria presenting as scleroderma and acrosclerosis in a sibling pair. Br J Dermatol 1977; 96: 663-68 7. Gunther W The porphyrias and erythropoietic protoporphyria. Aust J Dermatol 1967; 9: 23-29 8 Hofstad F. Seip M. Eriksen L Congenital erythropoietic porphyria with a hitherto undescribed porphyrin pattern. Acta Paediatr Scand 1973; 62: 380-84 9 Kushner JP, Barbuto AJ, Lee GR An inherited enzyme defect in porphyria cutanea tarda decreased uroporphyrinogen decarboxylase activity. J Clin Invest 1979; 58: 1089-97 10. Verneuil H de, Aitken G, Nordmann Y Familial and sporadic porphyria cutanea two different diseases Hum Genet 1978; 44: 145-51. 11. Elder GH, Lee GB, Tovey JA Decreased activity of hepatic uroporphyrinogen decarboxylase in sporadic porphyria cutanea tarda. N Engl J Med 1978; 299: 274-78 12. Smith SG The use of thin layer chromatography in the separation of frée porphyrins 6.
and porphyrin methyl esters Br J Dermatol 1975, 93: 291-95 Improved ethanol extraction procedure for determining zinc-protoporphyrin in whole blood. Clin Chem 1977;
13. Garden JS, Mitchell DG, Jackson KW, Aldous KM.
23: 1585-89 14. Sassa S Solish G. Levere RD, Kappas A. Studies in porphyria. IV. Expression of the gene defect of acute intermittent porphyria in cultured human skin fibroblasts and amniotic cells Pre-natal diagnosis of the porphyric trait J Expt Med 1975; 142: 722-31
15. Smith SG Rao KRN, Jackson AH The porphyrins of normal human urine, with a comparison of the excretion pattern in porphyria cutanea tarda Int J Biochem 1980, 12: 1081-84. 16. Benedetto AV. Kushner JP, Taylor JS Porphyria cutanea tarda in three generations of a single family N Engl J Med 1978, 298: 858-62. Eriksen L, Eriksen N Porphyrin distribution and porphyrin excretion in human congenital erythropoietic porphyria. Scand J Clin Lab Invest 1974; 33: 323-32. Salamanca RE de, Catalan T, Cruces MJ, Pena ML, Olmos A, Mas V The inheritance of porphyria cutanea tarda Int J Biochem 1980, 12: 869-72 19. Topi G D’Alessandro Gandolfo L Inheritance of porphyria cutanea tarda analysis of 14 cases in families Br J Dermatol 1977; 97: 617-28. 20. Grandchamp B, Deybach JC, Grelier M, Verneuil H de, Nordman Y. Studies of porphyrin synthesis in fibroblasts of patients with congenital erythropoietic porphyria and one patient with homozygous coproporphyria Biochim Biophys Acta 1980, 629: 577-86 Elder GH, Evans JO, Thomas N, et al. The primary enzyme defect in hereditary coproporphyria Lancet 1976, ii: 1217-19 17.
18.
21.
PURGATIVE ABUSE ASSOCIATED WITH REVERSIBLE CACHEXIA, HYPOGAMMAGLOBULINAEMIA, AND FINGER CLUBBING D. LEVINE
A. W. GOODE D. L. WINGATE
Gastroenterology and Surgical Units, The London Hospital, Whitechapel, London E1 1BB Laxative abuse may cause systemic and metabolic changes, but cachexia has not been reported as a predominant feature. A patient with finger clubbing and extreme wasting recovered when senna intake was stopped and nutritional care provided. A diagnosis had been made of acquired common variable hypogammaglobulinaemia with absence of circulating B lymphocytes. The immunological abnormalities were corrected after senna intake was stopped and lean body mass restored.
Summary
Case-History
_
_
A 64-year-old woman was admitted for management of diarrhoea and weight loss. She had lost more than 45% of her healthy weight and had become an invalid. She had had repeated urinary infections with renal stones over many years, but diarrhoea had been the chief symptom since 1972. Finger clubbing and hypokalaemia were observed in 1975. At that time faecal fat estimations were normal, but no immunological tests were conducted. Jejunal biopsy was normal and X-ray examination of the bowel revealed only a dilated colon. Persistent diarrhoea prompted further investigation at another teaching hospital in 1977. Hypokalaemia was again a feature, but she also had steatorrhoea (43 mmol/24 h of stool fat, normal 18 mmol/24 h). Giardia lamblia were seen both in jejunal biopsy sections and in jejunal aspirate. A peripheral blood-count showed microcytic anaemia, which was attributed to chronic blood loss from colonic polyps, later removed during colonoscopy. In addition to these tubular adenomas, colonic biopsy specimens showed melanosis. Serum albumin was 30 g/1 and there were persistently low serum levels of IgG (on occasion as low as 1’6g/1). IgM and IgA were never more than slightly reduced. Several urine samples contained excessive kappa and lambda light chains, but there was no abnormal band on serum electrophoresis. A bone-marrow aspirate was normal apart from reduced iron stores. Analysis of peripheral blood lymphocytes (method of Horwitz and Lobol) showed that 53% of circulating mononuclears were T cells, but B cells were absent. Repeated injections of immunoglobulin made no difference to the diarrhoea. Giardia lamblia was eliminated after a long course of metronidazole. On admission to the London Hospital in January, 1980, she weighed less than 24 kg (3 st 10 lb). Total body potassium was measured by a shadow shield whole-body counter, a method which relies on measuring y-radiation from natural radioactive 4oK, present as a fixed proportion (0’012%) of the stable potassium. Intracellular red-cell potassium concentration was within normal range, and total body potassium measurements indicated a 25% loss of lean body mass. Gross finger and toe clubbing was still present. A candida skin test was negative. Serum levels of IgG, IgA, and IgM were all reduced at 3 · 19, 0 · 67, and 0 - 40 g/1 respectively. Diarrhoea (average daily stool weight, 700 g normal fat) and hypokalaemia (average plasma level, 2 -3mmol/1) persisted for the first week in hospital. At that point over 200 ’Sennokot’ tablets were found in her locker, whereupon she agreed to stop taking senna and surrendered her supply. Compliance with this advice and increased food intake with enteral proprietary supplements (’Isocal’) led to rapid weight.gain. Serial measurements of total body potassium indicated an increase in lean body mass. As her weight rose, so did serum levels of
immunoglobulins, particularly IgG (see accompanying figure).
920
her illness. Both steatorrhoea and hypoproteinaemia have been associated with purgative abuse,5 but the mechanism is unclear. In our patient, giardiasis may also have played a part. Whatever the original reason for taking senna, purgative abuse eventually became a habit for which there was no
longer an overwhelming compulsion. Although the patient clearly surprised when confronted with the supply of senna, she then cooperated fully and there has been nothing since to suggest further abuse of purgatives. She was strikingly transformed from invalidism as a weak, wasted, and housebound woman to an active life as an apparently fit and well-groomed housewife. Chronic laxative abuse leading to severe disability does not necessarily carry a poor prognosis.
was
We are grateful to Prof. J. S. Orr and the staff of the Hammersmith Hospital for the serial whole-body potassium counts and to Dr D. Bainbndge for the final B and T lymphocyte counts. We are indebted to Dr Derek Jewell for information about the patient.
Changes in body-weight and serum IgG.
Requests for reprints should be
directed
to
D. L. W.
REFERENCES
Nine months later, a repeat lymphocyte analysis showed B cells in normal numbers, and an increased proportion of cells representing early stages of B-cell differentiation. T-cell numbers were slightly below the normal (see table). In an interview with a clinical psychologist, she gave a history of probable anorexia nervosa in early adult life, since when she had apparently retained the idea that a low bodyweight was desirable. Since discharge from hospital, she has taken 30 ml of magnesium sulphate mixture daily as a single dose and passed one normal motion each day. Finger clubbing has virtually disappeared and her bodyweight remains stable at about 35 kg (5 st 7 lb). Apart from constipation, increasingly painful vertebral osteoporosis is her only remaining trouble.
Discussion Neither hypogammaglobulinaemia nor B-cell deficit have been reported in association with laxative abuse or weight loss. The association of low IgG with repeated urinary infections remains speculative. When these infections began, she had no diarrhoea and had not lost weight, although she was probably already taking senna. Our findings support a previous finding of reversible finger clubbing and purgative abuse, though, in that case, serum immunoglobulins were normal. It is most likely that the immune deficits and clubbing were the result of cachexia and chronic diarrhoea, although a direct toxic action of senna cannot be discounted. Abnormalities of cell-mediated immunity, such as negative candida skin test, are known to follow severe weight loss.3,4 They usually disappear after recovery of normal body weight. The severe weight loss was probably due to two main factors: food intake was undoubtedly low for several years and increased considerably after stopping senna; and fat malabsorption was identified during at least the last two years of PERCENTAGE OF TOTAL LYMPHOCYTES
1. Horwitz DA, Hobo PI. J Clin Invest 1975; 56: 1464. 2. Silk DBA, Gibson JA, Murray CRH. Reversible finger clubbing in a case of purgative abuse. Gastroenterology 1975; 68: 790-94. 3. Carpenter Y, Delesperse G, Janne PA, Mendes da Coster P, Collet H Variations of immunocompetence compared to nitrogen balance in patients undergoing parenteral nutrition. Proceedings of International Society of Parenteral Nutrition. Kyoto, Japan. Acta Chir Scand 1975; 466: 122-23. 4. Law DK, Dudrick SJ, Abdon NI. Immunocompetence of patients with protein-calorie malnutrition. Ann Intern Med 1973; 79: 545 5. Heizer WD, Warshaw AL, Waldman TA, Laster L. Protein losing gastroenteropathy and malabsorption associated with factitious diarrhoea. Ann Intern Med 1968, 68: 839-52
Preliminary Communication PROPRANOLOL IN PREVENTION OF RECURRENT GASTROINTESTINAL BLEEDING IN CIRRHOTIC PATIENTS DIDIER LEBREC
OLIVIER NOUEL
JACQUES BERNUAU
MARTIN BOUYGUES JEAN-PIERRE BENHAMOU
BERNARD RUEFF Unité de Recherches de
Physiopathologie Hépatique (INSERM), Hôpital Beaujon, 92118 Clichy, France
Summary
Placebo
or
propranolol was given randomly
groups of 12 adults with cirrhosis who had recently bled from oesophageal or gastric varices or from acute gastric erosions. During three months’ follow-up 5 patients in the placebo and none in the propranolol group had recurrent gastrointestinal bleeding. to two
INTRODUCTION
CONTINUOUS oral administration of propranolol induces a sustained decrease in portal venous pressure in patients with cirrhosis.’ We report preliminary results of a controlled study of propranolol in the prevention of recurrent bleeding due to ruptured oesophageal or gastric varices or to acute gastric erosions in patients with cirrhosis. PATIENTS AND
M = mouse.
*Polyvalent. t Bearing kappa and lambda surface markers. tmouse rosettes (after treatment with neurammidase), representing early stages of B-cell differentiation and consistent with B-cell recovery.
METHODS
24 adults with histologically proven cirrhosis (alcohohc 21. hepatitis-B infection 1, unknown cause 2) were admitted after gastrointestinal bleeding due to ruptured oesophageal or gastro varices (in 17) or to acute gastric erosions (in 7). The additional criteria for inclusion in this study were: (1) the diameter c:
manifestations in those who inherit the gene for familial porphyria cutanea tarda,’, 10,16,18,19 which is inherited as an autosomal dominant characteristic. 2 of our patients came from Spain and the third was of Italian ancestry: these are two countries where familial porphyria cutanea tarda may be 18,19 commoner than in some other parts of Europe. However, further investigations are needed to exclude the possibility that HEP is caused by a new type of uroporphyrinogen decarboxylase defect. A patient who is homozygous for the gene that causes another type of autosomal dominant porphyria, hereditary coproporphyria, has been described.20 As with patient 3, this patient’s fibroblasts had a very low enzyme activity, whereas cells from heterozygotes responded normally to an ALA load .2’ The findings in living cells (fibroblasts) in these patients support the evidence obtained from in-vitro work that the enzymes that metabolise porphyrinogens are normally present in amounts that are far in excess of those needed to maintain haem synthesis.2’ Identification of cases of homozygous porphyria should enable more rapid progress to be made in determining the nature of the mutations in this group of conditions. We thank Mr W. H. Lockwood for much assistance with patient 3; Miss Carol Wyvill, Miss Rose Aston, and Mr C. Bastaricca for technical assistance, and staff of the biochemistry department, Royal Children’s Hospital, Melbourne, for porphyrin analyses. G. H. E. thanks the Medical Research Council for financial support.
Requests for reprints should be addressed to G. H. E., Department of BlOchemIstry, Welsh National School of Medicine, Cardiff CF4
Medical 4XN.
REFERENCES
Moore MR, Goldberg A Enzyme abnormalities in the porphyrias. Lancet 1977, ii: 699-701 2 Brenner DA, Bloomer JR The enzymatic defect in variegate porphyria. N Engl. JMed 1980, 302: 765-68. 3. Czarnecki DB Hepatoerythropoietic porphyria. Arch Dermatol 1980, 116: 307-11 4 Pinol Aguade J, Castells A, Indachochea A, Rodes J. A case of biochemically unclassifiable hepatic porphyria Br J Dermatol 1969; 81: 270-75. 5 Pinol Aguade J, Herrero C, Almeida J, et al. Porphyria hepatoerythrocytaire, une 1 Brodie MJ,
nouvelle forme de porphyrie Ann Dermatol Syphilol 1975, 102: 129-36. Simon N, Berko G, Schneider I. Hepato-erythropoietic porphyria presenting as scleroderma and acrosclerosis in a sibling pair. Br J Dermatol 1977; 96: 663-68 7. Gunther W The porphyrias and erythropoietic protoporphyria. Aust J Dermatol 1967; 9: 23-29 8 Hofstad F. Seip M. Eriksen L Congenital erythropoietic porphyria with a hitherto undescribed porphyrin pattern. Acta Paediatr Scand 1973; 62: 380-84 9 Kushner JP, Barbuto AJ, Lee GR An inherited enzyme defect in porphyria cutanea tarda decreased uroporphyrinogen decarboxylase activity. J Clin Invest 1979; 58: 1089-97 10. Verneuil H de, Aitken G, Nordmann Y Familial and sporadic porphyria cutanea two different diseases Hum Genet 1978; 44: 145-51. 11. Elder GH, Lee GB, Tovey JA Decreased activity of hepatic uroporphyrinogen decarboxylase in sporadic porphyria cutanea tarda. N Engl J Med 1978; 299: 274-78 12. Smith SG The use of thin layer chromatography in the separation of frée porphyrins 6.
and porphyrin methyl esters Br J Dermatol 1975, 93: 291-95 Improved ethanol extraction procedure for determining zinc-protoporphyrin in whole blood. Clin Chem 1977;
13. Garden JS, Mitchell DG, Jackson KW, Aldous KM.
23: 1585-89 14. Sassa S Solish G. Levere RD, Kappas A. Studies in porphyria. IV. Expression of the gene defect of acute intermittent porphyria in cultured human skin fibroblasts and amniotic cells Pre-natal diagnosis of the porphyric trait J Expt Med 1975; 142: 722-31
15. Smith SG Rao KRN, Jackson AH The porphyrins of normal human urine, with a comparison of the excretion pattern in porphyria cutanea tarda Int J Biochem 1980, 12: 1081-84. 16. Benedetto AV. Kushner JP, Taylor JS Porphyria cutanea tarda in three generations of a single family N Engl J Med 1978, 298: 858-62. Eriksen L, Eriksen N Porphyrin distribution and porphyrin excretion in human congenital erythropoietic porphyria. Scand J Clin Lab Invest 1974; 33: 323-32. Salamanca RE de, Catalan T, Cruces MJ, Pena ML, Olmos A, Mas V The inheritance of porphyria cutanea tarda Int J Biochem 1980, 12: 869-72 19. Topi G D’Alessandro Gandolfo L Inheritance of porphyria cutanea tarda analysis of 14 cases in families Br J Dermatol 1977; 97: 617-28. 20. Grandchamp B, Deybach JC, Grelier M, Verneuil H de, Nordman Y. Studies of porphyrin synthesis in fibroblasts of patients with congenital erythropoietic porphyria and one patient with homozygous coproporphyria Biochim Biophys Acta 1980, 629: 577-86 Elder GH, Evans JO, Thomas N, et al. The primary enzyme defect in hereditary coproporphyria Lancet 1976, ii: 1217-19 17.
18.
21.
PURGATIVE ABUSE ASSOCIATED WITH REVERSIBLE CACHEXIA, HYPOGAMMAGLOBULINAEMIA, AND FINGER CLUBBING D. LEVINE
A. W. GOODE D. L. WINGATE
Gastroenterology and Surgical Units, The London Hospital, Whitechapel, London E1 1BB Laxative abuse may cause systemic and metabolic changes, but cachexia has not been reported as a predominant feature. A patient with finger clubbing and extreme wasting recovered when senna intake was stopped and nutritional care provided. A diagnosis had been made of acquired common variable hypogammaglobulinaemia with absence of circulating B lymphocytes. The immunological abnormalities were corrected after senna intake was stopped and lean body mass restored.
Summary
Case-History
_
_
A 64-year-old woman was admitted for management of diarrhoea and weight loss. She had lost more than 45% of her healthy weight and had become an invalid. She had had repeated urinary infections with renal stones over many years, but diarrhoea had been the chief symptom since 1972. Finger clubbing and hypokalaemia were observed in 1975. At that time faecal fat estimations were normal, but no immunological tests were conducted. Jejunal biopsy was normal and X-ray examination of the bowel revealed only a dilated colon. Persistent diarrhoea prompted further investigation at another teaching hospital in 1977. Hypokalaemia was again a feature, but she also had steatorrhoea (43 mmol/24 h of stool fat, normal 18 mmol/24 h). Giardia lamblia were seen both in jejunal biopsy sections and in jejunal aspirate. A peripheral blood-count showed microcytic anaemia, which was attributed to chronic blood loss from colonic polyps, later removed during colonoscopy. In addition to these tubular adenomas, colonic biopsy specimens showed melanosis. Serum albumin was 30 g/1 and there were persistently low serum levels of IgG (on occasion as low as 1’6g/1). IgM and IgA were never more than slightly reduced. Several urine samples contained excessive kappa and lambda light chains, but there was no abnormal band on serum electrophoresis. A bone-marrow aspirate was normal apart from reduced iron stores. Analysis of peripheral blood lymphocytes (method of Horwitz and Lobol) showed that 53% of circulating mononuclears were T cells, but B cells were absent. Repeated injections of immunoglobulin made no difference to the diarrhoea. Giardia lamblia was eliminated after a long course of metronidazole. On admission to the London Hospital in January, 1980, she weighed less than 24 kg (3 st 10 lb). Total body potassium was measured by a shadow shield whole-body counter, a method which relies on measuring y-radiation from natural radioactive 4oK, present as a fixed proportion (0’012%) of the stable potassium. Intracellular red-cell potassium concentration was within normal range, and total body potassium measurements indicated a 25% loss of lean body mass. Gross finger and toe clubbing was still present. A candida skin test was negative. Serum levels of IgG, IgA, and IgM were all reduced at 3 · 19, 0 · 67, and 0 - 40 g/1 respectively. Diarrhoea (average daily stool weight, 700 g normal fat) and hypokalaemia (average plasma level, 2 -3mmol/1) persisted for the first week in hospital. At that point over 200 ’Sennokot’ tablets were found in her locker, whereupon she agreed to stop taking senna and surrendered her supply. Compliance with this advice and increased food intake with enteral proprietary supplements (’Isocal’) led to rapid weight.gain. Serial measurements of total body potassium indicated an increase in lean body mass. As her weight rose, so did serum levels of
immunoglobulins, particularly IgG (see accompanying figure).
920
her illness. Both steatorrhoea and hypoproteinaemia have been associated with purgative abuse,5 but the mechanism is unclear. In our patient, giardiasis may also have played a part. Whatever the original reason for taking senna, purgative abuse eventually became a habit for which there was no
longer an overwhelming compulsion. Although the patient clearly surprised when confronted with the supply of senna, she then cooperated fully and there has been nothing since to suggest further abuse of purgatives. She was strikingly transformed from invalidism as a weak, wasted, and housebound woman to an active life as an apparently fit and well-groomed housewife. Chronic laxative abuse leading to severe disability does not necessarily carry a poor prognosis.
was
We are grateful to Prof. J. S. Orr and the staff of the Hammersmith Hospital for the serial whole-body potassium counts and to Dr D. Bainbndge for the final B and T lymphocyte counts. We are indebted to Dr Derek Jewell for information about the patient.
Changes in body-weight and serum IgG.
Requests for reprints should be
directed
to
D. L. W.
REFERENCES
Nine months later, a repeat lymphocyte analysis showed B cells in normal numbers, and an increased proportion of cells representing early stages of B-cell differentiation. T-cell numbers were slightly below the normal (see table). In an interview with a clinical psychologist, she gave a history of probable anorexia nervosa in early adult life, since when she had apparently retained the idea that a low bodyweight was desirable. Since discharge from hospital, she has taken 30 ml of magnesium sulphate mixture daily as a single dose and passed one normal motion each day. Finger clubbing has virtually disappeared and her bodyweight remains stable at about 35 kg (5 st 7 lb). Apart from constipation, increasingly painful vertebral osteoporosis is her only remaining trouble.
Discussion Neither hypogammaglobulinaemia nor B-cell deficit have been reported in association with laxative abuse or weight loss. The association of low IgG with repeated urinary infections remains speculative. When these infections began, she had no diarrhoea and had not lost weight, although she was probably already taking senna. Our findings support a previous finding of reversible finger clubbing and purgative abuse, though, in that case, serum immunoglobulins were normal. It is most likely that the immune deficits and clubbing were the result of cachexia and chronic diarrhoea, although a direct toxic action of senna cannot be discounted. Abnormalities of cell-mediated immunity, such as negative candida skin test, are known to follow severe weight loss.3,4 They usually disappear after recovery of normal body weight. The severe weight loss was probably due to two main factors: food intake was undoubtedly low for several years and increased considerably after stopping senna; and fat malabsorption was identified during at least the last two years of PERCENTAGE OF TOTAL LYMPHOCYTES
1. Horwitz DA, Hobo PI. J Clin Invest 1975; 56: 1464. 2. Silk DBA, Gibson JA, Murray CRH. Reversible finger clubbing in a case of purgative abuse. Gastroenterology 1975; 68: 790-94. 3. Carpenter Y, Delesperse G, Janne PA, Mendes da Coster P, Collet H Variations of immunocompetence compared to nitrogen balance in patients undergoing parenteral nutrition. Proceedings of International Society of Parenteral Nutrition. Kyoto, Japan. Acta Chir Scand 1975; 466: 122-23. 4. Law DK, Dudrick SJ, Abdon NI. Immunocompetence of patients with protein-calorie malnutrition. Ann Intern Med 1973; 79: 545 5. Heizer WD, Warshaw AL, Waldman TA, Laster L. Protein losing gastroenteropathy and malabsorption associated with factitious diarrhoea. Ann Intern Med 1968, 68: 839-52
Preliminary Communication PROPRANOLOL IN PREVENTION OF RECURRENT GASTROINTESTINAL BLEEDING IN CIRRHOTIC PATIENTS DIDIER LEBREC
OLIVIER NOUEL
JACQUES BERNUAU
MARTIN BOUYGUES JEAN-PIERRE BENHAMOU
BERNARD RUEFF Unité de Recherches de
Physiopathologie Hépatique (INSERM), Hôpital Beaujon, 92118 Clichy, France
Summary
Placebo
or
propranolol was given randomly
groups of 12 adults with cirrhosis who had recently bled from oesophageal or gastric varices or from acute gastric erosions. During three months’ follow-up 5 patients in the placebo and none in the propranolol group had recurrent gastrointestinal bleeding. to two
INTRODUCTION
CONTINUOUS oral administration of propranolol induces a sustained decrease in portal venous pressure in patients with cirrhosis.’ We report preliminary results of a controlled study of propranolol in the prevention of recurrent bleeding due to ruptured oesophageal or gastric varices or to acute gastric erosions in patients with cirrhosis. PATIENTS AND
M = mouse.
*Polyvalent. t Bearing kappa and lambda surface markers. tmouse rosettes (after treatment with neurammidase), representing early stages of B-cell differentiation and consistent with B-cell recovery.
METHODS
24 adults with histologically proven cirrhosis (alcohohc 21. hepatitis-B infection 1, unknown cause 2) were admitted after gastrointestinal bleeding due to ruptured oesophageal or gastro varices (in 17) or to acute gastric erosions (in 7). The additional criteria for inclusion in this study were: (1) the diameter c: