Strittmatter WJ, Saunders AM, Schmechel D,
high-avidity binding to &bgr;-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proc Natl Acad Sci USA
1993; 90: 1977-81. 3 Wisniewski T, Golabek A, Matsubara E, Ghiso J, Frangione B. Apolipoprotein E: binding to soluble Alzheimer’s &bgr;-amyloid. Biochem Biophys Res Commun 1993; 192: 359-65. 4 Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science 1993; 261: 921-23. 5 Askanas V, Engel WK. New advances in inclusion-body myositis. Curr Opin Rheumatol 1993; 5: 732-41. 6 Askanas V, Engel WK, Bilak M, Alvarez RB, Selkoe DJ. Twisted tubulofilaments of inclusion body myositis muscle resemble paired helical filaments of Alzheimer brain and contain hyperphosphorylated tau. Am J Pathol 1994; 144: 1-11. 7 Weisgraber KH, Shinto LH. Identification of the disulfide-linked homodimer of apolipoprotein E3 in plasma: impact on receptorbinding activity. J Biol Chem 1991; 266: 12029-34.
Paracentesis for acute renal failure caused hepatic veno-occlusive disease
SIR—Veno-occlusive disease (VOD) complicating bone-
transplantation (BMT) is a frequent life-threatening complication occurring in 20-50% of patients with a death rate of up to 50%.1 It begins 1-3 weeks after transplantation with sudden weight gain, hepatomegaly, ascites, and hyperbilirubinaemia. If associated with uraemia, particularly if haemodialysis is necessary, the prognosis is especially poor with a death rate of 84% . We report the successful treatment of renal failure associated with severe VOD, well documented by pulsed doppler sonography, with a combination of paracentesis, recombinant tissue-plasminogen-activator, prostaglandin E2, and full-dose anticoagulation with heparin. A 31-year-old man was treated in January, 1993, for poor-prognosis acute lymphoblastic leukaemia. He achieved complete remission in March, 1993, after two cycles of myeloablative chemotherapy and received T-cell-depleted BMT from his HLA-identical sister in May, 1993, after conditioning by chemotherapy and radiotherapy. Cyclosporin was given for prophylaxis against graft-versus-host disease and heparin for prevention of VOD. The early post-transplant course was favourable. On day 13, liver and kidney function tests were normal. During the following days, urine output decreased, accompanied by urinary sodium of 17 mmol/L, weight gain, and increase in blood urea nitrogen. On day 17, despite diuretics, volume expansion with albumin, and introduction of dopamine, oliguria with pronounced ascites developed. Pulsed doppler sonography revealed inversion of portal venous flow without obstruction, supporting the diagnosis of VOD. Alteplase was administered at a dose of 10 mg on day 18, 30 mg on day 19,40 mg on day 20, and 30 mg on day 21 combined marrow
The aetiology of acute renal failure associated with VOD after BMT is not yet clearly understood. In our patient, the impressive recovery in diuresis and renal function after paracentesis suggests that the acute increase in intraabdominal pressure had interfered with the renal perfusion. The role of paracentesis is much debated in the treatment of cirrhosis; it is useful and safe in the management of refractory ascites but is not recommended in the hepatorenal syndrome even if transient improvement in renal function has been reported.4,s The use of recombinant tissue-plasminogenactivator was associated with a favourable outcome in 5 of 10 patients with severe VOD but the renal response was not as striking as the liver response.6 In our patient, renal recovery occurred before reduction in portal hypertension. The treatment of VOD includes recombinant tissue-plasminogenactivator associated with heparin and prostaglandin E2. Combination of these treatments in association with paracentesis was associated with a successful outcome. Neither side-effects nor bleeding were observed during the treatment period and paracentesis, to our knowledge, is not reported to be a dangerous procedure if done 6 hours after therapy. Patrick Saudan, Pierre-Yves Martin, Dominique Jaques, Philippe Schonenberg, Claudine Helg, Herve Favre Department of Medicine, Geneva University Hospital, 1211 Geneva 14, Switzerland 1
McDonald GB, Hinds MS, Fisher L, et al. Veno-occlusive disease of the liver and multiorgan failure after bone marrow transplantation: a cohort study of 355 patients. Ann Intern Med 1993; 118: 255-67. Zager RA, O’Quigley J, Zager RN, et al. Acute renal failure following bone marrow transplantation: a retrospecitve study of 272 patients. Am J Kidney Dis 1989; 3: 210-16. Luca A, Cirera I, Garcia-Pagan JC, et al. Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis.
Gastroenterology 1993; 104: 222-27. 4
Gines P, Arroyo V, Quintero E, et al. Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites: results ofa randomised study. Gastroenterology 1987; 93: 234-41. Levy M. Hepatorenal syndrome. Kidney Int 1993; 43: 737-53. Bearman SI, Shuhart MC, Hinds MS, McDonald GB. Recombinant human tissue plasminogen activator for the treatment of established severe venocclusive disease of the liver after bone marrow transplantation. Blood 1992; 10: 2458-62.
Cigarette smoking in Japan SIR-With respect to the letter from Takei (Dec 11, p 1491)and smoking in Japan, we enclose a photograph of a message displayed on a cigarette vending machine in a hotel lobby in Kyoto:
heparin. Within the first 48 hours, diuresis continued to decrease; blood urea nitrogen rose to 25-9 mmol/L, and liver with
deteriorated. The mean arterial pressure was 80 mm Hg and central venous pressure was maintained between 6 and 17 mm Hg. On day 20, paracentesis of 2920 mL of ascites was done and was followed over the next 12 hours by a diuresis of 4 L. Thereafter, a daily diuresis of 3-4 L was sustained with minimum diuretic prescription and renal function improved. At this point, pulsed doppler sonography still revealed inversion of portal venous flow and prostaglandin E2 (500 pg daily by continuous infusion) was started. A second paracentesis of 2800 mL was done on day 25. Dopamine and prostaglandin E2were stopped by day 26 and 47, respectively. Bodyweight returned to baseline by day 29. Biological indices gradually returned to normal. On day 32 pulsed doppler sonography revealed normal portal venous flow. On day 50 the patient was discharged with normal renal function. tests
Nussenzweig, Hermann M Biggs
NYU Medical Center, Department of Pathology, Michael Heidelberger Division of Immunology, New York, NY 10016, USA