379 CLINICAL COURSE OF PATIENTS WITH PTH CAH=chronic active hepatitis, CPH=chronic persistent hepatitis, ACH=acute hepatitis, CAH+S=CAH with moderate fibrosis with slender but not complete septa, CIRR=cirrhosis BX1 =biopsy at PTH presentation, BX2=biopsy 6-12 months from BX1, BX3 =biopsy 6-12 months from BX2. ALT= alanine aminotransferase. cholangiography. If any of these results were abnormal when the liver biopsy revealed a possible PTH, the patient was not thought to have PTH (2 patients, both with abnormal cholangiograms). All patients anti-HCV positive before liver transplantation remained positive after transplantation, despite chronic immunosuppression. 7 of the 30 patients (23%) developed PTH of unknown origin, which was presumed to be associated with chronic HCV infection. The mean time from transplantation to the first histological and clinical evidence of hepatitis was 95 days (50-210). Histological findings at the time of diagnosis of PTH and other details are shown in the table. In patient 7, the histological finding was of hepatocyte spot necrosis without portal or periportal infiltrate (table). A second and third liver biopsy was done after 6-12 months and were available in 4 of the 7 patients with PTH. The disease had progressed in 3 (no 1, 3, and 5). Two patients developed cirrhosis after, respectively, 9 and 18 months, and 1 (no 5) is waiting for a new graft because of a severely deteriorated graft function. Similarly to HBV infection, recurrent HCV infection is a possibility after liver transplantation. From the clinical point of view, the most interesting aspects are the frequency of PTH in anti-HCV positive recipients and the course. We observed PTH of unknown origin, and therefore presumably HCV-related, in almost 25% of our anti-HCV-positive recipients and more importantly the reinfection rapidly progressed with 2 patients already cirrhotic within 2 years from transplantation. The use of antiviral agents4 and/or non-specific immunoglobulinss are two prophylactic options that deserve to be investigated. Department of Surgery, Liver Transplantation Unit, and Department of Hepatology, Ospedale Niguarda, Milan, Italy L. S. BELLI G. F. RONDINARA F. ROMANI A. ALBERTI L. DE CARLIS G. IDEO L. BELLI 1. Read AE, Donegan E, Lake J, et al. Hepatitis C m patients undergoing liver transplantation. Ann Intern Med 1991; 114: 282-84. 2. Poterucha J, Rakela J, Lumeng L, Lee CH, Taswell HF, Wiesner RH. Diagnosis of chronic hepatitis C after liver transplantation by the detection of viral sequences with polymerase chain reaction. Hepatology 1992; 15: 42-45. 3. Martin P, Munoz SJ, Di Bisceglie AM, et al. Recurrence of hepatitis C virus infection after orthotopic liver transplantation. Hepatology 1991; 13: 719-21. 4. Reichard O, Andersson J, Schwartz R, Weiland O. Ribavirin treatment for chronic hepatitis C. Lancet 1991; 337: 1058-61. 5. Sanchez-Quijano A, Pineda JA, Lissen A. Prevention of posttransfusion NANB by non-specific immunoglobulins. Lancet 1988; i: 1245-48. Safety of vaccines in childhood SIR,-Dr Colville and Dr Pugh’s data (Sept 26, p 786) on a high frequency of postvaccination mumps meningitis in the UK have led to the stopping of the distribution of mumps vaccines containing the Urabe Am9 mumps strain in most European countries.! We hope that supplies of vaccine containing the Jeryl Lynn strain will be sufficient to continue mumps vaccination for all children. After vaccination it is not surprising that vaccine virus is found in body fluids, including cerebrospinal fluid (CSF). Although in the past physicians hoped that the mumps vaccine virus did not invade the central nervous system (CNS), Colville and Pugh and others have shown that the mumps vaccine strain is present in CSF more often than previously thought. Nevertheless, all children with positive findings in CSF after vaccination with the Urabe strain had a good outcome. The illness was milder and more transient than infection from the wild mumps virus and had no residual effects. Colville and Pugh provide no information about checks for other possible agents causing CNS infections after vaccination, such as herpes simplex virus (HSV) or human herpes virus-6 (HHV-6). However, the most important question is, are other types of virus or bacteria present in addition to the vaccine strain? Over the past 20 months we have examined 37 children with various diseases after immunisation with different vaccines (eg, measles/mumps/rubella; diphtheria/pertussis/tetanus; BCG; Haemophilus influenzae type B; oral poliovirus) to clarify the reason for atypical postvaccination courses.2 16 children proved to have single viral infections (rotavirus, HHV-6, parvovirus B19, Epstein- Barr virus, adenovirus, HSV, rubeola, influenza); 3 had double viral infection; 11 had bacterial infections (salmonella, staphylococcus, borrelia, mycobacterium, pneumococcus, neisseria, streptococcus, haemophilus); 3 had double mixed (viral/bacterial); and 1 had triple mixed (viral/bacterial/yeast) infections. The remaining 3 children had diagnoses of accidental intoxication, fragile X syndrome, and uncertain disease.* In most of these cases illness was temporally related to vaccination, but we believe that these infections were not causally related to the vaccine given. We thank Dr R. Mentel, Dr H. Herrmann, and Dr W. Seidel, Institute of Medical Microbiology, University of Greifswald for laboratory investigations. Department of Paediatrics, University Hospital, E M Arndt University, 2200 Greifswald, Germany SIEGFRIED WIERSBITZKY ROSWITHA BRUNS 1. Anon. Two MMR vaccines withdrawn. Lancet 1992; 340: 722. 2. Wiersbitzky S, Bruns R, Niendorf N. Reactive arthritis and immune vasculitis with cardiovascular shock after DPT vaccination? Kinderarztl Prax 1990; 58: 547-49. Body building, high-protein diet, and progressive renal failure in chronic glomerulonephritis SIR,-The benefit of low-protein diets in slowing the progression of chronic renal failure is debatable. In animal models of renal insufficiency, high-protein intake accelerates the development of glomerular injury.3’ We describe a patient with chronic glomerulonephritis and normal renal function who progressed rapidly to end-stage renal failure after eating a high-protein intake for rapid muscle gain. The patient was 17 years old in 1988, when he presented with macroscopic haematuria, nephrotic range proteinuria (3-5 g per day), normal blood pressure, and normal renal function findings (serum creatinine 78 pmol/L). Renal biopsy findings were consistent with Berger’s disease (segmental and focal glomerulonephritis with mesangial IgA deposits). No specific treatment was given. Thereafter, blood pressure and serum creatinine remained normal, while urinary protein remained above 2-5 g per day. He had no new haematuric episode. Serum creatinine was 83 umol/L in July, 1991. In January, 1992, this thin young man (1-81 m, 61 kg) began a muscle-building programme. Hoping for rapid augmentation of *Detailed table for 37 patients available from The Lancet on request.