OBJECTIVE: To study epidemiology and possible risk factors associated with the development of cryptosporidiosis among European patients with AIDS. METHODS: An inception cohort of 6548 patients with AIDS, consecutively diagnosed from 1979 to 1989, from 52 centres in 17 European countries was studied. Data on all AIDS defining events were collected retrospectively from patients' clinical records. Kaplan-Meier estimates, log rank tests and Cox proportional hazard models were used to examine for possible risk factors associated with cryptosporidiosis. RESULTS: Cryptosporidiosis was diagnosed in 432 (6.6%) patients, 216 at time of the AIDS diagnosis and 216 during follow-up. The probability of being diagnosed with cryptosporidiosis at AIDS diagnosis was significantly lower for intravenous drug users (1.3%) than for homosexual men (4.1%) and for patients belonging to other transmission categories (4.0%) (p < 0.001). The probability was also higher for patients from Central Europe compared with patients from South Europe (4.1% versus 2.5%, p = 0.005). The rate of developing cryptosporidiosis after the diagnosis of AIDS was 3 per 100 patient years of follow-up. The rate was significantly lower for intravenous drug users than for homosexual men (relative risk 0.34, 95% confidence limits 0.22-0.54) and for women compared with men (RR 0.43 (0.21-0.87)). The risk was higher in North Europe than in South and Central Europe. In a multivariate analysis only transmission category remained a significant predictor for the development of cryptosporidiosis. CONCLUSION: The development of cryptosporidiosis in AIDS patients may be associated with sexual risk behaviour.

This study examined the factors associated with the development of a first episode of Pneumocystis carinii pneumonia (PCP) in 5,025 patients with AIDS, including 1,976 patients with primary PCP at the time of AIDS diagnosis and 635 with primary PCP occurring subsequently. Compared with untreated patients, patients treated with zidovudine were at similar risk of developing PCP during the first year of therapy but were at greater risk after longer intervals of treatment. The following factors were associated with an increased risk of PCP (either at the time of AIDS diagnosis or thereafter): lack of primary PCP prophylaxis, male homosexuality/bisexuality, diagnosis of AIDS in northern Europe, and CD4 cell count below 200 x 10(6)/L at the time of AIDS diagnosis. Patients with severe weight loss had a 60% higher risk of developing PCP during follow-up than those without such weight loss. Thus, the occurrence of PCP depended on geographic location, mode of acquisition of human immunodeficiency virus and AIDS, degree of immunodeficiency, and use of various treatment regimens.

Objectives-To examine the pattern of survival and factors associated with the outcome of disease in patients with AIDS.Design-Inception cohort. Data collected retrospectively from patients' charts.Setting-52 clinical centres in 17 European countries.Subjects-6578 adults diagnosed with AIDS from 1 January 1979 to 31 December 1989.Main outcome measures-Survival after the time of diagnosis.Results-The median survival after diagnosis was 17 months, with an estimated survival at three years of 16% (95% confidence interval 15% to 17%). Patients diagnosed in southern Europe had a shorter survival, particularly immediately after the time of diagnosis, compared with patients diagnosed in central and northern Europe (survival at one year (95% confidence interval) 54% (52% to 56%) 66% (64% to 68%), 65% (63% to 66%), respectively. The three year survival, however, was similar for all regions. The regional differences in survival were less pronounced for patients diagnosed in 1989 compared with earlier years. Improved survival in recent years was observed for patients with a variety of manifestations used to define AIDS but was significant only for patients diagnosed with Pneumocystis carinii pneumonia. The three S ear survival, however, remains unchanged over time.Conclusions-Survival of AIDS patients seems to vary within Europe, being shorter in southern than central and northern Europe. The magnitude of these differences, however, has declined gradually over time. Short term survival has improved in recent years, but the long term prognosis has remained equally poor, reflecting the fact that the underlying infection with HIV and many of the complicating diseases remains essentially uncontrolled.

OBJECTIVE:To determine the association between elapsed time since starting zidovudine and survival in patients with acquired immunodeficiency syndrome (AIDS).DESIGN:Inception cohort and observational study of patients treated and not treated with zidovudine.SETTING:Fifty-one centers in 17 European countries.PATIENTS:A total of 4484 patients diagnosed as having AIDS from 1979 to 1989 who survived their initial AIDS-defining event and who had not started zidovudine before AIDS diagnosis.MAIN OUTCOME MEASURES:Use of zidovudine and mortality.RESULTS:Among patients who did not receive zidovudine, the death rate was approximately constant for the first 5 years after AIDS diagnosis. For patients treated with zidovudine, the death rate within the first year since starting zidovudine was markedly lower than for untreated patients who had developed AIDS at the same time (relative rate, 0.47; 95% confidence interval [CI], 0.42 to 0.51). For longer times since starting zidovudine, the association with reduced mortality rate was diminished, and for patients surviving more than 2 years since starting zidovudine, the death rate was greater than for untreated patients who had developed AIDS at the same time (relative rate, 1.35; 95% CI, 1.15 to 1.58). Adjustment for other prognostic factors failed to substantially affect this observation.CONCLUSIONS:When initiated after the time of AIDS diagnosis, zidovudine was associated with improved prognosis but for no more than 2 years after starting therapy.

A hemophilia B patient, seropositive for HIV antibodies since 1984, came to us in March 1989 with a severe necrotizing lesion of the nose. It was an erythematous lesion and looked like rhinophyma. Microbiological examination of the skin biopsy showed the presence of Cryptococcus neoformans. At the time of the study, the patient was in partial remission after 2 weeks of therapy with fluconazole per os 400 mg/day. He will be treated with the same therapy at maintenance dose (200 mg/day) for a long period.

IgM antibody to hepatitis B core antigen (anti-HBc IgM) was investigated by an antibody-capture radioimmunoassay (serum dilution 1∶4000) in serum samples from 31 untreated children with chronic hepatitis B who were followed prospectively for 1–7 years. At the start, all patients were positive for hepatitis B e antigen (HBeAg), and anti-HBc IgM was detected in 23 cases, including 15 out of 16 with chronic active hepatitis and 7 out of 14 with chronic persistent hepatitis. A significant positive correlation was found between anti-HBc IgM levels and severity of liver damage (P<0.05), while an inverse relationship was found between anti-HBc IgM levels and distribution of hepatitis B core (HBcAg) antigen in the liver as detected by immunofluorescence. In fact 75% of anti-HBc IgM positive patients showed a focal HBcAg pattern (less than 40% positive nuclei), whereas 87% of antibody negative cases exhibited a diffuse HBcAg expression (more than 60% stained nuclei). During follow-up, seroconversion from HBeAg to anti-HBe with subsequent remission of liver disease occurred in 82% of patients presenting with detectable levels of anti-HBc, including three out of seven cases with chronic persistent hepatitis, but in none of the cases that were initially negative (P<0.01). These results indicate that during the natural course of chronic hepatitis B in children, anti-HBc IgM levels in serum reflect the degree of host immune response to infected hepatocytes. The close correlation between anti-HBc IgM seropositivity and seroconversion from HBeAg to anti-HBe suggests that anti HBc IgM may have a prognostic value during the follow-up of children with chronic HBeAg positive hepatitis B.

During a prospective study of acute symptomatic viral hepatitis, started in 1978, 664 consecutive adult patients, including 223 drug abusers, fulfilled the diagnostic criteria (anti-HBc IgM positivity) for acute type B hepatitis. In order to evaluate the outcome of the disease, 443 patients were followed for up to 12 months after the onset. 2.4% of the infections became chronic; the rate did not significantly differ between drug addicts and non-drug abusers, suggesting that chronic hepatitis is a rare complication of acute symptomatic hepatitis type B. Ongoing liver damage after clearance of HBsAg from serum was observed in drug abusers only (14% of the cases). Clinical, biochemical and virological features of the acute phase in patients with ongoing infection were compared with those of uncomplicated cases. Anicteric hepatitis and lower transaminase values were significantly (p<0.05) associated to a chronic evolution of the disease, as well as a higher prevalence of HBV-DNA, DNA polymerase and HBcAg positivity in serum. Testing HBV-DNA and DNA polymerase early in the course of the infection appeared to be of high predictive value for the subsequent outcome of the illness.

During a seven-year survey of acute symptomatic viral hepatitis in Padua (Northern Italy), the epidemiological features of hepatitis A were evaluated in 207 consecutive patients (120 males, mean age 22.7 ± 11.4 years). The annual attack rate of the disease decreased significantly (p <0.05) between 1978 and 1979 (0.11/1000 inhabitants) and 1981 and 1984 (0.04–0.03/1000 inhabitants), mainly due to its declining prevalence in the pediatric age. In parallel with the shifting of hepatitis A towards adulthood, single sources of infection, mainly associated with adult life-style such as foreign travel and raw shellfish ingestion, have become more and more prominent. The spread of drug abuse has not influenced the epidemiology of hepatitis A in our area.

A 6-year-old girl, operated upon for an optic nerve astrocytoma (resection limited to the intraorbital portion of the nerve), developed 3 years later symptoms and signs of chiasmatic invasion. Nine years after surgery (1980), she suffered from pneumococcal meningitis, due to cerebrospinal rhinorrhea that had been present in the last few years. A repeated neuroradiological investigation showed the site of the fistula and cerebral ventricles of normal size. The case is argued for bulb-to-chiasm resection of an optic nerve glioma: a spontaneous cerebrospinal rhinorrhea with its potential dangers of meningitis seems to be one more complication of a limited resection of these tumors. It is felt that this is an unusual instance of spontaneous rhinorrhea from direct tumoral erosion. The diagnostic value of metrizamide cisternography for the assessment of presence and site of the fistulous leak is confirmed.

Epidemiological and clinical features of acute symptomatic hepatitis type B were evaluated in 51 otherwise healthy children and in 13 children receiving immunosuppressive treatment for leukaemia and malignancy, who were admitted to hospital with acute hepatitis B surface antigen (HBsAg) positive hepatitis during a period of 7 years. Blood transfusions, or intimate contacts with asymptomatic HBsAg carriers or with contaminated material during repeated admission to hospital were the possible sources of infection in the immunosuppressed patients, whereas percutaneous exposure was identified as the source in a minority of non-immunosuppressed patients. Features of the acute phase of the illness differed little between the two groups of patients (acute liver failure developed in one patient with leukaemia and in two untreated children). Conversely, chronic evolution was observed in 69% of immunosuppressed patients but in only 9% of untreated children and affected only patients born to HBsAg positive mothers (two of four patients) or patients presenting with papular acrodermatitis (both patients).