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Among 34 children with AIDS enrolled in a trial with 2'-3' dideoxyinosine (ddI), six (aged 1-6 years) developed liver abnormalities within 2-18 months after institution of ddI. Two children died of fulminant hepatic failure (one had also an adenovirus infection), and four had a striking elevation of alkaline phosphatases (AP: 1120-7000 IU/L). All of them received sulfa drugs and antifungic treatment with ketoconazole or fluconazole. Three had a serology positive for hepatitis C virus. The evolution of liver enzymes following withdrawal and rechallenge with ddI in the children with elevated AP was an indication of drug-induced toxicity in two patients. In both of the others, readministration of ddI did not cause any subsequent problems. Liver histology in the patients with fulminant hepatitis showed an extensive hepatic necrosis. Liver biopsy done in two other patients revealed a mild granulomatous hepatitis in one and nonspecific changes (i.e., steatosis and a mild inflammation) in the other. Hepatic toxicity has been described with ddI and other nucleoside analogs in adult patients. These six children had many potential causes of liver disease. It may be that ddI is not hepatotoxic per se but that it precipitates liver disease in predisposed patients. We recommend that liver functions be carefully monitored when using this drug.

The family situation of 122 children followed at the Necker hospital is analysed in this study: 40% of these children live with both parents, while 22% live with one parent, 10% with their maternal grand mother and 28% are under the care of the Aide Sociale à l'Enfance (Social Services for Children). At this time, less stable family situations and the separation of a child from his mother are not due to the child's HIV status but rather to the social and family context. A better knowledge of these factors is essential to prevent future family separation. Increased awareness and training in this context is urgently needed by the personnel in care of these children as the situation will undoubtedly become even more serious in the next few years.

This report describes the one-year results of a noncomparative study designed to assess the safety and tolerance of low-dose zidovudine (azidothymidine) given orally to 60 human immunodeficiency virus type 1-infected infants and children. At baseline, the mean age was 1.9 years (+/- 1.4), and all were symptomatic: 43% were P2A and 57% were P2B to F according to the Centers for Disease Control classification. All the patients received zidovudine for at least 6 months, and 52 of them (87%) completed a full year of therapy. The mean duration of follow-up was 346 days (+/- 42) (range, 183 to 366 days). The initial therapy consisted of four daily doses of 100 mg/m2 (400 mg/m2 per day, equivalent to 20 mg/kg per day). However, this treatment was modified when neutropenia or anemia was observed. Twenty-nine children (48%) remained at the initial therapy for the entire study. Zidovudine dosage was adjusted 92 times in the other 31 children (52%), mostly due to neutropenia (83%). Altogether, the time under full-dose therapy represented 81% of the total duration of the protocol for all patients. Children with mild symptoms, P2A at study entry, were more likely to remain under full-dose therapy than children with severe symptoms, P2B to F: the time under full-dose therapy represented 91% of the duration of the protocol for the former group and only 74% for the latter one (P less than .02). No clinical adverse experiences were attributed directly to zidovudine. Thirty-seven children were prescribed trimethoprim-sulfametoxazole as a prophylaxis for Pneumocystis carinii pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)

HIV infection of the newborn is now known to result mostly from mother-to-foetus transmission. The risk of transmission is at least 40 p. 100. However, the circumstances of passage are little known, and there is no maternal virological parameter capable of evaluating individual risks. The disease is more severe in children than in adults. Rare are the children who remain asymptomatic for more than 15 months; one out of three of them develop severe acquired immunodeficiency syndrome and die within the first 2 or 3 years of life. A specific encephalopathy is observed in about 30 p. 100 of the infected children. Kaposi's sarcoma is exceptional. Since there is no contagion between children, those who are in fairly good clinical condition should have a family and school life as normal as possible.

The clinical and immunologic abnormalities of 7 infants with Lymphadenopathy Associated Virus (LAV) infection are reported. Indicative immune changes, positive anti-LAV serologic test and/or virus isolation led to the diagnosis. In a case with a particularly severe form of the disease, whose mother died from AIDS, serologic tests and virus isolation were negative. Beside a case associated with blood transfusion, the familial and ethnic context helped the diagnosis. Clinical and biochemical features were close to those in adult AIDS, including hepatosplenomegaly, polyadenopathy, a decreased absolute number of OKT4(+) lymphocytes and hypergammaglobulinemia. The importance of cellular and sometimes also humoral immune deficiency was highly variable. For 4 patients, the severity of the immune deficiency allowed the diagnosis of AIDS. Occurrence of such an infection in the first months of life suggests a fetomaternal viral transmission; however, a postnatal contamination cannot be ruled out. Long-term prognosis is difficult to assess. It depends, among other factors, on the importance of the immune deficiency.

The clinical signs and immunological abnormalities in ten babies with lymphadenopathy associated virus infections (LAV) are described. We have made this diagnosis based on the association of specific immunological abnormalities, serological tests or the positive isolation of the virus. In one very severe case, whose mother died of AIDS, the serology and attempts to isolate the virus were both negative. Excluding the two post-transfusion cases, the ethnic and familial history always suggested the diagnosis. The clinical characteristics were very close to those in adults, being hepatosplenomegaly and generalized lymphadenopathy. There was an associated retardation of growth and weight gain. A decrease of the absolute number of OKT4(+) lymphocytes and hypergammaglobulinaemia were the abnormalities most frequently observed. The degree of immunodeficiency, both humoral and cellular was very variable. The existence of LAV infection during the first few months of life suggests a maternal-foetal transmission, but a post-natal infection cannot be eliminated. It is difficult to decide the long-term prognosis; it depends mainly on the degree of the immune deficiency.