Hamid Moallem

Ceftriaxone-related fatal hemolysis in an adolescent with perinatally acquired human immunodeficiency virus infection☆☆☆★

A 14-year-old girl with perinatally acquired human immunodeficiency virus infection had fatal intravascular hemolysis after intravenous administration of ceftriaxone. Laboratory studies confirmed the presence of an antibody against ceftriaxone in the serum and on the patients red blood cells. No evidence of sepsis, glucose-6-phosphate dehydrogenase deficiency or anaphylaxis was found.

HIV Type 1-Specific IgE in Serum of Long-Term Surviving Children Inhibits HIV Type 1 Production in Vitro

We previously identified a group of long-term pediatric survivors who had acquired HIV-1 through maternal transmission; had not received antiretroviral therapy; are now >8 years old, in good health, and with no opportunistic infections; and have not failed to thrive, although they have greatly decreased numbers of blood CD4+ T cells (<500/mm(3)). All the children have elevated total serum IgE levels (210-2475 IU/ml) and make anti-HIV-1 IgE or IgE directed against non-HIV-1 specificities (radioimmunoassay, Western blot assay); they have no detectable antigenemia. We have now studied the ability of anti-HIV-1 IgE in serum obtained from these children to regulate (1) production of HIV-1 by interleukin 2/phytohemagglutinin (IL-2/PHA)-stimulated peripheral blood mononuclear cells (PBMCs) taken from HIV-1-seronegative donors and infected with a T cell-tropic clone of HIV-1, and (2) transmission of a primary HIV-1 strain from adult AIDS patients to uninfected IL-2/PHA-stimulated PBMCs (p24 core antigen production). High levels of HIV-1 production were observed when PBMCs were cultured for 5 days in the presence of HIV-1-seronegative donor serum that was either IgE positive or IgE negative (IgE, >100 or <100 IU/ml, respectively). HIV-1 production also was observed when PBMCs were cultured with HIV-1-infected donor serum that either contained IgE directed against non-HIV-1 specificities or was IgE negative; these levels were 40% less than those seen with sera from the HIV-1-seronegative donors. Far greater inhibition of virus production was observed if the serum in culture contained anti-HIV-1 IgE (>95%). Virus neutralization did not appear to account for the inhibition obtained with anti-HIV-1 IgE-containing serum because virus production was not suppressed in cultures to which serum was added immediately preinfection (<10%), but was strongly suppressed when serum was added 1.5 hr postinfection (>95%). The inhibition of virus production obtained with serum containing anti-HIV-1 IgE was reversed when (1) serum was depleted of IgE (immunoaffinity), but not when it was depleted of IgG (protein G-Sepharose) before inclusion in culture postinfection, (2) anti-IgE, but not anti-IgG, was included in culture, or (3) serum was heat treated before culture. The results indicate that serum from certain HIV-1-infected pediatric long-term survivors contains agents that inhibit HIV-1 production in vitro, and that these agents include anti-HIV-1 IgE. They suggest that a cytotoxic event, rather than virus neutralization, plays an important role in anti-HIV-1 IgE-mediated inhibition of virus production.

Systemic lupus erythematosus in children with sickle cell disease

Coexistence of sickle cell disease (SCD) and systemic lupus erythematosus (SLE) has been reported in 11 patients. The authors describe five additional patients with SCD and symptoms initially attributable to SCD who were later found to have SLE. Patients were identified over a 10-year period (1991-2001) in a pediatric sickle cell population numbering approximately 350. All patients are African-American. Age at diagnosis of SLE was 9 to 17 years (median 11 years), and follow-up after diagnosis ranged from 6 months to 10 years (median 3 years). SLE cerebritis (n = 3), serositis (n = 4), and nephritis (n = 2) were common findings. Physicians should be alerted to the possible development of SLE in patients with SCD.

Chlamydia pneumoniae as a Cause of Respiratory Illness in Children with HIV Infection |[dagger]| 924

Chlamydia pneumoniae as a Cause of Respiratory Illness in Children with HIV Infection † 924

TREATMENT OF PERSISTENT ESOPHAGEAL ULCER IN A PEDIATRICS PATIENT WITH AIDS♦ 54

A 2 year old girl, perinataly infected with HIV Presented to University Hospital of Brooklyn with dysphagia and odynophagia to both liquids and solids. Her weight and height were at 10th percentile and she had lost 6 pounds over 7 weeks. Hepatosplenomegaly as well as swollen cervical, axillary and inguinal nodes were noted. Upper GI endoscopy revealed 6 esophageal ulcers from 0.5 cm to 6 cm in diameter with sharp smooth, raised borders and erythematous base at 8 cm above lower esophageal sphincter. Pending results of pathology/microbiology she was treated with IV acyclovir which she failed to respond. Diagnosis of Idiopathic esophageal ulcers was made and treatment with prednisone was started. Repeat endoscopy after 10 days revealed marked healing, but symptoms and endoscopic findings recurred within a month while prednisone was being tapered. She responded quickly to increased dose, but different attempts to wean her from steroids failed, and eventually she did not respond at all. She was then started on Thalidomide 100mg Q.D. ×2 weeks, on compassionate basis. Based on endoscopic findings which showed improvement, Thalidomide was continued with 100 mg TIW for 8 weeks. By the end of this period she started taking soft foods by mouth and was switched to 100 mg Thalidomide twice/week. She is currently on regular diet for the age without complaint. Her clinical/neurological findings as well as laboratory values including CD4 count did not change.