Life-threatening maternal and fetal macrocytic anemia from antiretroviral therapy.

BACKGROUND: Antiretroviral therapy is recommended for human immunodeficiency virus (HIV)-infected patients during pregnancy to reduce the vertical transmission to the newborn. Complications from this therapy are uncommon. CASE: A 38-year-old HIV-positive pregnant woman was treated with lamivudine and zidovudine. At 28 weeks of gestation, her hemoglobin had fallen to 4.6 g/dL with an mean corpuscular volume (MCV) of 126 microm. At 36 weeks the fetal biophysical profile was abnormal. A pale hydropic infant was delivered via emergency cesarean, with a hemoglobin of 2.1 gm and MCV of 131 microm. The newborn hemoglobin normalized after withdrawal of the neonatal retroviral therapy. CONCLUSION: Maternal-fetal macrocytic anemia may complicate antiretroviral therapy.

Exhaled nitric oxide and tracheal endothelin-1 in preterm infants with and without RDS.

We measured exhaled nitric oxide and tracheal aspirate endothelin-1 to determine relationships between these substances and alterations in pulmonary gas exchange during respiratory distress syndrome (RDS) in comparison to those obtained from control preterm infants without RDS. Eight infants with RDS had measurements made at 24 hr and again at 48-72 hr. Eight control infants were studied once at 24-48 hr of life. Exhaled gas was analyzed on-line, and minute excretion of NO (V(NO)) was calculated. ET-1 was determined by immunoassay. Median V(NO) at 24 hr in RDS was 0.405 nl/min/kg (range, 0.30 -0.79), which subsequently declined by 48-72 hr to 0.166 nl/min/kg (P < 0.01). The V(NO) in RDS infants was significantly higher than time-matched V(NO) in controls, with a median of 0.099 nl/min/kg (range, 0.03-0.27; P < 0.001). ET-1 was not correlated with initial V(NO) in the RDS or control patients. In conclusion, in RDS, V(NO) decreases as gas exchange improves. ET-1 is detectable in tracheal aspirate samples in both groups of infants.

Endogenous production of nitric oxide in endotoxemic piglets.

We sought to assess the relation between endotoxin-induced pulmonary hypertension and the production of nitric oxide (NO) in neonatal animals. Adult animals respond to endotoxin by increasing exhaled NO and plasma NO metabolites. The response of neonatal animals has not previously been reported. We administered 20 microg/kg of Escherichia coli lipopolysaccharide (LPS) to 12- to 18-day-old and to 5- to 7-week-old piglets. Pulmonary vascular resistance increased significantly in both age groups. Exhaled NO in the 12- to 18-day-old animals and in the 5- to 7-week-old piglets did not increase significantly. A similarly treated group of adult rats did show a significant increase in exhaled NO (2.6 +/- 1.0 to 109.5 +/- 54.3 ppb; p = 0.028). Plasma NO metabolite measurements followed the same pattern of no increase in both porcine groups, and a large increase in the rat group. However, immunostaining of lungs from 12- to 18-day-old piglets did reveal an increase in inducible NO synthase. These results suggest that piglets demonstrate a limited ability to modulate LPS-induced pulmonary hypertension by elevations in exhaled NO. They also demonstrate the differential response to LPS between species.