Arginine-induced insulin and growth hormone secretion in children with nutritional rickets.

We evaluated arginine-induced insulin and growth hormone (GH) secretion in ten children with vitamin D deficiency rickets and compared these values with those of eight age-matched control children. All rachitic children had biochemical (increased serum alkaline phosphatase activity and decreased calcium x phosphate product) and clinical evidence for rickets. After an intravenous infusion of arginine-HCl (10% solution, 0.5 g/kg), blood samples were obtained for the measurement of serum insulin and GH concentrations. The mean insulin level 30 min after the start of the infusion was 22.2 +/- 17.1 microU/ml for the rachitic children. This value is significantly below that for the normal children, 63.4 +/- 38.7 microU/ml (p = 0.004). Neither the fasting insulin level nor any others after the arginine infusion differed significantly from those for the control children. There were no significant differences in the fasting or the arginine-stimulated GH levels between the rachitic and control children. The concentrations of insulin-like growth factors did not differ between the two groups.

Serum insulin-like growth factors I and II concentrations and growth hormone and insulin responses to arginine infusion in children with protein-energy malnutrition before and after nutritional rehabilitation.

Serum insulin, growth hormone (GH), insulin-like growth factors (IGFs) I and II, cortisol, and albumin concentrations were measured in 15 children with kwashiorkor, 15 with marasmic-kwashiorkor, and 21 with marasmus, before and in the survivors, after nutritional rehabilitation, as well as in 10 underweight and eight normal Egyptian children. We also evaluated arginine-induced insulin and GH secretion. IGF-I concentrations were reduced in the three severely malnourished groups (0.07 +/- 0.03, 0.05 +/- 0.03, and 0.09 +/- 0.09 U/ml, respectively) but returned to normal after refeeding. IGF-II concentrations were low in the kwashiorkor (175 +/- 79 ng/ml), marasmic-kwashiorkor (111 +/- 57 ng/ml), and marasmic children (128 +/- 70.9 ng/ml) and returned to normal after nutritional rehabilitation. Basal GH levels were high in the three severely malnourished groups (21.9, 28.8, and 16.6 ng/ml, respectively) and returned to normal after refeeding (8.1, 6.5, and 6.0 ng/ml, respectively). GH responses to arginine were depressed in the three malnourished groups and improved significantly in marasmic-kwashiorkor and marasmic children after nutritional rehabilitation. Insulin responses to arginine were impaired in kwashiorkor, and marasmic-kwashiorkor children and improved significantly after refeeding. IGF-I levels correlated significantly with percent of expected weight (r = 0.52, p less than 0.001), percent of expected height (r = 0.42, p less than 0.001), and weight/(height)2 index (r = 0.34, p less than 0.01). IGF-I levels correlated positively with insulin levels (r = 0.421, p less than 0.001) and negatively with cortisol concentrations (r = -0.400, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Pregnancy hepatitis in Libya.

The death-rate from hepatitis in pregnant women in Libya is high. Of 922 hepatitis patients treated during 1975, 377 were males and 545 were females. The case fatality-rate was 0.53% for males and 7-67% for females. In 293 pregnant women it was 12-97% compared with 1-6% in 252 non-pregnant women. In pregnant women deaths occurred mainly in the last trimester. Although 18-4% of the male patients and 15-2% of the women were hepatitis B surface antigen (HBsAg) positive, no patient shown to be antigen-positive died. The frequency of hepatitis in the second half of the year fell both in pregnant women and in the general population, suggesting a warning hepatitis-A epidemic. The exact cause of the high mortality in pregnant women is not clear, but it may have a nutritional basis.

PIP: An outbreak of hepatitis especially virulent in pregnant women in Tripoli, Libya in 1975 is described. The case-fatality rate was 12.97% in 293 pregnant women, 1.6% in 252 nonpregnant women, and 0.53% in 377 men. Deaths in pregnant women usually occurred in 3rd trimester, often at the onset of labor. There was no evidence that pregnant women with jaundice were admitted in preference to non-pregnant women, or that age or parity was related to infection. Hepatitis B antigen was tested by counter immunoelectrophoresis and later by reverse passive hemagglutination and radioimmunoassay. The overall prevalence was 16.6%. In pregnant women it was 11.1%. None of the pregnant women who died were positive for HBsAg. Coma and an abrupt deterioration were often seen in the pregnant women who dies. The women ate a diet devoid in protein from meat, eggs or fish. The epidemic died down in the second half of the year. It was conjectured that virulent a non-A-non-B hepatitis virus caused this outbreak.