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Objective: A randomized, double-blind controlled study compared breastfeeding, partially- and extensively-hydrolyzed protein formulas (pHF and eHF) in their effect on cow' milk allergy (CMA) and atopic symptoms in infants at risk of allergy.Methods: Healthy, full-term infants were randomized to receive a whey pHF or a whey eHF, either exclusively from birth to 4 months of age or at weaning when mothers were willing to breastfeed child. The population consisted of 141 (ITT) and 104 (PP) children in the pHF group and 138 (ITT) and 90 (PP) in the eHF group, of whom respectively 40 (ITT) and 32 (PP) and 38 (ITT) and 31 (PP) were partially breastfed. At 4 months, a milk oral food challenge was performed and at 4 and 12 months, skin prick tests with various food antigens and plasma immunoglobulin concentrations were measured. Standard growth parameters were followed.Results: The incidences of CMA and of reactions to other food antigens were similarly low in all groups. Total IgE plasma concentrations increased between 4 and 12 months in all groups but increased significantly (p=0.048) less with pHF (16.92±47.11 kU/L) than with eHF (23.68±41.29 kU/L). There was an unexpectedly higher hemoglobin level in infants fed a pHF or an eHF compared to breastfeeding. Infants in all groups grew normally according to WHO standards.Conclusion: The whey pHF and the eHF reduced the risk of CMA and of atopic symptoms similarly. The pHF was superior in reducing IgE levels during the first year of life.

Phosphorus depletion which is a well known phenomenon occuring during diabetic keto-acidosis led to assess parathyroid hormone (PTH) secretion.32 children (mean age 9) admitted with diabetic keto-acidosis were studied. They required IV insulin 0.1 U/kg/day, IV rehydration (Cl Na 9%) and IV bicarbonates 14%. Only 3 needed a phosphorus supplement.Sequential serum native 1-84 PTH determinations (normal values 15-85 ng/ml) were done at day 1, 2, 8 and in outpatient clinic at day 30, as compared to all glucose and calcium metabolism serum parameters.An obvious hypoparathyroidism exists at day 1 (mean 11 ng/ml range 1-30), especially as regards to subnormal serum calcium and magnesium levels, and remains on day 2 despite of hyperglycemia and acidosis resolution.No statistical correlation was found with any glucose (serum glucose, bicarbonates…) or calcium (serum calcium, phosphorus, magnesium, 1, 25(OH)2D…). Serum FFH levels normalization was obtained at day 8 or more later at day 30.So a transient hypoparathyroïdism occurs in keto-acidosis, but its pathophysiology remains unclear.

Post natal hypoglycemia related to hyperinsulinism of diabetic women fetuses is presently the major complication of IDM. The aim of this study was to determine hyperinsulinism degree to lead to an appropriate metabolic management. Circulating immunoreactive C peptide provides a means of studying B cell function of IDM because insulin-antibudies cross the placenta; but its RIA requires some delay and so is not usefull in practice. So, other criteria were successively investigated, and were compared to blood C peptide nmol/l / glucose mmol/l ratio (0.12 ± 0.01 sem in control group). No significant correlation with maternal HbA1c % determined on prenatal period is found. There is no significant difference in serum glucosamine levels between IDM and controls. A statistical correlation (rs0.62 p < 0.05) with macrosomia index is found for an index > 1.2. It appeared a negative correlation (r 0.56 p < 0.001 n 35) with serum levels of branch chain aminoacicis which is thought to be an indirect index of hyperinsulinism; results were obtained in relative short time (24 h) : hyperinsulinism is found to a sum level< 200 mcmol/l. There is a close correlation with serum insulin determined by classical or recent quick RIA (r 0.08 p< 0.001 n 33). Results can be obtained within very short time (4 hours). So, actually, 3 repeated routine quick insulin RIA compared to relative blood glucose, offer a direct and rapid way to evaluate IDM hyperinsulinism and hypoglyeeomi c risk, rnak ing possible an appropriate management.

Pseudohypoparathyroidism (PsHP) is a rare disorder that might be caused by a defect in the stimulatory G-proteine (Gs), which transduce the PTH receptor signal to adenylate cyclase. We investigate 35 patients (29 children and 6 adults) with PsHP syndrome. Clinical features, Ellsworth-Howard test, serum level of intact PTH (PTHi) and Gs biological activity are studied. Gs activity is measured with a technic adapted from that of LEVINE we optimized to applicate in children (Assay variation : 10 %). 24 patients (68 %) have a PsHP type Ia with a decrease of Gs-unit activity, but we don't find any relation between Albright's osteodystrophy (AHO) and Gs-unit defect : 4 children are AHO - and 20 are AHO +, and 10 of them presented an associate hypothyroidism. 2 patients (6 %) have no response to infusion of exogenous PTH with an increased of Gs-unit activity and could be PsHP type Ib. Only one patient is PsHP type II with normal Gs-unit, serum PTHi level are increased in all patients (mean = 218 pg/ml, range 65 - 571) without difference between PsHP groups, or relation with Gs-unit activity. Other patients would be classified in pseudo-PsHP with decrease Gs - biological activity. In other hand, we studied 10 families, in 9 Gs-unit activity defect is found at least in 1 member (7 times mother, 1 both mother and father, 1 father). In conclusion, Gs-unit activity appears to be of interest in the investigation of PsHP syndrome.Supported by INSERM.

Post natal hypoglycemia is presently the major complication that occurs in infants of diabetic mothers (IDM) and this complication may be related to the hyperinsulinism state thought to be present in fetuses of diabetic women. Because of sudden and asymptomatic hypoglycemia, hypoglycemic risk persists in despite of present neonatal managment. We studied the somatostatin effect on transient hyperinsulinism of IDM in neonatal period. Five IDM were studied at this time. Synthetic cyclic somatostatin (provided by CLIN-MIDY Laboratories) was infused at the rate of 4 µg/kg/h, a glucose infusion (0.5 g/kg/h) was maintened throughout the study course. Plasma C Peptide (CPR) determined by radioimmunoassay (Mallinckrodt) may provide a mean of studying beta cell function in IDM because insulin antibodies cross the placenta. The cross reactivity with human proinsulin is about 10 %. Before somatostatin administration, plasma CPR was inapropriatly elevated for the blood glucose levels. Plasma CPR/glucose ratio was high. During somatostatin infusion plasma CPR dropped within the first hour and normal level was obtained before the fourth hour in three cases. Blood glucose was maintened over 5.5 mmol/1. Plasma CPR escaped from suppression just after somatostatin infusion although blood glucose moderatly rose. No side effect was observed. Our findings show that beta cells may be more sensitive than alpha cells to somatostatin suppression as previously suggested in nesidioblastosis.The parent gave informed consent and this study was approved by the ethical comittee.

Recent works have demonstrated an essentially inhibitory effect of vitamin D on IPTH secretion. We present an in vivo study, carried out in ricket patients, in an attempt to confirm previous observations and also contribute to a better physiopathological understanding of this affection. 13 and 23 months old advanced nutritional rickets patients who presented hypocalcemia and hypophosphoremia were initially treated exclusively with 25 HCC (DEDROGYLR) at a dose of 20 µg per day. The serum calcium and IPTH couple was assayed daily (IPTH determined by BW 211/41 antiserum). Serum hydroxylated vitamin D metabolites (25;24,25;1,25 HCC) were concurrently determined. Prior to administration, there were high IPTH levels corresponding to a low serum calcium titer. Following 25 HCC administration, a decrease in IPTH levels was observed in spite of the persistance of identical low serum calcium. This decrease attained a maximum value of 36 % at the 5th day. Furthermore, there was a decrease in alkaline phosphatases and urine cAMP excretion. During this initial IPTH fall no change in serum 24,25 HCC level was observed while 1,25 HCC increased and there was a negative correlation between IPTH and 1,25 HCC levels. Considering the fact that hypocalcemia is the only recognized stimulator of IPTH secretion, these findings are in agreement with the hypothesis that vitamin D metabolites and mainly 1,25 HCC have an inhibitory effect on parathyroid hormone secretion in nutritional rickets

35 infants, aged 13.4 ± 11.8 months with vitamin D deficiency rickets were included in the study. Calcemia, phosphorus, serum alkaline phosphatases (ALP) level and isoenzymes, osteocalcin, 25 and 1.25 dihydrovitamin D metabolites, biological activity of Gs protein were measured before and after treatment. Gs protein or stimulatory G protein transduce the signal form PTH receptor to adenylate cyclase. Quantitative analysis of Gs-unit biological activity was determined by a technic, we adapted and optimized from that of Levine to applicate in infants (Assay variation = 10 %). The procedure was based on the measure of cAMP generated in vitro. Normal range is 85-110 % of a Gs biological activity of control patients. We observed, as soon as 1 week after treatment a expected signifiant change in all parameter but ALP. Particularly, Gs-unit activity is constantly decreased but one (73 ± 15 %) and increased to normal range after treatment (98 ± 15 %) (p < 0.002). Low Gs-units activities observed were similar to those found in our experience about pseudohypoparathyroidism type Ia. Our results are consisting with a PTH renal resistance in infants with vitamin D deficiency rickets, which could be due to low biological activity of Gs protein, in relation with vitamin D metabolite or hyperparathyroidism.

Pseudohypoparathyroidism (PsHP) is a rare disorder that might be caused by a defect in the stimulatory G-proteine (Gs), which transduce the PTH receptor signal to adenylate cyclase. We investigate 35 patients (29 children and 6 adults) with PsHP syndrome. Clinical features, Ellsworth-Howard test, serum level of intact PTH (PTHi) and Gs biological activity are studied. Gs activity is measured with a technic adapted from that of LEVINE we optimized to applicate in children (Assay variation : 10 %). 24 patients (68 %) have a PsHP type Ia with a decrease of Gs-unit activity, but we don't find any relation between Albright's osteodystrophy (AHO) and Gs-unit defect : 4 children are AHO - and 20 are AHO +, and 10 of them presented an associate hypothyroidism. 2 patients (6 %) have no response to infusion of exogenous PTH with an increased of Gs-unit activity and could be PsHP type Ib. Only one patient is PsHP type II with normal Gs-unit, serum PTHi level are increased in all patients (mean = 218 pg/ml, range 65 - 571) without difference between PsHP groups, or relation with Gs-unit activity. Other patients would be classified in pseudo-PsHP with decrease Gs - biological activity. In other hand, we studied 10 families, in 9 Gs-unit activity defect is found at least in 1 member (7 times mother, 1 both mother and father, 1 father). In conclusion, Gs-unit activity appears to be of interest in the investigation of PsHP syndrome.Supported by INSERM.