Anemia in infants with congenital hypothyroidism diagnosed by neonatal screening.

Although anemia is a common finding in adult hypothyroid patients, there are no studies on anemia in hypothyroid infants. The aim of this study, therefore, was to review the hematologic status during the first year of life in 50 infants with congenital hypothyroidism detected through the regional neonatal screening program. The mean age at diagnosis was 23.7 +/- 6.5 days and treatment was initially begun with a mean L-thyroxine dose of 6.8 +/- 1.3 micrograms/kg/day. Clinical and haematological assessments were performed at diagnosis, 3, 6 and 12 months of age. The patients were divided in 2 groups based on whether T4 serum concentration at diagnosis was < 3 micrograms/dl (Group A) or > or = 3 micrograms/dl (Group B). Data for hemoglobin (Hb), hematocrit (Ht), red cells count (RCC), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), serum iron and ferritin were expressed as Standard Deviation Score (SDS). Although at diagnosis the mean value of Hb-SDS, Ht-SDS and RCC-SDS were in the low-normal range in both groups, at 3 months of age the values in Group A (Hb -1.9 +/- 0.79; Ht -2.34 +/- 1.02; RCC -1.56 +/- 1.25) were significantly lower than in Group B (Hb -1.14 +/- 0.78, p < 0.005; Ht -1.59 +/- 0.94, p < 0.05; RCC -0.55 +/- 1.32, p < 0.02). A rise of the Hb, Ht and RCC values was observed in both groups from 6 to 12 months. The mean values of MCV-SDS and MCH-SDS were in the normal range at diagnosis in both groups, decrease progressively at 3 and 6 months and returned to normal at 12 months of age; no differences were found between the 2 groups at any time. Mean Hb levels at 3 months of age were correlated with mean serum T4 at diagnosis (r = 0.30, p < 0.05). The present results indicate that anemia is a frequent finding in infants with congenital hypothyroidism and is depended on the degree of neonatal hypothyroidism and imply that hypothyroidism during development may produce persisting changes even after thyroid replacement has begun.

Bendazac and benzydamine for treatment of cataract: individualized therapy by the "BLOA test".

It was found that two chemically very close Non-Steroid Antiinflammatory Drugs (NSAID), bendazac and benzydamine, were able to reduce the Biological Liquid Oxidant Activity (BLOA) in vitro (bendezac) and in vivo (bendazac and benzydamine). Four hundred and seven patients were treated with bendazac and 599 with benzydamine. After a single dose oral administration they effected a BLOA Reducing Activity (BRA) ranging from 5% to over 20% in about 40% of cataractous patients. When these drugs were able to reduce the BLOA, they showed anticataract activity in about 50% and about 90% of patients according to the extent of BRA, i.e., less than 20% and greater than or equal to 20% of the basal value. This fact suggests that the anticataract agent is not the original NSAID (prodrug) but a NSAID metabolite or an elicited endogenous compound which produced the BLOA reduction. Individual BLOA could be reduced in vivo by benzydamine or bendazac, by both or by neither of them. This finding may be accounted for by selective biotransformation of each patient's original NSAID into the antioxidant anticataract compound. However, other possible mechanisms of the anticataract activity beside antioxidant activity might take place, such as protein and membrane stabilization, together with a not yet defined activation of enzymes within the lens effecting the reversal of cataractous opacity. Several side effects were apparent in short and long term treatments. The final conclusion of our study is that bendazac at a dosage ten-fold lower than that used in the clinics is anticataract drug when orally administered to "BLOA test selected" patients, at least for short term treatment of young, otherwise healthy humans with cortical cataract.