Blood histamine levels (BHL) in infants and children with respiratory and non-respiratory diseases.

BACKGROUND: Blood histamine levels are decreased after severe allergic reactions and in various chronic diseases. AIMS: To study blood histamine levels in infants and children with acute infectious and non-infectious, non-allergic, disease. METHODS: Blood histamine levels were investigated by a fluorometric method in infants and children admitted to hospital with bronchiolitis, non-wheezing bronchitis, acute infections of the urinary tract, skin and ear-nose-throat, gastroenteritis, or hyperthermia of unknown aetiology. Results of blood histamine levels and white blood cell counts were compared with those obtained for children recovering from benign non-infectious, non-allergic illnesses. RESULTS: As compared with control children, white blood cell numbers were significantly increased in children with acute infections of the urinary tract, skin and ear-nose-throat, and were significantly decreased in children with gastroenteritis. Blood histamine levels were significantly lower in children with gastroenteritis and hyperthermia than in children with other diseases and control children. It was not possible to correlate blood histamine levels and the number of blood basophils. CONCLUSIONS: BHL are significantly decreased in infants and children with acute gastroenteritis and hyperthermia of unknown aetiology. The mechanisms responsible for the decrease in blood histamine levels in children with gastroenteritis and hyperthermia are discussed

Central inhibition of stearoyl-CoA desaturase has minimal effects on the peripheral metabolic symptoms of the 3xTg Alzheimer’s disease mouse model

Abstract Evidence from genetic and epidemiological studies point to lipid metabolism defects in both the brain and periphery being at the core of Alzheimer’s disease (AD) pathogenesis. Previously, we reported that central inhibition of the rate-limiting enzyme in monounsaturated fatty acid synthesis, stearoyl-CoA desaturase (SCD), improves brain structure and function in the 3xTg mouse model of AD (3xTg-AD). Here, we tested whether these beneficial central effects involve recovery of peripheral metabolic defects, such as fat accumulation and glucose and insulin handling. As early as 3 months of age, 3xTg-AD mice exhibited peripheral phenotypes including increased body weight and visceral and subcutaneous white adipose tissue as well as diabetic-like peripheral gluco-regulatory abnormalities. We found that intracerebral infusion of an SCD inhibitor that normalizes brain fatty acid desaturation, synapse loss and learning and memory deficits in middle-aged memory-impaired 3xTg-AD mice did not affect these peripheral phenotypes. This suggests that the beneficial effects of central SCD inhibition on cognitive function are not mediated by recovery of peripheral metabolic abnormalities. Given the widespread side-effects of systemically administered SCD inhibitors, these data suggest that selective inhibition of SCD in the brain may represent a clinically safer and more effective strategy for AD