Effects of elevated carbon dioxide environment on calcium metabolism in humans.

BACKGROUND: Chronic respiratory acidosis induced by an elevated carbon dioxide (CO2) environment should provoke hypercalciuria with related total body and subsequent bone calcium losses. We examined this hypothesis in four healthy male volunteers, who were exposed during a 25-d period to an 0.7% CO2 environment within a deep diving isolation chamber. Three months later the same subjects were reexamined during a second campaign being exposed to a 1.2% CO2 atmosphere. METHODS: The subjects received a constant calcium intake (1.4 g.d-1) and vitamin D supplement (1000 IU.d-1) during both campaigns. Calcium balance (oral calcium intake minus urinary and fecal calcium output) was evaluated. Serum calcium concentrations and biomarkers of bone metabolism were measured, in order to evaluate bone turnover. Additionally, the response to an acute oral calcium load was examined as a sensitive measure of changes in calcium metabolism. RESULTS: Both, urinary calcium excretion (from 245 +/- 38 to 199 +/- 31 mg.d-1; mean +/- SE, 0.7% and 1.2%, respectively) and fecal calcium losses (from 1229 +/- 128 to 996 +/- 62 mg.d-1) were significantly reduced in the higher (1.2%) CO2 atmosphere. Although more calcium was retained in the body during the 1.2% than during the 0.7% CO2 campaign, serum calcium concentrations and biomarkers of bone formation were significantly lower in the higher CO2 campaign. Furthermore, bone resorption was slightly increased in the 1.2% experiment. CONCLUSION: Elevated CO2 atmosphere may dose-dependently preserve body calcium without a parallel improvement of bone substance.

[Iatrogenic Wernicke-Korsakow syndrome with unusual neurological deficits and MRI lesions]. / Iatrogenes Wernicke-Korsakoff-Syndrom mit ungewöhnlichen Symptomen und MRT-Veränderungen.

Wernicke-Korsakow Syndrome (WKS) is caused by thiamine (vitamin B1) deficiency and usually occurs in conjunction with chronic alcohol abuse. Our report concerns a 64-year-old, nonalcoholic, woman with no history of alcohol abuse, who became ill with WKS after 3 weeks of parenteral nourishment. As an unusual initial symptom she went blind in both eyes; this was followed a few days later by impaired consciousness and spastic tetraparesis. A cranial MRI examination showed symmetrical signal alteration (T2, FLAIR and diffusion weighting) in the medial thalamus, periaqueductal mesencephalon including the quadrigeminal plate, mamillary bodies and-most unusually-both paracentral gyri. Laboratory tests confirmed the diagnosis of WKS as significant thiamine deficiency was detected. Following several weeks of intravenous thiamine supplementation the MRI lesions were almost completely reversed but the neurological deficits regressed only partially.