{'fraction_non_alphanumeric': 0.027944111776447105, 'fraction_numerical': 0.017298735861610112, 'mean_word_length': 5.1138211382113825, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Use of oral calcium loading to characterize the hypercalciuria of young insulin-dependent diabetics.

To investigate the pathogenesis of the alterations in bone and mineral metabolism that are found in young insulin-dependent diabetics (IDDs), we performed a standard oral calcium load in 26 IDDs, 7-18 yr of age, and in 17 normal children, 9-18 yr of age. Eighty-five percent of the IDDs had second metacarpal cortical bone widths below the mean for matched controls. Calcium excretion in the IDDs fell along a continuous spectrum, ranging from normal to values consistent with renal hypercalciuria. Immunoreactive PTH was significantly (P less than 0.03) lower in the IDDs compared to that in the controls, and 24,25-dihydroxyvitamin D was significantly elevated (P less than 0.001). We were not able to document a significantly lower concentration of 1,25-dihydroxyvitamin D in the IDDs. Serum calcium, phosphate, and PRL levels were normal, as were creatinine (Cr) clearance and 24-hr urinary cortisol excretion. There was no apparent correlation between the fasting and postload urinary Ca to Cr and glucose to Cr concentration ratios. The accumulated data suggest that in many young IDDs, there is a component of intestinal calcium hyperabsorption which results in appropriate feedback responses by the parathyroid gland and vitamin D metabolic pathway(s). This imbalance between circulating PTH and vitamin D metabolites could result in defective bone remodeling and decreased cortical thickness.