{'fraction_non_alphanumeric': 0.029925187032418952, 'fraction_numerical': 0.005818786367414797, 'mean_word_length': 5.764044943820225, '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}}
Hypercalcemia in Addison's disease: calciotropic hormone profile and bone histology

Abstract. Three cases of hypercalcæmia secondary to acute adrenocortical insufficiency are described; all the patients had moderate to severe renal impairment, one being on chronic dialysis treatment with no residual diuresis. Parathyroid hormone (PTH) and 1,25 dihydroxyvitamin D [1,25(OH)2D] were low, indicating a suppressed PTH‐vitamin D axis. In the two patients with partial renal impairment, urine Ca excretion was increased, indicating increased load of the cation into the extracellular fluid (ECF), most probably from bone. Saline infusion, to correct any ECF depletion and to increase urine Ca excretion, could not fully correct the hypercalcæmia. Complete correction of plasma Ca levels was observed shortly after the institution of hormonal substitutive therapy. Despite the evidence of increased Ca mobilization from bone, bone biopsies in two patients did not show any signs of cell‐mediated bone resorption; instead, bone cell activity appeared to be suppressed. Thus, glucocorticoid deficiency appears to induce Ca mobilization from bone stores by mechanism(s) unrelated to bone remodelling processes.