{'fraction_non_alphanumeric': 0.021044427123928292, 'fraction_numerical': 0.003117692907248636, 'mean_word_length': 6.295454545454546, '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}}
Hypophosphatemia and encephalopathy in alcoholics.

The 69-years old alcoholic manwas admitted to their hospital with alcoholic ketoacidosis, rhabdomyolysis and acute renal failure, and was treated with intravenous glucose solution containing vitamin B { as well as by continuous hemodiafiltration (CHDF). The disturbance of consciousness which persisted despite the general improvement was normalized by correcting his hypophosphatemia. In general, alcoholic patients are in the state of phosphate depletion because of poor intake of phosphorus, secondary hyperparathyroidism due to calcium and vitamin D malabsorption and other factors, and its depletion is exacerbated abruptly by the increase of renal phosphate excretion associated with alcoholic ketoacidosis (2). Importantly, the therapeutic intervention such as the administration of glucose for rehydration or refeeding could potentially precipitate marked hypophosphatemia by redistribution, namely a shift in phosphate from the extracellular to the intracellular compartmentas a consequence of insulin-stimulated glycolytic activity. Therefore, a textbook (3) states that, for alcoholic patients with historical, physical, or biochemical evidence of malnutrition, intravenous fluids should contain phosphate to provide ap-