Abstract
The consumption of soft drinks is a crucial factor in determining persistent hypocalcemia. The aim of the study is to evaluate the biochemical mechanisms inducing hypocalcemia in a female patient with usual high consumption of cola drink and persistent hypocalcemia, who failed to respond to high doses of calcium and calcitriol supplementation. At baseline and after pentagastrin injection, gastric secretion (Gs) and duodenal secretion (Ds) samples were collected and calcium and total phosphorus (Ptot) concentrations were evaluated. At the same time, blood calcium, Ptot, sodium, potassium, chloride, magnesium concentrations, and vitamin D were sampled. After intake of cola (1 L) over 180 min, Gs and Ds and blood were collected and characterized in order to analyze the amount of calcium and Ptot or sodium, potassium, magnesium, and chloride ions, respectively. A strong pH decrease was observed after cola intake with an increase in phosphorus concentration. Consequently, a decrease in calcium concentration in Gs and Ds was observed. A decrease in calcium concentration was also observed in blood. In conclusion, we confirm that in patients with postsurgical hypoparathyroidism, the intake of large amounts of cola containing high amounts of phosphoric acid reduces calcium absorption efficiency despite the high doses of calcium therapy.
Highlights
The consumption of soft drinks, full of phosphoric acid, is a potential factor determining hypocalcemia, notably in patients with hypoparathyroidism
We describe the case of a patient with postsurgical hypoparathyroidism-related hypocalcemia who was treated with high doses of oral calcium and calcitriol supplements, without reaching a good control of calcium levels
This report describes a case of a patient with severe hypocalcemia secondary to iatrogenic hypoparathyroidism, who because of cola consumption was not responsive to high doses of oral calcium and calcitriol supplementation
Summary
The consumption of soft drinks, full of phosphoric acid, is a potential factor determining hypocalcemia, notably in patients with hypoparathyroidism. Postoperative hypoparathyroidism and subsequent hypocalcemia are the most frequent complications of total thyroidectomy. A small proportion of thyroidectomized patients receiving supplemental calcium therapy remains hypocalcemic [2, 3]. A 28-year-old woman was hospitalized in our Section of Endocrinology with severe and recurrent hypocalcemic crises (12 times/year). She had undergone total thyroidectomy 8 months before our observation, with postsurgical hypoparathyroidism. She was treated with oral calcium carbonate (10 g/day), calcitriol (2 μg/day), and levo-thyroxine (125 μg/day). Celiac disease was excluded based on negativity for serum antibodies (anti-tissue transglutaminase and anti-endomysial), small bowel biopsy, and genetic testing (human leukocyte antigen test). Attempts to normalize calcemia with other calcium formulations (calcium carbonate plus gluconate, calcium lactate, and calcium citrate) were unsuccessful
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