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Endocrine Abstracts (2022) 81 EP158 | DOI: 10.1530/endoabs.81.EP158

Centro Hospitalar do Tamega e Sousa, Endocrinology, Penafiel, Portugal.

Introduction: Milk-alkali syndrome is defined by the triad hypercalcemia, metabolic alkalosis and renal impairment, due to intake of calcium salts and absorbable alkali. It is the 3rd leading cause of hypercalcemia but often underdiagnosed. Patients with chronic hypoparathyroidism after total thyroidectomy have increased risk for this potentially life-threatening complication and its epidemiology is unclear. We present a case of milk-alkali syndrome in a patient with chronic hypoparathyroidism.

Case report: Female, 60 years-old. Chronic hypoparathyroidism and hypothyroidism after total thyroidectomy due to non-toxic multinodular goiter 2 years ago. Rheumatoid arthritis, chronic kidney disease and inferior limb deep vein thrombosis. Brown-Sequard syndrome 1 year ago due to cervical spine hematoma and submitted to vertebral laminectomy. Medication: levothyroxine 100 ug, calcitriol 0.25 ug id, calcium carbonate/cholecalciferol 1500 mg/400 UI 2id, acenocoumarol, methotrexate, and methylprednisolone 4 mg bid. She presented with nausea, vomiting and polydipsia for 4 days. She was dehydrated, BP 139/74 mmHg, HR 78 bpm, SatO2 99% (room air), temperature 36.4°C. Normal cardiopulmonary auscultation. No signs of acute abdomen and no peripheral oedema. Arterial blood gas analysis: pH 7.49, pCO2 59 mmHg, pO2 79 mmHg, HCO3− 38.6 mmol/l, iCa2+1.70 mmol/l. ECG: 57 bpm. Venous blood analysis: creatinine 2.5 mg/dl, urea 89 mg/dl, sodium 142 mmol/l, potassium 3.1 mmol/l, corrected total calcium 14.4 mg/dl, magnesium 2.3 mg/dl, phosphate 3.7 mg/dl, PTH <4 pg/ml, 25-hidroxicholecalciferol 5 nmol/l, TSH 0.81 uUI/ml, T4L 1.22 ng/dl, CRP 6 mg/dl, leukocyte count 10690/uL. Kidney ultrasound: non-obstructive bilateral echogenic foci. She was diagnosed with milk-alkali syndrome. Calcium and vitamin D supplements were suspended and started treatment with intravenous isotonic saline and potassium chloride, maintaining a good urine output. Calcium and creatinine levels improved progressively. Calcium carbonate/cholecalciferol 1500 mg/400 UI 2id and calcitriol 0.25 ug one every other day were restarted and she was discharged 4 days after. At the follow-up, she was asymptomatic with a corrected total calcium 8.7 mg/dl, phosphate 4.0 mg/dl and creatinine 1.37 mg/dl.

Discussion: In people exposed to large doses of calcium and alkali, normal kidney function and calcitriol suppression help maintain calcium and acid–base balance. However, once hypercalcemia develops, it perpetuates metabolic alkalosis, which itself decreases renal calcium excretion. Risk factors are older-age, chronic kidney disease, pregnancy and medication. Potential triggers are dehydration, volume depletion, infection, diets rich in pH-basic foods and altered medication dose. Our patient had chronic kidney disease, so when exposed to volume depletion and dehydration secondary to vomiting, she was unable to excrete excessive calcium. Additionally, the inability to decrease calcium absorption, due to exogenous calcitriol, in response to increased serum calcium levels might have aggravated hypercalcemia.

Volume 81

European Congress of Endocrinology 2022

Milan, Italy
21 May 2022 - 24 May 2022

European Society of Endocrinology 

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