Abstract Disclosure: K. Dash: None. P. Eswaran: None. K. Maharajan: None. S. Nangia: None. U. Ayyagari: None. 58 year old female with PV bleed was diagnosed as Carcinoma Cervix and recommended radical radiotherapy with 6 weeks of concurrent chemotherapy with Cisplatin and IV Magnesium premedication. Post 6th cycle of chemo, she presented with nausea, perioral and facial tingling, and lower limb cramps of one day duration. Investigations showed Serum Magnesium 0.4 mg/dl (range 1.6–2.5), Calcium 5.9 mg/dl (8.4-10.2), Potassium 3.3 mg/dl (3.5-5.5). She was treated with IV Calcium gluconate and discharged home post correction with serum Calcium 7.9, Magnesium 1.8, PTH 88.7. She was readmitted twice, 5 and 9 days later, with hypocalcemia, given IV Calcium Gluconate, and discharged post correction of serum calcium levels. She presented to Endocrine OP 2 days later, asymptomatic, serum Calcium 5.9, Magnesium 0.6, K 3.8. She was admitted and replacement commenced with IV Magnesium and Calcium. Over the next day her Calcium and Magnesium levels improved. She was stabilized on oral Calcium and Magnesium replacement and discharged. Calcium replacement was weaned over the next 2 weeks with stable serum Calcium levels on continuing oral Magnesium replacement to date. Cisplatin is a commonly used chemotherapeutic agent. It binds to the N7 reactive center on purine residues and causes DNA damage in cancer cells blocking cell division resulting in apoptotic cell death. This interaction with DNA and the formation of covalent adducts with purine DNA bases is the source of the cytotoxic effect of cisplatin. Therapy is associated with side effects including neuro-, nephro-, hepato-, and cardiotoxicity. Electrolyte disturbances including hypomagnesemia, hypocalcemia, hypokalemia, and hyponatremia are recognized in association with cisplatin therapy. The signs and symptoms of dyselectrolytemias may be nonspecific and a high index of suspicion is required to diagnose. Hypomagnesemia is described in up to 78% of patients on cisplatin due to magnesium wasting attributed to reduced magnesium reabsorption in the distal tubule and/or inadequate intestinal magnesium absorption. Magnesium is primarily an intracellular cation and stored in bone. Serum levels are a poor indicator of total body magnesium and serum concentrations <1.8 mg/dl indicate more severe underlying deficit. Hypocalcemia, possibly due to end organ unresponsiveness to PTH, frequently coexists with hypomagnesimia, and can be resistant to treatment unless hypomagnesimia is corrected. While hypomagnesimia stimulates PTH secretion, very low serum concentrations can induce a paradoxical block. Our case illustrates the importance of recognizing and correcting underlying hypomagnesimia to stabilize serum calcium levels. The normal PTH level, despite low serum Calcium, suggests hypomagnesimia impairing parathyroid gland function. Due to the acute presentation, and ongoing IV correction, we were unable to measure urinary magnesium excretion. Presentation: 6/1/2024
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