Session: MON 199-237-Disorders of Parathyroid Hormone & Calcium Homeostasis
Poster Board MON-225
Clinical case: A 54-year-old female with an 11-year history of T2DM presented with intractable nausea and vomiting presumed due to exacerbation of diabetic gastroparesis. She frequently visited emergency rooms or urgent care centers due to these symptoms and her clinical course deteriorated requiring frequent hospitalizations. A technetium gastric emptying study confirmed delayed emptying with 98% of gastric contents retained in the stomach two hours post-meal (normal <60%). Hemoglobin A1c was 7.1% on glyburide, metformin, and pioglitazone. A macrolide-based promotility regimen was contraindicated due to QTc interval prolongation, up to 492 milliseconds (<460 for women). Laboratory tests showed hypocalcemia and vitamin D insufficiency, with serum calcium concentration 8.1 mg/dl (8.6-10), ionized calcium (iCa) 4.2 mg/dl (4.6-5.3), 25-OH vitamin D 21 ng/ml (25-80), PTH 22 pg/ml (14-72), and magnesium 1.4 mg/dl (1.6-2.6). She started metoclopramide, gastroparesis diet, calcium and vitamin D supplementation and was discharged home. However, she returned 4 days later with recurrent nausea, vomiting. At the time of readmission, iCa remained low at 4.0 and QTc prolonged at 490. Treatment with calcitriol and calcium normalized hypocalcemia and QTc; then she started azithromycin. Although calcitriol and azithromycin were intended new medications at discharge, she did not fill these prescriptions. Several weeks later at an outpatient visit, her QTc was 472 and iCa 4.6. Gastroparesis symptoms were mildly improved on metoclopramide and gastroparesis diet, but she continued to have almost daily nausea. Therefore, calcitriol 0.25 mcg daily was re-prescribed. Three months later iCa and QTc normalized to 4.9 and 436, respectively. She took oral azithromycin suspension 200 mg/5ml, 5 ml daily, but developed diarrhea, and this resolved upon dose decrease to 1 ml daily. Gastroparesis symptoms greatly improved on azithromycin and frequency of hospitalizations declined. Two years later, she remains on calcitriol without hypocalcemia or QTc prolongation.
Conclusion: In this patient, hypocalcemia and prolonged QTc normalized on calcitriol, thereby permitting initiation of macrolide therapy, resulting in symptom improvement of diabetic gastroparesis.
Nothing to Disclose: SJH, MMM, SLR, SWI
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