PSAT227 Clinically Suspected Calcium Malabsorption and Secondary Hyperparathyroidism Due to Chronic Proton Pump Inhibitor Use in a Child

BACKGROUND: Proton Pump Inhibitors (PPI) are commonly in clinical practice as agents to treat multiple acid-related gastrointestinal disorders. Studies have shown that long-term PPI-based therapy may be associated with decreased bone mineral density that could be related to hypochlorhydria-associated malabsorption of calcium and gastrin-induced parathyroid hyperplasia. CLINICAL CASE: We report the case of a 6-year-old female born premature at 25 weeks, with global developmental delay, chronic lung disease, G-tube and tracheostomy dependent that was admitted for tracheal reconstruction surgery. She was on a PPI (lansoprazole) since the age of 4 years. She was found to have mild hypocalcemia 8.5 mg/dL (Ref 8.8-10.4 mg/dL), mild hypomagnesemia 1.5 mg/dL (Ref 1.6-2.6 mg/dL), and hyperparathyroidism 117 pg/dL (Ref 14-72 pg/dL). Her vitamin D 25 hydroxy level was 28 ng/dL (Ref<19 ng/dL) and vitamin D 1,25 dihydroxy 44.8 pg/dL (Ref 19.9-79.3 pg/dL). In addition, her bone x-ray showed evidence of demineralization, with nofracture. PTH (308.6, 429.4, 253.1pg/mL) continue to rise over the next 2 months despite normal Ca/vitamin D level. We suspected the etiology of hypocalcemia and hyperPTH was related to chronic PPI use. This was also associated with markedly elevated, hypergastrinemia of 574 pg/dL (Ref <100 pg/dL), PTHrp was not detectable. Due to high risk of aspiration, her pulmonologist noted that her PPI needed to be continued at the time. She was fed via G-tube and took Pediasure 1.4 L daily which contained elemental calcium of 32 mg/kg/day. Her vitamin D intake was 1000 units daily. However, we suspected that she had calcium malabosoprtion in light of hypochlorhydria and hypergastrinemia, both leading to hyperPTH. Subsequently, she was started on oral calcium citrate 1200mg daily as the absorption of calcium citrate is non PH dependent. One month later, her PPI was discontinued as well. She responded well to therapy and calcium normalized to 9.7 mg/dl (Ref 8.8-10.4 mg/dl) after 3 months, Gastrin 85 pg/dL (Ref<100 pg/dL) and PTH 90.1 pg/dL (Ref 14-72 pg/dL). CONCLUSION: Bone health status of patients on long-term PPI treatment should be addressed with particular attention to calcium/vitamin D intake. The possible mechanisms of hyperPTH and bone demineralization induced by PPIs include calcium malabsorption. In addition, hypochlohydria induced hypergastrinemia can also exacerbate hyperPTH by causing parathyroid hyperplasia. Bone health and mineral status of patients on long-term PPIs should be regularly monitored. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.