In some patients, significant calcium deficiency can culminate in hypocalcemia that presents with neuromuscular irritability, including perioral numbness, carpopedal spasm, frank tetany, and potentially generalized seizures or life‑threatening arrhythmias. Clinical data in children with hypocalcemic seizures suggest that, once acute stabilization is achieved, carefully dosed oral calcium can be as effective as continued intravenous calcium in maintaining serum calcium over the first 24–48 hours, with similar calcium levels and seizure‑recurrence rates reported between groups. The key clinical implication is that prompt recognition and correction of hypocalcemia, followed by an appropriate transition to ongoing oral calcium (and vitamin D when indicated), can help prevent recurrent tetany, seizures, and cardiac instability while longer‑term etiologies of calcium deficiency are addressed. This medication is commonly used for Stomach Acid.
Han, P., Trinidad, B. J., & Shi, J. (2015). Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox. ASN Neuro, 7(2). Uday S, Högler W. Nutritional rickets & osteomalacia: A practical approach to management. Indian J Med Res. 2020 Oct;152(4):356-367. Ashwin Reddy S. Ventricular Arrhythmia Precipitated by Severe Hypocalcaemia Secondary to Primary Hypoparathyroidism. Case Rep Cardiol. 2019 Apr 7;2019:4851073. Dhir H, Kumar D, Shah D, Batra P, Ahmed RS, Gupta P. Efficacy of Oral vs. Intravenous Calcium Supplementation for Continuation Therapy in Hypocalcemic Seizures: A Randomized, Controlled Trial. Indian J Pediatr. 2023 May;90(5):433-437.
Some side effects may be linked to nutrient depletion caused by this medication.
Long-term use of PPIs might raise the risk of calcium deficiency and weaken bones. A potential mechanism for this is chronic hypergastrinemia, a condition where the stomach produces excess gastrin due to PPI use. This can lead to parathyroid hyperplasia, where the parathyroid glands overproduce a hormone that pulls calcium from bones. Additionally, PPIs significantly reduce stomach acid production, which can hinder calcium absorption from food in the intestines. Individuals taking PPIs, especially individuals at higher risk of bone issues or those on long-term PPI therapy, should consider calcium supplementation to help protect against deficiency.
Research suggests that long-term use of medications that reduce stomach acid, like H2 blockers and PPIs, may be linked to vitamin B12 deficiency. Stomach acid plays a role in releasing vitamin B12 from food, and reduced acid levels caused by these medications could hinder proper B12 absorption. Some studies find an increased risk of B12 deficiency, particularly in older adults or those using these medications for extended periods. Individuals taking H2 blockers or PPIs long-term should consider vitamin B12 supplementation.
There is evidence that proton pump inhibitors (PPIs) might decrease vitamin C levels in the body. A study showed that even a short course of omeprazole, a common PPI, reduced vitamin C levels in healthy volunteers, regardless of their dietary intake. This suggests that PPIs may reduce the bioavailability of vitamin C, meaning the body has a harder time absorbing and using it. Vitamin C plays a crucial role in immune function and antioxidant defenses and therefore individuals using PPI therapy should consider supplementation with vitamin C to protect against a deficiency.
Studies find that proton pump inhibitors (PPIs) may increase your risk of magnesium deficiency. A large study involving over 100,000 participants found a significant association between PPI use and lower magnesium levels (hypomagnesemia). PPIs work by reducing stomach acid production, which can also play a role in magnesium absorption. Individuals taking PPIs, particularly long-term use, should consider magnesium supplementation to help protect against deficiency.