Primary Hyperparathyroidism in Celiac Disease: Diagnostic Challenges and Therapeutic Strategies.

Celiac disease (CD) is a primary immune-mediated enteropathy triggered by gluten ingestion in genetically predisposed individuals. Gluten ingestion results in villous atrophy of the small intestine and can lead to impaired absorption of multiple vitamins and nutrients, including vitamin D and calcium. This may result in vitamin D deficiency, a physiologic stimulus for parathyroid hormone (PTH) secretion, subsequently causing secondary hyperparathyroidism. Malabsorption and hyperparathyroidism in CD can contribute to metabolic bone disease (MBD), including osteopenia or osteoporosis. Correction of CD with a gluten-free diet (GFD) does not always reverse MBD. Although malabsorption in CD is a well-recognized cause of secondary hyperparathyroidism, some case reports have also suggested a potential association between CD and primary hyperparathyroidism (PHPT). In this literature review, we present evidence from observational studies, case series, and case reports that suggest a potential association or coexistence of CD and PHPT. Although the exact relationship between CD and PHPT remains unclear, limited evidence suggests that the two conditions may be related or may coexist independently of one another, with GFD treatment potentially unmasking underlying PHPT in patients with CD. One proposed mechanism is that vitamin D deficiency in CD reduces the vitamin D-mediated suppression of parathyroid cell proliferation, potentially contributing to the development of PHPT; however, current evidence remains insufficient to establish a causal relationship. PHPT and CD can contribute to MBD with increased fracture risk and adversely affect quality of life and overall health. Monitoring PTH, vitamin D, and calcium levels is important to identify persistent hyperparathyroidism and unmask underlying PHPT after correction of malabsorption. The literature review highlights a gap in our understanding of the pathogenesis linking these two conditions and underscores the need for future studies to elucidate their potential relationship. Because surgery is the only curative treatment modality for PHPT, patients with persistent hyperparathyroidism despite correction of malabsorption should be evaluated for possible concomitant PHPT, as they may require interdisciplinary management involving gastroenterologists, endocrinologists, and endocrine surgeons.