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Iatrogenic acute pancreatitis due to hypercalcemia in a child with pseudohypoparathyroidism
Insights
Hypercalcemia, often caused by vitamin D and calcium overtreatment, can lead to acute pancreatitis in children. This rare condition highlights the need to consider high calcium levels as a potential cause of pancreatitis in pediatric cases.
Area of Science:
- Pediatric Endocrinology
- Gastroenterology
Background:
- Pancreatitis in children is uncommon, and its association with hypercalcemia is rare and debated.
- Pseudohypoparathyroidism (PHP) is a condition involving parathormone (PTH) resistance, leading to hypocalcemia that requires calcium and vitamin D treatment.
Purpose of the Study:
- To report a rare case of acute pancreatitis in a child secondary to hypercalcemia.
- To discuss the potential pathogenetic role of hypercalcemia in pediatric pancreatitis.
Main Methods:
- Case report of a 6-year-old boy with pseudohypoparathyroidism.
- Clinical presentation, laboratory findings (amylase, lipase, calcium), and treatment review.
Main Results:
- The patient presented with severe abdominal pain and vomiting, with elevated amylase, lipase, and calcium levels.
- Hypercalcemia, likely due to overtreatment with calcium and vitamin D for pseudohypoparathyroidism, was implicated as the cause of acute pancreatitis.
Conclusions:
- Hypercalcemia, even in the context of treated pseudohypoparathyroidism, should be considered a potential cause of acute pancreatitis in children.
- Further research is needed to elucidate the mechanisms linking hypercalcemia to pancreatitis and to define the role of predisposing factors.
Abstract:
Pancreatitis due to hypercalcemia is very rare in children, and its pathogenetic role is still debated. The following report describes a case of acute pancreatitis secondary to hypercalcemia in a 6-year-old boy with pseudohypoparathyroidism treated with calcium and vitamin D. Pseudohypoparathyroidism is characterized by parathormone (PTH) resistance, high PTH levels and hypocalcemia which need to be corrected with calcium and vitamin D supplementation. The patient was admitted for severe abdominal pain and vomiting associated with high plasma amylase, lipase and calcium levels. Hypercalcemia due to vitamin D and calcium overtreatment was probably responsible for the acute pancreatitis in this case. High serum calcium levels seem to sensitize patients to pancreatitis, even if the mechanism through which it happens is not completely understood. Moreover, the importance of concomitant predisposing factors, either acquired or especially genetic, needs to be further defined. Even though a rare occurance in childhood, hypercalcemia should be considered as a cause of pancreatitis and it should be examined together with the other etiologies that may contribute to the development of this disease.
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