Recurrent severe hypercalcemia caused by bone marrow sarcoidosis

Recurrent hypercalcemia is a rare clinical condition that often signals underlying disease. Prior research has shown that conditions like sarcoidosis can cause hypercalcemia due to excessive vitamin D metabolism. However, the specific role of bone marrow sarcoidosis remains unclear. No prior work had resolved whether bone marrow involvement alone can lead to severe hypercalcemia. This uncertainty drove the need to investigate cases where organ involvement is absent. The angiotensin-converting enzyme (ACE) elevation is a known marker in sarcoidosis, but its significance in bone marrow-only cases is not well established. The connection between noncaseating granulomas and hypercalcemia is still debated in the literature. This gap motivated further exploration of isolated bone marrow sarcoidosis as a potential cause of hypercalcemia. Understanding the mechanism could help refine diagnostic criteria and treatment approaches.

The aim of this case report is to describe a patient with recurrent severe hypercalcemia and bone marrow sarcoidosis. The specific problem is the lack of awareness about bone marrow sarcoidosis as a standalone cause of hypercalcemia. The motivation is to highlight the diagnostic challenge when organ involvement is absent. The patient's clinical features suggest a need to consider bone marrow sarcoidosis in differential diagnosis. The study seeks to emphasize the role of noncaseating granulomas in calcium dysregulation. The absence of other organ involvement is unusual and requires further attention. The fluctuation of 1,25 dihydroxycholecalciferol levels is a key observation. This case may suggest a broader role for bone marrow sarcoidosis in endocrine disorders.

The study is a single-case analysis using clinical and laboratory data. Bone marrow biopsy was performed to identify granulomas. Serum calcium and parathyroid hormone levels were measured. 1,25 dihydroxycholecalciferol levels were tracked over time. Angiotensin-converting enzyme levels were assessed as a sarcoidosis marker. No imaging or functional tests were described in the abstract. The absence of other organ involvement was confirmed through standard diagnostic procedures. The normalization of calcium and vitamin D levels was monitored to evaluate treatment response.

The patient had multiple noncaseating granulomas in the bone marrow. Serum calcium levels were severely elevated. Parathyroid hormone levels were low, suggesting non-parathyroid hypercalcemia. 1,25 dihydroxycholecalciferol levels were initially high but normalized with calcium levels. Angiotensin-converting enzyme levels were elevated. No other organ involvement was detected. The granulomas were consistent with sarcoidosis pathology. The normalization of calcium and vitamin D levels suggests a reversible process.

The authors suggest that bone marrow sarcoidosis may be a rare cause of hypercalcemia. The absence of other organ involvement is notable in this case. The fluctuation of 1,25 dihydroxycholecalciferol levels supports a metabolic link. The low parathyroid hormone levels indicate a non-parathyroid mechanism. The elevated ACE level is consistent with sarcoidosis diagnosis. This case may suggest that bone marrow sarcoidosis should be considered in differential diagnosis. The normalization of calcium and vitamin D levels implies a treatable condition. The findings may propose a new clinical pattern of sarcoidosis-related hypercalcemia.