Endocrine Abstracts

Introduction: Hypercalcaemia is a metabolic disorder with multiple aetiologies including granulomatous diseases like sarcoidosis. This is a patient with renal sarcoidosis with fluctuating PTH levels following treatment with steroids, illustrating the interplay between steroid therapy and calcium homeostasis.

Case Presentation: A 61-year-old female with background of CKD presented with AKI secondary to severe hypercalcemia (3.8 mmol/l) with PTH of 4.2 (1.6-6.9 pmol/l) and Vit.D of 55(>50 nmol/l). Phosphate was 2.08mmol/l. After IV fluids and Pamidronate, she was referred to Nephrology and Endocrinology. ACE levels were elevated: 247 (20-70 IU/l). Imaging revealed bilateral axillary and inguinal lymphadenopathy with splenomegaly, but lymph node biopsy excluded lymphoproliferative malignancy. Urinary calcium excretion was elevated (17.44 mmol), with UCCR of 0.12, likely influenced by CKD. USS Neck and SESTAMIBI ruled out parathyroid adenoma. Possibility of renal sarcoidosis considered. As patient was not amenable to renal biopsy, high-dose corticosteroid therapy was initiated following which calcium, ACE levels and renal function normalized. Although the PTH was initially low normal, post glucocorticoids, a fluctuating pattern was seen and showed direct temporal association with dosing adjustments. Whenever the glucocorticoids were increased, the PTH trended up to reach levels as high as 17.2, with low normal calcium, with PTH dropping to normal with down titration of glucocorticoids.

Discussion: Hypercalcaemia in sarcoidosis is primarily driven by extrarenal synthesis of calcitriol by activated macrophages within granulomas, enhancing intestinal calcium absorption. Corticosteroid-induced suppression of calcitriol creates transient functional Vit-D deficiency, lowering calcium. Parathyroids respond physiologically by increasing PTH. This secondary hyperparathyroidism is not pathological but adaptive. This mechanism explains the fluctuations in PTH with steroid treatment.

Conclusion: Corticosteroid-associated suppression of calcitriol can trigger a physiological rise in PTH, leading to secondary hyperparathyroidism. Recognizing this adaptive response is crucial to avoid misdiagnosis of primary parathyroid disease and unnecessary interventions.