Case Study: Calcitriol Supplementation in the Management of Cushing’s Syndrome
Patient Profile: Ms. A, a 45-year-old woman, presented to our endocrinology clinic with a history of uncontrolled hypertension, central obesity, and unexplained weight gain over the past two years. She reported experiencing fatigue, muscle weakness, and easy bruising, which had progressively worsened despite lifestyle modifications and antihypertensive medications. Physical examination revealed classic features of Cushing’s syndrome, including moon facies, buffalo hump, and purple striae on her abdomen.
Diagnostic Workup: Ms. A’s initial laboratory evaluation confirmed the presence of hypercortisolism, with elevated 24-hour urinary free cortisol levels and lack of cortisol suppression on low-dose dexamethasone suppression test. Further investigations, including plasma adrenocorticotropic hormone (ACTH) levels and adrenal imaging, were consistent with a diagnosis of ACTH-independent Cushing’s syndrome secondary to an adrenal adenoma.
Treatment Approach: Given the functional nature of Ms. A’s adrenal adenoma and the risks associated with surgery, including adrenal insufficiency, she was deemed a candidate for medical management of Cushing’s syndrome. In addition to lifestyle modifications and antihypertensive therapy, we initiated pharmacological intervention with a cortisol-lowering agent and adjunctive therapy with calcitriol supplementation.
Calcitriol Supplementation: The rationale for incorporating calcitriol supplementation stemmed from its potential to modulate adrenal function and mitigate some of the metabolic and skeletal complications associated with Cushing’s syndrome. We initiated calcitriol therapy at a conservative dosage of 0.25 mcg daily, with close monitoring of serum calcium levels to prevent hypercalcemia.
Outcome and Follow-Up: Over the course of six months, Ms. A demonstrated significant improvements in her clinical symptoms and biochemical markers of Cushing’s syndrome. Her blood pressure normalized, and she reported a gradual reduction in abdominal girth and improvement in muscle strength. Laboratory parameters, including urinary free cortisol levels and glycemic control, showed notable improvements, reflecting the efficacy of cortisol-lowering therapy and calcitriol supplementation.
Moreover, serial bone mineral density (BMD) measurements revealed stabilization of bone loss, suggesting a potential protective effect of calcitriol on skeletal health in the setting of Cushing’s syndrome. Ms. A reported improved quality of life and expressed satisfaction with her treatment regimen, highlighting the importance of a multidisciplinary approach in managing complex endocrine disorders.
Discussion: This case underscores the utility of calcitriol supplementation as an adjunctive therapy in the management of Cushing’s syndrome. By targeting dysregulated adrenal function and addressing metabolic and skeletal complications, calcitriol supplementation complements traditional treatment modalities and enhances overall therapeutic efficacy.
However, it is essential to recognize the need for individualized treatment strategies and close monitoring of patients receiving calcitriol supplementation, particularly in the context of potential adverse effects such as hypercalcemia. Further research is warranted to elucidate the optimal dosage, duration, and safety profile of calcitriol supplementation in Cushing’s syndrome and refine its role in clinical practice.
Conclusion: Ms. A’s case highlights the transformative impact of a comprehensive treatment approach, integrating pharmacological intervention with calcitriol supplementation in the management of Cushing’s syndrome. By addressing the underlying hormonal imbalance and its systemic manifestations, clinicians can strive to optimize patient outcomes and improve quality of life for individuals affected by this challenging endocrine disorder.