Hyponatraemia and hyperpigmentation in primary adrenal insufficiency

Hyponatraemia is a frequently observed electrolyte imbalance, often linked to various pathologies. Prior research has shown that it can arise from conditions such as heart failure, liver disease, or hormonal dysregulation. However, the underlying cause is not always immediately clear. In some cases, it is attributed to the syndrome of inappropriate antidiuretic hormone secretion. This assumption can lead to misdiagnosis if other contributing factors are overlooked. The presence of additional symptoms such as hyperpigmentation and syncope may hint at a different etiology. No prior work had resolved the diagnostic overlap between paraneoplastic syndromes and primary adrenal insufficiency. That uncertainty drove the need for a more detailed endocrine evaluation. This gap motivated the investigation into whether adrenal insufficiency could be the true cause in this patient.

The aim of this case report is to highlight the importance of considering primary adrenal insufficiency in patients presenting with hyponatraemia and unexplained symptoms. The specific problem addressed is the potential misdiagnosis of hyponatraemia as a paraneoplastic syndrome. The motivation stems from the patient's history of cholangiocarcinoma, which initially led to the assumption of a paraneoplastic cause. The presence of hyperpigmentation and syncope raised suspicion for an endocrine disorder. The study aimed to determine whether adrenal insufficiency was the underlying cause. The researchers proposed that a thorough endocrine assessment would clarify the diagnosis. This approach is necessary to avoid inappropriate treatment strategies. The ultimate goal was to provide a correct diagnosis and initiate appropriate therapy.

The researchers conducted a clinical and endocrine assessment of the patient. They performed a physical examination to identify signs of adrenal insufficiency. The synthetic adrenocorticotropin hormone (ACTH) stimulation test was used to evaluate adrenal function. Blood samples were collected to measure ACTH levels. The test results were interpreted according to standard clinical guidelines. The patient's symptoms were monitored before and after treatment. Hydrocortisone and fludrocortisone were administered as replacement therapy. The response to treatment was evaluated through clinical and laboratory parameters.

The ACTH stimulation test showed an inadequate adrenal response, confirming primary adrenal insufficiency. ACTH levels were elevated, consistent with Morbus Addison. The patient's hyponatraemia resolved after initiating corticosteroid replacement. Hyperpigmentation also improved with treatment. Syncope episodes ceased following therapy. Laboratory values normalized within a few weeks. The patient's overall condition improved significantly. These findings suggest that adrenal insufficiency was the true cause of the patient's symptoms.

The authors propose that adrenal insufficiency should be considered in patients with hyponatraemia and unexplained symptoms. The presence of hyperpigmentation and syncope supports this diagnosis. The ACTH stimulation test is a reliable method for confirming adrenal insufficiency. Elevated ACTH levels further support the diagnosis of Morbus Addison. The response to corticosteroid replacement therapy confirms the effectiveness of treatment. This case highlights the importance of a thorough endocrine evaluation. The researchers suggest that early diagnosis can prevent complications. These findings may help guide future diagnostic approaches in similar cases.