Multifactorial Hyponatremia in Seronegative Myasthenia Gravis Without Thymoma

Introduction: Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by fluctuating muscle weakness. Particularly some seronegative variants of MG can present with subtle, bulbar-predominant symptoms that complicate diagnosis. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is a frequent cause of euvolemic hyponatremia, typically secondary to a neurologic or pulmonary disease, or a paraneoplastic syndrome such as a thymoma. We report a rare case of multifactorial hyponatremia with overlapping features of SIADH, increased total free water, and highly-suggestive seronegative MG, without an identifiable thymoma. Case Description: A 56-year-old male with CKD 3A, type 2 diabetes, HTN, and hypothyroidism presented with nausea, vomiting, generalized weakness, and fatigue. Initial labs were significant for severe hyponatremia (115 mmol/L) and elevated creatinine (1.86 mg/dL). Vitals were stable. Hyponatremia worsened (114 mmol/L) after 1L IV normal saline, raising concern for SIADH. Fluid restriction, salt tablets, and diuretics were initiated, which caused mild improvement of sodium. However, it worsened kidney function (2.56 mg/dL), suggesting he may have been hypovolemic. Over the next 3 days, the patient developed progressive bulbar symptoms—difficulty managing secretions and dysphonia. Imaging (CT of head, thorax, abdomen/pelvis) was unremarkable for an obvious paraneoplastic source, including thymoma. MG antibodies returned negative. IVIG, mestinon, and steroids were initiated for suspected seronegative MG, improving bulbar symptoms. Sodium improved with tolvaptan and enteral nutrition via tube feeds. Discussion: This case highlights a multifactorial etiology of hyponatremia—combining low solute/excess free water intake and likely SIADH triggered by autoimmune inflammation. Though SIADH in MG is commonly associated with thymoma, no malignancy was found, which is more unique in the literature. The patient’s liquid-heavy diet, due to bulbar-predominant symptoms, more likely contributed to hyponatremia by limiting solute intake. However, recent studies have shown that proinflammatory cytokines, such as IL-1β and IL-6, may also play a role in stimulating ADH secretion. This case highlights the importance of a comprehensive approach, considering both the primary autoimmune condition and secondary complication of hyponatremia.