Autoimmune small-vessel cerebral vasculitis is an uncommon but potentially reversible cause of rapidly progressive cognitive and neurological decline. Its presentation can be heterogeneous, often mimicking vascular, infectious or degenerative processes. Hyponatraemia due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) may occur as a secondary manifestation of hypothalamic involvement or systemic inflammation, compounding neurological dysfunction and complicating management. We describe a middle-aged woman who developed acute cognitive deterioration, emotional lability and gait disturbance secondary to newly diagnosed autoimmune small-vessel vasculitis with serological evidence of systemic autoimmunity, on a background of prior polyautoimmune diseases (type 1 diabetes mellitus and hypothyroidism). Despite resolution of inflammatory activity following high-dose corticosteroid therapy, profound hyponatraemia (serum sodium 110-120 mmol/L) persisted despite conventional measures (fluid restriction, salt supplementation and urea) and despite improvement in inflammatory activity following immunotherapy, consistent with refractory SIADH. Initiation of tolvaptan, a selective vasopressin V2-receptor antagonist, successfully resulted in gradual and sustained correction of serum sodium levels without over-rapid correction, osmotic demyelination or hepatic toxicity. Alongside longer-term immunosuppression with steroids and cyclophosphamide, this led to stabilisation of neurological and cognitive deficits. This case highlights the complexities of managing patients with cognitive and neuropsychiatric sequelae from autoimmune small-vessel central nervous system (CNS) vasculitis and the importance of evaluation and treatment of potential organic causes of cognitive impairment. To our knowledge, there are no prior published reports describing refractory SIADH in autoimmune small-vessel CNS vasculitis requiring V2-receptor antagonism. Awareness of this disease association and this effective therapeutic option allows earlier recognition and improved patient outcomes in similar cases.

A man in his early 60 s developed persistent hyponatremia following lumbar spine surgery complicated by traumatic brain injury with subarachnoid hemorrhage. Initial evaluation demonstrated hypotonic hyponatremia with inappropriately concentrated urine, consistent with the syndrome of inappropriate antidiuretic hormone secretio. Standard therapy including hypertonic saline and oral sodium supplementation resulted in only transient improvement. Given a history of secondary adrenal insufficiency due to long-term topical corticosteroid use, adrenal function was reassessed. An adrenocorticotropic hormone stimulation test confirmed secondary adrenal insufficiency. Initiation of hydrocortisone therapy led to sustained normalization of serum sodium. This case highlights the diagnostic difficulty of post-TBI hyponatremia and underscores the importance of considering adrenal insufficiency, even years after apparent recovery from steroid-induced hypothalamic-pituitary-adrenal axis suppression.

Paraneoplastic endocrine syndromes (PESs) are hormonal disturbances associated with malignancies that result from tumor-related production of hormone-like substances, immune-mediated mechanisms, or dysregulated signaling pathways. While they are well recognized in lung and neuroendocrine cancers, their relevance in gastrointestinal tumors remains less clearly defined. This narrative review synthesizes current knowledge on paraneoplastic endocrine manifestations in gastrointestinal malignancies, based on a structured search of the literature in major databases, including PubMed, Scopus, and Web of Science. The analysis focuses on clinically relevant syndromes such as hypercalcemia, Cushing-like manifestations, disorders of water balance, hypoglycemia, and acromegaly, with emphasis on underlying mechanisms, associated tumor types, diagnostic approaches, and therapeutic considerations. Available evidence indicates that gastrointestinal tumors can produce a range of biologically active substances, leading to diverse endocrine manifestations that may precede tumor detection and influence disease course. Among these, hypercalcemia and Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) are among the most frequently reported, while other syndromes, such as ectopic Cushing syndrome or tumor-related hypoglycemia, are less common but often associated with more severe clinical outcomes. Recognition of these manifestations has direct clinical implications, as they may support earlier diagnosis, contribute to prognostic assessment, and guide therapeutic management. Improved awareness and a multidisciplinary approach remain essential for optimizing outcomes in patients with gastrointestinal malignancies.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and central fever are rare and underrecognized manifestations of multiple system atrophy (MSA). Here, we report a 66-year-old woman who presented with a progressively evolving combination of parkinsonian features and pronounced autonomic dysfunction, fulfilling the diagnostic criteria for clinically probable MSA. Notably, she also developed two uncommon comorbidities: euvolemic hypotonic hyponatremia fulfilling the diagnostic criteria for SIADH, alongside episodic fever refractory to antipyretics in the absence of infection, but responsive to environmental cooling, consistent with central fever. These uncommon comorbidities underscore the involvement of hypothalamic and neuroendocrine regulatory pathways in MSA. This case broadens the well-recognized non-motor clinical spectrum of MSA and emphasizes the importance of considering central mechanisms when evaluating unexplained hyponatremia or fever in MSA. Awareness of these atypical manifestations may facilitate early recognition, guide targeted homeostatic management, and ultimately improve the quality of clinical care in MSA.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a disorder in which an excessive amount of antidiuretic hormone (ADH) is released, leading to water retention and subsequent hyponatremia. Delayed hyponatremia, typically beginning on postoperative day (POD) 4, is a well-recognized complication following transsphenoidal resection of pituitary tumors and is thought to result from excess release of stored ADH due to surgical trauma. In this rare case of early symptomatic hyponatremia secondary to SIADH, a 61-year-old postmenopausal woman with no significant past medical history developed symptomatic hyponatremia on POD 1 after elective transsphenoidal resection of a nonfunctioning pituitary neuroendocrine tumor. Her serum sodium reached a nadir of 126 mmol/L on POD 2. Urine osmolality was 961 mOsm/kg on POD 1, consistent with SIADH. She was treated with fluid restriction, intravenous 3% hypertonic saline, and salt tablets, with improvement in serum sodium prior to discharge on POD 4 on fluid restriction and salt tablets. This case highlights the importance of early clinical vigilance for hyponatremia following pituitary resection, as symptomatic hyponatremia can rarely occur in the early postoperative period.

The neurohypophysis (pars posterior) is the posterior lobe of the pituitary gland, located at the base of the brain. The embryological origin of this structure is the neuroectodermal infundibulum. The neurohypophysis comprises 2 primary regions, the pars nervosa and the infundibular stalk. The pars intermedia and median eminence are sometimes included. The neurohypophysis secretes the 2 peptide hormones, oxytocin and vasopressin. Oxytocin stimulates uterine contractions and milk ejection. Vasopressin, also known as antidiuretic hormone (ADH), prevents diuresis. These hormones are synthesized by magnocellular neurosecretory cells of the hypothalamus, specifically within the paraventricular and supraoptic nuclei. Axons from these neurons project to the neurohypophysis, transporting the hormones for storage and subsequent release into the neurohypophyseal capillaries, which deliver these neuropeptides to systemic circulation. Dysfunction of the posterior pituitary disrupts hormonal homeostasis, causing arginine vasopressin deficiency (AVP-D) and the syndrome of inappropriate antidiuresis (SIAD). Disorders resulting from oxytocin deficiency are rare and primarily associated with pregnancy, lactation difficulties, osteopenia, and hyperphagia. The posterior pituitary contains pituicytes. In the pars nervosa, these cells function as glial cells, providing structural support and modulating hormone release.

The clinical manifestations of lung cancer are diverse. Presentation initially as the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) is relatively uncommon. This article reports the diagnosis and treatment process of a 76-year-old male patient with hyponatremia, ultimately diagnosed with SIADH attributed to small cell lung cancer (SCLC). The patient presented with fatigue and significant hyponatremia. Comprehensive investigation excluded adrenal, thyroid, and other functional abnormalities. Combined with features including high urinary sodium, euvolemic status, and normal renal function, the findings were consistent with a diagnosis of SIADH. Subsequent imaging and pathological examinations revealed the etiology to be SCLC. Management included fluid restriction, sodium supplementation, and the use of tolvaptan. Subsequent chemotherapy and radiotherapy for the SCLC led to the gradual normalization of serum sodium. This article reviews the literature in conjunction with this case, summarizing the diagnostic approach to hyponatremia, as well as the diagnostic workup, pathophysiological mechanisms, and treatment strategies for SIADH, aiming to enhance the early recognition and comprehensive management of this condition.

The pars nervosa is a neuroendocrine structure that, along with the anterior lobe, intermediate lobe, and infundibular stalk, makes up the pituitary gland. This structure lies within the sella turcica, a saddle-shaped indentation in the sphenoid bone that lies posterior to the nasopharynx. The pars nervosa is responsible for the secretion of the neurohypophysial hormones oxytocin and arginine vasopressin into the systemic circulation. Because these hormones play important roles in the regulation of blood pressure and osmolarity as well as parturition and lactation, their regulated secretion is typically considered the primary physiologic function of the pars nervosa.

A boy aged 5 years and 2 months with a history of acute myeloid leukemia of more than 10 months was admitted. Twenty days after admission, he underwent an HLA 8/10-matched unrelated umbilical cord blood stem cell transplantation. On day 6 post-transplant, high fever and a generalized erythematous papular rash occurred, with elevations of liver enzymes and interleukin-6; pre-engraftment syndrome was diagnosed and symptoms improved after symptomatic treatment. On day 22 post-transplant, refractory hyponatremia occurred. After drug effects, infection, central nervous system lesions, other organ dysfunction, and renal salt wasting were excluded, syndrome of inappropriate antidiuretic hormone secretion (SIADH) was diagnosed. Fluid restriction, 3% sodium chloride infusion, and oral salt capsules were administered, and SIADH resolved completely as the pre-engraftment syndrome resolved. One pediatric case of SIADH after hematopoietic stem cell transplantation is reported, and published cases are summarized to inform early diagnosis and treatment.