Introduction: Disseminated histoplasmosis is a rare but important cause of adrenal insufficiency (AI), particularly in tuberculosis (TB)-endemic regions, where it may mimic granulomatous diseases. Adrenal involvement occurs in up to 80% of disseminated cases, although overt AI is less common. Reported cases described bilateral adrenal masses mimicking malignancy or TB, even in immunocompetent individuals. Addisonian crisis may be the initial manifestation, especially when the diagnosis is delayed. In TB-endemic settings, fungal infections are often overlooked, leading to delayed diagnosis and inappropriate therapy. Case: We reported a case of a 68-year-old male with underlying diabetes mellitus who presented with fever, cough, dysphagia, and weight loss for 1 month. He was empirically treated as smear-negative disseminated TB. On day 2 of therapy, he developed hypotension (80/50 mmHg), hypoglycemia (3.9 mmol/L), hyponatremia (Na 129 mmol/L), and hyperkalemia (K 5.1 mmol/L), suggestive of adrenal crisis, and was started on intravenous hydrocortisone. Serum cortisol prior to treatment was 61 nmol/L. Computed tomography (CT) imaging revealed bilateral lipid-poor adrenal lesions (right: 3.6 × 2.2 × 4.9 cm, Hounsfield Unit (HU) 36 and absolute washout 33%; left: 3.5 × 2.4 × 5.4 cm; HU 35 and absolute washout 17%), raising suspicion of infectious or malignant etiologies. Endoscopic ultrasound-guided biopsy demonstrated necrotizing granulomatous inflammation with budding fungal yeasts on Pituitary Apoplexy Score and GMS staining, consistent with Histoplasma capsulatum. TB and malignancy were excluded. He received amphotericin B for 14 days, followed by oral itraconazole for 1 year, and oral hydrocortisone replacement. At 1-year follow-up, adrenal lesions remained stable on CT images, and he continued to require hydrocortisone replacement. Conclusion This case highlights the importance of considering disseminated histoplasmosis as a differential diagnosis of bilateral adrenal masses with AI, especially with poor response to anti-TB therapy. Early tissue diagnosis is essential, as imaging findings are non-specific. Prompt recognition is critical to prevent life-threatening adrenal crisis and improve clinical outcomes.
Histoplasmosis ; Tuberculosis

Introduction: Hypocalcemia in patients with advanced malignancy is usually attributed to bone metastases, vitamin D deficiency, renal impairment, or antiresorptive therapy. Paclitaxel, a taxane-based chemotherapy agent widely used for breast cancer, is not commonly associated with calcium disturbances. Proposed mechanism includes renal tubular dysfunction, renal salt wasting, and disruptions in bone metabolism. In patients with underlying disorders of calcium homeostasis such as hypoparathyroidism, taxanebased chemotherapy such as Docetaxel and Paclitaxel may exacerbate calcium imbalance. We reported a case of recurrent hypocalcemia associated with paclitaxel therapy in a patient with metastatic breast cancer. Case: A 42-year-old female with metastatic breast cancer, involving the liver and bones, had previously undergone neoadjuvant chemotherapy, mastectomy, and adjuvant radiotherapy. Following the disease progression, she was commenced on weekly intravenous paclitaxel at a 20% dose reduction due to prior complications and underlying metabolic risk. She had a history of post-thyroidectomy hypoparathyroidism and had previously been intolerant to docetaxel during the neoadjuvant chemotherapy, which was complicated by hypocalcemia, likely secondary to renal salt wasting. During paclitaxel treatment, she developed recurrent symptomatic hypocalcemia, requiring multiple hospital admissions and repeated intravenous calcium gluconate infusions despite ongoing oral calcium and calcitriol supplementation, which were temporarily increased during the chemotherapy. These episodes occurred intermittently in temporal association with paclitaxel administration, with other causes of hypocalcemia were considered less likely. Conclusion Hypocalcemia associated with paclitaxel is rarely described in literature. This case highlights the importance of monitoring calcium level in patients receiving paclitaxel, particularly in those with pre-existing hypoparathyroidism.
Hypocalcemia ; Hypoparathyroidism ; Breast Diseases ; Paclitaxel

Introduction: Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant syndrome caused by mutations in the tumor suppressor gene MENIN, classically characterized by endocrine tumors of the parathyroid glands, pancreas, and pituitary. Beyond tumorigenesis, emerging evidence suggests a role for MENIN in immune regulation, with deficiency linked to CD4⁺ and CD8⁺ lymphocyte dysfunction and predisposition to autoimmunity. While autoimmune conditions such as thyroiditis and pernicious anemia have been described in MEN1, an association with autoimmune hemolytic anemia (AIHA) has not been previously reported. We describe a rare case of MEN1 associated with warm AIHA, highlighting a potential link between endocrine tumorigenesis and immune dysregulation. Case: A 56-year-old female presented with a 4-month history of lethargy, anorexia, weight loss, and painless jaundice. She is para 6 + 1, with no history of anemia in pregnancy, prior blood transfusions, or family history of hematological disorders. Examination revealed mild pallor, jaundice, and hepatomegaly without splenomegaly. She had a prior diagnosis of MEN1, with two hallmark features: primary hyperparathyroidism and a pancreatic neuroendocrine tumor. She underwent pancreatic enucleation, hemithyroidectomy, and hemiparathyroidectomy; histopathology demonstrated a benign thyroid nodule and parathyroid hyperplasia. Whole exome sequencing identified no pathogenic MEN1 mutation but revealed a c.1621A>G variant, classified as a non-deleterious polymorphism. Variants in TP53 and BRCA1 were also detected without phenotypic expression. Surveillance colonoscopy and mammography were unremarkable. Laboratory findings were consistent with warm AIHA, including elevated lactate dehydrogenase, indirect hyperbilirubinemia, low haptoglobin, reticulocytosis, and a positive direct Coombs test (immunoglobulin G). Peripheral blood film was nonspecific. She responded well to a tapering course of prednisolone. Conclusion This case highlights a possible association between MEN1 and autoimmune hemolysis. The presence of the MEN1 c.1621A>G variant, alongside TP53 and BRCA1 variants, raises the possibility of modifier effects influencing immune dysregulation. Further studies are needed to clarify this relationship.

Introduction: Hypothyroidism is the most common outcome following radioiodine (RAI) therapy for Graves’ disease, affecting up to 80% of patients, usually within 6 months. While symptoms are often nonspecific, musculoskeletal complaints may be the predominant or sole manifestation. Hypothyroid myopathy occurs in 30–80% of patients, typically causing myalgias, cramps, fatigue, and slowly progressive, symmetric proximal weakness with delayed reflex relaxation. We report an atypical case with subacute and evolving weakness after levothyroxine initiation. Case: A 43-year-old female with Graves’ disease underwent RAI therapy (25 mCi) and developed hypothyroidism 7 weeks later. She was started on levothyroxine 50 mcg daily. Two weeks into treatment, she presented with progressive proximal lower limb weakness (power 4/5), while distal strength and reflexes remained intact. Labs revealed elevated creatine kinase (259 U/L), hypokalemia (3.3 mmol/L), creatinine (57 µmol/L), and severe hypothyroidism (thyroid-stimulating hormone [TSH] 52.88 mIU/L, free thyroxine 4 [FT4] 7.79 pmol/L). Levothyroxine was increased to 100 mcg daily. Two weeks later, she developed proximal upper limb weakness (power 4/5), while lower limb strength had normalized. Nerve conduction studies and electromyography were unremarkable. Labs showed creatine kinase (244 U/L) and creatinine (58 µmol/L). As she remained hypothyroid (TSH 20.85 mIU/L, FT4 11.61 pmol/L), levothyroxine 100 mcg daily was continued. Her symptoms gradually improved alongside biochemical recovery (TSH 8.83 mIU/L, FT4 15.90 pmol/L) after 4 weeks, consistent with hypothyroid myopathy. Conclusion This case highlights an atypical subacute presentation of hypothyroid myopathy following RAI, with evolving weakness and transient worsening after starting thyroid hormone therapy. Although other serious causes should be excluded, clinicians must maintain a high index of suspicion to avoid unnecessary investigations and ensure timely optimization of thyroid hormone therapy, as clinical improvement parallels biochemical recovery.
Iodine Radioisotopes ; Muscular Diseases

Introduction: Thyroid storm is a life-threatening endocrine emergency with a mortality rate of 8–25% despite optimal therapy. Some patients exhibit a refractory phenotype characterized by rapid clinical deterioration and failure of conventional treatment, necessitating early escalation. Therapeutic plasmapheresis and lithium represent adjunctive therapies targeting different aspects of thyroid hormone physiology, yet their combined use remains underexplored. Case: A 55-year-old male with Graves’ disease, non-adherent to treatment since 2020, presented with fever, palpitations, and dyspnea for 2 days. He recently started on carbimazole 30 mg daily and propranolol 1 week prior. On examination, blood pressure was 158/74 mmHg, heart rate 180 bpm, Glasgow Coma Scale 15/15 with bibasal crepitations. Electrocardiogram showed atrial fibrillation at 168 bpm. His Burch-Wartofsky score was 95, consistent with thyroid storm. Standard therapy with propylthiouracil 250 mg QID, Lugol’s iodine, intravenous hydrocortisone 100 mg TDS, and carvedilol was commenced. However, after 3 days of treatment, he developed acute confusion and persistent fast atrial fibrillation requiring cardioversion. Liver function remained normal. Plasmapheresis was initiated on day 4 for six sessions. Propylthiouracil was switched to methimazole due to a declining white cell count from (5.5– 3.2 ×10⁹/L). Lithium 300 mg BD was added on day 13 due to inadequate free thyroxine 4 (FT4) reduction. After 1 week of combined therapy, FT4 decreased from 70 to 35 pmol/L. Conclusion Early recognition of refractory disease and timely escalation are critical as refractory thyroid storm carries high mortality, especially with cardiovascular and neurological involvement. When conventional therapy fails, plasmapheresis facilitates rapid clearance of circulating thyroid hormones and inflammatory mediators, while lithium inhibits thyroid hormone release, providing an alternative mechanism when thionamides alone are insufficient. Their combined use offers a synergistic approach and targets both circulating and intrathyroidal hormone pools, suggesting that early dual-modality intervention is essential to overcome therapeutic resistance and improve overall outcomes in refractory disease.
Lithium ; Thyroid Crisis ; Plasmapheresis