Introduction: Primary hyperparathyroidism (PHPT) is frequently asymptomatic or detected incidentally; however, delayed diagnosis may lead to severe skeletal complications. Early recognition is essential, as timely identification and management of parathyroid disease can prevent significant morbidity, although diagnosis may be challenging when clinical and imaging findings are inconclusive. Case: A 46-year-old female with severe bilateral hearing impairment presented to the orthopedic clinic with 3 years’ history of bilateral knee pain and was found to have a right intertrochanteric femur fracture following minimal trauma. She was referred for evaluation of suspected secondary osteoporosis. She has had intermittent constipation and long-standing oligomenorrhea since menarche. There was no history of childhood fractures or use of medications affecting bone metabolism. Examination revealed bilateral knee bowing. Initial evaluation considered metabolic bone disease, including Paget’s disease; however, skeletal survey showed no features suggestive of Paget’s disease or multiple myeloma. Biochemical investigations demonstrated persistent hypercalcemia (2.65–3.1 mmol/L) with inappropriately elevated intact parathyroid hormone (peak 7.62 pmol/L), consistent with PHPT. Serum phosphate was low-normal. Concomitant vitamin D deficiency (25-OH vitamin D 34.46 nmol/L) improved following replacement. Bone mineral density confirmed severe osteoporosis (lumbar spine T-score −5, z-score -4.1); (forearm −6.7, z-score -6.1) reflecting prolonged untreated disease. Neck ultrasound demonstrated a mixed solid-cystic lesion posterior to the right thyroid lobe, suggestive of a parathyroid adenoma. The TC-99 m Sestamibi scan showed no definite focal uptake. However, subsequent SPECT-CT revealed focal tracer uptake at the posterior right thyroid gland, consistent with a hyperfunctioning parathyroid gland. Parathyroidectomy was done. Postoperatively, the calcium level normalized. Conclusion Severe osteoporosis and fragility fracture occur, reflecting prolonged exposure to excess parathyroid hormone and significant skeletal morbidity. Early biochemical evaluation in unexplained severe osteoporosis is essential, as timely diagnosis and definitive management of parathyroid disease are critical to halt ongoing bone loss and prevent irreversible complications.
Hyperparathyroidism, Primary ; Osteoporosis

Introduction: Pituitary apoplexy is an acute endocrine emergency, as early recognition may influence the outcomes, often presenting with sudden headache, visual disturbances, ocular palsies, vomiting, or altered consciousness. Given that urgent surgical decompression is a common management, emerging evidence supports corticosteroid therapy in our patient with significant neuro-ophthalmic deficits. Case: A 65-year-old male with hypertension, dyslipidemia, type 2 diabetes mellitus, chronic kidney disease stage III, and ischemic heart disease presented with a 4-day history of fever, vomiting, bifrontal headache, and generalized abdominal pain. Initially, he was treated for presumed intraabdominal sepsis. On day 3 of admission, he developed acute right-sided complete ptosis with ophthalmoplegia involving cranial nerves III, IV, and VI. Prior to that, he had also reduced morning erections for 6 months before presentation. Biochemical evaluation revealed markedly reduced total testosterone (0.33 nmol/L) with inappropriately low–normal gonadotropins (luteinizing hormone 1.5 IU/L, follicle-stimulating hormone 2.3 IU/L), in keeping with secondary hypogonadism. Adrenocorticotropic hormone was suppressed, indicating secondary adrenal insufficiency. Thyroid function was preserved. Overall findings suggested partial hypopituitarism. Magnetic resonance imaging confirmed a cystic pituitary lesion measuring 1.4 × 2.6 × 1.8 cm with cavernous sinus involvement and features of pituitary apoplexy. His Pituitary Apoplexy Score was 4. He was offered surgical intervention but was not keen. He was treated with intravenous hydrocortisone, with rapid clinical improvement, including near-complete resolution of right eye ptosis and restoration of extraocular movements within 3 days, and was able to recover without surgery. The hydrocortisone was gradually tapered, and the patient was discharged well with Endocrine follow-up. Conclusion Timely corticosteroid therapy alone can result in rapid, near-complete neurological recovery in pituitary apoplexy, even with multiple cranial nerves involvement. In carefully selected patients without visual field compromise, conservative management may safely obviate the need for urgent surgical intervention, emphasizing the importance of early recognition and individualized treatment strategies.
Hydrocortisone ; Pituitary Apoplexy