Thyroid storm is an uncommon but life-threatening manifestation of hyperthyroidism which, unless appropriately treated by combined therapy, causes 30-60% of deaths in hospitalized patients. Mental deterioration leading to apathy and eventually coma is a rare clinical presentation of this pathology, frequently observed in the elderly. We present the case of a 77-year-old hypertensive woman who was hospitalized for fast onset of coma, probably due to the unusual combination of a hypernatremic hyperosmolar state and an unexpected thyroid storm (TS). Although not definitely ascertained, the possible etiology was the hyperthyroid phase of chronic autoimmune thyreopathy (Hashitoxicosis). Notably, the significant adjunctive role of thyroid hyperfunction in the pathogenesis of coma was confirmed by the fact that, although metabolic abnormalities were overcome, complete and satisfactory recovery of the patient's mental and physical condition occurred only with normalization of thyroid hormones by antithyroid treatment. Our case highlights the importance of properly evaluating thyroid function in elderly patients who show a sudden progressive impairment in their mental condition, for early detection of potentially fatal conditions such as thyroid storm or myxedematous coma.
Whether elderly patients with asymptomatic or minimally symptomatic primary hyperparathyroidism (PHPT) should be treated or not is still under debate. Several literature reports have shown improvements in terms of bone density and physical and mental well-being after surgical resolution of PHPT. Here, we present the case of a 93-year-old hypertensive woman, who had suffered for one year from cognitive impairment, accompanied during the last month by behavioral alterations (and polyuria and polydipsia), which resulted in sopor leading to hospitalization. A CT brain scan evidenced cortical atrophy and cerebrovascular disease, and biochemical analyses were remarkable for hypercalcemia (11.4-12.6 mg/dL, corrected for albumin levels) associated with increased parathormone levels (95.4-100.6 pg/mL). A diagnosis of PHPT was established. Densitometry evaluation of radius showed osteopenia. Withdrawal of psycho-therapy drugs and thiazidic, together with i.v. saline hydration and loop diuretics, significantly improved the patient's mental state and resolved behavioral alterations. As the patient and her relatives refused the surgical option, and the clinical situation improved after medical normalization of calcium levels, PHPT was managed conservatively, and calcium levels were maintained within the normal range through i.v. administration of zoledronate at 8-week intervals. Our case highlights the importance of considering hypercalcemia as the cause of onset of behavioral alterations and worsening of mental condition in elderly patients with cognitive decline. Therapy with bisphosphonates in patients with PHPT who are unfit for or refuse surgery seems advisable, but needs further study.
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