MON-073 - Progressive Endocrine Derangements Following Tuberculosis Meningitis - A Case Study

Endocrinologic derangements are known complications of tuberculosis (TB) meningitis, though cases usually involve one or two complications. In this case we report a patient with TB meningitis who developed syndrome of inappropriate antidiuretic hormone (SIADH), then central diabetes insipidus (DI) and central hypothyroidism.

31-year-old male presented with progressive headache, confusion, and visual changes. CSF cultures grew Mycobacterium tuberculosis, and he was diagnosed with disseminated TB with meningoencephalitis complicated by multifocal strokes. He was treated with rifampin and isoniazid, and required neurosurgical intervention for hydrocephalus, herniation, and cerebral edema.

During treatment and while still hospitalized, he developed euvolemic hypotonic hyponatremia, with sodium (Na) decreasing from 135 mmol/L to 118 mmol/L (range: 134–147 mmol/L) over a few days, and was clinically diagnosed as SIADH. An MRI brain showed mild hydrocephalus with periventricular edema, and hyponatremia was treated with fluid restriction and salt tabs. In 1 day Na increased to 130 mmol/L, and a head CT showed worsening hydrocephalus, mild bilateral uncal herniation, and diffuse cerebral edema. A day later, Na increased to 175 mmol/L, with dilute urine (167 mOsm/kg). Fluid restriction and salt tabs were discontinued, and water flushes were started.
The patient was started on 1 mcg of desmopressin intravenously for presumed DI with persistently elevated Na. This decreased urine output from 400 to 30 cc/hr (confirming central DI) and was necessary for 3 weeks until Na normalized.

About 1 month into the hospitalization, thyroid stimulating hormone (TSH) was 4.2 µU/mL (range: 0.700–3.800 µU/mL), free T4 was 0.5 ng/dL (range: 0.80–1.70 ng/dL), and levothyroxine 25 mcg daily was started. Repeat testing at 1 and 2 weeks showed TSH of 3.26 µU/mL and free T4 0.33 ng/dL. TSH and free T4 decreased continually, raising concern for malabsorption, requiring higher doses other forms of levothyroxine dosing. Eventually, levothyroxine 200 mcg/day via G tube maintained free T4 stable at 0.6–0.9 ng/dL with TSH at 0.085 µU/mL.

Months after initial diagnosis and receiving his last DDAVP dose, the patient had episodes of hyponatremia and hypernatremia (Na 119-162 mmol/L) with transient DI, requiring fluid restriction, brief hypertonic saline, and spot dosing of DDAVP.

While hypothyroidism and SIADH are established complications of TB meningitis, central DI is more rare. This case illustrates the extent of hypothalamic and pituitary damage and overlap that can occur with meningitis, with rapid and slower changes in electrolytes (like Na) and hormones (like TSH), requiring prompt diagnosis and treatment. TB meningitis warrants monitoring of sodium, fluid balance, thyroid function, and other hypothalamic-pituitary functions, especially in patients with evidence of evolving cerebral damage.

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