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Severe Euvolemic Hyponatremia Consistent With Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) During Localized Herpes Zoster in an Older Adult.

Source: PubMed, NCBI / U.S. National Library of Medicine

CureusRajendran Abinaya, Dhayalan Dhayanithi, Adapa SreedharPublished 7/1/2026Last synced 8/3/2026Status: syncedPMID: 42542621DOI: 10.7759/cureus.111926

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an uncommon but recognized complication of herpes zoster (varicella-zoster virus, VZV) infection, and diagnostic uncertainty may arise when hyponatremia develops after antiviral therapy is initiated. We report an 89-year-old patient with hypertension, chronic kidney disease stage 3, hyperlipidemia, and prior left nephrectomy for renal cell carcinoma who presented with right neck and upper arm pain, weakness, and a unilateral dermatomal vesicular eruption consistent with herpes zoster. Oral acyclovir was started at 800 mg five times daily. During hospitalization, serum sodium declined from 136 mEq/L to a nadir of 123 mEq/L despite discontinuation of hydrochlorothiazide. The patient remained clinically euvolemic, with urine sodium of 134 mEq/L and urine osmolality of 570 mOsm/kg, supporting SIADH. Thyroid-stimulating hormone and morning cortisol were normal. Fluid restriction < 1.2 L/day was ineffective. As the patient became symptomatic, and hypertonic saline (with removal of fluid restriction) produced no improvement, a single dose of tolvaptan produced rapid correction of serum sodium and improvement in mentation. The patient was subsequently maintained on sodium chloride tablet supplementation, fluid restriction, and a high-protein diet, with serum sodium improving to 135-136 mEq/L. This case describes severe hypotonic euvolemic hyponatremia meeting biochemical criteria for SIADH in the setting of localized

Abstract

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an uncommon but recognized complication of herpes zoster (varicella-zoster virus, VZV) infection, and diagnostic uncertainty may arise when hyponatremia develops after antiviral therapy is initiated. We report an 89-year-old patient with hypertension, chronic kidney disease stage 3, hyperlipidemia, and prior left nephrectomy for renal cell carcinoma who presented with right neck and upper arm pain, weakness, and a unilateral dermatomal vesicular eruption consistent with herpes zoster. Oral acyclovir was started at 800 mg five times daily. During hospitalization, serum sodium declined from 136 mEq/L to a nadir of 123 mEq/L despite discontinuation of hydrochlorothiazide. The patient remained clinically euvolemic, with urine sodium of 134 mEq/L and urine osmolality of 570 mOsm/kg, supporting SIADH. Thyroid-stimulating hormone and morning cortisol were normal. Fluid restriction < 1.2 L/day was ineffective. As the patient became symptomatic, and hypertonic saline (with removal of fluid restriction) produced no improvement, a single dose of tolvaptan produced rapid correction of serum sodium and improvement in mentation. The patient was subsequently maintained on sodium chloride tablet supplementation, fluid restriction, and a high-protein diet, with serum sodium improving to 135-136 mEq/L. This case describes severe hypotonic euvolemic hyponatremia meeting biochemical criteria for SIADH in the setting of localized herpes zoster, after consideration of concurrent hydrochlorothiazide exposure and temporally associated oral acyclovir.

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