The syndrome of inappropriate secretion of
antidiuretic hormone (
SIADH) associated with localized
herpes zoster is rarely reported and may be under-appreciated. We describe two diabetic men with
herpes zoster ophthalmicus (HZO) who developed
hyponatremia (114 and 116 mmol/L) during acute illness. Both were euvolemic and had elevated urine osmolality (435 and 368 mmol/kg.H(2)O) and
sodium (Na(+)) concentration (61 and 63 mmol/L) along with normal cardiac, renal, liver, and endocrine function consistent with the diagnosis of
SIADH. Thorough investigation for other causes of
SIADH, including detailed physical examination, laboratory studies, and computed tomography of the brain, chest, and abdomen, were negative. Despite
antiviral therapy (
acyclovir) for
herpes zoster,
ophthalmoplegia,
keratitis, and post-herpetic
neuralgia (PHN) developed. Even with fluid restriction and high
salt diet,
SIADH lasted for 3 to 4 months and resolved concomitantly with resolution of PHN, suggesting an association between
SIADH and HZO. These two cases raise the potential for
herpes zoster infection, especially HZO, to involve the regulatory pathway of ADH secretion, contributing to
SIADH. The presence of PHN, which reflects greater neural damage may, at least in part, explain the prolonged ADH secretion and
hyponatremia.