Syndrome of inappropriate secretion of antidiuretic hormone associated with localized herpes zoster ophthalmicus

Abstract

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.

Figure 1

Simplified schema of regulation of ADH secretion. The secretion of ADH is regulated by central and peripheral osmoreceptors as well as baroreceptors. Signals from peripheral receptors ascend via different nerves and relay in the brainstem. The nucleus tractus solitarius (NTS) in the brainstem processes signals from peripheral receptors and excites neurosecretory cells located in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) to release ADH. VZV reactivation in dorsal root ganglia (shown in ①) and the first branch of the trigeminal nerve may stimulate ADH secretion via NTS (shown in ②). The NTS is also thought to be involved in pain-induced ADH secretion. VLM, ventrolateral medulla.