Abstract

Diagnosis of Guillain–Barré syndrome (GBS) is established clinically and is supported by nerve conduction studies and cerebrospinal fluid examination. Renal function is usually not affected, but recent case reports have established a link between GBS and hyponatremia. A 60-year-old woman presenting with lower back ache since 3 days, became drowsy the next day and developed paraparesis and bulbar symptoms. Her sensorium and power deteriorated progressively over the next 2 days and she was brought to hospital in a drowsy state. She was found to have severe hyponatremia (Na+ at 113) and nerve conduction study (NCS) was son of AMAN. The patient was started on intravenous immunoglobulin and her sodium levels were corrected, and the patient recovered completely. The occurrence of hyponatremia in patients diagnosed with GBS is well described. However, there have been only two prior case reports in which hyponatremia had been observed before the manifestation of neuromuscular deficits. Our patient case is unique in that severe hyponatremia occurred simultaneously with neurologic symptoms and the diagnosis of GBS. In most cases reported in the literature, hyponatremia was noted after a diagnosis of GBS was established. The mean period of onset of syndrome of inappropriate antidiuretic hormone (SIADH) was 8.8 days after the onset of symptoms of GBS. In conclusion, this presentation raises the possibility that early changes in the autonomic nervous system triggered by GBS might lead to alterations in water and sodium balance that can precede symptomatic changes in the peripheral nervous system. Although rarely, but both GBS and its treatment, intravenous immunoglobulin, should be considered in the differential diagnosis of hyponatremia.

Highlights

  • Guillain–Barré syndrome (GBS) is an immunemediated polyneuropathy characterized by progressive, ascending, symmetric muscle weakness, and depressed or absent deep tendon reflexes

  • In a prospective study of 50 patients diagnosed with GBS, hyponatremia was noted in 48% of cases [6] and motor dysfunction preceded the onset of hyponatremia

  • The underlying etiology of this phenomenon is presumably related to secretion of antidiuretic hormone (SIADH), there has been considerable discussion on whether ‘pseudohyponatremia’ from intravenous immunoglobulin (IVIG) administration is playing a major role

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Summary

Introduction

Guillain–Barré syndrome (GBS) is an immunemediated polyneuropathy characterized by progressive, ascending, symmetric muscle weakness, and depressed or absent deep tendon reflexes. The normal regulation of antidiuretic hormone (ADH) secretion is mediated by the hypothalamus and autonomic nerve fibers Damage to those structures from the autoimmune process in GBS can alter ADH release patterns leading to autonomic dysfunction and SIADH. The other blood values including liver function tests and glucose levels were normal. The infusion rate was adjusted on the basis of her clinical response and serial electrolyte levels obtained six hourly She was started on intravenous immunoglobulin (IVIG) therapy on the fourth day of her illness. She was more alert on day 4 when her serum sodium level had had been gradually corrected to 124 mEq/l. At follow-up after 2 weeks she showed no residual motor deficits

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