ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2009) 19 P23

An unusual case of SIADH precipitated by chronic inflammatory demyelinating polyneuropathy

L Varadhan1,2, P Newman2 & D Barton2

1University Hospital North Staffordshire, Stoke on Trent, UK; 2Princess Royal Hospital NHS, Telford, UK.

Hyponatremia is one of the commonest electrolyte abnormality. Various neurological conditions including Guillain Barre syndrome could precipitate it. Very few citations in literature report SIADH in CIDP.

A 68-year-old gentleman was admitted with worsening confusion and unsteady gait following a flu like illness few weeks ago, with increasing drowsiness for 3 days. His past medical history included hypertension and benign prostatic hypertrophy, being treated with Bendroflumethiazide, Irbesartan, Atenolol, Naproxen and Tamsulozin. He had ongoing history of fluctuating myalgia and arthralgia and episodic paraesthesia in both legs for 8 months. A diagnosis of polymyalgia rheumatica (ESR 46) and subsequently non-specific inflammatory arthritis was made, for which he was treated with reducing dose of steroids for the preceding 4 months.

GCS on admission was 12/15, clinically euvolemic, hemodynamically stable and rest of initial assessment were normal. Biochemical assessment showed serum Sodium 100 mmol/l, serum osmolality 218 mOsm/l, urine osmolality 630 mOsm/l, urine sodium 45 mmol/l, with normal renal function. Differential diagnosis includes

  1. SIADH.
  2. Diuretic induced hyponatremia.
  3. Atypical pneumonia.
  4. Hypoadrenalism due to decreasing steroid doses.
  5. Naproxen induced tubulointerstitial disease.

Naproxen and diuretics were omitted and hydrocortisone initiated. Sodium levels improved gradually with fluid restriction and demeclocycline. Chest X-ray, CT head and Synacthen test were normal. Renal investigations, uric acid, B12, folate, myeloma screen, urine porphyria screen and thyroid function test were normal. Full neurological examination after initial improvement showed mixed upper and lower motor neuron signs with patchy sensory involvement. Paraneoplastic neuropathy was ruled out with whole body CT scan, paraneoplastic antigens and tumor markers. Nerve conduction study confirmed demyelinating disease with polyneuropathy consistent with CIDP. Anti ganglioside antibodies were negative

Conclusion: This is an unusual case where the diagnosis of CIDP was prompted from hyponatremia. Extensive investigations for other causes of SIADH were negative.

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