Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
SIADH in a Diabetic Patient with Severe Neuropathy
Kaoru InoueTaro WasadaMizuho NakagawaAkihiko TazoeHiroshi OnoToyoshi InoguchiFumio UmedaHiroshi Ibayashi
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Keywords: carbamazepine
JOURNAL FREE ACCESS

1987 Volume 30 Issue 2 Pages 181-185

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Abstract
A 55 year-old woman, who had had diabetes for 2 years, was admitted to our hospital because of marked emaciation (body mass index 13.6) and painful neuropathy. She was chronically ill and apathetic. With daily insulin treatment (14-16 U), her fasting blood glucose was 150 mg/dl and HbA1 9.6%. Renal and endocrine functions including the thyoid gland, the pituitary adrenocortical axis and the renin aldosterone system were normal. She had the clinical features of severe symmetric peripheral neuropathy. The MCV of posterior tibial nerve was 32.4 m/sec. The SCV of the sural nerve could not be evoked. The R-R interval variation during deep breathing was 2.3 beats/min. Biopsy of the sural nerve revealed a marked loss of both myelinated and unmyelinated nerve fibers, independent of fiber size. Her blood showed low Na concentrations (127-131 mEq/l) and hypo-osmolarity (236-256 mOsm/l). Water loading (20 ml/kg) failed to dilute the urine below the level of the plasma osmolarity and the plasma ADH was not significantly suppressed. Urinary Na output was relatively large (28-120 mEq /l) in the presence of hyponatremia. Interestingly, these abnormalities in the water loading test persisted for 2 months after discontinuation of treatment with carbamazepine, when serum Na had already been normalized. These findings suggest that a certain causal linkage may exist between inappropriate secretion of ADH and severe diabetic neuropathy.
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