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Thiazide-induced hyponatremia.

J E Johnson, L F Wright

    Southern Medical Journal
    |November 1, 1983
    PubMed
    Summary

    Thiazide diuretics can cause severe hyponatremia (low sodium) by affecting vasopressin secretion and potentially leading to intracellular osmolar inactivation. Prompt treatment with hypertonic saline resolved neurological symptoms in this case.

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    Area of Science:

    • Nephrology
    • Endocrinology
    • Neurology

    Background:

    • Thiazide diuretics are commonly prescribed for hypertension and edema.
    • Hyponatremia, a potential side effect, can lead to serious neurological complications.
    • Understanding the precise mechanism of thiazide-induced hyponatremia is crucial for patient management.

    Observation:

    • A 54-year-old woman presented with seizures and focal neurologic deficits attributed to hyponatremia from thiazide use.
    • Neurologic symptoms resolved promptly after correction with hypertonic saline.
    • Metabolic studies and rechallenge with hydrochlorothiazide were performed to elucidate the mechanism.

    Findings:

    • Abnormal vasopressin secretion was observed, indicated by elevated plasma vasopressin levels relative to plasma osmolality after a fluid challenge.
    • Rechallenge with chlorothiazide led to a rapid decrease in serum sodium and plasma osmolality, despite minimal urinary cation losses and stable body weight.
    • Intravenous electrolyte administration also triggered hyponatremia, suggesting a mechanism beyond simple external water and electrolyte imbalance.

    Implications:

    • The findings suggest that thiazide-induced hyponatremia may involve mechanisms beyond external water and electrolyte balance, such as osmolar inactivation.
    • The rapid onset of hypotonicity points towards intracellular processes contributing to severe hyponatremia.
    • This case highlights the importance of recognizing and promptly managing thiazide-induced hyponatremia to prevent severe neurological sequelae.

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