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1/5. Inappropriate antidiuretic hormone complicating histiocytic lymphoma.

    The syndrome of inappropriate antidiuretic hormone (IADH) often causes the hyponatremia that may be seen in patients with malignant disorders. Most physicians correctly associate IADH with small cell carcinoma of the lung. We describe two patients in whom IADH was caused by histiocytic lymphoma. One patient was thought to have small cell carcinoma of the lung on the basis of marrow infiltration and the IADH. When the proper diagnosis was made and therapy instituted, both patients responded, with rapid resolution of their disease and the IADH. The identification of the neoplasm that produces the IADH is important, since histiocytic lymphoma may mimic small cell carcinoma of the lung, yet may be very responsive with newer treatment regimens.
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2/5. SIADH: a serious side effect of psychotropic drugs.

    In this communication two cases of possibly drug induced hyponatremia secondary to amitriptyline and thioridazine have been reported. What is particularly important is the fact that in one, irreversible neurological symptoms were left as sequelae and in the other, the patient was in a coma and thus suffered from a potentially lethal complication. The physicians should be aware of this disturbing side effect while treating their patients with antidepressant and neuroleptic medications.
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3/5. The treatment of severe hyponatremia.

    Severe hyponatremia may be chronic (days) or acute (hours), symptomatic or asymptomatic. Severe chronic symptomatic hyponatremia (serum sodium concentration < 110 to 115 mM/liter) occurs most commonly in the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The treatment of this hyponatremia is a challenge to practicing physicians, in part because an overly rapid correction of hyponatremia may cause brain damage. The latter sometimes takes the form of central pontine myelinolysis (CPM). On the basis of available clinical and experimental literature, the rate of correction of this symptomatic hyponatremia should be no more than 0.5 mM per liter per hour, and the initial treatment should be halted once a mildly hyponatremic range of the serum sodium concentration has been reached (approximately 125 to 130 mM/liter). In contrast, severe chronic asymptomatic hyponatremia may be treated sufficiently by a fluid restriction. On the other hand, severe symptomatic acute hyponatremia should be treated promptly and rapidly, using hypertonic saline, to initially reach a mildly hyponatremic level.
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4/5. thymoma associated with syndrome of inappropriate antidiuretic hormone secretion and myasthenia gravis.

    We describe the association of malignant thymoma with the syndrome of inappropriate antidiuretic hormone secretion and myasthenia gravis. hyponatremia has not been reported associated with those tumors and our case should alert physicians about the potential for a life-threatening complication.
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5/5. Assessment of neuroendocrine dysfunction following traumatic brain injury.

    Posttraumatic neuroendocrine pathology may be a clinically significant complication following traumatic brain injury (TBI). Metabolic abnormalities are described after TBI in two cases. A 21 year old male injured in a motor vehicle accident admitted in a minimally responsive condition presented with fluctuating high sodium levels, undetectable serum testosterone, and depressed cortisol and thyroid function. Imaging revealed near complete avulsion of the pituitary stalk leading to panhypopituitarism. A 38 year old male admitted for occipital skull fractures and brain contusions presented with hyponatremia and low serum testosterone. Both patients required hormonal replacement and correction of electrolyte abnormalities. A screening protocol adapted for selected patients at risk for endocrine problems is described. While neuroendocrine screening is not advocated in all TBI patients, physicians should be aware of the importance of neuroendocrine dysfunction following TBI.
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