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Results for “Inappropriate ADH Syndrome”

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At least 19 recordsLinked to original sources
PubMed1992

Hyponatraemia and the inappropriate ADH syndrome in pneumonia.

We studied serum sodium, plasma osmolality and urinary sodium and osmolality on days 1, 3 and 5 of hospitalization of 100 children aged from 1 month to 12 years admitted with a diagnosis of pneumonia. Hyponatraemia (serum sodium concentration < or = 130 mmol/l) was found in 31 patients at the time of admission. The probable cause of hyponatraemia in 94% of cases was the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Symptoms and signs indicative of severe pneumonia were two to three times more frequent and the mean duration of tachypnoea, chest-wall retraction and hospital stay about one and a half times longer in children with hyponatraemia. Four children died (two on day 1, one on day 5 and one on day 8); all four had a serum sodium concentration < or = 125 mmol/l which persisted until death. Of the remaining 27 hyponatraemic children, serum sodium concentrations returned to normal on day 3 in 26, while in one hyponatraemia persisted until day 7. The recovery from hyponatraemia showed a good correlation with improvement in clinical signs of respiratory distress. The SIADH occurred in about one-third of the children hospitalized for pneumonia, and was associated with a more severe disease and a poorer outcome. Perhaps fluid restriction in these cases may improve the outcome.

Child↗
PubMed1979

Antidiuretic hormone excess.

Known physiologic mechanisms explain the elevated blood ADH levels observed in most patients with the syndrome of inappropriate ADH. Therefore the word "inappropriate" is a misnomer. It implies that the mechanisms that regulate ADH release are not functioning normally--which is not true. The term misleads the physician who, ideally, should determine why a patient has an excessive blood ADH level and initiate appropriate treatment. Patients with ectopic production of ADH and hyponatremia should be so labeled: "Hyponatremia due to ectopic ADH production." The term SIADH, if used at all, should be reserved for the rare patient with CNS injury or disease that causes increased ADH release and in which the hypothalamic center does not respond normally to afferent peripheral stimuli.

Blood↗
PubMed1992

Inappropriate antidiuretic hormone secretion in a patient with systemic sarcoidosis.

A 59 year old man presenting fever, serum hyponatremia and hypoosmolality in association with hyperosmotic urine was hospitalized in our unit in February 1988. We demonstrated evidence of systemic sarcoidosis and inappropriate secretion of antidiuretic hormone (ADH). The patient was treated with corticosteroid therapy for a period of about 1 year, with regression of signs of the inappropriate vasopressin secretion as well as the symptomatology related to systemic sarcoidosis. This study identified systemic sarcoidosis as a definite cause of "syndrome of inappropriate ADH secretion".

Arginine Vasopressin↗
PubMed1978

Pharmacologic studies in Bartter's syndrome: effect of DDAVP and indomethacin on renal concentrating operation. Part II.

We have investigated the effect of indomethacin and DDAVP on water excretion in a patient with familial Bartter's syndrome in whom urinary concentration was impaired during ad libitum fluid intake without any decrease in maximal concentrating ability. In response to indomethacin urine osmolality and free water reabsorption increased, simultaneously with the decrease in the excretion of prostaglandin E2. The indomethacin induced improvement was however less than that obtained after DDAVP with or without indomethacin. The results can be interpreted on the basis of either a direct "vasopressin-like" action of indomethacin or abolishment of the peripheral vasopressin--prostaglandin interaction. The clinical implication is that the theoretical possibility of indomethacin-induced inappropriate ADH syndrome should be borne in mind when a patient is treated with this drug on a long term basis.

Adult↗
PubMed1977

Release of antidiuretic hormone during mass-induced elevation of intracranial pressure.

There are complex osmotic and non-osmotic factors regulating release of antidiuretic hormone (ADH). A wide variety of intracranial pathological processes may trigger ADH release sufficient to produce clinically recognizable hyponatremia, or the "inappropriate ADH syndrome." We systematically studied one non-osmotic trigger, namely mass-induced elevated intracranial pressure (ICP). Initial experiments established baseline data in normal rhesus monkeys: anesthetized animals displayed appropriate rises and falls in immunoreactive urinary ADH in response to intravenously administered hypertonic and hypotonic infusions. Next, ballon catherters were implanted subdurally over temporal lobes and the animals were allowed to recover. The final experiment consisted of anethetizing the animals, monitoring arterial blood pressure and blood gases, and retrieving timed urinary specimens while continuously recording ICP during infusion-pump expansion of the subdural ballon. A nonlethal and a lethal series of ballon-expansion experiments were done. Control values of urinary ADH were 783 +/- 125 muU/15 min, and ICP was less than 10 mm Hg. During nonlethal mass expansion ADH output rose of 3433 +/- 269 millimicronU/15 min while ICP averaged 65 mm Hg (measured at completion of mass expansion). While the mass was maintained, hypotonic infusion produced unchanged urinary ADH output of 3452 +/- 277 muU/15 min. During lethal experiments, urinary ADH rose still higher to 4339 +/- 1887 muU/15 min associated with ICP averaging 100 mm Hg. We concluded that there is a direct relationship between the magnitude of ICP and the amount of ADH release, and that during elevated ICP the ADH release is not suppressed by hypotonic infusion.

Animals↗
PubMed1979

Vasopressin: deficiency, excess and the syndrome of inappropriate antiduretic hormone secretion.

The hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.

Demeclocycline↗
PubMed1978

Demeclocycline in the treatment of the syndrome of inappropriate antidiuretic hormone release: with measurement of plasma ADH.

A patient with the syndrome of inappropriate antidiuretic hormone release (SIADH) following head injury and meningitis was studied during treatment with demeclocycline, a drug known to produce a reversible nephrogenic diabetes insipidus. No changes were observed during six days of demeclocycline 1200 mg/24 hr but urine output increased significantly, with the production of a dilute urine, when the dose was increased to 2400 mg/24 hr. The patient lost weight, and all biochemical features of the syndrome were rapidly corrected despite an unchanged fluid intake and despite the persistence of high plasma levels of ADH. The rise in serum sodium was accompanied by mild sodium retention, as measured by external balance and exchangeable sodium. A complication of treatment was the development of acute renal failure possibly induced by a nephrotoxic effect of high circulating levels of demeclocyline. On stopping demeclocyline renal function returned to normal and, after some delay, SIADH returned, and was still present 9 months after initial presentation. This confirms earlier reports of the efficacy of demeclocycline in SIADH; but the authors advise caution against increasing the dose above 1200 mg/24 hr.

Demeclocycline↗
PubMed1979

Haloperidol-induced syndrome of inappropriate secretion of antidiuretic hormone.

Several psychotropic drugs have been associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We report here a patient who on two occasions developed clinically significant hyponatremia while receiving the antipsychotic drug, haloperidol. The criteria for the syndrome of inappropriate secretion of ADH were fulfilled and other causes of SIADH were excluded. We documented inability in this patient to excrete a water load while on haloperidol and normal ability in its absence. This case therefore illustrates SIADH due to haloperidol.

Haloperidol↗
PubMed1992

[Clinical-pharmacological case report: drug-induced inappropriate ADH secretion].

The syndrome of inadequate secretion of antidiuretic hormone (SIADH) following treatment with a tricyclic antidepressant is demonstrated using the example of a 70 year-old man admitted for weakness and cognitive disturbances. Because of incontinence he had been periodically treated since 1989 with imipramine (Tofranil) by his family doctor. On admission he was seriously hyponatriemic and had low plasmatic osmolality, significantly lower than urinary osmolality. Creatinine, urea and uric acid in serum were also below normal values. Like other drugs tricyclic antidepressants can rarely induce an increased release of ADH by direct hypothalamic stimuli. In this patient imipramine was terminated and within a few days of reduced fluid intake and substitution of sodium a sustained clinical improvement and normalisation of laboratory parameters was noted. The patient was discharged to his home after three weeks.

Aged↗