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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Antidiuretic hormone excess. 10 2

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.
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PMID:Vasopressin: deficiency, excess and the syndrome of inappropriate antiduretic hormone secretion. 10 6

Metabolic abnormalities compatible with inappropriate secretion of ADH developed during the course of severe viral pneumonia in a 17-year-old Navy recruit. With a regimen of strict fluid restriction, normalization of these abnormalities occurred. Marked leukopenia and hypoxia were also present, but gradually improved with resolution of the pneumonia. Inappropriate ADH secretion has been associated most often with bacterial pneumonia and this patient represents one of the few with viral pneumonia complicated by this syndrome. While the previous cases were assoicated with influenza virus, this patient was infected with adenovirus-7 which is endemic in the military recruit population.
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PMID:Inappropriate secretion of antidiuretic hormone associated with adenovirus pneumonia. 17 45

A 61 year old woman presented with profound hyponatremia and markedly low serum osmolality. Urine osmolality was greater than the serum osmolality, an abnormality that was corrected by water restriction, suggesting inappropriate ADH secretion. Although there were no physical signs of Cushing's syndrome, her serum potassium level was low and markedly elevated levels of plasma and urine corticosteroids were not altered by the administration of large amounts of dexamethasone, suggesting the ectopic ACTH-MSH syndrome. Plasma levels of immunoreactive ACTH and beta-MSH were elevated. At autopsy, a metastastic oat cell carcinoma of the lung, not detected antemortem by chest roentgenograms and bronchoscopy, was found. Immunoreactive ADH, ACTH and beta-MSH were detected in the primary tumor and in metastases to the liver. beta-MSH was also detected in the spleen, in which metastases were observed. This is the first documented case of the simultaneous production of ADH, ACTH and beta-MSH by neoplastic tissue associated with clinical manifestations of the syndrome of inappropriate ADH secretion and the ectopic ACTH-MSH syndrome.
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PMID:Ectopic production of antidiuretic hormone (adh), adrenocorticotrophic hormone (ACTH) and beta-melanocyte stimulating hormone (beta-MSH) by an oat cell carcinoma of the lung. 18 5

The authors report two cases and consider the various physiopathological mechanisms of inappropriate hypersecretion of antidiuretic hormone. An exploration including clearance of free water and, in some cases, estimation of ADH before and after a water load, then before and after administration of ethyl alcohol, permits one to determine the mechanism. It seems advisable to reserve the term Schwartz-Bartter syndrome to paraneoplasic syndromes linked to ectopic and autonomous secretion of ADH.
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PMID:[Inappropriate secretion of antidiuretic hormone: true and false Schwartz-Bartter syndrome. Apropos of 2 cases]. 19 21

1. Studies on eight patients were performed to clarify the mechanism(s) of altered sodium metabolism and volume regulation in SIADH. The mechanism controlling water excretion was also studied to determine whether there is evidence that altered osmoregulation may be the basis for inappropriate ADH secretion in some patients. 2. These studies show that cumulative sodium balance and aldosterone secretion rates in patients with SIADH are negatively correlated with water intake. There is also a negative correlation between aldosterone secretion and urinary sodium excretion. In the absence of normal urine diluting ability, this increased excretion of sodium becomes a mechanism that allows an increased quantity of water to be excreted despite the persistence of an ADH effect on the renal tubules. 3. Within the range of hyponatremia observed in our studies, changes in serum sodium concentration were accounted for by changes in solute and water balance. One patient, who was potassium deficient during the studies, retained large quantities of sodium and potassium that could not be accounted for by an increase in either serum osmolality or body weight. These observations suggest that intracellular osmotically active solute is either lost or "inactivated" in some manner as intracellular potassium is replenished. 4. Marked impairment of urine diluting ability was demonstrated in all patients. However, two patients with SIADH associated with pulmonary tuberculosis exhibited graded responses to water loading, which suggests that ADH secretion may have been suppressed as serum osmolality was progressively reduced. Whether this can be attributed to a basic alteration or "re-setting" or osmoreceptor function, or is merely an indication that greater than normal reductions of serum osmolality are required to inhibit potent nonosmotic stimuli, remains to be determined.
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PMID:The syndrome of inappropriate antidiuretic hormone secretion (SIADH): pathophysiologic mechanisms in solute and volume regulation. 44 60

We have experienced with 50 cases of parasellar tumors, four cases of which had persistent thirst, polydipsia, polyuria, and reversible temporary hyponatremia secondary to hypernatriuresis. The mechanism of the syndrome in these four cases could not be explained by either that of the syndrome of hypernatremia or of the so-called SIADH. We tentatively named this syndrome as "CEREBRAL POLYURIC HYPONATREMIA" and the criteria of this syndrome as as follows: 1) persistent thirst, polydipsia polyuria, 2) reversible temporary hyponatremia secondary to hypernatriuresis, 3) exception of the following items--administration of uretic drugs, renal and adrenal dysfunction, hyperglycemia, hyperlipemia, overadministration of water, and poor administration of NaCl. The mechanism of this syndrome is presumed as follows: 1) compression by a tumor or surgical attack to the anterior hypothalamus, 2) disturbance of the mechanism of ADH secret-on, 3) extrasecretion of natriuretic factor possibly produced in the anterior hypthalamus, and 4) preservation of the thirst center.
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PMID:[Cerebral polyuric hyponatremia--discussion of a new syndrome with disturbance of electrolyte balance of central origin (author's transl)]. 55 42

Inhibition of ADH-secretion and transient water diuresis was observed as acute effects of radio-frequency lesions in the septal region of goats. The water diuresis was not compensated for by drinking and therefore rapidly induced pronounced hypernatremia and hypovolemia. The development of hypovolemia was accompanied by a rise in plasma renin activity. Lesions of the same kind, but extending into the preoptic region near the medial portion of the supraoptic nuclei induced the inability to excrete excessive water characteristic of SIADH. Determinations of plasma arginine vasopressin suggested that the lesions causing SIADH did not produce any noticeable increase in basic ADH-secretion. The results suggest that impulses from juxtaventricular receptors regulating ADH-release and water intake to a considerable extent are transmitted via the septal region, and that elimination of this impulse traffic is sufficient to turn water balance to the negative side. However, reflex volumetric inhibition of the ADH-secretion does not seem to be mediated by pathways passing through the septal region.
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PMID:Transient water diuresis and syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by forebrain lesions of different location. 71 63

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.
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PMID:Pathophysiologic and pharmacologic alterations in the release and action of ADH. 81 77

The syndrome of inappropriate ADH secretion ("SIADH") was first recognized 1935 by Roth et al. and described in detail 1957 by Schwartz et al. The clinical symptoms (hyponatremia, hypertonicity of urine and inability to excrete a water load) are caused by inadequately elevated ADH secretion under a variety of situations and diseases. Some recent work was focused on the pathogenesis of this syndrome and new clinical findings (low plasma levels of uric acid and potassium) as well as special forms ("SIADH" without elevated vasopressin levels in plasma) are thought to be of relevance. New therapeutical recommendations will be discussed.
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PMID:[The syndrome of inappropriate secretion of vasopressin (SIADH) (author's transl)]. 85 83


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