Syndrome Of Antidiuretic Hormone Research Articles

Inappropriate Antidiuretic Hormone Syndrome in Craniofacial Surgery by Michel F. Brones, M.D., Henry K. Kawamoto, Jr., M.D., D.D.S., and Justin Renaudin, M.D.

Received for publication April 16, 1982. Derek A. Bruce, M.B., Ch. B. Division of Neurosurgery The Children's Hospital of Philadelphia 34th Street and Civic Center Boulevard Philadelphia, Pa. 19104

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.

Malignant pituitary adenoma. A cause of sphenoid hyperostosis and monocular blindness.

Malignant pituitary adenomas are extremely rare and comprise less than 5% of all pituitary tumors. A 65-year-old woman had rapid loss of vision and a chiasmal syndrome. Investigation revealed panhypopituitarism, and hyperostosis of the greater wing of the sphenoid bone and x-ray film evidence suggested a tuberculum sella meningioma. When a craniotomy was performed, a pituitary adenoma was found. The patient's death one month later was caused by an abnormal antidiuretic hormone (ADH) syndrome and pulmonary emboli. Pathological examination revealed an invasive pituitary adenoma, involving the optic nerves and cavernous sinus. The hyperostosis seemed to correlate well with the tumor infiltration. There were, however, no clinical or radiological findings that were diagnostic of malignant pituitary adenomas. The diagnosis of malignant adenomas should be considered when visual loss is rapid or when there are signs of extension into the cavernous sinus.

Inappropriate Antidiuretic Hormone

Comments and Corrections1 March 1973Inappropriate Antidiuretic HormoneROBERT D. GILBERT, M.D.ROBERT D. GILBERT, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-3-462_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The report of Miller and Moses (Ann Intern Med77:715-721, 1972) documenting the usefulness of the radioimmunoassay of urinary antidiuretic hormone (ADH) was impressive. But their data do not support their conclusion, as paraphrased in their abstract: "The urinary ADH response to water loading allows the certain diagnosis of inappropriate ADH syndrome. . . ." Although the antidiuretic hormone excretion was dramatically different from "normal" in their patients with the syndrome, no data on patients with hyponatremia and congestive heart failure, myxedema, or cirrhosis were presented. In fact, these diagnoses were rightly excluded on clinical grounds from... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Division of Computer Research and Technology National Institutes of Health Bethesda, Maryland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1973Volume 78, Issue 3Page: 462-462KeywordsAntidiuretic hormoneCirrhosisExcretionHeart failureHyponatremiaRadioimmunoassays Issue Published: 1 March 1973 PDF downloadLoading ...

Urinary Antidiuretic Hormone in Polyuric Disorders and in Inappropriate ADH Syndrome

Abstract Urinary antidiuretic hormone (ADH) excretion was measured by radioimmunoassay in patients with polyuric disorders and with the inappropriate ADH syndrome. The hormone was undetectable in p...

Plasma arginine vasopressin in the syndrome of inappropriate antidiuretic hormone secretion

Plasma arginine vasopressin (AVP) was measured by a specific and sensitive method during standard neurohypophyseal function tests in seven patients with inappropriate antidiuretic hormone syndrome. Four patients had oat cell carcinoma of the lung, two had remote head trauma and one had acute intermittent porphyria. Plasma AVP after dehydration was within the normal range in six patients but was not completely suppressed by hydration as in normal subjects. Plasma AVP levels rose appropriately after the administration of nicotine and hypertonic saline solution. One patient with metastases near the hypothalamus had markedly elevated AVP levels. The maintenance of a normal plasma AVP level and the fall to some degree after hydration in patients with and without tumor suggest that the hormone secretion is controlled, at least in part, by volume- and osmoreceptors.

Inhibition of antidiuretic hormone secretion by diphenylhydantoin.

INCREASED secretion of antidiuretic hormone (ADH) has been implicated in many hyponatremic disorders associated with impaired water excretion. This increased ADH release may be due to nonosmotic stimulation in response to volume depletion, to certain pharmacological agents, or frequently to an ADH secretion secondary to tumors, pulmonary disease, or central nervous system (CNS) disease. 1 The only previously known chemical inhibitor of ADH release other than water is ethanol. 2 More recently, Lee et al 3 have shown that diphenylhydantoin corrected the impaired water excretion of two patients with the syndrome of inappropriate ADH secretion. To further clarify the mechanism of ADH inhibition by diphenylhydantoin sodium (Dilantin) we have studied the effect of this drug in six patients with the inappropriate ADH syndrome and in eight normal subjects. Materials and Methods All clinical studies were performed in the Clinical Research Center of the University of Southern California School

Inappropriate vasopressin secretion and carcinoma of the pancreas

A fifty-nine year old man with a bronchogenic carcinoma (oat cell) demonstrated inappropriate antidiuresis: persistent urine hyperosmolality with marked serum hypoosmolality and hyponatremia in the presence of a normal blood volume, correction of hyponatremia with water restriction and excessive natriuresis with normal renal and adrenal function. Resection of the primary lung tumor did not ameliorate the antidiuretic hormone (ADH) syndrome. At autopsy, performed four months postoperatively, metastatic lung cancer was present in the liver and a separate tumor (adenocarcinoma) was found in the pancreas. Extracts of the pancreatic neoplasm contained very high levels of arginine vasopressin (380 milliunits (mU) per mg.) as demonstrated by both radioimmunoassay and biologic assay. Extracts from the primary lung tumor, lymph nodes involved by the lung tumor and metastatic lung tumor in the liver contained no detectable antidiuretic activity in both assays. In addition, pharmacologic analysis of the pancreatic carcinoma revealed a considerable quantity of oxytocin (500 mU per mg.). The values for arginine vasopressin (AVP) and oxytocin observed in the pancreatic neoplasm are in the same range as those present in the human neurohypophysis.

Inappropriate Antidiuretic Hormone Secretion in Carcinoma of the Lung

Four cases with inappropriate antidiuretic hormone syndrome associated with carcinoma of the long are reported. It is concluded that certain tumors manifest a capability to synthesize and release a substance similar to antidiuretic hormone which enhances water reabsorption, leading to dilution and expansion of the extracellular fluid volume. These changes in the extracellular fluid volume stimulate the third factor mechanism which depresses proximal tubular sodium reabsorption, resulting in a continued renal salt loss despite the existing hyponatremia. The simple restriction of fluid intake to 500–750 ml per day along with an adequate intake of sodium will result in correction of the hyponatremia and relief of the distressing symptoms. Permanent cure is possible when complete removal of the tumor is technically feasible.

Inappropriate Antidiuretic Hormone Syndrome and Carcinoma of Pancreas with Demonstration of Tumor Antidiuretic Activity.

Excerpt A 59-year-old man with a bronchogenic carcinoma (oat cell) demonstrated inappropriate antidiuresis on the basis of [1] persistent urine hyperosmolality with marked serum hypoosmolality and ...

The role of adrenocorticoids in the inappropriate antidiuretic hormone syndrome.

Twenty patients with all of the characteristics of the inappropriate antidiuretic hormone (ADH) syndrome were observed at the Los Angeles County General Hospital in the past 2 years. The varied causes, including chest lesions, central nervous system disorders, and unclassified causes and frequency, suggest that it is certainly not a rare syndrome. Bioassay for ADH in the majority of cases tested showed increased biologic activity in serums or tumors. The defect in acute water load excretion was correctable by intravenous diphenylhydantoin in the cases not due to autonomous tumor. Glucocorticoid administration failed to correct hyponatremia in patients with the syndrome as compared with patients with hyponatremia secondary to hypopituitarism. The failure of high doses of glucocorticoids to affect the syndrome suggests that, at least in patients with inappropriate or autonomous ADH secretion, glucocorticoids do not act as inhibitors of ADH release. Mineralocorticoids in high doses may correct the hyponatremia, and an "escape" phenomenon with a resumption of increased urinary sodium may ensue. Aldosterone excretion may be normal and important in minimizing sodium losses as shown by the inhibition of aldosterone-mediated sodium retention and aggrevation of the sodium loss by aldosterone inhibitors. Creatinine clearance was generally normal, and there was no correlation between variation in glomerular filtration rate and urine sodium excretion. The presence of normal creatinine clearance and aldosterone excretion with persistent urine sodium loss, in spite of hyponatremia, suggests that the sodium diuresis is due to some "third factor" other than increased glomerular filtration or hypervolemic inhibition of aldosterone. The mechanism of sodium loss in this syndrome appears to be similar to the escape phenomenon occurring with high doses of mineralocorticoids and may be related to proximal tubular rejection of sodium secondary to an expanded intravascular volume.

Correction of an Inappropriate ADH Syndrome by Tumor Resection

Paraendocrine or humoral syndromes associated with tumors of nonendocrine origin have received a great deal of attention in the past decade. Several of the more striking symptom complexes or syndromes include hypoglycemia, polycythemia, hyperthyroidism, hypercalcemia, Cushing's syndrome, and the inappropriate antidiuretic hormone (ADH) syndrome, the latter most commonly observed with bronchogenic carcinoma. In the past few years, several well described cases of lung tumor associated with the inappropriate secretion of ADH have appeared in the literature. 1-18 Although the occurrence of hyponatremia with carcinoma of the lung was first noted and described by Winkler and Crankshaw 19 in 1938, it was not until 1957 that Schwartz et al 1 further elucidated the pathogenesis of the syndrome with experimental evidence of the inappropriate secretion of ADH. The present report describes a patient in whom a bronchogenic carcinoma was resected resulting in complete correction of associated inappropriate antidiuresis. The syndrome subsequently reappeared