Inappropriate Antidiuretic Hormone Release Research Articles

Imaging of the sella in the syndrome of inappropriate secretion of antidiuretic hormone.

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) results either from ectopic production or inappropriate release of antidiuretic hormone from the neurohypophysis. Although magnetic resonance imaging (MRI) has provided new insights into the morphological changes of the hypophysis in health and disease, no previous studies have evaluated its use in SIADH: The aim of this study was to evaluate the MRI appearance of the neurohypophysis in patients with SIADH: Retrospective case-control study. Tertiary care teaching hospital. We studied retrospectively eight patients with SIADH who had been hospitalized in Boston's Beth Israel between 1984 and 1994 and who had MRI scans including the sella turcica. We also evaluated prospectively the MRIs of the heads of 23 consecutive control patients who had no pituitary pathology and no serum osmolality or electrolyte abnormalities. Clinical evaluation as well as sagittal and axial T1-MR images. Presence or absence of the high intensity signal of the neurohypophysis. In seven out of eight patients (87.5%) the normal high intensity signal of the neurohypophysis was not present. In one patient (12.5%), two interpreting radiologists disagreed about its presence. The high intensity signal was present in the neurohypophysis of 20 out of 23 controls (87.5%). Our data indicate an association of SIADH with the absence of the normal hyperintense signal of the neurohypophysis, confirming the usefulness of MRI as a tool to visualize ADH processing. These data also raise the possibility that the absence of the high intensity signal may be useful diagnostic tool in cases of SIADH that are difficult to diagnose clinically. Additional studies to correlate this signal with various forms of SIADH will be needed.

Air leaks and vasopressin release.

Eleven very low birthweight babies being ventilated for respiratory problems during the first week of life developed air leaks on 22 occasions. On 16 out of 19 occasions the infants showed increases in urinary excretion of vasopressin after these events and on 10 occasions out of 13 there was a rise in the plasma arginine vasopressin concentration. The peripheral signs of the syndrome of inappropriate antidiuretic hormone release were seen on only one occasion in response to the sometimes high vasopressin concentrations.

Tobacco Smoking and Hyponatremia in Psychiatric Patients

To the Editor.— In his article, Dr Blum 1 states that in his study of ten compulsive drinkers he found that episodes of hyponatremia developed only in heavy smokers. We have previously looked at this question of heavy smokers and hyponatremia and polydipsia. 2 In our study, we found that most of the patients who presented with hyponatremia and severe neurological dysfunction were heavy smokers. However, when compared with normonatremic schizophrenics, the rate of smoking was not different. Many studies concerning hyponatremia and schizophrenia do show that these patients may have inappropriate release of antidiuretic hormone (ADH) associated with their polydipsia. Factors that cause this release of ADH remain uncertain. Studies with ADH levels and their relationship to smoking would be helpful to settle this matter.

Water diuretic effect of intravenously administered 9-deoxo-16, 16-dimethyl-9-methylene-PGE2 in conscious man.

The stable prostaglandin analogue 9-deoxo-16, 16-dimethyl-9-methylene-PGE2 (9-methylene-PGE2) was infused intravenously (0.5 ml/min) in the dosage of 20 micrograms/min for 2 h in conscious euhydrated man. The administration of 9-methylene-PGE2 rapidly induced an increase in urine flow (from 1.2 +/- 0.07 to 5.35 +/- 1.07 ml/min) concomitantly with a decrease in urine osmolality (from 827 +/- 40 to 193 +/- 44 mOsm/kg). Parallel to this tubular reabsorption of sodium (Na+), calcium (Ca2+) and magnesium (Mg3+) increased and that of potassium (K+) decreased as shown by a reduction in the clearance for respective ion divided by the clearance of inulin. Apparently the water diuresis was mediated by an inhibition of arginine vasopressin's (AVP) antidiuretic effect. The mechanism behind the increase in renal tubular reabsorbtion of Na+ could possibly be a 9-methylene-PGE2 mediated modulation of the renal aldosterone effect. However the protocol followed did not provide any evidence for this, or any other explanation of the observed renal retention of Na+, Ca2+ and Mg2+. The results reported here indicate that 9-methylene-PGE2 may have a future use as a water diuretic agent in patients suffering from water retention and dilutional hyponatraemia such as seen in the syndrome of inappropriate antidiuretic hormone (AVP) release commonly known as SIADH or Schwartz-Bartter's Syndrome.

The prostaglandin-analogue-9-deoxo-16,16-dimethyl-9-methylene-PGE2 inhibits the antidiuretic effect of vasopressin (AVP) in the conscious sheep.

The effects of intravenous infusions of the stable prostaglandin analogue 9-deoxo-16,16-dimethyl-9-methylene-PGE2 (9-methylene-PGE2) in a dosage of 10 or 24 micrograms/min were studied in the consicious euhydrated, dehydrated, and hyperhydrated with the simultaneous administration of exogenous arginine vasopressin (AVP), sheep. The infusions decreased urine osmolality and increased urine flow and renal free water clearance. The results indicate that 9-methylene-PGE2 exhibits its diuretic effect by antagonizing the antidiuretic action of AVP. In the hyperhydrated sheep receiving AVP the syndrome of inappropriate antidiuretic hormone release (SIADH) was simulated. As the prostaglandin analogue effectively blocked the antidiuretic effect of the AVP-administration it appears that 9-methylene-PGE2 may play a future role as a diuretic agent, especially in conditions characterized by water retention and dilutional hyponatremia such as SIADH.

EEG-Veränderungen bei einer Patientin mit akuter intermittierender Porphyrie und einem Schwartz-Bartter-Syndrom (SIADH)

A 24-year-old female with gastrointestinal disturbances, nausea and vomiting, had a convulsion with loss of urine and bitten lips on the 5th day of hospitalization. A significant decrease of sodium and potassium levels and lowered osmolality of the serum as well as urinary hyperosmolality permitted the diagnosis of the so-called syndrome of inappropriate antidiuretic hormone release (SIADH) of unknown aetiology, described by Schwartz-Bartter. Twice short tests for porphyria were negative; then the elevated porphyrin precursors collected in 24 h urine indicated the existence of an acute intermittent porphyria. A clinical follow-up and improvement were demonstrated by the EEG findings. Since animal experiments and pathohistological findings indicate that porphyrin metabolites such as delta-amino laevulinic acid and porphobilinogen may influence inhibitory and neurosecretory structures in central nervous tissue and interfere with GABA, cerebral hyperexcitability as well as disturbance of electrolytes may be explained. Finally, the question of whether the EEG changes are due to the significant electrolyte disturbances or are typical signs of acute intermittent porphyria is discussed.

Routine tests in malignancy

It is not infrequent that routine chemical tests performed on patients with malignancies show a number of abnormalities. These can be considered in three catagories: Specific effects —biochemical changes usually resulting from the effects of substances released from malignant cells: hyponatraemia associated with inappropriate antidiuretic hormone release, hypokalaemia associated with ectopic adrenocorticotropin production, hypercalcaemia associated with the production of parathormone or other calcium mobilizing substances, hyper/hypocalcaemia associated with malignant deposits in the bone, hypoglycaemia associated with certain sarcomas, and increased alkaline phosphatase and/or lactate dehydrogenase activities associated with certain tumours. Compromised organ function —chemical evidence of organ function failure resulting from direct malignant involvement, occurring as a result of substances released by the malignant cells, or complicating therapy directed against the malignancy. Non-specific tissue damage —as a result of malignant involvement or associated therapy, malignant and/or normal cells can release various substances, such as proteins and enzymes, that can be detected in increased amounts in the circulation. With techniques such as multivariant analysis certain routine tests can be used to diagnose the presence of hepatic metastases etc. Various examples of these abnormalities will be shown. Although not usually of major diagnostic importance, such changes in routine tests performed in patients with malignancy are useful in following the progress of their disease, particularly during treatment.

Abnormal iron and water metabolism in acute intermittent porphyria with new morphologic findings

A fifty year old white man with no history of liver disease, alcoholism or iron therapy experienced his first attack of acute intermittent porphyria characterized by severe postural hypotension, severe abdominal pain, pink urine, intermittent disorientation with hallucinations, excessive diaphoresis and hyponatremia (values to 115 mEq/L). Although studies of urine and blood suggested the syndrome of inappropriate release of antidiuretic hormone (SIADH), blood volume was markedly reduced to 45.2 ml/kg (normal blood volume for males = 67.0 ± 6.5 ml/ kg) with a normal hematocrit value and a normal aldosterone secretion rate. Overactivity of the sympathetic nervous system was documented chemically by measurement of epinephrine excretion (48 and 56 μg/twenty-four hours, normal less than 20 μg/twenty-four hours) and norepinephrine excretion (102 and 112 μg/twenty-four hours, normal less than 80 μg/twenty-four hours). Death occurred suddenly and was thought to have resulted from an arrhythmia. At autopsy the histologic changes in the liver were unusual for acute intermittent porphyria. There was prominent generalized hemosiderosis which spared nodular areas of regeneration. The origin of the excessive concentrations of iron in the liver, spleen and marrow is unknown. In the supraoptic and paraventricular nuclei there was about a two-thirds reduction in the expected number of neurosecretory cells, mild astrocytic gliosis and vacuolar changes in most of the remaining neurosecretory cells. The significance of these findings is discussed.

Subdural hematoma. With inappropriate antidiuretic hormone secretion.

CEREBRAL salt-wasting describes the findings of hyponatremia and excessive renal sodium excretion in patients with various affections of the central nervous system (CNS). Formerly, these electrolyte alterations in patients with cerebral disease were ascribed to a decrease in corticotropin (ACTH) secretion or to direct interference with the neural control of renal tubular sodium reabsorption.1,2In 1957, Schwartz and co-workers3reported similar electrolyte findings in two patients with bronchogenic carcinoma and suggested that abnormal or inappropriate release of antidiuretic hormone (ADH) was the pathogenic abnormality. Since then, the syndrome of inappropriate ADH secretion (SIADH) has been documented in patients with inflammatory, vascular, degenerative, and traumatic disorders of the CNS. Moreover, recent reports indicate that this is by no means a rare syndrome.4,5 Regardless of the underlying cerebral disease, the clinical picture may be dominated by the neurologic manifestations associated with hyponatremia. Apathy, weakness, dizziness, and headaches

The effect of diet in variegate (South African genetic) porphyria

Studies of the effect of diet on porphyrin and porphyrin precursor excretion in two patients with variegate (mixed or South African genetic) porphyria demonstrate that these are inversely related to the intake of carbohydrate and/or protein in the diet. During the course of severe dietary restriction, symptoms developed, suggesting an acute attack of the disease in both patients. In one patient, this was accompanied by the syndrome of “inappropriate release of antidiuretic hormone” into the circulation. Symptoms and biochemical findings rapidly reversed with intravenous glucose administration. These data imply that hepatic δ-aminolevulinic acid synthetase is induced in variegate porphyria and is subject to what has previously been called the “glucose effect.”

The syndrome of inappropriate secretion of antidiuretic hormone

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been examined and reviewed. Typically, it is characterized by hyponatreinia without dehydration, urinary sodium loss and hypertonicity of the urine. Atypically, urinary sodium loss may be absent and urinary tonicity may be below that of serum; the only requirement is that the urine be less than maximally dilute. The syndrome is found with various tumors, notably oat cell carcinoma of the bronchus, which probably produce antidiuretic substance directly, and in a wide variety of disorders affecting the central nervous system or the lungs, in which there is probably abnormal release of endogenous antidiuretic hormone. The syndrome is also seen occasionally in patients with adrenal, thyroid or pituitary insufficiency. The possible role of the inappropriate release of antidiuretic hormone in all these disorders and in the hyponatremia which can occur postoperatively or in congestive heart failure or cirrhosis, requires further definition by new, specific assay technics.

Acute intermittent porphyria: New morphologic and biochemical findings

This paper presents the results of postmortem morphologic and biochemical studies on a patient with acute intermittent porphyria (AIP); there was evidence suggesting the syndrome of inappropriate antidiuretic hormone (ADH) release. Examination of the brain revealed injury to the median eminence and bilateral loss of neurones of the supraoptic and paraventricular nuclei. This represents the first correlation of a specific hypothalamic lesion with the syndrome of inappropriate ADH release. The activity of hepatic δ-aminolevulinic acid synthetase (ALA synthetase), a mitochondrial enzyme which normally is rate-limiting for porphyrin biosynthesis, was increased sevenfold above normal. The high level of this enzyme explains the increased porphyrin precursor excretions seen in AIP. Three general mechanisms, including an operator constitutive mutation, have been discussed as possible explanations of the induction of hepatic ALA synthetase.

Postoperative Hyponatremia with the Inappropriate Release of Antidiuretic Hormone

Postoperative Hyponatremia with the Inappropriate Release of Antidiuretic Hormone

Postoperative Hyponatremia with the Inappropriate Release of Antidiuretic Hormone

Postoperative Hyponatremia with the Inappropriate Release of Antidiuretic Hormone

BRONCHOGENIC CARCINOMA WITH INAPPROPRIATE ANTIDIURETIC ACTIVITY IN PLASMA AND TUMOR.

SINCE the original description of the syndrome of bronchogenic carcinoma complicated by inappropriate antidiuresis in 1957,2 18 cases have been reported in detail.2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Because of the similarity between these patients and normal subjects who are chronically given large doses of exogenous antidiuretic hormone, it has been assumed that the antidiuresis results from inappropriate secretion of this hormone. However, this hypothesis has not been confirmed by direct demonstration of circulating plasma antidiuretic activity. Also uncertain is the source of the hypothesized antidiuretic activity. Possibilities include the inappropriate release of pituitary antidiuretic hormone by the tumor as a result of interference with . . .

Self-Induced Water Intoxication. Case Study of a Chronically Schizophrenic Patient with Physiological Evidence of Water Retention due to Inappropriate Release of Antidiuretic Hormone

Self-Induced Water Intoxication. Case Study of a Chronically Schizophrenic Patient with Physiological Evidence of Water Retention due to Inappropriate Release of Antidiuretic Hormone

The syndrome of hyponatremia and renal sodium loss probably resulting from inappropriate secretion of antidiuretic hormone.

Case Reports1 December 1959THE SYNDROME OF HYPONATREMIA AND RENAL SODIUM LOSS PROBABLY RESULTING FROM INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONEH. J. ROBERTS, M.D.H. J. ROBERTS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-51-6-1420 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis paper reports a patient with a bronchogenic carcinoma who developed profound hyponatremia and hypochloremia in association with considerable loss of both sodium and chloride in the urine. Clinically he was found to have normal renal and adrenal function and at autopsy the kidneys and the adrenals showed no significant pathologic change.Two earlier instances of this particular syndrome were included in the report by Schwartz et al. in 1957.1It was the opinion of these investigators that this unusual electrolyte derangement could best be explained by a sustained and inappropriate secretion of antidiuretic hormone, and that this disorder was...Bibliography1. SchwartzBennettCurelopBartter WBWSFC: A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone, Am. J. Med. 23: 529, 1957. CrossrefMedlineGoogle Scholar2. PorterFrantz MRVK: Tumors associated with hypoglycemia—pancreatic and extrapancreatic, Am. J. Med. 21: 944, 1956. CrossrefMedlineGoogle Scholar3. Donaldsonvom EigenDwight RMPRRW: Gastric hypersecretion, peptic ulceration and islet-cell tumor of the pancreas (the Zollinger-Ellison syndrome): report of a case and review of the literature, New England J. Med. 257: 965, 1957. CrossrefMedlineGoogle Scholar4. BerlinerLevinskyDavidsonEden RWNGDGM: Dilution and concentration of the urine and the action of antidiuretic hormone, Am. J. Med. 24: 730, 1958. CrossrefMedlineGoogle Scholar5. LeafBartterSantosWrong AFCRFO: Evidence in man that urinary electrolyte loss induced by Pitressin is a function of water retention, J. Clin. Investigation 32: 868, 1953. CrossrefMedlineGoogle Scholar6. PaullPecoraCooperLawson AMDVPHA: Bradycardia and syncope as early manifestations of bronchogenic carcinoma, New England J. Med. 248: 773, 1953. CrossrefMedlineGoogle Scholar7. WiermanClagettMcDonald WHOTJR: Articular manifestations in pulmonary diseases, J. A. M. A. 155: 1459, 1954. CrossrefMedlineGoogle Scholar8. BrickGlazer IBL: Marked eosinophilia with cancer: a poor prognostic sign, Ann. Int. Med. 35: 213, 1951. LinkGoogle Scholar9. WeltSeldinNelsonGermanPeters LGDWWPWJJP: Role of central nervous system in metabolism of electrolytes and water, Arch. Int. Med. 90: 355, 1952. CrossrefGoogle Scholar10. Cort JH: Cerebral salt wasting, Lancet 1: 752, 1954. CrossrefGoogle Scholar11. Wise BL: Relation of brain stem to renal electrolyte excretion, Proc. Soc. Exper. Biol. and Med. 91: 557, 1956. CrossrefMedlineGoogle Scholar12. EpsteinLevitin FHH: "Cerebral salt-wasting": an example of sustained inappropriate release of antidiuretic hormone, abstract, J. Clin. Investigation 38: 1001, 1959. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: West Palm Beach, Florida*Received for publication August 18, 1958.Requests for reprints should be addressed to H. J. Roberts, M.D., 1525 North Flagler Drive, West Palm Beach, Florida. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byLung Cancer MarkersPituitary insufficiency, inappropriate antidiuretic hormone (ADH) secretion, and carcinoma of the bronchusParaneoplastic syndromes Resulting from elaboration of ectopic hormones, antigens and bizarre toxinsAuswirkungen der renalen Insuffizienz auf die Zusammensetzung der Cerebrospinalflüssigkeit, den Stoffwechsel des ZNS und zentralnervöse FunktionenDie zentralnervöse klinische Symptomatologie der akuten und chronischen NiereninsuffizienzStörungen der HarnkonzentrierungHormonal Syndromes Associated with NeoplasiaCase 30-1967The syndrome of inappropriate secretion of antidiuretic hormoneAn investigation into the cause of hyponatremia in the syndrome of inappropriate secretion of antidiuretic hormoneInappropriate Renal Sodium Loss Reverted by Vena Cava ObstructionHENRY O. HEINEMANN, M.D., JOHN H. LARAGH, M.D., F.A.C.P.Hyponatremia from inappropriate antidiuretic hormone elaboration in carcinoma of the lungPARANEOPLASTIC DISORDERS“Inappropriate” secretion of antidiuretic hormone without corresponding hyponatraemia in cerebral pathologyHypoadrenocorticotropism with Hyponatremia, Resembling Antidiuretic Hormone ExcessJOSEPH L. GRANT, M.D., F.A.C.P., ALASTAIR MACDONALD, STEPHEN R. BROVENDER, M.D., NICHOLAS YANKOPOULOS, M.D.Physiology of the kidneyDisorders of renal functionBronchogenic Carcinoma with Inappropriate Antidiuretic Activity in Plasma and TumorA review of unusual systemic manifestations associated with carcinomaCarcinoma of the Lung with Inappropriate AntidiuresisHyponatremia and the inappropriate secretion of antidiuretic hormoneHyponatremia and bronchogenic carcinoma associated with renal excretion of large amounts of antidiuretic materialElectrolyte disturbances associated with cancerHYPONATREMIA IN ACUTE INTERMITTENT PORPHYRIA PROBABLY RESULTING FROM INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE*Use of a low-sodium formula as an improved Karell diet, with emphasis upon the outpatient management of heart failure and lymphedemaAldosterone in Cerebral Salt WastingThe Clinical and Physiologic Significance of the Serum Sodium ConcentrationUnstable osmolar homeostasis with and without renal sodium wastageIdiopathic, episodic inappropriate secretion of antidiuretic hormoneAbnormal electrolyte and water metabolism in acute intermittent porphyriaHypo- and HypernatremiaLOUIS G. WELT, M.D., F.A.C.P.Cerebral HyponatremiaSodium BalanceHyponatremia and Renal Wasting of Sodium in Patients with Malfunction of the Central Nervous System 1 December 1959Volume 51, Issue 6Page: 1420-1426KeywordsAntidiuretic hormoneAutopsyBlood plasmaBradycardiaChloridesHyponatremiaKidneysPathogenesisSodiumUrine ePublished: 1 December 2008 Issue Published: 1 December 1959 PDF downloadLoading ...