Disease relevance of Inappropriate ADH Syndrome

• Because dDAVP acts only on the V2 receptors, these data suggest that the higher urate clearance observed during hyponatremia related to SIADH is not only the consequence of an increased "effective vascular volume," but that V1-receptor stimulation also contributes to it, by a mechanism that remains to be determined [1].
• In 14 patients with bronchogenic carcinoma, but without overt SIADH, plasma levels of arginine vasopressin were significantly higher than in normal subjects (p less than 0.001) [2].
• The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) occurred during an excerbation of multiple sclerosis (MS) [3].
• The inappropriate secretion of AVP was evident in the patients with SIADH and hypopituitarism, and hydrocortisone replacement normalized urinary excretion of AQP-2 and renal water excretion in those with hypopituitarism [4].
• Despite the mitigating effect of decreased renal sensitivity to AVP, the SIADH seen in these patients appears to contribute to the development of water intoxication caused by polydipsia [5].

High impact information on Inappropriate ADH Syndrome

• High plasma atrial natriuretic peptide independent of sodium balance in SIADH [6].
• SIADH in a patient receiving sertraline [7].
• We describe an elderly woman who presented with significant hyponatremia caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) during therapy with amiodarone [8].
• This modification of tubular handling of uric acid is considered to be induced by the increase in the "effective vascular volume". This study was designed to determine if V1-receptor stimulation participates in the development of a high uric acid clearance rate as in SIADH, in which the antidiuretic hormone acts on V1 and V2 receptors [1].
• SIADH associated with fluoxetine and sertraline therapy [9].

Chemical compound and disease context of Inappropriate ADH Syndrome

• As observed in the SIADH, cirrhotic patient with high FE uric acid have raised FE urea only when salt excretion is low [10].
• Although tuberculosis is considered a cause of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), circulating vasopressin has been documented in only a few cases [11].
• More cases of SIADH with fluoxetine [12].
• This was clearly shown during the long-term treatment of a third patient with SIADH who was taking 30 g urea/day during 11 weeks [13].
• Although he had been taking haloperidol, the SIADH responded to fluid restriction alone [14].

Biological context of Inappropriate ADH Syndrome

• It is concluded that urea is a good alternative in the treatment of patients with SIADH who presented with persistent hyponatremia despite the restriction of water intake [13].
• Up-regulation of AQP-2 mRNA expression was found, but this up-regulation was significantly less in the SIADH rats compared with the dDAVP-excess rats (153.5 +/- 29.8% vs. 323.7 +/- 23.8% on day 7, P < 0.05) [15].
• To investigate the hypothesis that atrial natriuretic peptide (ANP) is related to the natriuresis in SIADH, serum samples were obtained from 8 neurosurgical patients with intracranial disease seen consecutively who fulfilled the traditional clinical and laboratory criteria for SIADH [16].
• A patient with malignant thymoma is reported, in whom the syndrome of inappropriate antidiuretic hormone secretion (SIADH) occurred 36-48 hours after being given cis-Dichlorodiammineplatinum II (CPPD) with a mannitol diuresis [17].
• Clinicians should be aware of the possibility that carboplatin may cause SIADH, and should carefully monitor electrolyte balance after chemotherapy [18].

Anatomical context of Inappropriate ADH Syndrome

• The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been reported rarely in systemic lupus erythematosus (SLE) with central nervous system disease [19].
• Because the syndrome of inappropriate antidiuretic hormone (SIADH) is a state of disturbed body fluid volume regulation and altered sodium balance we sought to determine if recently described volume regulatory factors were stimulated in SIADH [20].
• Risk factors for SIADH included young age, transplantation from an HLA-mismatched or unrelated donor, cord blood transplantation, and graft-versus-host disease prophylaxis with methyl prednisolone [21].
• With respect to the underlying mechanisms of SIADH in the cases, we considered two factors; 1) dysfunction of the feedback system in ADH secretion via intrathoracic volume receptors caused by changes in intrathoracic circulation, and 2) primarily functional abnormalities in the limbic system which could influence hypothalamic osmoreceptors [22].
• By administering vinblastine on days 1 and 4 (instead of days 1 and 2, as suggested in the high-response regimen consisting of vinblastine, bleomycin, and cis-platinum) we have found better bone marrow tolerance and have not noticed the inappropriate ADH syndrome [23].

Gene context of Inappropriate ADH Syndrome

• Thus, V2 receptor blockade could be of interest in several water-retaining diseases such as the syndrome of inappropriate antidiuretic hormone secretion (SIADH), liver cirrhosis and congestive heart failure and deserves to be widely explored [24].
• Either hypervolemia or hypotonicity may diminish the post-receptor signaling of AVP in renal collecting duct cells, under the chronic AVP excess state found in SIADH [15].
• CONCLUSION: AVP-induced alterations of rBSC1 expression, as well as those of AQP2, are involved in the pathogenesis of SIADH [25].
• We describe two infants whose clinical and laboratory evaluations were consistent with the presence of SIADH, yet who had undetectable arginine vasopressin (AVP) levels [26].
• We have previously suggested that IL-6-stimulated AVP secretion may be the origin of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in inflammatory conditions [27].

Analytical, diagnostic and therapeutic context of Inappropriate ADH Syndrome

• Eight subjects unable to excrete ingested free water normally (three patients with SIADH and five healthy humans after intranasal administration of desmopressin) underwent a standard oral water loading test [28].
• Seven of nine patients with overt SIADH, studied after fluid deprivation, showed an increase in plasma arginine vasopressin coincident with an increase in plasma osmolality (r = +0.8, p less than 0.01); in one patient, plasma arginine vasopressin returned to the original level following rehydration [2].
• OBJECTIVES: a) To determine if antidiuretic hormone (ADH) is elevated in patients undergoing spinal fusion, especially in those who have clinical evidence of syndrome of inappropriate antidiuretic hormone (SIADH); b) to evaluate the relationship between ADH secretion and the secretion of atrial natriuretic peptide (ANP) [29].
• Two patients with squamous cell carcinoma of the head and neck are reported in whom the syndrome of inappropriate antidiuretic hormone (SIADH) secretion occurred transiently during the rapid cytolytic phase of tumor destruction after chemotherapy with cis-platinum diamminedichloride and bleomycin [30].
• In animal models of the syndrome of inappropriate antidiuresis (SIADH), sustained administration of vasopressin and water results in free-water retention and progressive hyponatremia for several days, which is then followed by escape from the vasopressin-induced antidiuresis [31].

References