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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↗
PubMed1983

Management of the syndrome of inappropriate antidiuretic hormone secretion in small cell lung cancer.

From 1976 to 1980, 18 of the 250 patients (7%) seen with small cell carcinoma of the lung had clinically evident inappropriate secretion of antidiuretic hormone (ADH). Hyponatremia was usually severe (116 +/- 7 meq/l), and eight patients showed symptoms of water intoxication at the time of diagnosis. Of the eight patients who had plasma ADH measured at diagnosis, seven had elevated values (mean 52.0, range 16.1 - greater than 250 pg/ml). Intensive combination chemotherapy produced objective tumor responses in all patients, and syndrome of inappropriate ADH secretion (SIADH) resolved in 16 of 17 evaluable patients within three weeks of initiation of treatment. ADH values after therapy were normal, and all patients maintained a normal serum sodium during the period of tumor remission in spite of unrestricted fluid intake. All 17 evaluable patients have developed progressive cancer, but only 10 have manifested recurrent SIADH. Patient survival was similar to the overall population of small cell carcinoma patients without SIADH. The indirect methods of treatment for SIADH (fluid restriction, demeclocycline, lithium, urea) are frequently of transient value while awaiting a response to chemotherapy or in patients with resistant tumors. However, the initial treatment of choice for SIADH associated with small cell carcinoma of the lung is combination chemotherapy.

Adult↗
PubMed1999

[Hypo-osmolar hyponatremic syndromes: physiopathology and clinical aspects].

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.

Adrenal Insufficiency↗
PubMed1992

Disorders of antidiuretic hormone secretion.

Depending upon the age and sex of a human, water constitutes 55% to 80% of the body's weight and provides a milieu vital for survival. Water imbalance is common among the critically ill. Excessive increases or decreases in body water can be lethal. There are numerous pathologic and iatrogenic causes for water imbalance, the most troublesome being disorders of antidiuretic hormone (ADH) secretion. Antidiuretic hormone plays a pivotal role in conserving water by increasing reabsorption of water by the kidney. Without the influence of ADH (as is seen in diabetes insipidus), a person would be required to ingest between 5 and 15 L of water daily to match urinary losses. Conversely, excessive ADH secretion would reduce urine output in adults to as little as 500 mL per day, dangerously diluting blood volume and expanding intracellular volume. This is what causes the symptoms of the syndrome of inappropriate ADH (SIADH). The care of patients who are critically ill and have disorders of ADH secretion can be challenging. The challenge lies in the recognition and treatment of the disorder. A collaborative team approach helps patients achieve and maintain the delicate balance of body fluids.

Diabetes Insipidus↗
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↗
PubMed1983

Spontaneous remission of cranial diabetes insipidus due to concomitant development of ADH-producing lung cancer--an autopsied case.

The very rare occurrence of an ADH-producing small cell carcinoma of the lung in a 52 year old male patient with cranial diabetes insipidus since childhood is described. In this case diabetes insipidus disappeared concomitantly with development of lung cancer and re-appeared with shrinkage of the lung tumour by radiation therapy. Further progressive expansion of the primary and metastatic tumours induced the syndrome of inappropriate ADH secretion once again (SIADH). This deterioration in the clinical course was reflected in the plasma levels of ADH and neurophysins. The existence of vasopressin in the tumour tissue was also demonstrated by means of an immunohistochemical staining technique combined with anti-vasopressin serum.

Carcinoma, Small Cell↗
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↗
PubMed2004

Sinonasal neuroendocrine carcinoma in association with SIADH.

BACKGROUND: Neuroendocrine carcinoma (NEC) is a rare malignancy of the nasal cavity or paranasal sinuses. The syndrome of inappropriate ADH secretion (SIADH) has not been previously reported in association with this cancer. METHODS: We report a 30-year-old woman with histologically confirmed neuroendocrine carcinoma who also demonstrated SIADH. After successful chemotherapy and radiotherapy treatment for the neoplasm, her SIADH resolved. A literature search found eight cases of olfactory neuroblastoma (ONB) associated with SIADH, four of which resolved after treatment of the malignancy. RESULTS: Treatment of the underlying malignancy resulted in the immediate resolution of the SIADH. CONCLUSIONS: We report the first case of SIADH associated with NEC, which resolved after treatment of the cancer. A direct cause and effect between ONB/nasal NEC and SIADH has been established in previous reports.

Adult↗
PubMed1990

Phase I trial of intravenous vinzolidine (LY 104208) given on a biweekly dosing schedule.

Vinzolidine (VZL) is a semisynthetic vinca alkaloid with broad antitumor activity in animal models of malignancy but had unpredictable toxic effects when given orally to humans. To minimize the toxic effects due to potential erratic gastrointestinal absorption, this drug was restudied in man as an intravenous preparation given as a rapid injection every two weeks. The maximum tolerated dose (MTD) on this schedule was 9.0 mg/m2 with unpredictable leukopenia (usually occurring 5-14 days post treatment but appearing erratically), constipation, paralytic ileus, and inappropriate ADH syndrome as major toxicities. Nonhematologic toxicities were dose-limiting. Repetitive dosing at two week intervals was associated with leukopenia at D 14-15 in some but not all patients treated above 5.0 mg/m2 precluding further treatment on schedule. In contrast, the oral MTD of this agent in our prior studies was 45 mg/m2 with no evidence of delayed leukopenia. Intrapatient variability of toxicity was small; interpatient variability of toxicity was substantial and did not correlate with prior therapy. Because of the presence of delayed hematologic toxicity on repetitive dosing schedules, intravenous VZL should be given on a dosing schedule longer than 14 days. No antitumor activity was seen in this study.

Adult↗
PubMed1998

SIADH following laparoscopic cholecystectomy.

PURPOSE: To present an unusual case of inappropriate antidiuretic hormone secretion syndrome after a minor surgical procedure in a healthy patient. CLINICAL FEATURES: A 71-yr-old woman underwent uneventful laparoscopic cholecystectomy for gallstones under general anaesthesia. Fifty-two hours post operatively she began convulsing and was found to have a serum sodium concentration as low as 112 mmol.L-1. Serum osmolality, urinary sodium concentration and urine osmolality suggested a diagnosis of inappropriate antidiuretic hormone secretion. Subsequent treatment with anticonvulsants followed by strict fluid restriction which increased serum sodium concentrations led to rapid recovery. CONCLUSION: The syndrome of inappropriate ADH secretion has several well documented causes including major surgery. Few episodes have been described following minor surgery in healthy patients and the only possible risk factor evident in this patient could be her advancing years.

Aged↗