Syndrome of inappropriate secretion of antidiuretic hormone produced by vincristine toxicity (with bioassay of ADH level)

Suskind, Robert M.; Brusilow, Saul W.; Zehr, J. E.

doi:10.1016/s0022-3476(72)80381-0

Cited by 68 publications

(18 citation statements)

References 4 publications

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“…The hypothesis advanced to explain SIADH in this patient is that fibers containing spheroids played a role in disturbing the inhibitor mechanism of the supraoptic nucleus neurosecretion.The fact that a peripheral neuropathy is frequently associated in patients suffering from vinca alkaloid-related SIADH is an indirect argument for this neurological toxicity. Abnormally elevated serum and urine antidiuretic hormone (ADH) levels have been found concomitantly with clinical hyponatremia-associated SIADH in several patients, corroborating this hypothesis [55,62,63,81]. Finally Tomita et al [67] suggest that the kallikrein-kinin system may play a role in the development of excessive natriuresis in the SIADH induced by vincristine.…”

Section: Vinca Alkaloidsmentioning

confidence: 80%

“…In the case of SIADH, an adapted treatment must be applied. Water restriction [11,12,22,27,30,39,42,55,62,63,71,76,77,81], hypertonic saline perfusion more or less associated with furosemide [25,33,54,62,70], and demeclocycline [40,49] have been used against SIADH secondary to a chemotherapeutic agent. Urea and lithium are also potential effective therapies in case of SIADH [13, 14, 79] but were not used in these described cases.…”

Section: Discussionmentioning

confidence: 99%

“…The route of administration of the drugs is classically intravenous but in three patients, hepatic arterial infusion of vinblastine was associated with the occurrence of SIADH [21]. The cases described are generally reversible, both for hyponatremia and for its associated symptoms [1,12,17,25,44,52,55,60,62,63,71,76,80,81], but not in every case. One case of a 6-month-old boy treated with vincristine, Adriamycin and cytarabine was fatal in the context of a SIADH.…”

Section: Vinca Alkaloidsmentioning

confidence: 99%

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Hyponatremia related to medical anticancer treatment

Berghmans

1996

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Hyponatremia is a common potential complication in cancer patients. It can be related to anticancer medical therapy. Vincristine, vinblastine, cisplatin and cyclophosphamide are the chemotherapeutic agents most frequently associated with hyponatremia. More recently, analogs such as carboplatin and ifosfamide have also been incriminated. Hyponatremia is also associated with new immunomodulators (interferon, interleukin-2 and levamisole) and monoclonal antibodies. The mechanism by which all these drugs act on the sodium steady state is only partially known. The syndrome of inappropriate antidiuretic hormone secretion is described secondary to vinca alkaloids and cisplatin and possibly with alkylating agents. Renal salt wasting is described with platinum compounds.

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Section: Vinca Alkaloidsmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Vinca Alkaloidsmentioning

confidence: 99%

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Hyponatremia related to medical anticancer treatment

Berghmans

1996

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“…In several cases, these symptoms were clearly related to severe hyponatremia and an inappropriate secretion of the antidiuretic hormone, arginine vasopressin (13)(14)(15)(16). While this complication might be explained by toxic alterations of peripheral osmoreceptors (17), the precise mechanism by which vincristine causes CNS injury in patients with no underlying metabolic abnormalities is not known.…”

Section: Discussionmentioning

confidence: 99%

Acute encephalopathy associated with continuous vincristine sulfate combination therapy: case report

1985

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Neurotoxicity is a well-recognized and commonly observed side effect associated with the use of vincristine sulfate in cancer chemotherapy. The clinical manifestations of vincristine neuropathy cover a wide spectrum of peripheral neurologic dysfunctions that have been described to be reversible and cumulative in most instances (1, 2). Paresthesias, loss of tendon reflexes, and progressive weakness are the most common clinical features (3, 4). Sensory impairment, cranial nerve palsies, gastrointestinal disturbances, and autonomic dysfunctions including atonic bladder, impotence, and orthostatic hypotension may occur (5). Acute CNS complications, usually presenting as generalized seizures, are extremely rare and only a few cases have been reported which were without underlying biochemical or structural abnormalities (1, 5-9). We describe the case of a woman with multiple myeloma, who developed fulminant encephalopathy following 4 days of continuous vincristine, adriamycin, and day 1-4 pulse dexamethasone (VAD) combination therapy.

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“…Hyponatraemia, occasionally associated with convulsions, has also been described and attributed to inappropriate antidiuretic hormone (ADH) secretion (Fine, Clarke, and Shore, 1966;Slater, Wainer, and Serpick, 1969). Some of these patients had raised ADH levels (Suskind, Brusilow, and Zehr, 1972;Robertson, Bhoopalam, and Zelkowitz, 1973;Stuart et al, 1975). Recovery from the acute toxic effects of the drug occurred in all the reported cases, except in that of Weiden and Wright (1972) where the patient died of bronchopneumonia after vincristine-induced paraplegia.…”

mentioning

confidence: 99%