Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Presented is the case of an elderly woman who developed severe hyponatremia while taking tricyclic antidepressants. She met the criteria for the syndrome of inappropriate antidiuretic hormone secretion induced by drugs. Her symptoms of lethargy, weakness, and gastrointestinal disturbances developed insidiously, allowing the hyponatremia to reach severe levels before a diagnosis was made. A variety of psychoactive drugs, most prominently tricyclic antidepressants, have been reported to produce hyponatremia idiosyncratically in elderly persons.
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PMID:Hyponatremia due to antidepressant medications. 663 32

A smoking patient presented with altered mental status, left sided weakness, and an opacity on the chest roentgenogram. During hospitalization he developed hyponatremia, which was corrected with hypertonic saline solution, fluid restriction, and demethylchlortetracycline. The clinical presentation and the laboratory findings supported the diagnosis of the syndrome of inappropriate secretion of antidiuretic hormone. This was believed to be associated with the pulmonary carcinosarcoma documented at necropsy.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in association with pulmonary carcinosarcoma. 712 Apr 55

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

A 73-year-old man with alcoholic liver cirrhosis was admitted to our hospital because of massive hematemesis. He was treated with continuous intravenous infusion of vasopressin of 0.2 U/min. 22 hours after the infusion, he complained of myalgia, muscle weakness and skin mottling in the extremities. The skin lesion extended to the back. The serum CK and myoglobin levels were elevated to 52,280 IU/L and 84,400 ng/ml respectively. The urinary myoglobin level was elevated to 732,000 ng/ml. On the fifth hospital, he died of bleeding from the esophageal varices. Autopsy examination demonstrated necrosis of the skeletal muscle cells and myoglobin casts in the renal tubules. Our patient was probably hypersensitive to vasopressin because of underlying liver dysfunction. The massive myonecrosis might be induced from the following conditions; overreactive vasopressin-induced vasoconstriction resulted in ischemic muscle damage, and hypersensitive sarcoplasmic reticulum released excessive Ca2+ followed by muscle hypercontraction as seen in malignant syndrome or malignant hyperthermia.
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PMID:[A case of rhabdomyolysis with administration of intravenous vasopressin]. 866 38

In this prospective study, a series of 1812 consecutive mild head injured adult patients who visited the hospital emergency department were assessed. Twenty-eight patients (1.5%) deteriorated after head injury; 23 of these (1.3% of the series) required surgical intervention. Five patients (0.3%) deteriorated due to non-surgical causes [post-traumatic seizure 2, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) 3]. Most of the deterioration occurred within the first 24 hours (57%). Post-traumatic headache was found in 280 patients (15.5%) and 84 patients (4.6%) suffered post-traumatic vomiting. The relative risk is calculated. Age over 60, presence of drowsiness, focal motor weakness, post-traumatic headache and vomiting has increased risk of deterioration (p < 0.001). This study suggests that post-traumatic headache and vomiting deserve more clinical attention rather than being considered as post-traumatic syndrome only.
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PMID:Relative risk of deterioration after mild closed head injury. 874 3

Primary adrenal insufficiency (PAI) is a relatively rare but serious condition that can lead to signs and symptoms ranging from mild generalized weakness and fatigue to fulminant shock and death. We present the case of a previously healthy 31-year-old man who developed PAI while undergoing rehabilitation after a severe traumatic brain injury (TBI). The patient suffered a TBI with comminuted skull fractures, bifrontal confusions, and bilateral epidural hematomas in a jet-ski accident. Acute hospitalization was prolonged by several medical complications, and the patient was admitted for subacute rehabilitation 1 month after his injury with cognitive deficits, persistent agitation, confusion, generalized weakness, and poor endurance for therapy. His weakness, fatigue, and orthostasis did not improve with attempts at gradual remobilization. The patient also had persistent anorexia, nausea, and hyponatremia despite various treatment regimens. Endocrinology workup showed normal anterior pituitary function but an abnormal response to adrenocorticotropic hormone (ACTH) stimulation, leading to the diagnosis of PAI. The patient was treated with prednisone and fludrocortisone, which resulted in improvement in clinical symptoms followed by rapid gains in all functional areas. No previous descriptions of PAI following head injury were found in the medical literature. It is important for physiatrists to be aware of this entity because symptoms of adrenal insufficiency can be similar to those commonly seen with TBI alone. PAI may also be confused with other endocrine disorders more frequently seen after TBI such as the syndrome of inappropriate antidiuretic hormone secretion. Recognition and appropriate management of adrenal insufficiency can lead to significant clinical and functional gains.
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PMID:Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. 908 56

Myotonic dystrophy (DM) is an autosomal dominant disorder causing myotonia, progressive muscle weakness, and endocrine abnormalities including hypothalamic-pituitary-adrenal (HPA) axis hyperresponsiveness to CRH-mediated stimuli. This ACTH hyperresponsiveness appears directly related to the underlying genetic abnormality. Naloxone (Nal)-mediated CRH release causes ACTH release in normal humans and an ACTH hyperresponse in DM. Alprazolam (APZ) attenuates the ACTH release in response to Nal in normal individuals, probably by inhibiting CRH release. This study investigates the effects of APZ on Nal-induced HPA axis stimulation in DM. The ACTH response to Nal in DM subjects was significantly reduced by APZ. Despite this DM patients have a relative resistance to APZ inhibition of Nal-induced ACTH/cortisol release. APZ caused a smaller percentage reduction in AUC for ACTH in DM compared with controls. These findings provide further insight into the mechanism(s) of the HPA axis abnormalities in DM. In DM, there may be an increase in tonic opioid inhibition to CRH release with compensatory increases in stimulatory pathways. Alternatively, these patients may have a basal increase in pituitary vasopressin levels or an enhanced AVP/CRH synergistic mechanism at the level of the corticotroph.
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PMID:Inhibition of naloxone-stimulated adrenocorticotropin release by alprazolam in myotonic dystrophy patients. 966 54

Vincristine, referred to as a vinka alkaloid, has been used as a component of the various chemotherapeutic regimens. The major side effects of the usual dosage of vincristine are bone marrow suppression, gastrointestinal disorder, and neurotoxicity. A 53-year-old cervical cancer patient received 14 mg (4 mg/m2/day for 2 days) of vincristine instead of vinblastine because of the similarity between the two names. Then life threatening toxicities including paresthesias, bone marrow depression, severe oral mucositis, paralytic ileus, bladder atony, myalgia, muscle weakness, high fever, derangements of various organs (liver, heart), hypertension, and insomnia were encountered. But hypotension and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) were not observed. Other than paresthesias in the extremities, the patient recovered completely from toxic impairments with intensive symptomatic and supportive care. In order to prevent the administration of the overdosed drug, it would be advisable for chemotherapy to be administered only by an experienced physician who is able to check the dose and concentration.
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PMID:Overdose of vincristine: experience with a patient. 968 18

We describe a patient who had metastatic carcinoma of the stomach and severe headaches, weakness, and diplopia. The patient had meningeal carcinomatosis that was confirmed by examination of the cerebrospinal fluid after computed tomography of the brain was normal. Weakness was explained by the finding of hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). We believe this is the first reported case of meningeal carcinomatosis in which stomach carcinoma caused SIADH. The differentiation between SIADH and cerebral salt wasting due to malignant tumors is emphasized.
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PMID:Meningeal carcinomatosis and syndrome of inappropriate antidiuretic hormone in a patient with metastatic carcinoma of the stomach. 982 97

A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone associated with amyotrophic lateral sclerosis in respiratory failure. 1038 39


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