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)

A 44-year-old female with 16-year history of rheumatoid arthritis visited Akiru Hospital with complaints of a thirst, a dry mouth and a general fatigue. One week prior to admission, the patient manifested excessive thirsty feeling, a body weight loss and a sleepless by the polyuria. She has been given 5-10 mg of prednisolone and 240 mg of lobenzarit disodium (CCA) in a day for 11 months. A hematologic examination showed no abnormality, and the examination of her serum showed the following values: BUN, 9.3 mg/dl; creatinine, 0.9 mg/dl; sodium, 139 mEq/l; chloride, 102 mEq/l; potassium, 3.9 mEq/l; osmolality, 290 mOsm/l. Plasma antidiuretic hormone (ADH) level increased slightly (6.0 pg/ml). Examination of her urine revealed specific gravity, 1.005; no trace of glucose, protein, blood and ketones; normal sediment; and osmolality, 209 mOsm/l. The patient was given exogenous ADH (10 units of vasopressin tannate in oil, intramuscularly) to obtain a diagnosis, and she was found to be unable to concentrate her urine more than 1.008 in the specific gravity. A water restriction, as a test for diabetes insipidus, also failed to concentrate her urine in the specific gravity and in the osmolality. Together with these findings, the patient was diagnosed to be a diabetes insipidus, and CCA was seemed to account for the disease. This unfavorable effect of CCA appeared to be reversible, since the patient recovered her urinary concentrating ability after the medication of CCA was discontinued.
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PMID:[Lobenzarit disodium (CCA)--induced diabetes insipidus in a patient with rheumatoid arthritis]. 141 95

Two cases of rheumatoid arthritis, who developed severe hyponatremia after treatment with non-steroidal anti-inflammatory drugs (NSAID) are presented. Early diagnosis was followed by rapid correction with hypertonic saline. It is suggested that NSAIDs, like piroxicam, diclofenac and indomethacin, may be added to the list of drugs which can induce syndrome of inappropriate antidiuretic hormone (SIADH).
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PMID:Water intoxication associated with non-steroidal anti-inflammatory drug therapy. 359 60

We experienced three patients who have collagen diseases with respiratory failure accompanied by hyponatremia. They were one systemic lupus erythematosus patient with interstitial pneumonia, one rheumatoid arthritis patient with acute pneumonitis, and one dermatomyositis patient with pulmonary fibrosis and organizing pneumonia. In all 3 patients, hyponatremia appeared along with a decrease in arterial O2 partial pressure (PaO2) and the hyponatremia tended to improve when the PaO2 increased after inhalation of oxygen, even though their respiratory failure were not improved. In dermatomyositis patient, serum Na levels were over-corrected after increase in PaO2. The serum and urine osmolality, serum antidiuretic hormone (ADH) levels and clinical pictures demonstrated a presence of inappropriate secretion of ADH (SIADH) in all 3 cases when hyponatremia and hypoxia appeared. A close association between hyponatremia and hypoxia observed in 3 patients strongly suggested that their SIADH were associated with hypoxia since SIADH could be demonstrated by hypoxia. Therefore, it is important to realize that hypoxia-induced hyponatremia will be promptly corrected to hypernatremia by an oxygen inhalation, which could cause a lethal central pontine myelinolysis.
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PMID:[Three cases of respiratory failure of collagen diseases accompanied by syndrome of inappropriate secretion of antidiuretic hormone (SIADH)]. 780 Dec 3

Nephrogenic diabetes insipidus (NDI) occurred in a 43-year-old woman who had received lobenzarit disodium for the treatment of rheumatoid arthritis (RA). Her urine output was initially 3 l/day and urine osmolarity was 203 mOsm/l. Based on a sodium chloride loading test and a vasopressin loading test, she was diagnosed as having lobenzarit-induced NDI. Seven days after the cessation of the use of lobenzarit disodium, polydipsia and polyuria disappeared, and the vasopressin test showed a normal response. These findings suggest that lobenzarit induces a reversible form of NDI as a side effect. The reports of lobenzarit-induced NDI in Japan during the past seven years are also reviewed.
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PMID:Nephrogenic diabetes insipidus induced by lobenzarit disodium treatment in patients with rheumatoid arthritis. 868 99

We describe symptomatic hydrocephalus and secondary syndrome of inappropriate antidiuretic hormone as clinical manifestations of vertical atlantoaxial subluxation in a patient with severe rheumatoid arthritis. We found no reports of this association as a complication of rheumatoid cervical involvement. We discuss the difficulties of differential diagnosis and treatment in this patient.
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PMID:Hydrocephalus and secondary syndrome of inappropriate antidiuretic hormone due to rheumatoid vertical atlantoaxial subluxation. 878 47

Two rheumatoid arthritis (RA) patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) during the course of infection are herein reported. One patient developed SIADH during the course of a localized cutaneous herpes zoster infection while the other developed SIADH in conjunction with Staphylococcus simulans septicemia. We consider that the development of SIADH was strongly associated with superimposed infections in the underlying RA. This is the first report discussing the association of SIADH and infections in RA patients in which SIADH is diagnosed by measurement of plasma ADH.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in elderly patients with rheumatoid arthritis associated with infections: report of two cases. 883

Adjuvant arthritis (AA) is an experimental model for rheumatoid arthritis, and is induced most easily in inbred Lewis rats by an intradermal injection of heat-killed Mycobacterium tuberculosis (MT) in incomplete Freund's adjuvant. Susceptivity to the arthritis in Lewis rats is thought to be related to a defect in their responses of the hypothalamo-pituitary-adrenal (HPA) axis to the disease. Because the use of an inbred strain is necessary for our immunological studies, we examined in Lewis rats changes in behavior, the HPA axis, and sympathetic nerve activities during development of the adjuvant arthritis. Following intradermal injections of heat-killed MT in adjuvant, the arthritis began to develop on day 12, reaching its maximum severity on day 21, and remained at the level for over a month. The body temperature rose from day 0 to 5 (the primary phase--before the onset of the arthritis). It then fell to normal temperature, and again rose from day 10 to 21 (the secondary phase--with fully developed arthritis). The behavioral (physical activity, food, and water intake) and hormonal parameters [plasma adrenocorticotropic hormone (ACTH) and corticosterone levels] also changed in two phases, similar to those observed in the temperature responses. No change in plasma vasopressin level was observed. Sympathetic nerve activities, assessed by changes in plasma noradrenalin levels, increased more in the primary than in the secondary phase. The possible causes for the biphasic changes associated with development of arthritis are discussed.
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PMID:Biphasic changes in behavioral, endocrine, and sympathetic systems in adjuvant arthritis in Lewis rats. 884 5

Interleukin-6, an inflammatory cytokine, is characterized by pleiotropy and redundancy of action. Apart from its hematologic, immune, and hepatic effects, it has many endocrine and metabolic actions. Specifically, it is a potent stimulator of the hypothalamic-pituitary-adrenal axis and is under the tonic negative control of glucocorticoids. It acutely stimulates the secretion of growth hormone, inhibits thyroid-stimulating hormone secretion, and decreases serum lipid concentrations. Furthermore, it is secreted during stress and is positively controlled by catecholamines. Administration of interleukin-6 results in fever, anorexia, and fatigue. Elevated levels of circulating interleukin-6 have been seen in the steroid withdrawal syndrome and in the severe inflammatory, infectious, and traumatic states potentially associated with the inappropriate secretion of vasopressin. Levels of circulating interleukin-6 are also elevated in several inflammatory diseases, such as rheumatoid arthritis. Interleukin-6 is negatively controlled by estrogens and androgens, and it plays a central role in the pathogenesis of the osteoporosis seen in conditions characterized by increased bone resorption, such as sex-steroid deficiency and hyperparathyroidism. Overproduction of interleukin-6 may contribute to illness during aging and chronic stress. Finally, administration of recombinant human interleukin-6 may serve as a stimulation test for the integrity of the hypothalamic-pituitary-adrenal axis.
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PMID:The pathophysiologic roles of interleukin-6 in human disease. 944 73

Corticotropin-releasing hormone (CRH) is a major regulator of the hypothalamic-pituitary-adrenal axis (HPA) and principal coordinator of the stress response. As in stress, intracerebroventricular administration of CRH suppresses the immune system indirectly, via glucocorticoid and/or sympathetic system-mediated mechanisms. Also, during inflammatory stress, the cytokines TNF alpha, IL-1, and IL-6 stimulate hypothalamic CRH and/or vasopressin secretion as a way of preventing the inflammatory reaction from overreacting. Recently, CRH receptors were described in peripheral sites of the immune system, and CRH was found to promote several immune functions in vitro. We demonstrated a direct role of CRH in the inflammatory immune process in vivo, by first studying the effect of systemic CRH immunoneutralization in an experimental model of carrageenin-induced aseptic inflammation in Spague-Dawley rats. We extended these observations to other forms of experimental inflammation, including streptococcal cell wall polysaccharide- and adjuvant-induced arthritides and peptide R16 (epitope of the interphotoreceptor retinoid-binding protein)-induced uveitis in Lewis rats. We also studied human disease states, including rheumatoid arthritis, Hashimoto thyroiditis, and ulcerative colitis. Inflamed tissues contained large amounts of IR CRH, reaching levels similar to those observed in the hypophyseal portal system. We also demonstrated the presence of CRH mRNA and CRH receptors in inflammatory cells and identified the mast cells as a major immune target for CRH. In addition to production by immune cells, the peripheral nervous system, including the postganglionic sympathetic neurons and the sensory fibers type C, appears to contribute to IR CRH production in inflammatory sites. The production of CRH from the postganglionic sympathetic neurons may be responsible for the stress-induced activation of allergic/autoimmune phenomena, such as asthma and eczema, via mast cell degranulation. Antalarmin, a novel nonpeptide CRH receptor antagonist, displaced 125I-labeled ovine CRH binding in rat pituitary, frontal cortex, and cerebellum, but not heart, consistent with antagonism at the CRHR1 receptor. In vivo antalarmin significantly inhibited CRH-stimulated ACTH release and carrageenin-induced subcutaneous inflammation in rats. Thus, antalarmin and other related compounds that antagonize CRH at the level of its own receptor have therapeutic potential in some forms of inflammation directly mediated by type 1 CRH receptors and promise to enhance our understanding of the many roles of CRH in immune/inflammatory reactions.
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PMID:Corticotropin-releasing hormone and inflammation. 962 33

We describe a 74-year-old man with rheumatoid arthritis (RA) who developed syndrome of inappropriate secretion of antidiuretic hormone (SIADH) 1.5 months after commencement of mizoribin prescription when his arthritis was improved. He noticed nausea and headache and serum Na fell as low as 118 mEq/l. Normal urinary Na excretion without hypotension or hemoconcentration negated the possibility of dehydration resulting from urinary Na loss. Serum antidiuretic hormone (ADH) remained elevated at 0.59 pg/ml in spite of a significant reduction in serum osmolality to 254 mosm/kg. He had no organic disease likely to cause SIADH. Despite infusion of hypertonic saline, his serum Na was not restored to normal. Shortly after mizoribin withdrawal, his serum Na increased significantly from 128 to 139 mEq/l and plasma osmolality from 265 to 287 mosm/kg. ADH hypersecretion in relation to plasma osmolality was reversed by mizoribin withdrawal, suggesting that bredinin might adversely induce SIADH. Additional predisposing factors were the patient's age and difficulty in urination due to benign prostatic hypertrophy. In summary, we report herein the first case of SIADH believed to be an adverse effect of mizoribin, which may therefore needed to be added to the list of drugs which can induce SIADH.
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PMID:A case of SIADH induced by mizoribin administration. 1239 45


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