Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mycophenolate mofetil, a pro-drug for mycophenolic acid, is an investigational immunosuppressive compound that is being developed for the treatment of rheumatoid arthritis (RA). The drug and its primary metabolite, mycophenolic acid, inhibit the de novo pathway of purine biosynthesis and have greater anti-proliferative effects on lymphocytes than on other rapidly dividing cells. Significant clinical improvement has been seen in many mycophenolate mofetil-treated RA patients who have been refractory to treatment with a variety of disease-modifying anti-rheumatic drugs (DMARDs). Treatment with mycophenolate mofetil reduces rheumatoid factor titres, immunoglobulin (IgG, IgM, and IgA) levels, and the total number of T cells (CD2) in RA patient peripheral blood; in addition, lymphocyte mitogen responses are inhibited and delayed hypersensitivity skin test reactivity is decreased. A dose of 2 g daily is more effective than lower doses, including several pulsing regimens. The most frequent adverse events reported by patients on mycophenolate mofetil are gastrointestinal, mainly nausea, vomiting, abdominal pain, and diarrhea. RA studies have demonstrated no clinically significant nephrotoxicity, hepatotoxicity, or bone marrow toxicity attributable to mycophenolate mofetil.
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PMID:Therapy of rheumatoid arthritis with mycophenolate mofetil. 832 35

A case of itraconazole-induced hypokalemia with pulmonary aspergilloma is reported. A 68-year-old female who had been followed for rheumatoid arthritis, gastric ulcer and pulmonary aspergilloma was admitted to our hospital because of a cough, low grade fever and hemosputum. She was treated with itraconazole (100 mg/day) for pulmonary aspergilloma of the left upper lobe. Fifty seven days after starting the treatment, her serum potassium was 2.33 mEq/l. Since there was no history of diarrhea, vomiting or abuse of drugs known to cause hypokalemia, itraconazole- induced hypokalemia was suspected. Thirty one days after the discontinuation of the treatment with itraconazole, her serum potassium increased to 3.57 mEq/l without potassium supplement. The lymphocyte stimulation test for itraconazole was negative. This case suggests that serum potassium should be monitored in the patients treated with itraconazole.
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PMID:[A case of itraconazole-induced hypokalemia with pulmonary aspergilloma]. 858 96

Methotrexate, a folic acid antagonist, is approved by the US Food and Drug Administration for use in rheumatoid arthritis, psoriasis, and various types of cancer, including choriocarcinoma, and has also been used to terminate ectopic pregnancies. Misoprostol, a prostaglandin, is approved for the prevention of gastric ulcers induced by nonsteroidal anti-inflammatory drugs. In France, the UK, and Sweden, misoprostol and another prostaglandin is used with mifepristone (RU486) to induce abortion in early pregnancy. Recent articles in the press have suggested that in early pregnancy, an intramuscular injection of methotrexate and oral or vaginal administration of misoprostol offers a medical alternative to a surgically induced abortion. This paper describes the mechanisms of action, pharmacokinetics, clinical use, and adverse effects of the two drugs. It is concluded that an intramuscular injection of methotrexate followed up to seven days later by the intravaginal administration of misoprostol can terminate an early intrauterine pregnancy. Headache, nausea, vomiting, diarrhea, and prolonged bleeding have occurred. However, in the few studies published to date, no serious complications have been reported.
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PMID:Methotrexate and misoprostol for abortion. 860 22

We described a case of rheumatoid arthritis (RA) with selective IgA deficiency. A 69 year-old female with RA was admitted because of gall bladder cancer, and also had selective IgA deficiency which serum IgA level was less than 5.0 mg/dl, and IgA 1 and IgA 2 subclasses were not detected. Prior to the operation, she was given red cell compatible blood transfusion because of severe anemia. After 30 min of transfusion, she developed chill, nausea, vomiting and hypotension. These anaphylactic reactions might be induced by the presence of anti-IgA antibody, since the level of this antibody titers in her serum was elevated, assessed by the methods of ELISA and Western blotting. Although a case of RA associated with selective IgA deficiency, and also with elevated serum anti-IgA antibody level is extremely uncommon, attention should be paid to the presence of anti-IgA antibody in patients with selective IgA deficiency to avoid any unexpected anaphylactic reactions.
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PMID:[A case report of selective IgA deficiency in rheumatoid arthritis and anti-IgA antibody induced anaphylactic transfusion]. 985 51

A 63-year-old woman who started to have polyarthralgia in December 1993 has been diagnosed as rheumatoid arthritis (RA) and treated with muscular injection of gold sodium thiomalate. She began to have nausea, vomiting, anorexia and watery diarrhea in October 1995. A year later, she had to receive intravenous infusion on admission since more frequent watery diarrhea occurred more than ten times within a day. On admission in our hospital in December 1996, she had proteinuria in addition to gastrointestinal symptoms. The biopsy specimen from stomach, duodenum and kidney proved systemic amyloidosis associated with RA. In spite of steroid-pulse, dimethyl sulfoxide (DMSO) and colchicine therapy, profound proteinuria in nephrotic syndrome was continued in association with hypoproteinemia, anasarca and renal failure. She was treated on hemodialysis and intravenous hyperalimentation (IVH) until November 1997 when A-V shunt operation on left forearm was performed. However, the shunt was not available for HD and she suffered from septicemia and died on December 1997. This patient was a rare case of secondary systemic amyloidosis associated with RA in early clinical course.
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PMID:[A case of secondary systemic amyloidosis associated with rheumatoid arthritis after 3-year disease duration]. 1033 14

Preclinical and clinical studies of phosphodiesterase 4 inhibitors have shown that these agents may find utility in a wide range of inflammatory disorders, including asthma, chronic obstructive pulmonary disease, atopic dermatitis, rheumatoid arthritis, multiple sclerosis and various neurological disorders. The future of this class of drugs will depend upon the ability to demonstrate a reasonable safety margin against emesis and other typical phosphodieserase (PDE4) side effects, as well as in identification of the inflammatory disorder(s) most relevant to PDE4 inhibition.
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PMID:Phosphodiesterase 4 inhibitors as novel anti-inflammatory agents. 1041 56

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Antineoplastic drugs caused various and frequent adverse drug reactions (ADR) in connection with their pharmacodynamics. Methotrexate (MTX) ADRs are preferably gastrointestinal disorders and hepatotoxicity (hepatic enzyme abnormalities). The aim of this study was to detect and analyse ADR induced by low-dose MTX treatment in rheumatology. We observed 94 patients, 63 with rheumatoid arthritis and 31 with psoriatic arthritis. All patients were co-medicated with nonsteroidal anti-inflammatory drugs (NSAID) as Diclofenacum, Indomethacinum, Piroxicamum and 51% with glycocorticosteroides. During the follow-up study we collected 18 case-reports with ADR for 17% of the patients. From the patients with registered ADR, 11 was treated with standard dose of 7.5 mg MTX for a week and 7 patients received from 10 to 15 mg for a week. The distribution of the cases according patients' gender was 9 females and 7 males. Prevail individuals in age groups' 41-50 and over 61 years. The most frequent adverse drug reactions were leucopenia, trombocytopenia, skin reactions and gastrointestinal disorders as vomiting, melaena, epigastrial pain, etc. The primary risk connected with long therapy of low doses MTX is hepatotoxicity that diagnose and treatment are painful and expensive. As a result of the appearance of ADR in 5 patients the therapy with MTX was not changed, in two cases MTX is stopped timely or the dosage is changed and in the rest 11 patients MTX was excluded from the therapeutic scheme.
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PMID:Low dose treatment with methotrexate-adverse drug reactions survey. 1105 96

Phosphodiesterase (PDE) enzymes are responsible for the inactiviation of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Phosphodiesterase 4 (PDE4) is a cAMP specific phosphodiesterase expressed in inflammatory cells such as eosinophils. Inhibition of PDE4 results in an elevation of cAMP in these cells, which in turn downregulates the inflammatory response. The anti-inflammatory effects of PDE4 inhibitors have been well documented both in vitro and in vivo in a range of animal models. The potential use of PDE4 inhibitors as anti-inflammatory agents for the treatment of diseases such as asthma, chronic obstructive pulmonary disease (COPD) and multiple sclerosis (MS), has received considerable attention from the pharmaceutical industry but to date, there are no selective PDE4 inhibitors on the market. Early PDE4 inhibitors, such as rolipram suffered from dose limiting side effects, including nausea and emesis, which severely restricted their therapeutic utility. Second generation compounds such as cilomilast have been identified with reduced side effect liability. Indeed, cilomilast is showing good therapeutic effects in clinical trials for asthma and COPD and represents the most advanced selective PDE4 inhibitor for any indication. The utility of this class of inhibitor in other inflammatory diseases is less well advanced. However, data in animal models of rheumatoid arthritis (RA) and MS suggests that there is also significant potential for PDE4 inhibitors as treatments for these diseases and the results of clinical trials in these disease areas are eagerly awaited.
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PMID:Update on the therapeutic potential of PDE4 inhibitors. 1177 17

The present paper describes the historical use of cannabis, starting with its use in Assyria and China. Recent advances in the understanding of the molecular basis of cannabis action are explained, including the identification of the cannabinoid receptors CB(1) and CB(2), as well as the isolation of endogenous cannabinoids from the brain and periphery. The use of delta(9)-tetrahydrocannabinol as an anti-vomiting and anti-nausea drug for cancer chemotherapy, and as an appetite-enhancing agent is described. Clinical work in multiple sclerosis, which may lead to the approval of tetrahydrocannabinol as a drug for this condition, is presented. Preclinical and clinical investigations with cannabidiol, a non-psychotropic cannabis constituent, are also described. Recent work with cannabidiol in animal models of rheumatoid arthritis may lead to clinical investigations. A synthetic cannabinoid, HU-211 (Dexanabinol), is in advanced clinical stages of investigation as a neuroprotectant in head trauma. The above clinical approaches may ultimately lead to the realization that cannabinoids are valuable clinical drugs in numerous fields.
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PMID:The cannabinoids: an overview. Therapeutic implications in vomiting and nausea after cancer chemotherapy, in appetite promotion, in multiple sclerosis and in neuroprotection. 1185 68


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