Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An opportunity to investigate the role of anti-acetylcholine receptor antibody (anti-AcH R-antibody) in neonatal myasthenia gravis was presented when an infant was born to a symptomatic myasthenic mother who elected to breast feed the child. Pyridostigmine bromide determinations in plasma and breast milk were made by quantitative gas liquid chromatography. Anti-AcH R-antibody was assayed by an immunoprecipitation method. Simultaneous maternal blood and milk samples did not suggest concentration of pyridostigmine bromide in milk or significant transfer of medication through demand breast feeding. Weakness was not noted in the neonate in spite of high levels of anti-AcH R-antibody demonstrated in her blood. Presence of a markedly elevated anti-AcH R-antibody in a pregnant patient symptomatic with myasthenia gravis does not necessarily predict a clinically affected offspring, nor does the elevated antibody in the infant, presumably acquired transplacentally, necessarily result in clinical symptomatology in the newborn period.
 ...
PMID:The role of anti-acetylcholine receptor antibody in neonatal myasthenia gravis. 75 66

Forty patients with irritable bowel syndrome were randomly allocated to treatment with octylonium bromide (20 mg TID) or cimetropium bromide (50 mg BID) in a double-blind trial lasting for six weeks. Drugs were taken before meals, according to a double-blind schedule. Clinical evaluations were made of digestive and other symptoms, objective findings (pain at palpation, contracted colon, tympanites), and overall effectiveness of treatment. Statistically significant decreases in severity of abdominal pain and subjective scores for bowel habits were obtained in both groups. The only statistically significant differences between treatments were in nondigestive symptoms (asthenia, palpitations, tremor, headache, etc.), which improved more in the cimetropium bromide group. No severe side effects were observed in either treatment group.
 ...
PMID:Double-blind study of a new antimuscarinic, cimetropium bromide, in patients with irritable bowel syndrome. 352 59

More than 2200 subjects were enrolled in the MorphiDex (MS:DM) development program, with a 1:1 (weight:weight) ratio of morphine sulfate (MS) to dextromethorphan hydrobromide (DM). Of the 1400 subjects exposed to MorphiDex, more than 350 subjects were treated for at least 6 months, and over 200 subjects were treated for a year or longer. The clinical population comprised an approximately equal number of men (46.2%) and women (53.8%), ranging in age from 16 to 96 years, and mostly Caucasian (91.8%). The most frequent (54.8%) daily dose of MorphiDex for subjects enrolled in the clinical program was 120 mg or less. Slow DM metabolizers took significantly lower daily doses of MorphiDex than rapid metabolizers without a significant difference in the incidence of adverse events. Plasma bromide concentrations were low and showed a wide margin of safety for both slow and rapid DM metabolizers. There were no clinically significant treatment-related changes in clinical laboratory tests, neurological examinations, or vital signs. The most common adverse events seen in the multiple dose controlled studies were nausea, dizziness, vomiting, somnolence, constipation, confusion, asthenia, headache, and pruritus. With long-term treatment, the prevalence of adverse events was greatest during the first month of MorphiDex exposure and then decreased over time. The incidence of constipation remained fairly constant over time.
 ...
PMID:Long-term safety of MorphiDex. 1068 40

Sarin (O-isopropylmethylphosphonofluoridate) is a highly toxic nerve agent produced for chemical warfare. Sarin is an extremely potent acetylcholinesterase (AchE) inhibitor with high specificity and affinity for the enzyme. Death by sarin is due to anoxia resulting from airway obstruction, weakness of the muscles of respiration, convulsions and respiratory failure. The main clinical symptoms of acute toxicity of sarin are seizures, tremors and hypothermia. Exposure to sarin during incidents in Japan in 1994, 1995 and 1998, and possible exposure to low levels of sarin during the Gulf War, resulted in the deaths and injury of many people in Japan and caused possible long-term health effects on Gulf War veterans. Symptoms related to sarin poisoning in Japan still exist 1-3 years after the incident and include fatigue, asthenia, shoulder stiffness and blurred vision. Sarin produced seizures in rats and pigs. Recent studies showed that long-term exposure to low levels of sarin caused neurophysiological and behavioral alterations. Toxicity from sarin significantly increased following concurrent exposure to other chemicals such as pyridostigmine bromide. Further research to examine effects of sarin on the cellular and the molecular levels, gene transcription, endocrine system as well as its long-term impact is needed.
 ...
PMID:Sarin: health effects, metabolism, and methods of analysis. 1238 97