Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026827 (hypotonia)
 5,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-eight consecutive patients were investigated for spontaneous chest pain without symptoms of effort angina, previous myocardial infarction or other signs of cardiac disease, to determine the incidence of oesophageal spasm. The character of the chest pain, its context and the results of resting ECGs were analysed. An ECG recorded during chest pain was available in 23 cases and exercise stress testing was performed in 43 cases. Coronary angiography was carried out in all patients. The coronary arteries were normal or showed little change in 44 patients. Further investigations were ordered: oesophageal manometry (42 cases), echocardiography 44 cases) and ergometrine provocation tests (44 cases). The patients were then divided into 4 groups: 23 patients (40 p. 100) with coronary artery disease; either atheroma (14 cases) or spasm (9 cases); 8 patients (13,5 p. 100) with non-coronary cardiac pathology (myocardial hypertrophy or mitral valve prolapse); 15 patients (26 p. 100) with oesophageal spasm alone; 12 patients (20,5 p. 100) with no obvious organic disease. Often simulating spontaneous angina, clinically and electrocardiographically, oesophageal spasm may sometimes be distinguished (6 out of 15 cases) by the finding of painful dysphagia on swallowing ice-cold liquid. The condition is confirmed by oesophageal manometry which shows abnormalities of oesophageal contraction. In addition, 13 out of 15 patients in our series had hypotonia of the gastro-oesophageal sphincter. Dyskinetic phenomena and this hypotonia should be taken into consideration in the treatment of this condition.
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PMID:[Esophageal spasm: a common cause of spontaneous precordial pain]. 643 62

For patients the author has observed, the majority of complaints following an acute pyrethroid intoxication disappeared after the end of exposure. Residuals frequently observed after more than 2 years were: (1) cerebro-organic disorders (reduced intellectual performance with 20-30% reduction of endurance during mental work, personality disorder), visual disturbances, dysacousia, tinnitus; (2) sensomotor-polyneuropathy most frequently in the lower legs; (3) vegetative nervous disorders (paroxysmal tachycardia, pollakisuria, increased heat-sensitivity, orthostatic hypotonia and reduced exercise tolerance due to circulatory disorder). Non-neurological symptoms include deficiency of cellular and humoral immune system established by laboratory findings: opportunistic infections, especially Candida-infections of the gastro-intestinal tract, relapsing infections of the urinary and respiratory tract, the latter often aggravating to respiratory obstruction. Most of the patients exhibit positive epi- or intracutantest against pyrethroids or pyrethrines, and acquainted sensitivity also to other antigens. Many of these patients exhibit pathological autoimmune diagnostical findings and developed autoimmune diseases as for instance scleroderma-like syndrome, myasthenia-like syndrome with progredient muscle atrophy, autoimmun-hemolysis and autoimmun-thrombocytopenic purpura.
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PMID:Chronic sequelae and irreversible injuries following acute pyrethroid intoxication. 1041 93