Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149520 (acute cholecystitis)
 2,784 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute elevation of the ST segment in several ECG leads was observed in seven patients with bacterial shock during the course of therapy. Six patients had bacterial pneumonia, one had acute cholecystitis, and none had a previous history of heart disease. At the onset of the ST elevation, all patients were receiving dopamine infusion, which in four of them was inadvertently increased shortly before the ECG changes, the ST elevation was not associated with chest pain, pericardial friction rub, or acute changes in the heart rate, or arterial blood pressure. In four patients the maximum ST elevation was greater than or equal to 5 mm. In each instance the ST segment returned to the isoelectric line within 24 hours, and subsequent development of Q waves or changes in the QRS was not observed. Although the existence of an acute pericarditis or an acute myocarditis as possible causes of the ST elevation cannot be fully ruled out, the sudden onset, prominent magnitude, and brief duration of the ST elevation are perhaps more indicative of an acute ischemic event, possibly related to a transient coronary vasoconstriction induced by the dopamine infusion.
 ...
PMID:Acute and transient ST segment elevation during bacterial shock in seven patients without apparent heart disease. 706 10

Blood samples obtained from 97 consecutive patients admitted to the hospital for chest pain were analyzed for taurine concentrations. The mean value of the maximum taurine concentration in whole blood from AMI patients were greater than the mean value of the maximum taurine concentration in patients without AMI. There was no difference in plasma taurine levels between AMI and non-AMI patients, indicating that a cellular component(s) of whole blood was sequestering taurine. The increased blood taurine concentrations in the AMI patients evolved over the course of 70 hr and paralleled the increase in total CK levels. Blood taurine concentrations, in general, did not rise in patients who had chest pain of unknown etiology, skeletal muscle trauma, pleuritic pain, SVT/VT plus CV, acute pericarditis, acute cholecystitis, or angina pectoris. It is concluded that blood but not plasma taurine concentrations rise after acute myocardial injury and tend to be higher the more extensive the infarction. The mechanism of the blood taurine rise is unknown, but a myocardial source is probable. Also, there is evidence that the myocardium selectively leaks taurine, and not other amino acids. Monitoring blood taurine concentration in AMI may provide useful diagnostic and prognostic information.
 ...
PMID:Elevated blood taurine levels in acute and evolving myocardial infarction. 731 Feb 26