[Actinomycosis of the liver (a case report)].
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Actinomycosis↗
Biomedical subjects
A Isakov
Publications and source records attributed to A Isakov.
Serum myoglobin levels in patients with ischemic myocardial insult.
Serum myoglobin levels were studied in 178 consecutive patients admitted for chest pain due to ischemic cardiac injury. Serum myoglobin level was compared with the clinical condition, electrocardiographic changes, and serum creatine kinase levels. Elevated serum myoglobin concentration was present in all patients with acute myocardial infarction, as defined by World Health Organization, Geneva, criteria, and, in addition, in about 50% of patients with so-called acute coronary insufficiency. On this basis we could define two different groups of patients with acute coronary insufficiency: cases exhibiting elevated serum myoglobin levels (group 1) and those with normal levels (group 2). In group 1 although creatine kinase levels were in the normal range, they were significantly higher than in group 2. Four patients from group 1 developed heart failure and another a typical acute myocardial infarction during hospitalization, whereas no patients of group 2 had such complications. In patients with acute myocardial infarction, the elevation of serum myoglobin preceded that of creatine kinase in most cases. Myoglobin release appears to be related to infarct size, the highest levels were found in extensive myocardial infarction and less marked elevations in cases of subendocardial infarction and in half of the cases with acute coronary insufficiency. It is proposed that serum myoglobin is a reliable measure of myocardial necrosis and serves to detect a hitherto undefined population of small-size acute myocardial infarction, with its attendant clinical and prognostic implications.
Coronary Disease↗
Serum myoglobin in detection of myocardial necrosis in patients with "coronary insufficiency".
Myoglobin, an oxygen-binding protein, is synthesized exclusively in striated and cardiac muscle, and is normally found in blood. Serum myoglobin determination has been used in the diagnosis of acute myocardial infarction. Experimental work has shown that myoglobin is released only after muscular necrosis. This prospective study included 101 patients: 62 with acute coronary insufficiency, 16 with acute myocardial infarction, and 23 controls. In all the patients with infarction the serum myoglobin levels were elevated. None of the controls showed serum myoglobin above normal. In patients with coronary insufficiency the peak serum myoglobin ranged from normal to 280 ng/ml. Half of all the patients with coronary insufficiency had a significant elevation of serum myoglobin (p less than 0.001). The obvious explanation of this finding is that myocardial necrosis to some extent develops in cases of so-called coronary insufficiency. Furthermore, this study confirms previous findings that serum myoglobin assessment constitutes a very early marker of myocardial damage.
Acute Disease↗
Cardiac rupture in patients with acute myocardial infarction.
The occurrence of myocardial rupture was evaluated in an unselected population of 1,737 patients with acute myocardial infarction (AMI). Patients with cardiac rupture after AMI were compared with age- and sex-matched control patients with fatal AMI not related to rupture and with AMI survivors discharged home. Rupture was found in 40 patients (15.7 percent of hospital deaths), or 2.3 percent of all cases of AMI. At the highest risk for rupture were women aged 60 to 69, although the age distribution did not differ significantly from that of patients dying of other causes. More patients with myocardial rupture had hypertension during hospitalization, persistent pain, and inferior wall myocardial infarction when compared with controls. The majority (95 percent) of cardiac ruptures occurred within the first six days, 40 percent within the first 24 hours after the onset of symptoms. Approximately 20 percent of ruptures were diagnosed as subacute; in only two was surgical intervention attempted unsuccessfully. The high-risk group of patients should be carefully monitored within the first six days after the onset of symptoms of AMI in an effort to prevent myocardial rupture.
Adult↗
Pseudomonas aeruginosa septicemia following endoscopic retrograde cholangiopancreatography with a contaminated endoscope.
Within a 3-week period, 2 patients developed Pseudomonas aeruginosa septicemia after endoscopic retrograde cholangiopancreatography. A contaminated endoscope which was found to be the source of the outbreak was later successfully disinfected. The importance of proper disinfection of such equipment cannot be overemphasized.
Aged↗
Reversible, nonoliguric acute renal failure in a patient with rheumatoid arthritis and renal amyloidosis.
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Acute Kidney Injury↗
Legionnaires' disease: a case acquired in Israel.
What is probably the first case of presumably nosocomial Legionnaires' Disease (LD) in Israel is described in a 56-yr-old man hospitalized for acute myocardial infarction. The patient developed bilateral pneumonia and hemorrhagic pleural effusion. The diagnosis of LD was confirmed by serological examinations that showed a significant increase and decrease in IgM- and IgG-type antibodies to Legionella pneumophila serogroups 1 and 3. The patient recovered on antibiotic treatment which included erythromycin.
Anti-Bacterial Agents↗
Positive inotropic effect in the heart produced by acetylcholine.
The effect of acetylcholine on cardiac muscle contractility and hemodynamics was investigated in human atrial strips and in isolated working rat heart. Activation of the muscarinic receptor in the heart muscle is generally known to result in negative chronotropic and inotropic effects. In our study, positive inotropic effects of acetylcholine (ACh) were observed in both human right atrial strips and in the working rat heart. Exposure of the human right atrial strips to ACh (10(-7)-10(-4) M) produced a dose dependent tri-phasic (positive-negative-positive) inotropic effect in approximately 40% of the strips. In muscle strips that exhibited only a negative inotropic effect, a positive response was observed following washout of ACh. Both positive and negative effects were antagonized by atropine. Exposure of the paced working rat heart to ACh (10(-7) - 10(-5) M) resulted in a dose dependent decrease in mean coronary flow followed by depression in cardiac function. When the heart was initially treated with the vasodilator adenosine (2 x 10(-6) M), exposure to ACh (10(-7) - 10(-5) M) had no effect on coronary flow and produced a dose dependent augmentation of all cardiodynamic indices: left ventricular pressure, isovolumic pressure, cardiac output, maximal aortic flow and stroke work. This positive response was antagonized by atropine. Exposure of the rat ventricular strips increased the formation of [3H]phosphoinositide breakdown products (e.g. inositol phosphates IP, IP2, IP3). These observations demonstrate that cholinergic muscarinic stimulation may produce positive inotropic effects in both human and rat cardiac muscle. Furthermore, our results suggest that IP3 may be a mediator in this process.
Acetylcholine↗
[The urinary excretion of renal prostanoids in children with chronic obstructive pyelonephritis in vesicoureteral reflux before and after antireflux operations].
The excretion of renal prostaglandins (PGE, PGF2 alpha, 6-keto-PGE1 alpha and TKB2) was studied in 45 children with chronic obstructive pyelonephritis in the presence of vesicoureteral reflux with account for the disease stage (partial remission--group I; total clinical and laboratory remission--group II) in various periods of surgical corrections of the impaired urodynamics in the area of vesicoureteral segments (in the early postoperative period of 12-14 days after the surgery; in the follow-up period of 6-12 months after the surgery). Preoperative observation of Group I children revealed a significant decrease in urinary PGF2 alpha excretion in the presence of an increase in the circadian TKB2 and 6-keto-PGF1 alpha excretion, whereas the patients from Group II who had normal levels of TKB2 and 6-keto-PGF1 alpha excretion, the levels of PGE and PGF2 alpha were lowered. The retention of sodium was documented in both groups. There was a total recovery of renal sodium and water excretion 6-12 months after the surgery. Children without the urinary syndrome (group II) demonstrated normalization of all secreted prostanoids, whereas in those with pronounced severity of pyelonephritis (group I), the excretion of sodium and diuresis were likely to be provided by hyperproduction of vasodilating sodium and diuretic PGE.
Adolescent↗