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Biomedical subjects

J Fuchs

Publications and source records attributed to J Fuchs.

At least 217 records · Page 12Linked to original sources
PubMed1988

Total lactate dehydrogenase and its isoenzymes in serum of patients with non-small-cell lung cancer.

Values for total lactate dehydrogenase (LD, EC 1.1.1.27) activity in serum and LD isoenzymes were determined at diagnosis in 273 patients with non-small-cell lung cancer, 85 of whom were in stage 1, 92 in stage 2, and 96 in stage 3. We divided the patients into three groups, based on their total serum LD values: less than 225 U/L (normal reference range), 226-500 U/L, and greater than 500 U/L. Overall values for LD were above normal at diagnosis for 69% of the patients, being moderately increased in 63 patients and highly increased in 125. Eighty percent of the patients in stage 1 had normal values for LD at diagnosis, but 88% of the patients in stage 2 and 94% of the patients in stage 3 had above-normal LD values at diagnosis. In 55% of the patients in stage 2 and 73% of the patients in stage 3, LD activity was highly increased. In the patients with normal values for total LD, the proportions of the LD isoenzymes were normal. In the patients with increased LD, the isoenzyme proportions were increased for LD-4 and LD-5, up to twice the normal values. The sensitivity of LD in detection of lung cancer was 60% for LD at the cutoff point of 250 U/L in comparison with normal controls, and 47% for LD at the cutoff point of 310 U/L in comparison with the benign lung disease group of patients (95% specificity). We conclude that total LD in serum may be a direct indicator of clinical stage and tumor burden in patients with non-small-cell lung cancer.

Adenocarcinoma↗
PubMed1988

[Various effects of secretin and pentagastrin on peripheral venous blood gas analysis].

Until recently, vasomotor effects of gastrointestinal polypeptide hormones have been observed primarily in animal experimentation. 33 volunteers were observed to survey the influence of secretin (1 CU/bw./h) and pentagastrin (0.75 micrograms/bw/h) on peripheral blood gas concentrations and on the acid/base balance. Compared to a control group, secretin caused a significant increase in pO2 and in O2 saturation (p less than 0.05). In contrast to secretin, pentagastrin caused a significant decrease in the pO2 as well as in the O2 saturation (p less than 0.05) pCO2, pH and HCO3 were not significantly affected by either secretin or pentagastrin. These results can be interpreted as possible direct vasodilatative/constrictive as well as local metabolic effects of secretin and pentagastrin.

Adult↗
PubMed1988

Atypical patterns of lactate dehydrogenase isoenzymes in acute myocardial infarction.

Total lactate dehydrogenase (LD; EC 1.1.1.27) activity in serum and LD isoenzymes were quantified in 190 patients with acute myocardial infarction (AMI) 24, 48, and 72 h after admission. In 90% of the 570 blood specimens an LD isoenzyme pattern typical of AMI (LD-1/LD-2 greater than 0.76) was found. The other 56 blood specimens showed an LD isoenzyme pattern atypical of AMI (LD-1/LD-2 less than 0.76). They were divided into three groups: 28 specimens with isomorphic pattern (relative increase in all five LD isoenzymes); 18 with relatively increased LD-3 proportion (greater than 35%); and 10 specimens with increased LD-5 proportion (greater than 10%). No difference was found in mean total LD activity in serum between the typical isoenzyme group and the three atypical groups. The LD isomorphic pattern was found in 60% of AMI patients complicated by cardiogenic shock. Fifty percent of AMI patients admitted with pulmonary edema showed increased LD-3 proportion and half of the patients with AMI and congestive heart failure, predominant right, demonstrated increased LD-5 proportion. We conclude that although most patients with AMI present at diagnosis with a typical LD isoenzyme pattern, it is important to recognize that some may present with atypical LD isoenzyme patterns, which may be associated with specific AMI complications.

Adult↗
PubMed1988

Significance of isolated increases in total lactate dehydrogenase and its isoenzymes in serum of patients with bacterial pneumonia.

Total lactate dehydrogenase (LD, EC 1.1.1.27) activity in serum and LD isoenzymes were quantified at the time of diagnosis in 320 patients with bacterial pneumonia. In eighty, LD activity was increased, but this was accompanied by either other pathological results for liver-function tests or associated diseases that could explain it. The remaining 240 patients were divided into four groups, based on their total serum LD values: group A, less than 225 U/L (normal limit); group B, 226-350 U/L; group C, 351-499 U/L; and group D, greater than 500 U/L. Total LD was above normal at diagnosis in 40% of the patients. Recovery time was twice as long in group D as in groups A, B, and C. In five patients from group D, the pneumonia reflected underlying lung cancer. In groups B and C, the LD-3 ratio was increased in comparison with group A; in group D, LD-4 and LD-5 were increased up to twice the normal limit. Evidently nearly half of patients with bacterial pneumonia may show isolated increases in total LD activity (mostly LD-3) in serum. In cases with high activity, prolonged recovery time is expected. Intensive follow-up and extensive investigation are warranted in these patients, because some may have underlying lung cancer.

Aged↗
PubMed1988

The efficiency of lactate dehydrogenase isoenzyme determination for the diagnosis of acute myocardial infarction.

Values for total lactate dehydrogenase (LDH; EC 1.1.1.27) activity and LDH isoenzymes 1 and 2 were determined in 80 patients with acute myocardial infarction (AMI) and in 40 without AMI every 24 hours up to 15 days after admission, when total serum LDH level returned to normal. The sensitivity, specificity, and efficiency of three LDH isoenzyme factors (LDH-1, greater than 90 U/L; LDH-1 greater than LDH-2; LDH-1/LDH ratio, greater than 0.4) for diagnosing AMI were assessed in three groups of patients according to total serum LDH values--group A, LDH level over 600 U/L; group B, 400 to 599 U/L; group C, 225 to 399 U/L--and in five groups of patients according to the time after admission--(1) first 48 hours; (2) three to five days; (3) six to eight days; (4) nine to 11 days; (5) 12 to 15 days. All three factors were found to be highly efficient for diagnosing AMI (91.5% to 97.5%) in groups A and B, but the most efficient factor in each group was LDH-1 value above 90 U/L. In group C, the only efficient factor was the LDH-1 value over 90 U/L (96%). The most efficient factor for diagnosing AMI in relation to time after admission up to 15 days after AMI was the LDH-1 value over 90 U/L (96% to 97.5%). The factors LDH-1 greater than LDH-2 and LDH-1/LDH above 0.4 were more efficient in patients up to five days after AMI (91.5% to 97.5%) than in patients six to 15 days after admission. We conclude that the most efficient LDH value for diagnosing AMI is the absolute value of LDH-1 above 90 U/L. Its superiority over other LDH isoenzyme values is best documented in a group of patients six to 15 days after admission and with only slight to moderate elevation of total serum LDH values (225 to 399 U/L).

Adult↗
PubMed1988

Patterns of lactate dehydrogenase isoenzymes in serum of patients with acute pulmonary edema.

Total lactate dehydrogenase (LD; EC 1.1.1.27) activity in serum and proportions of LD isoenzymes were quantified on admission and discharge in 170 selected (from 240) patients with acute pulmonary edema (APE). The patients were divided into group A, 75 patients with normal LD values (less than 225 U/L); and groups B-E, with increased LD activity in serum: group B, 40 patients with increase in the proportion of LD-3 (greater than 38%); group C, 12 patients with increased LD-5; group D, 36 patients with an isomorphic pattern of LD isoenzymes; and group E, seven patients with LD-1/LD-2 greater than 0.75. Nine patients in group C (75%) had also signs of right-sided congestive heart failure, 30 in group D (83%) had hypotension on admission, and six in group E (86%) had signs of recent myocardial infarction. Evidently, half of patients with APE may show increased total LD activity in serum at the time of admission. LD isoenzyme proportions should be determined in such patients, because there is no one typical pattern of LD isoenzymes and some LD isoenzyme patterns may be associated with specific clinical situations.

Acute Disease↗
PubMed1987

Circulating aggregated platelets in coronary artery disease.

Circulating aggregated platelets were assessed in 30 patients with stable angina, 22 with unstable angina and 50 with acute myocardial infarction (AMI). Fifty healthy volunteers and 20 noncardiac patients served as controls. One milliliter of venous blood was separated into 2 solutions: 1 composed of ethylenediamine tetraacetic acid (EDTA) and formalin containing reversible and aggregates and 1 composed of EDTA alone containing irreversible aggregates only. By direct microscopic readings the percentage of platelets forming aggregates/1,000 counted platelets was determined in the 2 solutions. The number of reversibly aggregated platelets was estimated by subtracting the percentage of aggregated platelets in the second solution from that in the first solution. In patients with stable angina the percentage of aggregated platelets was higher than in control subjects (15 +/- 4% vs 7 +/- 2%, p less than 0.001). Most aggregated platelets (72% and 76%, respectively) were irreversibly aggregated. In the unstable angina group the percentage of aggregated platelets was similar to that of the AMI group (24 +/- 13% and 24 +/- 10%) and significantly higher than in the stable angina group. Only 11% and 17% of aggregated platelets in patients with stable angina and AMI were irreversibly aggregated and 89% and 83% of them were reversibly aggregated. Participation of platelets in the pathogenesis of unstable angina and AMI may be related to the early reversible phase of platelet activation.

Angina Pectoris↗
PubMed1987

Possible role of fibrinogen in the aggregation of white blood cells.

In order to verify whether leukocyte aggregation correlated with aggregation of other cellular elements during inflammation, we examined the state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood and red cell aggregation. Correlation was found to be significant as was the correlation between LAA and fibrinogen, and with the fibrin/fibrinogen degradation products concentration during various inflammatory states. In vitro leukocyte aggregation was decreased when the cells were suspended in autologous heat defibrinogenated plasma as compared to cells suspended in autologous native plasma. Heat aggregated fibrinogen but not native fibrinogen caused leukocyte aggregation in vitro. Finally, Arvin defibrinogenation in rabbits reduced the state of LAA in endotoxinemic rabbits. Integrating all this information, we assume that fibrinogen participates not only in the aggregation phenomena of red cells and platelets, but also in those of leukocytes.

Animals↗
PubMed1987

A multiparameter analysis of the perfused rat heart: responses to ischemia, uncouplers and drugs.

In perfused rat hearts alterations of aortic flow and mitochondrial membrane potential resulting from uncoupling of oxidative phosphorylation, hypoxia and treatment with a cardioprotective drug (2-mercaptopropionylglycine (MPG) have been studied. Mitochondrial membrane potential was followed by surface fluorimetry on DASPMI stained hearts. This fluorochrome specifically stains mitochondria in living cells; fluorescence intensity is related to the electrochemical gradient. Aortic flow turned out to be a much more sensitive indicator of heart function than ventricular pressure or mitochondrial membrane potential. No direct relationship exists between mitochondrial membrane potential and ATP production under the different metabolic conditions. Two phases of hypoxic mitochondrial damage have been deduced: the first results in derangement of ATP synthases while membrane potential is maintained, the second in irreversible damage of mitochondrial membranes with loss of membrane potential.

Adenosine Triphosphate↗
PubMed1987

Myocardial infarction in young adults under 30 years: risk factors and clinical course.

The clinical features and course of 30 patients (26 men and 4 women) under 30 years of age (mean age 27.3 years) with an acute myocardial infarction (MI) are described. The most common risk factor among this group of patients was smoking in 20 patients (66%). The prevalence of the other risk factors was low: hyperlipidemia in four patients and family history of ischemic disease in another four patients, diabetes mellitus, hypertension, and obesity each in one patient. Seven patients (23%) had none of the conventional risk factors. Three patients were exerting themselves prior to the onset of their MI pain; all of them had normal coronaries. Five patients experienced chest pain prior to MI, among them only two experienced classical angina pectoris. Eighteen patients underwent uncomplicated MI. The complications in the other 12 during the acute MI were rhythm disturbances in eight and congestive heart failure in four. Cardiac catheterization was performed in 25 patients. The occurrence of zero, one, or multivessel disease was equal. The 30 patients were followed up from six months to 15 years (mean 7 years). In 18 patients circulating aggregated platelets were measured one year after the MI. Elevated values were found in all of them (mean +/- SD 34.9 +/- 9.1%). In 6 of the 18, all heavy smokers, extreme values were found in the range of 39-55%. Three out of the 30 patients died within five years after their first MI. The other 15 patients developed complications, most of them angina pectoris. Five patients were hospitalized for reinfarction. None of the 30 underwent aortocoronary bypass operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Plasma viscosity and haematocrit in the course of acute myocardial infarction.

Plasma viscosity and haematocrit were determined in 44 patients with acute myocardial infarction on the 1st, 2nd, 3rd and 10th day of hospitalization. The highest haematocrit value for the entire group was found on the 1st day of acute myocardial infarction--43.3 SD +/- 4.6% declining progressively to 38.8 SD +/- 3.5% on the 10th day (P less than 0.001). Plasma viscosity for the entire group was normal on the first day of acute myocardial infarction (1.44 SD +/- 0.10 cp) and started to increase on the second day (1.51 SD +/- 0.16 cp, P less than 0.001). A relationship was found between reinfarction or death (17 patients) occurring during hospitalization and changes in haematocrit and plasma viscosity. In this group plasma viscosity rose to 1.63 SD +/- 0.19 cp on the second day of acute myocardial infarction (P less than 0.001 vs plasma viscosity value on the first day). This elevation persisted on the third day. Haematocrit values in this group were 47.9 SD +/- 3.6% on the first day of acute myocardial infarction declining progressively and significantly afterwards. In the remaining patients both plasma viscosity and haematocrit were normal and did not change. No correlation of plasma viscosity and haematocrit were found when tested for other clinical complications, sex, age, maximal creatine phosphokinase values and coronary risk factors. We suggest that variations in haematocrit and plasma viscosity during acute myocardial infarction exist in a group of patients in whom reinfarction or death occurs. The changes in haematocrit and plasma viscosity precede the complications by 4-8 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Room temperature ADP induced first stage hyperaggregation of human blood platelets: a previously undescribed phenomenon and its relationship to spontaneous cold induced platelet aggregation.

ADP induced human platelet aggregation was shown to be accentuated when tested at 20-30 degrees C as increased sensitivity and as a greater change of optical density although second stage aggregation and the release reaction did not occur. This previously undescribed phenomenon is defined as room temperature ADP induced first stage hyperaggregation. Aggregation, which occurs under the above mentioned conditions with a quantity of ADP insufficient to maintain the aggregation (usually less than 1.5 micron), is reversible when the temperature is raised to 37 degrees C. After rewarming to these temperatures, second stage aggregation appeared in the presence of larger quantities of ADP (usually more than 2 microns) and could be blocked by aspirin. The absence of the release reaction was demonstrated with a lumi-aggregometer. Spontaneous cold induced platelet aggregation seen after chilling platelets to 0-4 degrees C is shown to be a distinct phenomenon.

Adenosine Diphosphate↗
PubMed1987

Acute transmural myocardial infarction in elderly patients hospitalized in the coronary care unit versus the general medical ward.

The hospital records of 126 patients over 75 years of age with transmural myocardial infarction initially treated in the coronary care unit were compared with a concurrent similar group of 94 patients admitted directly to the general medical wards. The in-hospital mortality rate for both groups together was 40%. The mortality rate within the coronary care unit was 24% as compared with 46% in the ward group (P less than 0.005). However, the mortality rate for the coronary care unit group as a whole (including those patients later transferred to the general ward) was 35 versus 46% in the ward group. Congestive heart failure and cardiogenic shock were the most frequent complications in both groups (47 and 30%, respectively), and they were the main cause of death. Patients with these complications were less likely to be successfully resuscitated, even in the coronary care unit. The overall incidence of serious ventricular arrhythmias and complete heart block was similar to that reported for younger patients. Eleven patients in the coronary care unit group were successfully resuscitated from these arrhythmias and eight survived to be discharged from hospital. In contrast, only two patients in the ward group were successfully resuscitated and eight (9%) patients died suddenly and the fatal event could not be diagnosed. We concluded that elderly patients with an acute myocardial infarction can benefit from early admission to a coronary care unit.

Aged↗
PubMed1987

Prosthetic valve endocarditis caused by Acinetobacter calcoaceticus subsp. lwoffi.

Acinetobacter spp. are uncommon etiologic agents of prosthetic valve endocarditis. Two patients with Acinetobacter calcoaceticus subsp. lwoffi prosthetic valve endocarditis are described. The patients were successfully treated with antibiotics (cefotaxime sodium and gentamicin sulfate); thus, we suggest medical treatment rather than early valve replacement in this particular type of infection.

Acinetobacter Infections↗
PubMed1987

Improvement of myocardial function after global hypoxia by protection of the inner mitochondrial membrane.

In the present study the hypothesis is tested that hypoxia causes morphological damage to the inner mitochondrial membrane and that this damage can be reversed by modification of the reoxygenated perfusate. Using the working rat heart model, hearts in group I (n = 40) were subjected to a 30 min normothermic, normoxic phase and a 90 min hypoxic phase, followed by 60 min reoxygenation. Hearts in group II (n = 32) were also subjected to a 30 min normoxic and a 90 min hypoxic phase. However, after 30 min of reoxygenation 1.5 mmol/l 2-mercaptopropionylglycine (MPG) was injected in the reoxygenated solution in order to test its ability to improve mitochondrial function. Mitochondrial function was assessed by measuring oxygen uptake (ST3), ST4, respiratory control index (RCI), ADP/O and oxidative phosphorylation rate (OPR). In addition mechanical function (heart rate, aortic and coronary flow, cardiac output, stroke volume) was monitored along with ultrastructural parameters. 90 min of hypoxia caused a deterioration of all parameters with persistent impairment in hemodynamic, morphologic and biochemical functions after 60 min of reoxygenation (group I). The role of the ATP-synthetases in the pathogenesis of oxygen-paradox is discussed. In contrast, the MPG-enriched reoxygenated solution (group II) improved hemodynamics, ultrastructure and mitochondrial function significantly (alpha = 0.05). It is concluded from these data that the ATP-synthetases are damaged during oxygen-deficiency and that MPG may be a useful drug for protecting the inner mitochondrial membranes during reoxygenation.

Adenosine Diphosphate↗