Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapeutic efficacy of cephacetrile (CEC) in bacterial pneumonia was evaluated in contrast with that of cefazolin (CEZ) by a double blind method. Both drugs were administered via intravenous route at a dose of 1 g twice daily for 14 days. 1) Of 81 patients, each 2 from both groups were eliminated from the study because of unknown results. In CEC group, 36 out of 38 obtained a slightly effective or better results (94.7% of effectiveness). In CEZ group, 31 out of 39 showed a similar result and there was no significant difference between the two groups. 2) In more detail, CEC achieved significantly better results in AaDo2 and cardiac insufficiency than CEZ, and this trend was also seen in dyspnea. 3) Regarding background factors, pretreatment severity was slightly in favor of CEC. However, so long as supplementary analysis is concerned, we could not find any relation between the pretreatment severity of symptom and drug efficacy or improvement of symptom. 4) Since there was a slight bias in the background factors, it is difficult to conclude that CEC is better than CEZ in terms of effectiveness. However, we consider CEC is superior to CEZ if compared in details. 5) Both drugs had the same incidence of side effect (6.25%, 3/48 in both groups). When clinical efficacy of CEC in bacterial pneumonia is evaluated together with the incidence of side effect, we may consider that CEC is an effective antibiotic agent equal to or better than CEZ.
 ...
PMID:[A clinical evaluation of the effect of cephacetrile on bacterial pneumonia. A comparative test with cefazolin by a double blind method (author's transl)]. 79 86

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co
 ...
PMID:Pulmonary and pleural complications of cardiac disease. 268 66

Clinico-instrumental investigations were performed in 52 patients with virus-bacterial pneumonia in different periods of disease and 10-12 mos after discharge from hospital. Considerable changes in the hemodynamics of the lesser and greater circulation and left ventricular myocardial contractility preserving for a long time, particularly in a grave form of disease, were revealed. In long-term periods hypertension in the pulmonary artery system persisted. It could result in the occurrence of occult heart failure.
 ...
PMID:[Hemodynamics in viral-bacterial pneumonia in middle-aged patients]. 360 97

Periodontitis, a prime cause of tooth loss in humans, is implicated in the increased risk of systemic diseases such as heart failure, stroke, and bacterial pneumonia. The mechanisms by which periodontitis and antibacterial immunity lead to alveolar bone and tooth loss are poorly understood. To study the human immune response to specific periodontal infections, we transplanted human peripheral blood lymphocytes (HuPBLs) from periodontitis patients into NOD/SCID mice. Oral challenge of HuPBL-NOD/SCID mice with Actinobacillus actinomycetemcomitans, a well-known Gram-negative anaerobic microorganism that causes human periodontitis, activates human CD4(+) T cells in the periodontium and triggers local alveolar bone destruction. Human CD4(+) T cells, but not CD8(+) T cells or B cells, are identified as essential mediators of alveolar bone destruction. Stimulation of CD4(+) T cells by A. actinomycetemcomitans induces production of osteoprotegerin ligand (OPG-L), a key modulator of osteoclastogenesis and osteoclast activation. In vivo inhibition of OPG-L function with the decoy receptor OPG diminishes alveolar bone destruction and reduces the number of periodontal osteoclasts after microbial challenge. These data imply that the molecular explanation for alveolar bone destruction observed in periodontal infections is mediated by microorganism-triggered induction of OPG-L expression on CD4(+) T cells and the consequent activation of osteoclasts. Inhibition of OPG-L may thus have therapeutic value to prevent alveolar bone and/or tooth loss in human periodontitis.
 ...
PMID:Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection. 1099 85

We studied 316 adults with community-and hospital-acquired bacterial pneumonia admitted from January 1998 to July 2003. Of these, 66 (20.9%) died. Classified by age, none under 70 died, but mortality increased to 22.6% in the 70-79 age group, 31.6% in the 80-89 age group and 24.2% in the group over 90. Mortality was 3.4% (6/177) for mild pneumonia, 32.0% (24/75) for moderate pneumonia, and 56.3% (36/64) for severe pneumonia. Mortality in hospital-acquired pneumonia (69.1%) was significantly higher than that in community-acquired pneumonia (10.7%). This may result from the higher percentage of moderate by and severe by ill patients who contracted hospital-acquired pneumonia, since 80% of those with hospital-acquired pneumonia were in the moderate and severe group compared to 36.4% of those with community-acquired pneumonia. For antibiotic regimens, mortality was 18.2% to 36.4% for patients who underwent Penicillins-Cephems therapy compared with 51.6% to 66.7% for Carbapenems-Quinolones therapy. The reasons for these differences remain unclear. Our study indicates that severity of illness, age, and antibiotic therapy were factors correlated with death from pneumonia. Underlying diseases such as respiratory failure, chronic heart failure, cerebrovascular disease, renal failure, malignancy, and senile dementia may also be associated with mortality.
 ...
PMID:[Prognostic and risk factors in patients hospitalized with bacterial pneumonia]. 1756 15