Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients developed an acute respiratory distress syndrome characterised by clinical and radiological signs of pulmonary oedema, a protein-rich oedema, severe hypoxemia refractory to oxygen therapy, contrasting with normal left ventricular filling pressures and indicating increased permeability of the alveolo-capillary membrane, 24 to 72 hours after the onset of acute myocardial infarction. After having excluded the usual causes of the acute respiratory distress syndrome, the authors suggest that acute myocardial infarction, especially when extensive, may cause a lesion of the alveolo-capillary membrane by an unknown mechanism. Treatment consisted in mechanical ventilation with positive expiratory pressures in 3 cases and with continuous positive pressure during spontaneous respiration in the third patient and in relay with controlled ventilation in the other two. These techniques of ventilation improved the hypoxemia and led to complete cure in all cases without evolution to pulmonary fibrosis. In addition to mechanical ventilation, all patients were given systematic antibiotic therapy because of the possibility of an infectious etiology while waiting for the results of microbiological and serological testing and because of the high risk of superinfection which plays an essential part in the outcome of the condition. The immediate response to treatment was favourable in all cases. One patient died suddenly of cardiogenic shock two weeks after this episode. The other patients are still alive 39, 38 and 20 months after infarction. The importance of the diagnosis of the acute respiratory distress syndrome in the acute phase of myocardial infarction resides in its therapeutic implications which are quite different to those of cardiogenic shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress syndrome in the initial phase of myocardial infarction in adults]. 212 17

The radiologic appearance of atypical cardiogenic pulmonary edema (ACPE) is presented in 10 cases admitted from 1983 to 1985, with age ranges from 74 to 89, and with diagnosis of ischemic heart disease, with myocardial infarction in 50% of them. Clinically they had asthenia, adynamia and anorexia in 80%, cough and weight loss in 50%. All of them had tachycardia, pulmonary rales and 50% pericardial rub. ECG showed in 80% anterior subepicardial ischemia, 60% posteroinferior subepicardial ischemia, 60% bifascicular block, and 50% left anterior fascicular block. Chest films were interpreted at first as pulmonary fibrosis in 90% of the cases with superior lobe involvement in 50%. Heart enlargement was present in 50%. A chronic lung disease was disclosed on clinical and pulmonary physiological grounds. It is concluded that asthenia, adynamia and anorexia were atypical manifestations of heart failure in the elderly. Silent myocardial infarction was observed in half of our patients and it was complicated with pericardial involvement in 50%. Irregular distribution of fluids in pulmonary edema was attributed to anatomic changes in elder lung. These atypical behaviour of pulmonary edema, has been misinterpreted on radiologic basis with pulmonary infection, tumours, metastasis or fibrosis. Those radiologic changes disappeared or improved in 72 hrs. with treatment of left ventricular failure.
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PMID:[Radiologic characteristics of cardiogenic pulmonary edema in the elderly]. 296 66

The utility of flecainide acetate was evaluated in 93 patients by means of electrophysiologic studies before and after intravenous flecainide administration to determine long-term efficacy. Twenty patients had a prior history of at least one cardiac arrest and 73 patients had sustained ventricular tachycardia (VT). The mean radionuclear ejection fraction was 32 +/- 5%. Flecainide was evaluated in 93 patients, with 44 patients no longer having VT following flecainide (47% efficacy). Procainamide was evaluated in 69 patients; 24 patients had an adverse reaction to reaction to procainamide and 28 of the 69 patients were protected on procainamide (40% efficacy). The mean serum concentration of flecainide achieved in the protected group was 298 +/- 36 ng/ml and 4.3 micrograms/ml for procainamide. Both flecainide and procainamide significantly prolonged refractoriness, lengthened QRS duration, while only procainamide increased the QT interval. All 93 patients were discharged on antiarrhythmic therapy, 42 on flecainide, 27 on other antiarrhythmic therapy guided by electrophysiologic testing, and 24 on amiodarone (when all other agents failed). Six of the 42 patients on flecainide complained of adverse side effects, but none were severe enough to warrant stopping therapy. Of the 42 patients on flecainide, four (9%) died suddenly over 18 +/- 4 months. Twenty-seven patients were on other therapy; eight of these have died, three suddenly (11%), four with myocardial infarctions, and one due to congestive heart failure. Twenty-four patients started amiodarone; 11 have died, five (21%) suddenly, four of congestive heart failure, one of pulmonary fibrosis, and one with myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic flecainide therapy selected by electrophysiology testing of intravenous flecainide. 311 Dec 36

Of 582 patients who underwent percutaneous nephrolithotomy, 4% had complications. The most common complications were fever (23%) and bleeding necessitating transfusion (12%). Extravasation was seen in 7% of patients and transient ureteral obstruction in 6%. Other complications included pneumothorax or hydrothorax, pneumonia/atelectasis, paralytic ileus, nephrostomy-tube dislodgment or urine drainage from the flank lasting more than 1 week, significant infection, urinoma formation, renal pelvic laceration, ureteral avulsion, ureteropelvic or ureteral stricture, bowel injury, or escape of stone fragments into the retroperitoneum. Seven patients (1%) required immediate surgery: four to repair renal pelvic lacerations, one to repair a ureteral avulsion, and two to control bleeding after nephrostomy-tube removal when embolization failed. Four patients required delayed surgery for ureteral or ureteropelvic junction strictures, which may have been caused by a tissue reaction to the stones rather than by the procedure itself. There were two deaths--one from respiratory failure in a patient with severe interstitial pulmonary fibrosis and chronic renal failure and the other from myocardial infarction in an obese diabetic patient with hypertension.
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PMID:Complications of percutaneous nephrolithotomy. 349 9

Between Jan 1, 1968, and Dec 31, 1980, 108 previously untreated patients with Hodgkin's disease pathologic stages (PSs) IA (29 patients) and IIA (79 patients) initially received radiotherapy alone. One postoperative death (due to pulmonary embolus) (0.9%) occurred, with one serious complication (0.9%). Between 1968 and 1973, patients were randomized to receive either involved field radiation treatment (RTIF) or extended field radiation treatment (RTEF). Since 1973 all patients have received RTEF, 4,000 cGy in four to five weeks, with a median follow-up of 7.4 years. Complete remission (CR) was achieved in 102 patients (94.4%), with no significant difference according to treatment or stage. Of the complete responders, 25 patients relapsed: 5/15 RTIF and 20/87 RTEF (P = .6). Twenty-one of 25 relapsing patients achieved a second CR. Disease free survival rates at five and ten years constituted: PS IA, 78.6% for both; PS IIA, 74.8% and 73.1% (P = .6); RTEF, 76.7% for both; RTIF, 73.3% and 66.7% (P = .7). Eighteen patients have died: eight of recurrent lymphoma, two of pulmonary embolus, one each of myocardial infarction, pulmonary fibrosis, and acute nonlymphocytic leukemia (ANLL) (following salvage chemotherapy), and one of diffuse histiocytic lymphoma (DHL). Four patients died in remission of unrelated causes. Actuarial survival rates at five and ten years constituted: PS IA, 95.7% and 72.4%; PS IIA, 89.6% and 81.4% (P = .3); RTIF, 93.7% for both; RTEF, 90.7% and 71.2% (P = .2). Age, sex, number of sites, and mediastinal involvement did not influence the outcome. Acute toxicity was modest and more frequent among those receiving RTEF (P = .08). Chronic toxicity (onset more than 30 days after completion of treatment) was identified in 16 patients: 1/16 RTIF; 15/92 RTEF (P = .5). Three patients developed a second malignancy: one carcinoma of the cervix in situ; one ANLL (following salvage chemotherapy); and one DHL of the stomach. At least 75% of patients with PS IA and IIA Hodgkin's disease were cured by radiation alone, with a risk of secondary malignancy following radiation alone of 0.9%. Since the majority of relapsing patients were successfully salvaged by chemotherapy, radiation alone appears to be the initial treatment of choice in this group of patients.
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PMID:Pathologic stages IA and IIA Hodgkin's disease: results of treatment with radiotherapy alone (1968-1980). 400 15

In a 70 years old worker in the bauxite industry in Surinam, who died of myocardial infarction, bauxite deposits were found in the lung in areas of mild pulmonary fibrosis. The identification and the localization within these areas of the bauxite deposits was determined by a histochemical mineralization technique and by scanning electron microscopy and electron microprobe analysis. The possible relationship between the presence of bauxite in the lung tissue and the pulmonary fibrosis is discussed.
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PMID:Deposition of bauxite dust and pulmonary fibrosis. 652 33

Monoclonal antibodies (mAb) have revolutionised many areas of medicine, particularly research and diagnostics. Murine, human and humanized mAb have all been developed. The most important clinical applications to date have been in the fields of transplantation and oncology. Experimental and limited clinical trials suggest mAb are emerging as a new therapeutic strategy in the critically ill. Antibodies against a variety of bacteria or their products are potentially useful in gram-positive and gram-negative shock. Anti-cytokine and anti-neutrophil adhesion molecule mAb may be effective not only in septic shock but also in other conditions associated with acute inflammation and cytokine release, e.g., acid aspiration, ischaemia/reperfusion injury (myocardial infarction, haemorrhagic shock, aortic aneurysm repair). Antibodies inhibiting neutrophil adhesion may also be efficacious in asthma, pulmonary fibrosis, meningitis and cerebral malaria. The use of these and other mAb in intensive care is an exciting prospect and future clinical studies will determine the extent of their role in the management of the critically ill.
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PMID:Monoclonal antibodies--immunotherapy for the critically ill. 812 30

Mutation of myocardial mitochondrial DNA was investigated in human left ventricles obtained at autopsy using the polymerase chain reaction (PCR). Seventeen autopsy cases were examined, including patients with diabetes mellitus, myocardial infarction, cardiomyopathy, cancer, and other diseases. Two cases of diabetes mellitus, 2 of myocardial infarction, and 1 of pulmonary fibrosis showed a 7.4 kb deletion of myocardial mitochondrial DNA. Primer shift PCR confirmed that an amplified DNA fragment had not been obtained by misannealing of the primers. It is unclear how much these findings are related to the severity or prognosis of the various diseases, but they indicate that mutation of myocardial mitochondrial DNA can occur in other diseases besides cardiomyopathy, although the influence of aging could not be excluded.
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PMID:Mitochondrial DNA deletion in human myocardium. 845 72

This study investigated cardiac disorders in 25 patients with diagnoses of progressive systemic sclerosis based on the criteria of the American College of Rheumatology. All were women, and the mean age was 59 +/- 11 (range 41-80) years old. The duration of the disease was 11 +/- 9 (range 3-40) years. The following complications were seen; Raynaud's phenomenon in all, esophageal disorders in 11, pulmonary fibrosis in 9, diabetes mellitus in 3, high blood pressure in 6, hyperlipidemia in 7, and positive anticardiolipin antibody in 8. Electrocardiography (ECG) and echocardiography were performed to assess the cardiac disorders. Abnormal ECG was seen in 11 patients (44%) and abnormal echocardiograms in 16 patients (64%). ECG abnormalities included incomplete right bundle branch block in 8 (32%), low voltage in 3 (12%), supraventricular arrhythmia in 3 (12%), ventricular arrhythmia in 1 (4%) and septal myocardial infarction pattern in 1 (4%). Echocardiographic abnormalities included valvular diseases in 13 (52%) and pericardial thickening in 7 (28%). No relationship was found between ECG and echocardiographic abnormalities. Echocardiographic abnormalities were more frequently observed in patients with positive anticardiolipin antibody (7/8, 88%) than in those with negative anticardiolipin antibody (9/17, 53%). Especially, pericardial thickening was seen in 63% (5/8) of positive patients, in comparison to 12% (2/17) of the negative patients (p < 0.05). Patients with progressive systemic sclerosis may have several cardiac disorders including conduction disturbances, low voltage ECG, valvular diseases and pericardial thickening. Pericardial thickening has a close relationship with positive anticardiolipin antibody.
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PMID:[Cardiac disorders associated with progressive systemic sclerosis]. 991 57

Hepatocyte growth factor (HGF) was purified as a potent mitogen for rat hepatocytes in primary culture and is believed to be the most physiological hepatotrophic factor that triggers liver regeneration. HGF is one of the largest disulfide-linked cytokines, consisting of a 60-kDa heavy chain and a 35-kDa light chain. Human HGF is synthesized as a single polypeptide chain precursor of 728 amino acid residues that has an appreciable homology with plasminogen, and it is processed proteolytically to release an N-terminal signal peptide of 31 amino acids and to generate an active heterodimer after secretion. The novel serine protease HGF activator and urokinase-type plasminogen activator (u-PA) are responsible for the latter extracellular processing. HGF stimulates the proliferation of rat hepatocytes in primary culture at concentrations as low as 10 pM. It also stimulates the growth of various epithelial cells, endothelial cells, and some kinds of mesenchymal cells. HGF inhibits the proliferation of several tumor cell lines and induces apoptosis of some of them. It also has motogenic, morphogenic, anti-apoptotic, angiogenic, and immunoregulatory activities. The receptor of HGF is the product of c-met proto-oncogene with tyrosine kinase activity that mediates the transduction of multiple biological signals of HGF. During liver regeneration, HGF gene expression in the liver, spleen, and lung and HGF levels in the blood and liver increase prior to the induction of liver DNA synthesis. Liver regeneration is markedly inhibited by continuous administration of a neutralizing anti-HGF antibody. HGF production in cultured cells is induced by PKC-activating agents, cAMP-elevating agents, PKA-activating agents, growth factors, and inflammatory cytokines; and it is inhibited by TGF-beta, glucocorticoids, 1,25-dihydroxyvitamin D3, and retinoic acid. There are many reports on potential application of HGF as a therapeutic agent for organ diseases that are difficult to cure such as liver cirrhosis, chronic renal failure, pulmonary fibrosis, myocardial infarction, and arteriosclerosis obliterans utilizing its potent growth-stimulating activity for a wide variety of cells. ELISA kits for assays of serum and plasma HGF levels are clinically used to prognosticate the development of fulminant hepatic failure.
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PMID:[Function and regulation of production of hepatocyte growth factor (HGF)]. 1206 Nov 40


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