Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low formaldehyd-concentrations were measured in three Cologne schools (mean 1 = 0,4425; mean 2 = 0,5725; mean 3 = 0,1292 ppm). As the main sources of emission were identified formaldehyd-urea-bound chip-plates in acoustic-ceilings and wainscots. To study the connection between the complaints of pupils and CH20-emissions 1594 pupils of these schools were questioned using a specially elaborated questionnaire. The questions concerned multiple complaints and disturbances of health as well as their anamnesis in chronological relationship with school attendance. Compared to controls consisting of 497 pupils of a school, where no CH2O-emitting chip-plates were used, the inquiry showed a significant increase (p less than 0,00005) of so-called functional disturbances (headache, disorder of concentrating ability, dizziness, nausea), affections of the respiratory tract (irritation of the mucosa of the nose and the pharynx, dry cough) and irritation of the conjunctiva. In regard to the anamneses, the difference between the investigation-group and the control-group was even more significant and additional complaints such as somnipathy, abdominal pain, skin disease were observed frequently. Comparing the normal distribution of so-called functional disturbances in pupils found in literature, the examined group of this study showed an even higher rate of the relative accumulation. The repeated investigation in one school (n = 328) 8 months after removal of the emission-sources demonstrated a very clear reduction of complaints by an average of 71,2 per cent.
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PMID:[Damages to health in schools. Complaints caused by the use of formaldehyde-emitting materials in school buildings]. 737 30

The increase of non specific surgeries in transplanted patients may be related to the better survival achieved by the efficacy of immunosuppressive therapy and improved surgical and intensive care conditions. Therefore, the anaesthetist may be mandated to give anaesthesia in such patients, treated in hospitals which are not involved in transplantation procedures. The ignorance of the main physiologic and pharmacological changes in the new grafted organ as well as the knowledge of high risks of rejection or infection contribute to the anxiety often encountered in front of these patients. The denervated heart is unable to respond to stimulations requiring the integrity of autonomic neural mechanisms. Modulation of cardiac output depends on intrinsic activity (Frank-Starling mechanism) and therefore of end diastolic volume (preload). The denervated transplanted lung shows inability to elicit cough reflex; the latter is totally abolished in case of tracheal anastomosis. These physiologic changes have no deleterious effects on early cardiac and pulmonary functions following transplantation. In the same way, renal, liver or pancreatic functions are restored after respective replacement. However chronic rejection occurs frequently in 50% of patients in a mean time of 5 years following surgery except for liver transplanted patients which seem to be better protected. It results in a progressive decrease in organ function tests. The preoperative assessment requires primary contact with the transplant center. This communication should give precious information about the last biological and functional results as well as about the immunosuppressive therapy. Standard preoperative investigations include measurements of haemoglobin, urea, electrolyte and creatinine concentrations, liver tests, ECG, chest X-ray and coagulation pattern. Previsible difficult intubation should be detected in case of previous pancreas transplantation. Immunosuppressive therapy and other treatments should not be disrupted until surgery. Usual premedication may be used. Previsional peroperative transfusion requires specific packed red blood cells, fresh frozen plasma and platelets in order to reduce CMV contamination and GVH reactions. Locoregional or general anaesthesia may be used with respect to usual contraindications. Special attention should be given in cardiac transplanted patients in order to maintain adequate preload. As atropine is ineffective, bradycardia may be treated by isoprenaline. Patients with lung transplants require a reduction of vascular loading and of hydratation and early postoperative pulmonary physiotherapy. Pancreas transplanted patients often suffer from severe cardiac diseases (coronaropathy). The immunosuppressive therapy modifies the pharmacological behavior of many anaesthetic agents. Ciclosporine enhances mainly the effects of muscle relaxants. Peroperative invasive monitoring requires full aseptic techniques. Invasive monitoring should be discussed in terms of benefit-risk ratio.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Anesthesia for non-specific surgery in a post-transplantation patient]. 833 62

We herein report the case of a subject exposed to urea fumes. After exposure, the subject immediately experienced throat and chest burning. A few hours later, she had cough, dyspnea and wheezing during exercise. The functional pulmonary testing performed two months later showed non-specific airway responsiveness. Bronchoscopy with broncho-alveolar lavage and bronchial biopsies was performed. Biopsies showed injury of the epithelial layer that was atrophic and devoid of ciliated cells. There was fibrosis of connective tissue as well as an inflammatory infiltrate. Immunohistochemistry stains showed that most of the inflammatory cells were T-lymphocytes. There were no degranulated eosinophils. The subject was given inhaled steroids. Four months later, bronchial responsiveness was normal.
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PMID:[Bronchial irritation syndrome following inhalation or urea. Histologic and immunohistochemical evaluation]. 903 5

Benazepril (BP), an angiotensin convertive enzyme inhibitor, was administered orally once daily for 4 weeks to 31 dogs with mild to moderate (NYHA functional classes II and III) congestive heart failure caused from mitral insufficiency (MI). There were no significant changes in clinical signs, electrocardiogram findings, radiographical observations and plasma biochemical results in 11 dogs treated with placebo for 4 weeks. In 31 dogs treated with BP, appetite increased, and mean scores of heart failure signs, such as activity, exercise tolerance, cough and respiratory effort, were significantly improved. No dog displays signs suggesting systemic hypotension. One dog died suddenly on the 26th day of treatment with BP. This dog had good vigor and appetite till the evening before the death, and cough and exercise tolerance had been gradually improving. The heart rate and ECG parameters of BP treated dogs did not change significantly, but length of long axis of the heart decreased. In plasma biochemical tests, plasma urea nitrogen (UN) levels did not change significantly, and plasma creatinine (CRE) levels increased slightly within the normal ranges during BP trial. Two dogs had higher plasma UN levels with slightly higher plasma CRE levels, but had normal general condition and other biochemical results. Plasma ACE activity decreased to 57.3% of pre-treatment level at 4 weeks after BP treatment. It is concluded that BP monotherapy was efficacious at least in dogs with relatively low grade congestive heart failure caused by MI.
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PMID:Efficacy of monotherapy with benazepril, an angiotensin converting enzyme inhibitor, in dogs with naturally acquired chronic mitral insufficiency. 927 44

A 59-year-old man with chronic obstructive pulmonary disease (COPD), atrial fibrillation, and gout developed acute dyspnea, cough, and diffuse muscle aches and pains. He had commenced colchicine (0.6 mg b.i.d. p.o.), for the first time, one month earlier for recurrent gout attacks. Clinical examination revealed atrial fibrillation, an exacerbation of his pulmonary disease, tender muscles, especially calves, and diffuse muscle weakness. Laboratory results included creatinine phosphokinase 6961 U/l (1% MB), microscopic hematuria, myoglobinuria, elevated creatinine 1.6 mg/dl, and blood urea nitrogen 17 mg/dl. COPD and atrial fibrillation were treated and colchicine was discontinued. The patient made a full recovery. This 2nd reported case of colchicine induced rhabdomyolysis is the first reported in the treatment of gout.
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PMID:Colchicine induced rhabdomyolysis. 933 Sep 53

The CASSIS study was a double-blind multicentric controlled Czech and Slovak study focused on treatment of chronic heart failure with the ACE inhibitor spirapril; it was conducted for 12 weeks. The present work analyzes the second year of the extended open part of the study when all patients (n = 168) were treated with 3 mg or 6 mg spirapril. A small proportion of the patients was treated with 12 mg spirapril. The objective of the study was to test the long-term effectiveness and tolerance of spirapril. The general mortality was analyzed throughout the whole two-year period. The results revealed an unchanging total mortality, analyzed after three-month intervals, during the whole two-year period. Also the functional improvement of the patients according to NYHA which occurred after the first three months of treatment was preserved during the second year. Spirapril proved to be a well tolerated ACE-inhibitor. The authors did not observe angioneurotic oedema in any of the patients. Hypotension and cough were recorded in 0.6% of the patients. The incidence of undesirable laboratory effects was also low and the majority was due to the basic disease. Creatinine did not rise significantly and a rise of urea was observed only in a small number of patients. Liver functions and haemogram did not change during treatment. The results of the second year of erxtension indicate that spirapril is a very effective and safe ACE-inhibitor which will extend in a significant way therapeutic means in patients with chronic heart failure.
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PMID:[Therapy of heart failure with spirapril--the open phase of the CASSIS study. Analysis of the 2nd year extension of the CASSIS study]. 960 64

Theophylline toxicity has been recognized since its introduction into clinical medicine. Clarithromycin is a new oral macrolide antibiotic with excellent antibacterial activity and rare adverse effect. Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. We report a case of acute renal failure due to acute rhabdomyolysis caused by the interaction of theophylline and clarithromycin. A 72-year-old man visited our hospital because of coughing and a sore throat continuing for 1 week. He was diagnosed as having the common cold with a bronchial asthmatic symptom and was prescribed 200 mg/day of sustained-release theophylline for the treatment of asthma for 7 days. One week later, he visited our hospital again. Radiographic study of the chest revealed mild interstitial pneumonia and 200 mg/day of sustained-release theophylline and 400 mg/day of clarithromycin were administrated concomitantly. Five days after the second visit, the patient was admitted to our hospital because of generalized twitching, muscular weakness, high fever and serious general condition. He experienced generalized muscular twitching and tremor. Blood urea nitrogen was 106.1 mg/dl, serum creatinine was 7.4 mg/dl, serum creatinine kinase (CK) was 36,000 IU/l (normal 15-130 IU/l), CK isozyme revealed the following ratio: BB 0%, MB 1% and MM 99%. He was diagnosed as having acute renal failure with rhabdomyolysis caused by the interaction of theophylline and clarithromycin. Hemodialysis therapy was started. After 5 weeks, his serum creatinine was markedly decreased. It is well-known that clarithromycin enhances the serum concentration of theophylline by inhibition of the cytochrome P450-dependent pathway in hepatocytes. Theophylline toxicity may be enhanced when clarithromycin is administrated concomitantly, especially to elderly patients with dehydration.
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PMID:[A case of acute renal failure with rhabdomyolysis caused by the interaction of theophylline and clarithromycin]. 1044 97

Absidiosis was produced experimentally in 18 buffalo calves by intravenous inoculation of spores of Absidia corymbifera. Infected animals exhibited dullness, depression, partial anorexia and an initial pyrexia and coughing during the first week and two animals died on each of 9, 13 and 16 days post infection (DPI). The haemoglobin concentration and total erythrocyte count showed no appreciable change from their basal values at any stage of the experiment. However, the erythrocyte sedimentation rate and total leukocyte count increased significantly in the infected animals. The differential leukocyte count revealed a relative neutrophilia from 5 to 20 DPI. There was a significant increase in the serum total proteins, blood urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase, serum alkaline phosphatase, total immunoglobulins and circulating immune complexes in the infected animals as compared to the controls. In the sera of the infected animals, specific Absidia corymbifera IgM and IgG antibodies were detected from 3 DPI to 6 DPI respectively by Dot-EIA. Type I and type III skin hypersensitivity were detected from 10 DPI and type IV hypersensitivity from 15 DPI onwards. The gross and microscopic pathological lesions were seen mainly in the lungs, in all except one of the affected animals. This animal died 9 DPI and mycotic granulomas were also seen in its heart and kidneys. The microscopic lesions in the lung took the form of well-developed granulomas.
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PMID:Sequential clinical, haematological, biochemical, immunopathological and histopathological alterations in buffalo calves (Bubalus bubalis) intravenously infected with Absidia corymbifera. 1044 50

We report a case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive, rapidly progressive glomerulonephritis(RPGN). A 60-year-old woman was admitted to our hospital for evaluation of RPGN. Laboratory evaluation revealed microhematuria, proteinuria(800 mg/day), anemia, renal failure(blood urea nitrogen 27 mg/dl, serum creatinine 2.2 mg/dl), cryoglobulinemia, hypocomplementemia, positive MPO-ANCA(232 EU), and hepatitis C virus infection(GOT 58 IU/l, GPT 38IU/l, HCV-RNA(PCR) 1,200 kcopy/ml, serotype 1). After admission, the patient's renal function and anemia deteriorated rapidly, then prednisolone(30 mg/day) was started. After treatment her renal function gradually improved, then a renal and liver biopsy was performed. The renal biopsy revealed six sclerosing fibrous crescentic glomeruli in twelve glomeruli. Immunofluorescent examination revealed granular deposits of IgG, C3, and fibrinogen along the glomerular basement membrane and mesangial matrix. The pathogenesis of RPGN in this case may relate to the deposition of immune complexes in the glomeruli because immunofluorescent examination was revealed to be the immune-complex type, but not pauci immune type nephritis. Liver histology revealed chronic active hepatitis with mild piecemeal necrosis and did not reveal vasculitis. Although her renal function was improved after treatment with prednisolone, she suffered from pulmonary manifestations(dry cough etc.) on the 120th hospital day. Suddenly she died because of pulmonary hemorrhage on the 180th hospital day. These findings suggest that various HCV-induced immunological abnormalities, such as positive MPO-ANCA, cryoglobulinemia and hypocomplementemia, play an important role in the pathogenesis of this RPGN, although we could not demonstrate deposition within glomeruli of immune complexes containing HCV. The effect of interferon therapy on such immunological abnormalities remains to be documented. Since interferon is known to have immunomodulatory effects, we selected corticosteroid therapy. Future studies need to focus on the optimal treatment strategy for hepatitis C virus-associated glomerulonephritis.
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PMID:[A case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive rapidly progressive glomerulonephritis]. 1089 95

The patient, a 78-year-old Asian male, was brought to the hospital because of acute shortness of breath that had progressively worsened over the course of the day. He complained of a nonproductive cough and claudication after walking 1 block. His past medical history was significant for mild renal insufficiency (serum creatinine 1.5--2.0 mg/dl), the etiology of which was never explored. Although there was a recent history of mild to moderate hypertension, at presentation his blood pressure was noted to be 240/118 mm Hg in both arms. His physical exam at the time of admission was remarkable for grade II hypertensive retinopathy, an S4 gallop, periumbilical systolic bruits, audible femoral arterial bruits and absent distal lower extremity pulses. Initial complete blood count, serum electrolytes and cardiac enzymes (including lactate dehydrogenase) were normal. His blood urea nitrogen and serum creatinine concentrations were 51 and 3.6 mg/dl, respectively, and his urinalysis showed 1+ protein (both by dipstick and sulfasalicylic acid) with a "benign" sediment (0--1 WBC/HPE, 1--2 RBCs/HPF) with occasional granular casts. His electrocardiogram, apart from demonstrating left ventricular hypertrophy with secondary ST-T wave abnormalities, showed no acute changes; his chest X-ray demonstrated cardiomegaly and pulmonary vascular congestion. He was intubated and subsequently treated with increasing parenteral doses of furosemide (40--240 mg) and a nitroglycerine drip (up to 15 mcg/min). Over the course of the first 48 h, his blood pressure was gradually lowered to 170/100 mm Hg. His urine output increased from 20 ml/h to 125/ml/h, and his respiratory status improved, allowing him to be extubated. In spite of adequate control of his blood pressure in the ensuing days (150--170/80--90 mm Hg), his renal function continued to deteriorate. Renal sonography (without Doppler) demonstrated a right kidney of 9.6 cm and a left kidney of 9.3 cm in length without evidence of hydronephrosis. Both kidneys were noted to be echogenic. Assays for antinuclear antibodies and antineutrophilic cytoplasmic antibodies were negative, and the patient's serum complement levels were normal. For several days after his admission, his serum creatinine gradually rose to 10.7 mg/dl, and hemodialysis was initiated for uremic encephalopathy. Because of the high index of suspicion for renal artery stenosis as the case of both his hypertension and renal failure, a renal angiogram was performed. It revealed a 90% occlusion of the right renal artery with ostial involvement and a 70% occlusion of the left renal artery; both kidneys had poor distal renal vasculature and there was marked atherosclerotic disease of the aorta. After being hemodialyzed for 3 treatments, his renal function began to improve spontaneously. His serum creatinine returned to 3.4 mg/dl, and a subsequent 24-hour urine demonstrated a creatinine clearance of 20 ml/min and an excretion of 1.2 g of protein. Following his discharge from the hospital, his renal function remained unchanged for 3 years, and his blood pressure was easily controlled on monotherapy with a long-acting calcium channel blocker. He recently died from pneumonia.
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PMID:Atherosclerotic Renovascular Disease. 1186 67


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