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

We encountered two cases of legionella pneumonia which ran a dramatic course and isolated Legionella dumoffii from one patient and Legionella pneumophila serogroup 5 from the other patient. The patient from whom L. dumoffii was isolated was a 59-year-old male with no basic disease. He presented chill, fever, coughing and other symptoms, starting on July 3, 1986, his disease was diagnosed as pneumonia at the clinic of his company. The patient was then introduced and admitted to our hospital. On admission chest radiography disclosed zonal pneumonia with an unclear border in the right superior lobe of the lung; a beta-lactam preparation was administered, but no effect was obtained and the lung lesion showed a rapid advance. From this condition, we suspected legionella pneumonia and changed the therapy to treatment with erythromycin and rifampicillin. Despite this, no improvement occurred and the patient died on the 26th hospital day. Colonies like Legionella colonies were separated from a total of seven specimens of biopsy aspirated matter from the airway and autopsy collected lung abscess and tracheal secretions, and the bacterium was identified L. dumoffii based on the biochemical and serological properties. In addition, the patient's serum was found to have an increased antibody titer against L. dumoffii. Based on these findings, the patient's disease was diagnosed as pneumonia as caused by L. dumoffii, a relatively rare bacterium as a member of the genus Legionella. The patient from whom Legionella pneumophila serogroup 5 was isolated was an 81-year-old man with basic diseases such as heart failure, anemia and hypothyroidism. He presented fever, general fatigue, anorexia and other symptoms, starting around June 2, 1987; pneumonia was suspected and the patient was urgently admitted to our hospital. The patient died of pneumonia of unknown cause on the second hospital day. To clarify the cause, autopsy was conducted; a large number of colonies like Legionella colonies were noted in the lung tissue. Identification test was then conducted and the bacterium was identified as L. pneumophila; we concluded that the patient's pneumonia had been caused by the identified bacterium L. pneumophila. The isolate was further subjected to slide agglutination test and identified as L. pneumophila serogroup 5.
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PMID:[Legionella dumoffii and Legionella pneumophila serogroup 5 isolated from 2 cases of fulminant pneumonia]. 250 80

Myotonia is defined as a persistent contraction of skeletal muscles after their stimulation. This contracture is not prevented or relieved by regional anaesthesia or muscle relaxants. The sensitivity to non-depolarizing muscle relaxants is usually normal. Suxamethonium, neostigmine, hypothermia, a rise in kalaemia should be avoided. There have been case reports of malignant hyperthermia in patients with myotonia congenita. Dystrophia myotonica is the second most frequent of the inherited muscle diseases, after Duchenne's dystrophy. The severity of the disease is due more to the muscular atrophy and the multiple organ involvement than to the abnormal contraction. Atrioventricular heart block and dysrhythmias are more common than heart failure. Prolonged apnoea and pneumonia are the main risks of anaesthesia. In severe cases, exists a restrictive respiratory insufficiency which is preceded by a fall in the maximum expiratory pressure. Dysphagias and inefficient coughing may occur early. An increased susceptibility to hypnotic drugs and opiates is a common feature. Spontaneous sleep apnoeas should be sought before anaesthesia, especially by using pulse oximetry. The anaesthetic implications are reemphasized.
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PMID:[Anesthesia in myotonia]. 253 24

This report reviews the tolerability profile of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, in the treatment of patients with congestive heart failure. Data have been collected from 546 patients treated with enalapril for up to 9 months in clinical trials other than the Cooperative North Scandinavian Enalapril Survival Study. Results in patients treated with enalapril (n = 193) or placebo (n = 195) in double-blind, controlled clinical trials show that the incidences of death, serious adverse experiences, and adverse experiences requiring discontinuation of double-blind therapy, as well as the overall incidence of such experiences, were similar in the 2 groups. However, certain adverse experiences that are related to the mechanism of action of ACE inhibitors were seen more often after enalapril than after placebo treatment. Dizziness and hypotension were the most frequent adverse experiences reported in patients with heart failure treated with enalapril. The most frequent laboratory adverse experiences were increases in blood urea nitrogen and serum creatinine levels. hyperkalemia was also seen in patients receiving enalapril. It is possible to identify patients at risk of these experiences before initiating treatment with enalapril and to take certain measures (such as withholding or reducing the dose of diuretic drugs and discontinuing potassium supplements or potassium-sparing diuretic drugs) to reduce the likelihood that hypotension, increases in blood urea nitrogen and serum creatinine levels, or hyperkalemia will occur. Angioedema, a recognized adverse effect of ACE inhibitors, was not seen in the clinical trials reviewed here. Cough , another recognized adverse effect of these agents, was seen infrequently and rarely resulted in the discontinuation of enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerability of enalapril in congestive heart failure. 253 64

27 cases of uremia with abnormal appearances on the chest films were analysed. The results showed that the clinical features were cough, expectoration dyspnea and hemoptysis. However, the degree of these symptoms was relatively mild as judged from the amount of pulmonary edema found on the chest films. The chest X-ray finding in these group of patients were characterized by pulmonary blood stasis, interstitial edema of the lung and edematous alveoli. The pathogenesis of uremic lung was said to be related to blood urea nitrogen and creatinine retention and the concurrent presence of left side heart failure may also play a role. Hemodialysis and other comprehensive treatments could help the patients with uremic lung for relief the symptoms. But the fundamental managements to improve the prognosis for this disease are early treatment of the primary renal diseases, in order to prevent the occurrence of renal failure. Kidney transplantation should be advised.
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PMID:[The uremic lung]. 263 29

Drug interactions common to all angiotensin-converting enzyme (ACE) inhibitors include those with thiazide diuretics and other antihypertensive agents. Interactions involving specific ACE inhibitors include captopril-digoxin, resulting in decreased clearance of digoxin from plasma in patients with heart failure, and captopril-probenecid, causing a decrease in captopril clearance. Tissue kinins, such as bradykinin, are metabolised by ACE inhibitors. Interactions involving bradykinin include captopril-indomethacin, in which an attenuation of the antihypertensive effects of captopril is manifest. Interestingly, neither enalapril nor lisinopril appear to show this interaction with indomethacin. Kinin-based interactions may also be important in the genesis of ACE inhibitor-induced cough and skin rash. Renal dysfunction affects the pharmacokinetics and pharmacodynamics of all ACE inhibitors, necessitating dosage reduction. Hepatic impairment is of less clinical importance, causing a delay in the onset of action of enalapril with initial doses, but probably having little relevance to long-term therapy.
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PMID:Drug interactions with ACE inhibitors. 267 38

A 61-year-old man was admitted to our hospital with complaints of cough and left back and chest pain. He had suffered from left tuberculous pleurisy at the age of 20 years. Chest X-ray film and CT revealed atelectasis of the left lung, a left hilar mass and an irregular left atrial wall. Depressed P-Ta segment in the inferior limb and anterior chest leads and an abnormal P wave were found on ECG. Transbronchial lung biopsy showed squamous cell carcinoma. After radiation therapy, the patient complained of chest oppression. ECG revealed a normalized P-Ta segment deviation, markedly elevated ST segment in the inferior limb and lateral chest leads and a depressed ST segment in the anterior chest leads. These findings persisted until his death. An obscure appearance of the pericardium and an echogenic intramyocardial mass in the posteroinferior and lateral wall were evident by echocardiography. The patient died due to heart failure. Postmortem needle biopsy showed scattered intramyocardial tumor cell nests with keratinization. CPK, GOT and LDH were within normal limits throughout the course, but CPK-MB was slightly increased. Cardiac metastasis with an ECG appearance similar to that of acute myocardial infarction has been rarely reported. Our present case showed peculiar feature including 1) ECG findings similar to atrial and ventricular myocardial infarction, and 2) an echogenic intramyocardial mass and an ill-defined pericardium on echocardiography. These findings suggested direct invasion of squamous cell carcinoma of the lung to the ventricular myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Report of a case of lung cancer with metastasis to the myocardium which showed electrocardiographic findings similar to acute myocardial infarction and intramyocardial mass on echocardiography]. 274 Jun 46

Pancreatitis may be associated with thoracic complications, notably chronic massive pleural effusion (CMPE) and, rarely, pseudocysts with mediastinal extension (PME) and enzymatic mediastinitis (EM). Our personal experience with 14 cases of thoracic complications (nine CMPE, two PME associated with pleural effusion, and three EM of 670 patients who underwent surgery; of these, 191 had acute and 479 had chronic pancreatitis) during 16 years (1970-1986) is reported. In the patients with CMPE, the initial symptoms were progressive dyspnea eventually associated with cough and chest pain. In the PME cases, there was dysphagia associated with left subscapular pain and left chest pain. The initial signs in the patients with EM were sudden dyspnea, cyanosis, retrosternal pain, tachycardia, and acute heart failure. A fistula between the pancreatic ductal system and the pleural cavity in seven of the nine patients with CMPE was demonstrated by intraoperative pancreatography and/or cystography. On the contrary, preoperative endoscopic pancreatography demonstrated the sinus tract in only three of the seven. In both cases of PME, computed tomography (CT) provided a correct diagnosis that was confirmed at surgery. In the patients with EM, the diagnosis was suggested by the clinical appearance and was confirmed by the chest roentgenogram and by CT. All patients had operations after varying periods of unsuccessful 2-4-week-long conservative treatment. One patient with infected ascites died postoperatively. There were no thoracic recurrences of pancreatic disease among the other patients at a 10-month-10-year follow-up observation after surgery.
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PMID:Thoracic complications of pancreatitis. 275 44

The relationship between angiotensin converting enzyme inhibitors (ACE inhibitors) and the development of cough was studied in 80 patients. Cough developed in 25 (31%). Seventeen patients had detailed respiratory investigations of whom 12 developed a new cough. Five of the 12 patients had a remission on placebo and recurrence on rechallenge. Cough does occur with ACE inhibitors but there are other possible causes of cough such as asthma, bronchitis, smoking and heart failure. The true incidence of new cough with ACE inhibitors is uncertain at present.
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PMID:Angiotensin converting enzyme inhibitors and cough. 283 99

To identify and measure the incidence of adverse effects of the angiotensin converting enzyme inhibitor enalapril 13,713 patients were studied for one year by prescription-event monitoring. Precise information about the duration of treatment was available for 12,543 patients. The frequency of many events was calculated, including dizziness (483 patients; 3.9%), persistent dry cough (360; 2.9%), headache (310; 2.5%) hypotension (218; 1.7%), and syncope (155; 1.2%). Less common reactions included angioedema, urticaria, and muscle cramps. Altogether 1098 (8%) patients died and the notes of 913 of them (83%) were obtained for detailed scrutiny. With the exception of a few patients with renal failure who deteriorated during treatment (reported on separately), no death was attributed to enalapril. Enalapril was considered to be effective, even in patients with advanced cardiac failure. These results for enalapril are reassuring and provide further evidence of the value of prescription-event monitoring.
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PMID:Postmarketing surveillance of enalapril. I: Results of prescription-event monitoring. 284 1

Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. The dosage must be adjusted according to renal function, in order to prevent accumulation and toxicity. In addition to patients with renal insufficiency, patients at high risk are those with a stimulated renin-angiotensin-aldosterone system, i.e. patients with renovascular hypertension or heart failure. Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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PMID:[Angiotensin-converting enzyme inhibition: side effects and risks]. 285 Jun 87


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