Gene/Protein Disease Symptom Drug Enzyme Compound
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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

A 70-year-old woman presented with a skin rash, chronic headaches, congestive cardiac failure, and a moderate pericardial effusion. These were attributed to systemic lupus erythematosus (SLE). She responded to a moderate dose of corticosteroids. SLE though rare in the elderly is a disorder that should not be forgotten.
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PMID:Systemic lupus erythematosus--not to be forgotten in the elderly. 757 Jan 22

In all patients hospitalized in one single hospital due to acute myocardial infarction (AMI) during a period of 21 months, we describe the prognosis in relation to smoking habits and other risk indicators with death. Of 862 AMI patients, 37% reported smoking at the onset of AMI. Of the patients who smoked at the onset of AMI and who survived the first year, 53% reported having quit smoking. Patients who had quit smoking reported fewer symptoms of chest pain (p < 0.01), headache (p < 0.01) and dizziness (p < 0.001) as compared with patients who continued to smoke after one year. Of the patients who had quit smoking, the mortality during the subsequent 4 years was 17% as compared with 31% for patients who continued to smoke (p < 0.05). However, patients who quit smoking less frequently had a previous history of myocardial infarction and congestive heart failure. When correcting for such dissimilarities, quitting smoking did not remain significantly associated with prognosis.
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PMID:Smoking habits in consecutive patients with acute myocardial infarction: prognosis in relation to other risk indicators and to whether or not they quit smoking. 758 61

Carvedilol is a beta-adrenoceptor antagonist which also causes peripheral vasodilation primarily via alpha 1-adrenergic blockade. Carvedilol produces its antihypertensive effect partly by reducing total peripheral resistance by blocking alpha 1-adrenoceptors and by preventing beta-adrenoceptor-mediated compensatory mechanisms. This combined action avoids many of the unwanted effects associated with traditional beta-blocker or vasodilator therapy. In clinical trials published to date, most of which enrolled small numbers of patients, the antihypertensive efficacy of carvedilol administered once daily was similar to that of atenolol, labetalol, pindolol, propranolol, metoprolol, nitrendipine (in elderly patients), slow release nifedipine or captopril in patients with mild-to-moderate essential hypertension. Combined therapy with carvedilol 25 mg and hydrochlorothiazide 25 mg, nicardipine 60 mg or slow release nifedipine 20 mg has an additive antihypertensive effect. Carvedilol and atenolol at similar doses were equally effective at reducing blood pressure in patients who had previously not responded adequately to hydrochlorothiazide monotherapy. As a result of its multiple mechanisms of action, carvedilol is suited for the management of specific groups of hypertensive patients, such as those with renal impairment. In patients with non-insulin-dependent or insulin-dependent diabetes mellitus carvedilol does not appear to affect glucose tolerance or carbohydrate metabolism. Initial studies have demonstrated that carvedilol and slow release nifedipine have similar efficacy in patients with stable angina pectoris and there is evidence that carvedilol has a beneficial haemodynamic effect in patients with congestive heart failure (NYHA class II or III) secondary to ischaemic heart disease. A postmarketing surveillance study has shown that carvedilol is generally well tolerated with only 7% (164/2226) of patients (83% of the total number received 25mg daily for 12 weeks) withdrawing from treatment because of adverse events. Vertigo, headache, bronchospasm, fatigue and skin reactions were the most common events causing withdrawal. Thus, clinical experience to date suggests that carvedilol is likely to be a valuable addition to the options currently available for treating patients with mild-to-moderate essential hypertension, and may offer particular benefit in specific populations of hypertensive patients.
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PMID:Carvedilol. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. 768 74

Earlier nonselective alpha 1-adrenergic blocking drugs such as phentolamine and phenoxybenzamine are now restricted to the pharmacological management of alpha 1-adrenergic crisis and phaeochromocytoma. Prazosin, the first selective alpha 1-blocker approved for the treatment of hypertension, became available in the mid-1970s. Additional alpha 1-blockers such as doxazosin and terazosin have been introduced during recent years. The undesirable effects of all members of this class are similar. Most adverse events can be attributed to reversible competitive antagonism of postsynaptic alpha 1-adrenergic receptors in tissues that sustain high levels of alpha-adrenergic sympathetic tone, e.g. resistance arteries, capacitance veins and the urinary bladder outflow tract. Orthostatic hypotension with a sensation of intense faintness and occasional syncope, can occur shortly after the initial dose. Aggravating factors include upright posture, intravascular volume depletion and concurrent administration of other medications that lower blood pressure, including all other classes of antihypertensive drugs. The problem is reduced or avoided by the choice of low starting doses, beginning treatment at bedtime and by minimising other risks. Among overall adverse effects, asthenia, dizziness, faintness and syncope predominate and occur in 10 to 20% of patients, leading to discontinuation of therapy in about half that number. Infrequent adverse events include headache, drowsiness, palpitations, urinary incontinence and priapism. Some patients experience a 1 to 2kg bodyweight gain which may be associated with secondary hyperaldosteronism. Tolerance appears to develop to the benefits of alpha 1-blockade in patients with congestive heart failure, but not in hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effects of alpha 1-adrenergic blocking drugs. 791 78

The purpose of this study was to evaluate the effects of the alpha 1-blocking agent terazosin on blood pressure (BP) and blood lipids in a large, variant population of patients with hypertension. A total of 16,917 patients with hypertension were evaluated at 2214 primary and community care facilities; 7808 of these patients had not been treated previously for hypertension; 3928 were switched to terazosin from another antihypertensive agent; and 5181 received terazosin in addition to an agent that had not controlled their hypertension. Terazosin produced highly significant reductions in systolic (-18.2 +/- 0.2 mm Hg) and diastolic (-13.2 +/- 0.1 mm Hg) BP when used as monotherapy (mean dose, 3.1 mg; range, 2 to 10 mg) without causing a significant increase in heart rate. Equal antihypertensive efficacy was demonstrated in men, women, blacks, and whites of all ages, with particular benefit to elderly patients (> or = 65 years of age) with systolic hypertension. Comparative studies indicated that terazosin had equal antihypertensive efficacy in combination with diuretics, beta-blockers, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors. Patients who had not responded to monotherapy with one of these classes of antihypertensive drugs showed significant reductions of BP after terazosin, in the following average doses, was added to diuretics, 3.1 mg; beta-blockers, 3.4 mg; calcium channel blockers, 3.3 mg; and ACE inhibitors, 3.4 mg. Terazosin produced highly significant reductions in blood levels of total cholesterol (-5.0%), triglycerides (-6.1%), and low-density lipoprotein cholesterol (-7.6%) without change in high-density lipoprotein cholesterol when used as monotherapy. Similar favorable effects on blood lipid levels were demonstrated when terazosin was used in combination with all other classes of antihypertensive drugs. The greatest reductions in blood cholesterol (-9.2%) were observed among patients with hyperlipidemia (total cholesterol > or = 240 mg/dL). Terazosin maintained its antihypertensive efficacy and was well tolerated by patients with a variety of concomitant diseases, including congestive heart failure, peripheral vascular disease, chronic obstructive pulmonary disease, benign prostatic hyperplasia, diabetes, and obesity. Adverse effects occurred in 17.9% of patients and caused 2.2% to drop out of the study. The most frequent adverse effects were dizziness (4.8%), headache (2.5%), and asthenia (2.4%). Only 0.4% suffered syncope and 0.2% impotence. These data demonstrate the usefulness of terazosin as monotherapy or add-on therapy for treatment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha 1-blockade for the treatment of hypertension: a megastudy of terazosin in 2214 clinical practice settings. 792 16

Ramipril is a long-acting nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor introduced for clinical use about a decade ago. Ramipril is a prodrug that undergoes de-esterification in the liver to form ramiprilat, its active metabolite. Ramipril rapidly distributes to all tissues, with the liver, kidneys and lungs showing markedly higher concentrations of the drug than the blood. After absorption from the gastrointestinal tract, rapid hydrolysis of ramipril occurs in the liver. In the therapeutic concentration range, protein binding of ramipril and ramiprilat is 73 and 56%, respectively. Ramiprilat binds to ACE with high affinity at concentrations similar to that of the enzyme and establishes equilibrium slowly. Although ramipril is metabolised by hepatic and renal mechanisms to both a glucuronate conjugate and a diketopiperazine derivative, most of the drug is excreted in the urine as ramiprilat and the glucuronate conjugate of ramiprilat. Elimination from the body is characterised by a relatively rapid initial phase with a half-life of 7 hours and a late phase with a half-life of about 120 hours. No clinically significant pharmacokinetic interactions between ramipril and other drugs have been reported. The drug has been generally well tolerated with the most prevalent adverse effects being dizziness (3.4%), headache (3.2%), weakness (1.9%) and nausea (1.7%). Ramipril is an effective and well tolerated drug for the treatment of hypertension and congestive heart failure in all patients, including those with renal or hepatic dysfunction, and the elderly.
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PMID:Clinical pharmacokinetics of ramipril. 813 99

Angiotensin converting enzyme inhibitors (ACEI) are established drugs for the treatment of congestive heart failure. Cases of symptomatic hypotension, especially on the first day of treatment, have been reported occasionally. The database we analysed consisted of 1,177 patients, mean age approximately 70 yrs, with congestive heart failure NYHA functional class II or III. These patients were treated and observed prospectively according to a uniform protocol, starting therapy with 2.5 mg enalapril and measuring blood pressure at hourly intervals for eight hours thereafter. 94.6% of the patients experienced no symptomatic hypotension, 4.75% moderate symptoms (e.g. dizziness, headache) and 0.59% severe symptoms (e.g. fainting, collapse, renal failure). For the analyses of risk factors a large number of baseline variables were analysed univariately to select those significant for inclusion in a multivariate stepwise logistic regression. Alternatively the CART-(classification and regression tree) technique was used. Both techniques showed diastolic blood pressure < or = 70 mmHg to be the single most significant risk factor. CART-analyses showed also pretreatment with nitrates and systolic blood pressure < or = 120 mmHg to be of prognostic relevance. Thus CART is a valuable complement when looking for prognostic factors.
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PMID:CART and logistic regression analyses of risk factors for first dose hypotension by an ACE-inhibitor. 814 29

The efficacy of flosequinan 100 mg once daily was evaluated in 15 patients with severe congestive heart failure (New York Heart Association [NYHA] class II-IV) who had not responded adequately to digoxin and diuretics. Efficacy assessments using non-invasive techniques included exercise capacity, haemodynamics and left ventricular function. Determinations were made after 3 and 21 days' treatment, and compared with baseline. Flosequinan significantly increased exercise capacity by 27% after 3 days (+79 seconds, p = 0.015) and by 43% after 21 days (+123 seconds, p = 0.0007) and was accompanied by an increase in heart rate (+7.2 beats/min, p = 0.03; +9.1 beats/min, p = 0.03, respectively). Cardiac index and cardiac output were also significantly increased but only after 21 days' treatment (+0.3 l/min/m2, +16% and +0.5 l/min, +14%, respectively; both p = 0.008). Flosequinan was well tolerated, with headache being the most frequently reported adverse event and only 1 patient being withdrawn. One patient died but this was not unexpected in a group of patients with severe heart failure. Using non-invasive techniques this study demonstrated that in patients with severe chronic congestive heart failure, flosequinan increased exercise capacity and cardiac output, the latter being achieved mainly by an increase in heart rate.
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PMID:A non-invasive evaluation of flosequinan on haemodynamics and exercise capacity in chronic congestive heart failure. 822 97

Pheochromocytoma is a catecholamine secreting tumor originating from the adrenal medulla (up to 90%), or from the chromaffin tissue along the paravertebral sympathetic chain. The hallmark of pheochromocytoma is paroxysmal hypertension associated with diaphoresis, headache, tremulousness, and palpitations. The triad of diaphoresis, tachycardia, and headache in hypertensive patients is highly suggestive of pheochromocytoma. Other symptoms like flushing, nausea, vomiting, personality changes, and visual disturbances may however cast doubt on the diagnosis of pheochromocytoma. Death resulting from pheochromocytoma is usually due to congestive heart failure, myocardial infarction, or intracerebral hemorrhage. Although less than 0.1 percent of patients with hypertension have a pheochromocytoma, nearly 50 percent of the mortality with unsuspected pheochromocytoma occurred during anesthesia and surgery or parturition. Patients of unsuspected pheochromocytoma have higher risk for surgery, because some mandatory pre-op medical treatments might have been ignored. It is also a challenge to anesthesiologists to handle unsuspected hypertensive crisis during anesthesia and surgery. We presented such a case of unexpected Pheochromocytoma which was mis-diagnosed by the surgeon and was treated as an ordinary adrenal gland tumor and was scheduled for surgical operation. When the patient was undergoing excision of the tumor, manipulations of the tumor initiated an tremendous elevation of the blood pressure. Upon reviewing her history of normotension with visual disturbance, nausea and restlessness, she was immediate treated as with a pheochromocytoma. Appropriate managements were applied to control her abnormally high fluctuating blood pressure with success and with no complications or adverse effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthetic management of intraoperatively diagnosed pheochromocytoma--a case report]. 830 54


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