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PubMed1999

Antiplatelet agents in the prevention of cardiovascular morbidity and mortality in older patients with vascular disease.

Antiplatelet drugs have been demonstrated to reduce the incidence of myocardial infarction (MI), stroke or vascular death in patients with vascular disease. There are no data suggesting that antiplatelet therapy acts differently in older people than in younger people and recommendations based on randomised clinical trials are probably generalisable to older people. Aspirin (acetylsalicylic acid) has been shown to reduce the incidence of non-fatal MI, nonfatal stroke and vascular death in patients with acute MI, a previous MI, angina pectoris or peripheral occlusive arterial disease (POAD), and to reduce cardiovascular morbidity and mortality in patients with a prior ischaemic stroke or transient ischaemic attack (TIA). It has also been shown to reduce the incidence of thrombus formation after coronary artery bypass graft surgery and percutaneous transluminal angioplasty, and in patients with atrial fibrillation and heart valve replacements. Deep vein thrombosis and pulmonary embolism after surgery are also prevented by aspirin. The available data allows the following recommendations to be made. Aspirin 160 to 325 mg daily should be administered to older men and women without contraindications to aspirin who have acute MI, prior MI, unstable or stable angina pectoris, ischaemic stroke, TIA or POAD, and continued indefinitely to reduce the risk of MI, stroke or vascular death. Aspirin should be started in patients before or immediately after revascularisation, and after heart valve replacement. Older men and women with nonvalvular atrial fibrillation who have contraindications to oral anticoagulant therapy but no contraindications to aspirin should be treated with aspirin 325 mg daily. It is reasonable to treat older men and women without contraindications to aspirin with aspirin 160 to 325 mg daily if they are at high risk for developing new coronary events. The incidence of stroke, MI or vascular death in patients after a stroke or TIA is reduced by ticlopidine. Therefore, ticlopidine 250 mg twice daily may be used in older men and women with a history of stroke or TIA who do not respond to or who cannot tolerate aspirin. Patients at high risk for coronary artery stent thrombosis benefit from combined therapy with aspirin plus ticlopidine. The annual incidence of ischaemic stroke, MI or vascular death was significantly reduced by clopidogrel in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial. Therefore, clopidogrel 75 mg daily may be used in older men and women with symptomatic atherosclerosis who do not respond to or who cannot tolerate aspirin to reduce the incidence of ischaemic stroke, MI or vascular death. It should be noted that the acquisition cost for either ticlopidine or clopidogrel is considerably greater than that for aspirin. Most data indicate that the combination of aspirin and dipyridamole is not more effective than aspirin alone in preventing vascular events, and available data do not support the use of sulfinpyrazone in patients with vascular disease.

Aged↗

PubMed1991

Pharmacokinetic interactions between theophylline and other medication (Part I).

Many drugs have been found to increase or decrease the clearance of theophylline, probably by interaction with one or more of the variants of the cytochrome P450 drug-metabolising system. Theophylline may be particularly susceptible to alteration of its clearance because of the particular form(s) of the P450 system involved, because its metabolism is saturable, and/or because 90% of its elimination is via metabolism. Its clearance has been found to be decreased (typically by around 25%, but often by far more) by erythromycin, troleandomycin (triacetyloleandomycin), roxithromycin, enoxacin, ciprofloxacin, pefloxacin, norfloxacin, ofloxacin, fluoroquinolone T-3262, pipemidic acid, cimetidine, etintidine, propranolol, verapamil, diltiazem, nifedipine, furosemide (frusemide), at least some anovulent agents, viloxazine, allopurinol, ticlopidine, idrocilamide, thiabendazole, disulfiram, influenza- and BCG-vaccination, interferon, and caffeine (half-life increase). In contrast, theophylline clearance (clearance/bioavailability) was found to be increased by isoprenaline (isoproterenol), terbutaline, some corticosteroids, phenytoin, phenobarbital, activated charcoal, felodipine moricizine, benzodiazepines and sulfinpyrazone - typically by about 25%, but sometimes by as much as 80% or more. For several of these concomitant medications, however, only some of the published studies can substantiate an influence, which may highlight the sensitivity of some interactions to particular experimental and/or clinical conditions, e.g. with terbutaline, erythromycin, ciprofloxacin, norfloxacin, ofloxacin, phenobarbital, cimetidine, verapamil, diltiazem, nifedipine, anovulents, allopurinol and influenza vaccination. Moreover, reports both of inhibition and of induction of theophylline clearance by each of rifampicin and isoniazid have appeared. Nevertheless, under investigation many medications have not been found to perceptibly influence theophylline disposition kinetics, e.g. ephedrine, orciprenaline (metaproterenol), prednisone, prednisolone, temelastine, terfenadine, mequitazine, picumast, repirinast, josamycin, midecamycin, miocamycin, spiramycin, amoxicillin, ampicillin, cefalexin, cefaclor, ceftibuten, cotrimoxazole (trimethoprim plus sulfamethoxazole), tetracycline, doxycycline, lomefloxacin, fluoroquinolones NY-198 and AM-833, nalidixic acid, lincomycin, metronidazole, certain antacids, ranitidine, roxatidine, pirenzepine, rioprostil, metoclopramide, metoprolol, atenolol, nadolol, medroxyprogesterone, dextropropoxyphene (propoxyphene), piroxicam, ozagrel, mebendazole and ascorbic acid.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗

PubMed1985

Erythromelalgia caused by platelet-mediated arteriolar inflammation and thrombosis in thrombocythemia.

Erythromelalgia was the presenting symptom in 26 of 40 patients with thrombocythemia in its primary form or when associated with polycythemia vera. The localized painful burning, redness, and warm congestion in the extremities could be accurately documented with thermography. Skin punch biopsy samples taken from the affected areas showed typical arteriolar inflammation, fibromuscular intima proliferation, and thrombotic occlusions. Erythromelalgia often progressed to ischemic acrocyanosis or necrosis in toes or fingers. Complete relief of pain and restoration of microvascular circulation disturbances was obtained with the cyclo-oxygenase inhibitors aspirin and indomethacin, but not with sodium-salicylate or the platelet inhibitors dipyridamole, sulfinpyrazone, ticlopidine, and dazoxiben. The erythromelalgia was alleviated during busulfan-induced remissions of thrombocythemia and its recurrence coincided with relapsing thrombocythemia. These observations suggest a causal relationship between erythromelalgia and thrombocythemia, in which platelet-mediated inflammatory and occlusive arteriolar changes play a part in the etiology of erythromelalgia.

Adult↗

PubMed1994

Medical treatment for stroke prevention.

PURPOSE: To review the effectiveness of medical treatments for stroke prevention in patients at elevated risk for stroke. DATA SOURCES: English-language articles published after 1977 and indexed in MEDLINE under the following Medical Subject Heading terms: anticoagulants, aspirin, dipyridamole, ticlopidine, or sulfinpyrazone, combined with cerebrovascular disorders. STUDY SELECTION: Randomized controlled trials of anticoagulant or platelet antiaggregant treatment reporting subsequent stroke and myocardial infarction, death, or complications in persons with asymptomatic carotid stenosis or bruit, transient ischemic attack (TIA), previous stroke, nonvalvular atrial fibrillation, or other vascular diseases. DATA EXTRACTION: Of 900 articles identified, 33 were selected by two independent reviewers and abstracted for outcome events and person-years of follow-up. RESULTS: In patients with nonvalvular atrial fibrillation, warfarin is highly effective in reducing stroke and death but may result in more complications. Aspirin appears to be less effective and less risky than anticoagulation. In patients with TIA or minor stroke, both aspirin and ticlopidine reduce the risk for stroke. In patients who have had myocardial infarction, warfarin is effective but had high complication rates in the reviewed studies. Aspirin slightly reduces the risk for stroke. CONCLUSIONS: Warfarin is strongly recommended for persons with nonvalvular atrial fibrillation who are older than 60 years or who have additional risk factors for stroke. Aspirin is recommended for persons at elevated risk for bleeding while receiving anticoagulants. For persons with TIA or minor stroke, aspirin should be used first. Patients who do not respond to or tolerate aspirin or who have had a major stroke are reasonable candidates for ticlopidine. For patients who have had myocardial infarction, aspirin is recommended for the prevention of secondary myocardial infarction but not of stroke.

Aspirin↗

PubMed1994

Interactions of warfarin with drugs and food.

PURPOSE: To evaluate the quality of studies about drugs and food interactions with warfarin and their clinical relevance. DATA SOURCES: MEDLINE and TOXLINE databases from 1966 to October 1993 using the Medical Subject Headings warfarin, drug interactions, and English only. STUDY SELECTION: All articles reporting original data on drug and food interactions with warfarin. DATA EXTRACTION: Each report, rated independently by at least two investigators (using causality assessment), received a summary score indicating the level of assurance (level 1 = highly probable, level 2 = probable, level 3 = possible, and level 4 = doubtful) that a clinically important interaction had or had not occurred. Inter-rater agreement was assessed using a weighted kappa statistic. RESULTS: Of 793 retrieved citations, 120 contained original reports on 186 interactions. The weighted kappa statistic was 0.67, representing substantial agreement. Of 86 different drugs and foods appraised, 43 had level 1 evidence. Of these, 26 drugs and foods did interact with warfarin. Warfarin's anticoagulant effect was potentiated by 6 antibiotics (cotrimoxazole, erythromycin, fluconazole, isoniazid, metronidazole, and miconazole); 5 cardiac drugs (amiodarone, clofibrate, propafenone, propranolol, and sulfinpyrazone); phenylbutazone; piroxicam; alcohol (only with concomitant liver disease); cimetidine; and omeprazole. Three patients had a hemorrhage at the time of a potentiating interaction (caused by alcohol, isoniazid, and phenylbutazone). Warfarin's anticoagulant effect was inhibited by 3 antibiotics (griseofulvin, rifampin, and nafcillin); 3 drugs active on the central nervous system (barbiturates, carbamazepine, and chlordiazepoxide); cholestyramine; sucralfate; foods high in vitamin K; and large amounts of avocado. CONCLUSIONS: Many drugs and foods interact with warfarin, including antibiotics, drugs affecting the central nervous system, and cardiac medications. Many of these drug interactions increase warfarin's anticoagulant effect.

Animals↗

PubMed1981

Intravenous prostacyclin in thrombotic thrombocytopenic purpura.

A therapeutic trial of prostacyclin (PGI), was done in a patient with thrombotic thrombocytopenic purpura resistant to treatment with antiplatelet drugs and plasmapheresis. Despite marked thrombocytopenia and continued treatment with aspirin, sulfinpyrazone, and dipyridamole, the urinary excretion of 2,3-dinor-thromboxane B2, a major thromboxane urinary metabolite, was within the normal range (90.3 to 368 pg/mg creatinine) at 96 pg/mg creatinine. Because of its potent antiaggregatory properties and the possibility of a defect in endogenous PGI2 production in thrombotic thrombocytopenic purpura, synthetic PGI2 (4 to 10 ng/kg-1 . min-1) was infused intravenously, first for 72 hours and then continuously for 18 days. Prostacyclin markedly reduced the excretion of 2,3-dinor-thromboxane B2, and the platelet count rose steadily to reach 100 000/mm3 by the eighth day of the second infusion. The patient remains in clinical remission, on no therapy, 7 months later. A controlled evaluation of PGI2 in thrombotic thrombocytopenic purpura is warranted. Apparent therapeutic failure in previous cases may have resulted from inadequate prolongation of PGI2 infusion.

Adult↗

PubMed1999

Diagnosis and management of gout.

Gout is a disease resulting from the deposition of urate crystals caused by the overproduction or underexcretion of uric acid. The disease is often, but not always, associated with elevated serum uric acid levels. Clinical manifestations include acute and chronic arthritis, tophi, interstitial renal disease and uric acid nephrolithiasis. The diagnosis is based on the identification of uric acid crystals in joints, tissues or body fluids. Treatment goals include termination of the acute attack, prevention of recurrent attacks and prevention of complications associated with the deposition of urate crystals in tissues. Pharmacologic management remains the mainstay of treatment. Acute attacks may be terminated with the use of nonsteroidal anti-inflammatory agents, colchicine or intra-articular injections of corticosteroids. Probenecid, sulfinpyrazone and allopurinol can be used to prevent recurrent attacks. Obesity, alcohol intake and certain foods and medications can contribute to hyperuricemia. These potentially exacerbating factors should be identified and modified.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2006

Medication errors with the use of allopurinol and colchicine: a retrospective study of a national, anonymous Internet-accessible error reporting system.

OBJECTIVE: To more closely assess medication errors in gout care, we examined data from a national, Internet-accessible error reporting program over a 5-year reporting period. METHODS: We examined data from the MEDMARX database, covering the period from January 1, 1999 through December 31, 2003. For allopurinol and colchicine, we examined error severity, source, type, contributing factors, and healthcare personnel involved in errors, and we detailed errors resulting in patient harm. Causes of error and the frequency of other error characteristics were compared for gout medications versus other musculoskeletal treatments using the chi-square statistic. RESULTS: Gout medication errors occurred in 39% (n = 273) of facilities participating in the MEDMARX program. Reported errors were predominantly from the inpatient hospital setting and related to the use of allopurinol (n = 524), followed by colchicine (n = 315), probenecid (n = 50), and sulfinpyrazone (n = 2). Compared to errors involving other musculoskeletal treatments, allopurinol and colchicine errors were more often ascribed to problems with physician prescribing (7% for other therapies versus 23-39% for allopurinol and colchicine, p < 0.0001) and less often due to problems with drug administration or nursing error (50% vs 23-27%, p < 0.0001). CONCLUSION: Our results suggest that inappropriate prescribing practices are characteristic of errors occurring with the use of allopurinol and colchicine. Physician prescribing practices are a potential target for quality improvement interventions in gout care.

Adverse Drug Reaction Reporting Systems↗

PubMed1991

Clinical trials in stroke prevention.

The randomized clinical trial has no satisfactory substitute in the evaluation of preventive treatment for stroke-threatened patients, and is the gold standard also in studies designed to test strategies which may reduce the impact of brain damage after ischemic stroke has occurred. Stroke data banks and contemporary non-randomized comparisons are imperfect or flawed as bench-marks against which to judge treatments for these types of patients. Flaws in the design, execution and analysis of randomized clinical trials have been eliminated gradually over the past 35 years. On the basis of the existing trials in stroke prevention it may be stated that anticoagulants are effective in patients with non-rheumatic atrial fibrillation and after myocardial infarction. No other uses of anticoagulants in preventing ischemic stroke have been proven. Acetylsalicylic acid between 325-1300 mg/d will prevent stroke; lower doses have not been proven of value. Ticlopidine is effective. Benefit for dipyridamole, suloctidil or sulfinpyrazone has not been shown. Cerebral by-pass surgery has not been shown to have any role in stroke prevention in arteriosclerotic cerebral vascular disease. Carotid endarterectomy is still undergoing careful evaluation.

Cerebrovascular Disorders↗

PubMedDate not supplied

Cyclosporin A drug interactions. Screening for inducers and inhibitors of cytochrome P-450 (cyclosporin A oxidase) in primary cultures of human hepatocytes and in liver microsomes.

In previous papers we demonstrated that cyclosporin A (CsA) was specifically oxidized in rabbit and human liver by cytochrome P-450IIIA. We therefore anticipated that any drug that is an inducer or an inhibitor of this cytochrome should lead to interaction with CsA when given in association with it. In order to confirm this hypothesis, primary cultures of human hepatocytes and human liver microsomes were used to "reproduce" in vitro clinically significant interactions observed between CsA and drugs known either as specific inducers (i.e., rifampicin) or as specific inhibitors (i.e., erythromycin) of P-450IIIA. Our results were in close agreement with the clinical reports. Human hepatocytes maintained in primary cultures for 72 hr in the presence of 50 microM rifampicin exhibited increased levels of P-450IIIA, determined by Western blot using specific antibodies, and concomitant increase in CsA oxidase activity, determined by HPLC analysis of extra and intracellular media. Conversely, these cultures exhibited erythromycin concentration-dependent decreases in CsA oxidase activity when incubated in the presence of 5, 20, and 100 microM erythromycin. In addition, a Lineweaver-Burk analysis of the erythromycin-mediated inhibition of CsA oxidase activity in human liver microsomes revealed competitive inhibition (with Ki of 75 microM) as expected, this macrolide being a specific substrate of P-450IIIA. Using this experimental approach, 59 molecules representative of 17 different therapeutic classes were screened for inducers and inhibitors of CsA oxidase activity. Our results allowed us to elucidate the molecular mechanism of previously observed, but unexplained, drug interactions involving CsA, and to detect drugs that should interfere with CsA metabolism as inducers or inhibitors. Drugs detected as potential inducers of CsA oxidase included: rifampicin, sulfadimidine, phenobarbital, phenytoin, phenylbutazone, dexamethasone, sulfinpyrazone, and carbamazepine. Drugs detected as potential competitive inhibitors included: triacetyloleandomycin, erythromycin, josamycin, midecamycin, ketoconazole, miconazole, midazolam, nifedipin, diltiazem, verapamil, nicardipine, ergotamine, dihydroergotamine, glibenclamide, bromocriptine, ethynylestradiol, progesterone, cortisol, prednisone, prednisolone, and methylprednisolone. Finally, cefoperazone, cefotaxime, ceftazidime, isoniazide, doxycycline, spiramycin, sulfamethoxazole, norfloxacin, pefloxacin, vancocin, trimethoprim, amphotericin B, valproic acid, quinidine, cimetidine, ranitidine, omeprazole, diclofenac, aspirin, paracetamol, debrisoquine, guanoxan, captopril, furosemide, acetazolamide, sparteine, gliclazide, and imipramine were found not to interfere with the hepatic metabolism of CsA.

Blotting, Western↗

PubMed1991

Gout and hyperuricemia.

Accurate diagnosis is essential since gout is overdiagnosed by a factor of three. Asymptomatic hyperuricemia is not associated with adverse consequences and should not ordinarily be treated. The acute attack of gout responds to any nonsteroidal anti-inflammatory drug, and antihyperuricemic therapy with allopurinol, probenecid or sulfinpyrazone is effective in lowering uric acid and preventing further attacks. Except for prophylaxis, colchicine is not recommended for the treatment of gout because of unacceptable levels of toxicity. Diet therapy, once a mainstay of treatment, is usually not indicated since drug therapy alone is far more efficacious.

Chronic Disease↗

PubMed1990

Platelet inhibitor therapy. Agents and clinical implications.

Platelets are central to the pathophysiology of an array of vascular disorders. Current platelet-inhibitor drugs reduce platelet aggregation through one of three pathways but do not prevent initial platelet adhesion. The most extensive clinical experience is with aspirin, an irreversible inhibitor of cyclooxygenase. Aspirin is clinically effective and has few gastrointestinal side effects if used at a dosage of 150 to 300 mg per day. Large clinical trials have documented the benefits of aspirin in arterial thromboembolic disease. It is effective in the primary and secondary prevention of myocardial infarction, including patients with unstable angina; reduces the acute thrombotic complications of coronary angioplasty and revascularization surgery; and also reduces cerebral ischemic events in patients with cerebrovascular disease. Aspirin is less effective for thrombi arising from the venous system or intracardiac chambers, which respond well to anticoagulants. Dipyridamole and sulfinpyrazone are most effective at preventing thrombosis on prosthetic surfaces. Dipyridamole reduces emboli from mechanical prosthetic valves when combined with warfarin and, unlike aspirin plus warfarin, does not increase bleeding complications. Newer agents such as ticlopidine and the thrombin inhibitor, hirudin, appear promising but require further evaluation. Because thrombin plays a critical role in mechanisms of arterial thrombosis, its inhibition appears promising for future therapy.

Adult↗

PubMedDate not supplied

[Hemolytic anemia in patients with heart valve prosthesis].

This article analyzes the historic evolution of the Starr-Edwards prosthesis manufacture and its association to hemolysis. It describes also the information related to bioprosthesis and hemolysis. The mechanisms involved in mechanical hemolysis are discussed (turbulent flux, red cells trapping, construction material and autoimmunity). Reviews the pathophysiology and criteria for clinical and laboratory diagnosis of hemolysis. We describe the value of the quantitation of unconjugated bilirubin, free plasmatic hemoglobin, DHL and it's DHL1 iso enzyme, methemalbumin and urinary hemosiderin for the specific diagnosis of this entity. Finally we comment on the utility of bed rest, cellular maturity inductors, propranolol and sulfinpyrazone therapy for the control of the hemolytic process.

Anemia, Hemolytic↗

PubMed1990

Restenosis after percutaneous transluminal coronary angioplasty--anatomic and pathophysiological mechanisms. Strategies for prevention.

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) probably results from pathophysiological mechanisms that are initiated during PTCA. Platelet deposition or exposed subendothelial connective tissue initiates complex blood element and vessel wall interactions that are not completely understood and leads to a proliferative response at the site of injury. The incidence of restenosis is also related to clinical, anatomic, and procedural variables. An increased frequency of restenosis is seen in patients who have recent onset of angina, unstable angina, or vasospastic angina, and in those who have diabetes. Stenoses in the proximal left anterior descending coronary artery, the ostium of the right coronary artery, and the proximal portion of a bypass vein graft have higher rates of restenosis than lesions at other sites. Restenosis can be predicted by an incomplete PTCA, which is identified by a high residual pressure gradient across the stenosis. Mechanical and pharmacological methods of preventing restenosis are under investigation. Intravascular stenting with expandable metal sleeves and laser angioplasty have shown encouraging results. Longer balloon inflation time can help prevent early elastic recoil. Platelet inhibitors (e.g., aspirin, dipyridamole, and sulfinpyrazone) do not appear to have an effect on restenosis. Agents, however, that interfere with platelet deposition at the PTCA site and that modify the effect of platelet-derived growth factor and medial cell proliferation show promise for control of restenosis.

Angioplasty, Balloon, Coronary↗

PubMed1990

Antiplatelet agents in coronary artery disease.

Coronary artery disease pathophysiology and platelet physiology are summarized, and the use of antiplatelet drugs in coronary artery disease is reviewed. Aspirin, sulfinpyrazone, and most other nonsteroidal anti-inflammatory agents alter platelet function by inhibiting the activity of cyclooxygenase, an enzyme necessary for the production of prostaglandins. Drugs that inhibit thromboxane synthetase or antagonize thromboxane A2 at the receptor level are under investigation. Prostacyclin and dipyridamole inhibit platelet function by elevating the concentration of cyclic AMP in platelets, but proof of their efficacy is limited. Most clinical trials of antiplatelet drugs in coronary artery disease have been small and of short duration; many have demonstrated short-term benefits, but long-term benefits are less obvious. Retrospective studies of patients before initial myocardial infarction suggest that regular aspirin ingestion may reduce the occurrence of cardiovascular complications. In prospective trials, the benefit of aspirin therapy for primary prevention of coronary artery disease was balanced by an increased likelihood of stroke. For secondary--after initial infarction--prevention of cardiovascular complications, the administration of aspirin and other antiplatelet agents has consistently decreased the rate of nonfatal myocardial infarction, overall mortality, or both. In the Second International Study of Infarct Survival, patients treated with streptokinase plus aspirin showed the greatest reduction in mortality, while each drug alone was associated with significantly lower mortality than placebo. Aspirin may improve clinical outcome in patients with or without previous myocardial infarction or with unstable angina pectoris. The daily dose should not exceed 325 mg. Antiplatelet therapy should not be used in patients at high risk for bleeding.

Coronary Disease↗

PubMed1988

Role of eicosanoids in the kappa-carrageenin rat tail thrombosis.

Pretreatment of rats by the cyclooxygenase inhibitors diclofenac, phenylbutazone, and aminophenazone did not influence kappa-carrageenin (KC) rat tail thrombosis (RTT) whereas pretreatment by aspirin, at high doses, and particularly sulfinpyrazone decreased RTT frequency, PGI2 or iloprost i.v. injection showed strong RTT preventing effects as it was also seen by thromboxane synthesis inhibitors (benzydamine, imidazole) at high doses. The PAF antagonist BN 52020 weakly protected. Lipoxygenase inhibitors (quercetin, oxphaman a.o.) proved ineffective. Therefore, thromboxane/PGI2 balance and partly PAF seem to be involved in the mechanism of KC RTT.

Aminopyrine↗

PubMed1989

[Clinical aspects of treatment and preventive treatment with thrombocyte aggregation inhibitors in cerebrovascular diseases].

Inhibitors of thrombocyte aggregation are generally accepted in the therapy and prophylaxis of ischemic cerebrovascular disease. The frequency of re-infarction, morbidity and mortality after TIA, PRIND and minor stroke is influenced favourably. There are controversial opinions, however, about the usefulness for patients suffering from completed strokes. In patients with progressive stroke, cerebral embolism of cardiac source, or non-infective thrombosis of sinuses or cerebral veins, inhibitors of thrombocyte aggregation are used if anticoagulation therapy is not possible. Additionally, they are applied in cases of infective thrombosis of sinuses or cerebral veins, after termination of anticoagulation therapy, after cardiac valve replacement, and after surgical reconstructions of craniocervical vessels. Acetylsalicylic acid is the clinically best examined substance; its effect--especially in males--was proven by numerous prospective trials. A combined treatment with dipyridamole, sulfinpyrazone or other drugs seems to be unnecessary. A daily dose of not more than 300 to 325 mg acetylsalicylic acid is recommended for prophylaxis after ischemic cerebral events; in connection with that dose severe gastrointestinal side effects are hardly to be expected. Whether even lower doses would yield the same prophylactic effects will have to be clarified by further studies.

Aspirin↗

PubMed1989

[The effect of anti-inflammatory agents on the granulocyte enzymes elastase and cathepsin G].

Effect of Nonsteroidal Anti-inflammatory Drugs on the Activity of Elastase and Cathepsin G from Human Polymorphonuclear Leukocytes. Several anti-inflammatory drugs display qualitative and quantitative different effects upon elastase and cathepsin G. Phenylbutazone, oxyphenbutazone, sulfinpyrazone and diclofenac-sodium proved to be the most efficient inhibitors of elastase and cathepsin G. A less marked inhibition of the proteinases of granulocytes was observed when indomethacin, ketoprofen, naproxen, pirprofen and tiaprofenic acid were tested. Acetylsalicylic acid, dexamethasone and oxaceprol were ineffective. Marked inhibition by these drugs was only observed at concentrations greater than those found naturally in the synovial fluid. Therefore it remains unknown, wether or to what extent an inhibition of the elastase and cathepsin G contributes to or participates in the therapeutic effects of nonsteroidal antirheumatic drugs.

Anti-Inflammatory Agents, Non-Steroidal↗