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L Puccetti

Publications and source records attributed to L Puccetti.

At least 19 recordsLinked to original sources
PubMed2003

T cell activation and enhanced apoptosis in non-ST elevation myocardial infarction.

Recent studies have shown that inflammation plays a major role in coronary plaque destabilization and in the induction of thrombosis in acute coronary syndromes. The aim of this study was to evaluate circulating lymphocyte activation and apoptosis in patients with non-ST elevation myocardial infarction (NSTEMI) in comparison with subjects with stable angina and with age-matched healthy controls. We considered T cell subpopulations, T cell surface HLA-DR and CD69 expression (evaluated by flow cytometry), lymphomonocyte spontaneous apoptosis (evaluated by ELISA), and IL2 production (evaluated by ELISA) in peripheral blood within 6 hours of onset of NSTEMI. We also investigated Fas expression on T cells (evaluated by flow cytometry) and FasL mRNA (evaluated by RT-PCR), as well as Fas functionality. In NSTEMI patients we found a significant increase of HLADR+ CD3+ and CD69+CD4+ cells. Spontaneous apoptosis was significantly increased in NSTEMI patients in comparison with the two control groups and was associated with an increased expression of Fas, an increased susceptibility to Fas agonist (CH11), and a normal production of IL2 in cell cultures. These data suggest that the enhanced apoptosis is due to a mechanism of "active" antigen-driven death, induced by the expression of death cytokines and not by the failure of cell growth factors. We conclude that peripheral lymphocytes are activated in NSTEMI and undergo an enhanced programmed cell death due to activation mechanisms. It is likely that lymphocyte activation occurs before the onset of acute ischemia and contributes to the plaque rupture and to the myocardial ischemic insult.

Apoptosis↗
PubMed2003

Different effect induced by treatment with several statins on monocyte tissue factor expression in hypercholesterolemic subjects.

Platelets and monocytes are involved in atherothrombosis via tissue factor expression. Moreover, they are activated in hypercholesterolemia, a classic risk factor for atherothrombosis. Cholesterol-lowering drugs (statins) reduce cardiovascular risk either by decreasing cholesterol or non-lipidic actions, such as platelet and monocyte activity. The aim of our study was to evaluate the effect of several statins on platelet and monocyte activity in hypercholesterolemic subjects. Platelet activity (P-selectin, cytofluorimetric detection), tissue factor levels (ELISA) and activity (detected in whole blood and cellular preparations by a specific clotting assay) were measured in hypercholesterolemic subjects (41 males, 23 females, aged 34-65 years, total cholesterol 6.86+/-0.60 mmol/l) treated with atorvastatin 10 mg, simvastatin 20 mg, fluvastatin 40 mg, or pravastatin 40 mg for 6 weeks. P-selectin and tissue factor expression in whole blood and isolated cells were increased in hypercholesterolemic subjects with respect to controls (all P<0.001). Simvastatin, atorvastatin, and fluvastatin reduced monocyte procoagulant activity in whole blood and P-selectin (P<0.01). Tissue factor antigen and activity in isolated cells were further reduced (all P<0.05) independently of cholesterol lowering. Pravastatin decreased tissue factor expression in whole blood in direct relationship to reduction of P-sel and cholesterol (P<0.05). Our data show a different impact of several statins on monocyte tissue factor expression in whole blood, suggesting a possible role of decreased platelet activity and a direct action on monocytes. In contrast, pravastatin decreased monocyte procoagulant activity with relation to cholesteroldependent modifications of platelet function.

Adult↗
PubMed2002

Cardiac papillary fibroelastoma: an unusual source of cerebral embolism solved with local fibrinolysis.

Fibroelastoma is an infrequent tumor affecting mainly cardiac valves. Before echocardiography, it was an occasional autoptic finding. With the development of ultrasonographic techniques, it is currently possible to carry out diagnosis in vivo. We report the case of a young woman with cerebral ischemia who was successfully treated by intra-arterial fibrinolysis with complete clinical resolution. Transesophageal echocardiography (TEE) identified a papillary fibroelastoma on the posterior leaflet of the mitral valve. Surgical excision of the tumor was performed. Sudden cerebral or peripheral embolization is frequently linked to thrombotic material which surrounds the neoplasm, and thus can be successfully treated with local fibrinolysis.

Female↗
PubMed2002

Relationship between serum complement and different lipid disorders.

Inflammatory and lipid factors share an important role in atherosclerosis. Recent studies showed the concomitant presence and increase of complement components and lipids both in the atherosclerotic plaque and the circulating blood. The aim of this study was to examine the relationship between the complement system and lipid disorders. We evaluated the circulating complement terminal complex C5b-9, a clear sign of complement activation, in three groups of 30 patients the first with hypercholesterolemia, the second with hypertriglyceridemia (associated with low values of HDL-cholesterol), the third with low levels of HDL-cholesterol compared with an equivalent group of matched normolipemic subjects. We found a significant increase of sC5b-9 in each group of patients compared with controls. The mean sC5b-9 level in the hypercholesterolemic population was 366.2 +/- 141.2 ng/ml (P<0.01), 395.4 +/- 118.2 ng/ml in the hypertrygliceridemic group (P<0.01), 414.8 +/- 126.4 ng/ml in the low HDL-chol subjects (P<0.01), and 182.0 +/- 40.8. ng/ml in the control group. Regression analysis showed a significant direct correlation between sC5b-9 and triglycerides (r=0.64), and a significant inverse correlation between sC5b-9, HDL-chol (r=-0.74), and apo-A1 (r=-0.68); no significant relationship was found between sC5b-9 and cholesterol. We suggest that complement activation is associated with the various lipid disorders and is more important in those dyslipidemic conditions in which other factors may be involved. In particular, hypertriglyceridemia may be associated with endothelial and fibrinolytic disturbances, and the decrease of HDL may induce the failure of the regulatory proteins transported by the same HDL.

Adult↗
PubMed2002

Effects of carvedilol on left ventricular remodeling and systolic function in elderly patients with heart failure.

BACKGROUND: Recent studies have shown that carvedilol therapy in patients with heart failure improves clinical outcome and survival, however, the effects of such treatment on left cardiac morphology and function in elderly patients with severe heart failure has not been widely studied. AIM: The purpose of this study was to establish the effect of carvedilol at short- and long-term on left ventricular size and performance with mono- and two-dimensional echocardiography, in subjects with dilated cardiomyopathy, NYHA III functional class, low LV ejection fraction (EF < 35%) and mean age of > 70 years. METHODS: We studied 48 patients, previously randomized to treatment with either carvedilol or placebo, and we performed echocardiographic evaluation at the start, and after 3 and 12 months. Left ventricular diameters, LV mass and fractional shortening were calculated by Deveraux formula; left ventricular volumes and ejection fraction were measured by area-length formula; pulmonary pressure was calculated by tricuspid reflow. RESULTS: After 3 months, only LV end-diastolic diameter was lower in the carvedilol group compared to the placebo group. Nevertheless, after 12 months, patients on carvedilol treatment showed a LV geometric and functional improvement compared to placebo. We found significant differences in: diastolic (P < 0.01) and systolic diameters (P < 0.001); on LV mass (P < 0.002); on LV systolic volume (P < 0.03); and on LV ejection fraction (P<0.01). Pulmonary pressure was also reduced in beta-blocker subjects (P < 0.001). CONCLUSIONS: Carvedilol therapy for 12 months reduced LV diameters and volumes. Thus, improving cardiac remodeling and LV systolic function in elderly patients with severe heart failure. Several months of therapy are required for these favorable effects to occur, as these changes do not occur in the short term.

Adrenergic beta-Antagonists↗
PubMed2002

Time-dependent effect of statins on platelet function in hypercholesterolaemia.

BACKGROUND: Reduction of platelet activity induced by statins has been described as a positive effect exerted by such molecules on vascular thrombotic events. However, the relations among cholesterol (LDL-C) reduction, the timing of the antiplatelet effect, the involved mechanisms and the doses of each statin able to reduce platelet function are not actually well known. The aim of our study was to evaluate the impact of simvastatin (20 mg day-1), atorvastatin (10 mg day-1), fluvastatin (40 mg day-1) and pravastatin (40 mg day-1) on platelet function in hypercholesterolaemic subjects with relation to (LDL-C), oxidized-LDL (ox-LDL) and antiport mechanism modifications. MATERIALS AND METHODS: Sixteen subjects were assigned to each treatment (40 males, 24 females, mean age 48.7 +/- 13.4, LDL-C 5.13 +/- 0,23 mmol L-1) and evaluated for platelet surface P-selectin (P-sel), lipid profile, ox-LDL, platelet-associated ox-LDL (Pox-LDL), platelet cholesterol content, antiport mechanisms, and intracellular and systemic NO synthase every 7 days for one month. RESULTS: Our data show a strong relation between enhanced P-sel and Pox-LDL (r = 0.68, P < 0.01). Simvastatin, atorvastatin, fluvastatin and pravastatin reduce platelet activity after 1, 2, 3 and 4 weeks of treatment, respectively (P < 0.001, P < 0.001, P < 0.01, P < 0.05). Pox-LDL are modulated early by simvastatin, atorvastatin and fluvastatin Pox-LDL (r = 0.66, 0.65 and 0.52; P < 0.001, 0.001 and 0.01, respectively) whereas LDL-C and ox-LDL reductions associated to modifications of antiport activity act later. Moreover, they are the most relevant finding in pravastatin-related subjects. CONCLUSIONS: Our data suggest a different impact of several statins on platelet function, which is initially related to interference with Pox-LDL rather than LDL-C reduction.

Adult↗
PubMed2001

Effect of diet and treatment with statins on platelet-dependent thrombin generation in hypercholesterolemic subjects.

BACKGROUND AND AIM: Platelets are strictly involved in arterial thrombosis and their hyperactivity has been shown in hypercholesterolemia. It has been reported that drugs affecting cholesterol metabolism (statins) decrease cardiovascular events by lowering lipid levels or by means of non-lipidic actions such as the direct inhibition of platelet function. The aim of this study was to detect the effect on platelet-dependent thrombin generation (PDTG) of a reduction in cholesterol obtained by means of a lipid-lowering diet or treatment with statins. METHODS AND RESULTS: We compared PDTG (T0) in 144 hypercholesterolemic subjects (94 males and 50 females of child-bearing age, mean age 48.2 +/- 13.8, plasma total cholesterol 6.93 +/- 0.64, high density lipoprotein cholesterol 1.25 +/- 0.14, triglycerides 1.15 +/- 0.19 mmol/L) and 70 normolipidemic controls (37 males and 33 females, mean age 43.1 +/- 12.6. After six weeks on an appropriate diet, the patients were randomised to receive different statin therapies if there was no reduction in their lipid profile and/or PDTG (T1). They were re-evaluated six weeks later, and the drug doses were maintained or increased on the basis of the variables (T2). A final evaluation was made after a further six weeks (T3). All of the data were evaluated using ANOVA and Spearman's correlation coefficent. The results showed increased PDTG in hypercholesterolemic subjects (418.2 +/- 29.2 mIU/mL, p < 0.001 vs controls). Diet alone did not reduce PDTG (380.2 +/- 28.5 mIU/mL, p = 0.226 vs controls). At T2, simvastatin and atorvastatin significantly decreased PDTG (P < 0.001 vs T0-1) and low-density lipoprotein cholesterol (LDL-C). No correlation was found between the two variables in the simvastatin group (r = 0.16). Cerivastatin reduced PDTG without significantly decreasing LDL-C (p < 0.001 and p = 0.476, r = 0.14). Pravastatin and fluvastatin significantly reduced thrombin generation only at T3 (40 mg/day); pravastatin was also associated with a decrease in LDL-C (p < 0.01, r = 0.66). CONCLUSIONS: Our results confirm an increased PDTG in patients with type IIa hyperlipoproteinemia, which is not reduced by diet. Statins at different doses significantly decrease PDTG but do not correlate with a reduction in LDL-C.

Adult↗
PubMed2001

Different mechanisms of fibrinolysis impairment among dyslipidemic subjects.

To determine whether there is a correlation between fibrinolytic activity and dyslipidemia, we performed a study of 72 subjects (20 patients with hypercholesterolemia, 20 with hypertriglyceridemia, 12 with isolated low high-density lipoprotein (HDL)-cholesterol (mean age 47.7 +/- 6.3, body mass index 24.7 +/- 0.4) and 20 healthy controls. Plasminogen activator inhibitor-1 (PAI-1), tissue-plasminogen activator activity and plasmin-antiplasmin complexes (PAP) were detected at baseline and after venous occlusion test. We also measured at baseline lipidic pattern, soluble E and P selectins (sE-sel, sP-sel), prothrombin factor 1+2 (F1+2), lipoprotein(a), factor VII, plasma insulin, fibrinogen, homocysteine, and thrombin activable fibrinolysis inhibitor (TAFI) activity. Fibrinolysis was significantly reduced in hypertriglyceridemic patients compared with hypercholesterolemic patients and control subjects (PAP, p < 0.01 and p < 0.001) and was associated with increased PAI-1 (at baseline and after venous occlusion test, p < 0.001). sP-sel, F1 +2 and TAFI were not significantly different compared with controls, while hypercholesterolemic subjects showed a significant increase in these parameters (p < 0.001), which were related to decreased PAP only at the upper low-density lipoprotein (LDL)-cholesterol levels (>160 mg/dl) (p < 0.001, r = -0.76). Moreover, there was no significant difference in PAI-1 activity (at baseline and after venous occlusion test) compared with controls. In conclusion, endothelial dysfunction was the main mechanism of decreased fibrinolysis in subjects with hypertriglyceridemia and low HDL-cholesterol, while enhanced thrombin generation and TAFI activity were the main determinants in hypercholesterolemia.

Adult↗
PubMed2000

Role of platelets in tissue factor expression by monocytes in normal and hypercholesterolemic subjects. In vitro effect of cerivastatin.

Thrombosis is a complication of atherosclerosis and monocytes play a determinant role either in the progression of atherosclerotic plaque or in blood coagulation by way of tissue factor expression. Platelets play a direct role in thrombosis and a hyperfunctional state has been described in hypercholesterolemic subjects. Moreover, platelets seem to be able to enhance monocyte activity. Cholesterol-lowering molecules (statins) are reported to reduce cardiovascular risk, either by decreasing the circulating level of cholesterol or by non-lipidic actions such as the reduction of monocyte and platelet activity. The aim of our study was to investigate the influence of platelets on the expression of tissue factor by monocytes and the effect induced by cerivastatin. We measured tissue factor levels by ELISA and the procoagulant activity of stimulated monocytes by a clotting assay on cellular preparations and whole blood in 40 hypercholesterolemic subjects (22 male, 18 female, mean age 52.7 +/- 12 years, total cholesterol 251.6 +/- 19.9 mg/dl) before and after cerivastatin addition. Tissue factor expression was enhanced in hypercholesterolemic subjects compared with normal subjects (31.6 +/- 7.6 vs. 23 +/- 5.8 pg/cells, P < 0.01). The presence of platelets increased the amount of tissue factor (55.3 +/- 7.3 pg/cells, P < 0.001) and cerivastatin reduced the expression of tissue factor in isolated monocytes, in the mixed cellular system, and in whole blood (19.6 +/- 4.1 pg/cells, P < 0.001). In conclusion, tissue factor expression by monocytes is enhanced in hypercholesterolemic subjects compared with normal controls. Platelets enhance monocyte production of tissue factor, and cerivastatin is able to counteract this prothrombotic mechanism.

Adult↗
PubMed2000

Complement activation in hypercholesterolemia.

BACKGROUND AND AIM: Inflammatory and lipid factors share an important role in atherosclerosis. This study evaluates their relations in dyslipidemic subjects. METHODS AND RESULTS: We compared the complement system (serum hemolytic activity CH50, C3 and C4 fractions and terminal complex sC5b-9) in 30 hypercholesterolemic patients with elevated cholesterol and decreased HDL-cholesterol levels, 30 normolipemic patients with clinical atherosclerosis and 30 matched normal subjects. In addition we evaluated the circulating immune complexes containing cholesterol (chol-CIC) on the assumption that they might be important in complement activation, and the circulating levels of the adhesion molecule ICAM-1 (sICAM-1) as a sign of endhotelial dysfunction. We found a significant increase of sC5b-9 (but not of CH50 and C3, C4) in the hypercholesterolemics compared with the other groups. The plasma sC5b-9 level was inversely and significantly related to HDL-chol (regression analysis), whereas no direct significant relation was found between sC5b-9 and cholesterol. Chol-CIC were also significantly increased in this group. The atherosclerosis patients also presented a significant increase of sC5b-9. Lastly, both patient groups displayed a significant increase of sICAM-1. CONCLUSIONS: We suggest that complement activation in dyslipidemics may be induced by their increased immune complexes. However, the decrease of complement regulatory proteins carried by HDL is another important factor, while complement changes may be related to variations of other humoral and cell systems (endothelium, coagulative/fibrinolytic system), whose involvement is suggested in our study by the changes of sICAM-1.

Adult↗
PubMed1999

Systemic adenosine increase during cold pressor test is dependent on sympathetic activation.

1. Following local vasoconstriction-inducing stimuli, such as the cold pressor test (CPT), significant changes occur in haemodynamics, with a rise in arterial blood pressure and heart rate (HR) due to the activation of the sympathetic nervous system. Among the compensatory mechanisms to local ischaemia, the endogenous nucleoside adenosine (ADO) has been suggested to play a relevant role by contributing to sympathetic stimulation. The possibility was investigated that CPT-induced increases in plasma ADO levels were not only an expression of the increased production of ADO in the ischaemic area, but also a consequence of systemic sympathoexcitatory mechanisms, thus showing a bidirectional involvement of the mechanisms of ADO formation. 2. The CPT was performed in 15 volunteers and mean arterial blood pressure (MABP) and HR were evaluated, together with plasma levels of noradrenaline (NA) and ADO in the tested and contralateral arm. The 15 subjects were then divided into three groups of five that were treated with either 5 mg transdermal clonidine weekly, 100 mg atenolol daily or 600 mg aminophylline twice daily. After 1 week treatment, the same test was repeated in the respective groups. 3. The CPT induced a rise in MABP and HR and an increase in plasma levels of NA and ADO. Increases in ADO were more pronounced in the tested arm. Clonidine blunted the haemodynamic response and NA release, while increases in ADO increase were reduced to a greater extent in the contralateral arm rather than the tested arm. Atenolol only affected MABP and HR without any effect on NA and ADO levels. Theophylline did not show any effect on CPT-induced changes. 4. In conclusion, local vasoconstriction and ischaemia induced in one arm following CPT are associated with haemodynamic changes dependent on the activation of the sympathetic system. The observed increase in plasma levels of ADO seems to be, in part, a direct expression of local responses to ischaemia (pre-dominant in the tested arm), but also appears as the consequence of systemic sympathoexcitatory mechanisms. Such increases in ADO are not dependent on a beta 1-adrenoceptor-mediated mechanism. Finally, theophylline, at a therapeutic dose, has no effect on the response to CPT.

Adenosine↗
PubMed1997

[Effectiveness and tolerability of heparan sulfate in the treatment of superficial thrombophlebitis. Controlled clinical study vs sulodexide].

One of the most interesting glycosaminoglycans (GAGs) is heparansulphate, known as the physiological activator of antithrombin III and involved in the maintenance of the antithrombotic potential of uninjured endothelium. The aim of our study was to evaluate the tolerability and effectiveness of heparansulphate with respect to sulodexide, another GAG suitable for the treatment of venous diseases. The study was performed in a open-label, controlled, with parallel and randomized groups, design. Thirty patients (aged 32-72 years) suffering from superficial thrombophlebitis were treated for two weeks with heparansulphate 100 mg t.i.d. or sulodexide 250 LSU b.i.d., both given orally. Some coagulative and fibrinolytic parameters (PT; aPTT; fibrinogen; euglobulin lysis time; t-PA; PAI-1; ATIII; alpha 2-antiplasmin; D-Dimer and platelets count) were assayed at the beginning and at the end of the study. Moreover signs and symptoms of disease (skin trophism; local pain; itch and oedema) were assessed. Heparansulphate and sulodexide were able to reduce signs and symptoms with similar degree and to significantly modify t-PA, alpha 2-antiplasmin and ATIII levels without any difference between treatments. Our issues show that heparansulphate can be useful in superficial thrombophlebitis management.

Adult↗
PubMed1996

A placebo-controlled study on urokinase therapy in systemic sclerosis.

A 4-month randomized placebo controlled trial on urokinase therapy in 36 consecutive systemic sclerosis patients randomly treated with urokinase or placebo was conducted. While patients on placebo did not show any significant improvement, in those following urokinase therapy there was a noticeable improvement in skin sclerosis observed via hand-print and ultrasonography of the skin. Vascular involvement improved: this was demonstrated by capillaroscopy results, showing an improvement in pattern and signs of revascularization and the resolution of skin ulcers. Vascular damage is a typical occurrence in systemic sclerosis cases and various vasoactive drugs are used symptoms for some such as Raynaud's syndrome or skin ulcers. At the moment these drugs seem to constitute the most effective therapy, and have few side effects. We have found only one previous study utilizing urokinase therapy for acute digital ischemia in systemic sclerosis. Our study is the first in which urokinase therapy has been used for the treatment of systemic sclerosis in a large number of patients.

Adult↗
PubMed1995

D-penicillamine and gold salt treatments were complicated by myasthenia and pemphigus, respectively, in the same patient with rheumatoid arthritis.

A 53-year-old woman with rheumatoid arthritis developed myasthenia gravis after 6 months of therapy with D-penicillamine. Nineteen months after D-penicillamine was discontinued and 12 months after the beginning of gold therapy, she developed pemphigus vulgaris. This is the first reported case of gold-induced pemphigus in rheumatoid arthritis. This study further underlines the complex interactions between the effects of treatment with sulfhydryl-disulfide exchange drugs and the altered immunological system of patients affected by rheumatoid arthritis.

Antirheumatic Agents↗
PubMed1994

Polymyositis-like syndrome in hypothyroidism: report of two cases.

An increase of muscle enzymes in hypothyroidism has sometimes been correlated with a polymyositis-like syndrome and hypothyroid patients have been misdiagnosed and mismanaged as suffering from polymyositis. Actually, muscle symptoms, such as aches and pain, stiffness, weakness and cramps or, more rarely, hypertrophy, are observed in hypothyroidism and increased serum muscle enzyme values, particularly the level of creatine phosphokinase (CPK), indeed seem to suggest polymyositis. The muscular groups most commonly affected by the above mentioned symptomatology are those of the shoulder and pelvic girdles. In this report two hypothyroid patients complaining of muscle symptoms, whose serum muscle enzymes were particularly elevated, are described. In the first case the patient had been suffering from pain and weakness of the thenar eminence for about 4 months. The clinical features suggested a diagnosis of Carpal Tunnel Syndrome, but thyroid function tests revealed primary hypothyroidism. In the second case the patient had been afflicted with muscular weakness of the shoulder girdle for 2 months and was unable to keep his arms raised over his head. A study of thyroid function demonstrated a picture of hypothyroidism. Both patients were treated with L-thyroxine and in a relatively short time biochemical parameters improved remarkably, and the symptoms disappeared. The hypothesis that a muscular effort of long duration by hypothyroid patients may have been responsible for the muscular damage and the symptoms may explain why only a few hypothyroid patients develop a clinical picture similar to polymyositis.

Adult↗
PubMed1994

Double-blind comparison of the efficacy and safety of etodolac SR 600 mg u.i.d. and of tenoxicam 20 mg u.i.d. in elderly patients with osteoarthritis of the hip and of the knee.

Etodolac SR is the sustained-release formulation of etodolac, an effective anti-inflammatory drug used in the treatment of various rheumatic diseases. The efficacy and safety of etodolac SR were compared with those of tenoxicam in 120 elderly patients with radiographic and clinical evidence of active osteoarthritis (OA) of the knee and/or the hip. This was a double-blind, double-dummy, randomized, parallel-group, multicentre study conducted at 4 Italian rheumatic-disease units. Sixty patients received 600 mg of etodolac SR once daily (u.i.d.) for 8 weeks; the remaining 60 patients received 20 mg of tenoxicam u.i.d. Significant improvements in all 6 efficacy parameters (viso-analogic scale of the global pain, pain at active movements, night pain, joint tenderness, joint motility, and Lequesne's algofunctional index) were observed within each of the treatment groups even after the first 2 weeks of therapy. There were no significant differences in the therapeutic response between the two groups for any efficacy parameters. Adverse reactions, mostly regarding the G-I tract, were significantly more frequent in the tenoxicam group than in the etodolac group: 23.3% vs 8.3% respectively, albeit in the majority of the cases they were not considered to be so severe as to cause the interruption of the study. There were no clinically important changes from baseline in laboratory tests performed during the study. Endoscopy of the upper G-I tract was performed both at baseline and after 8 weeks of therapy in 30 patients per treatment group in order to obtain a reliable comparative evaluation of the G-I safety of the two drugs. Both drugs were found to be well tolerated; only 2 ulcers were observed after therapy in both groups, but minor lesions were more frequently detected in the mucosa of the stomach in the patients who received tenoxicam. The cumulative endoscopic index that reflected both the erosive and the haemorrhagic lesions found in the stomach taken as a whole was significantly (p < 0.03) higher after therapy in the tenoxicam group. These results indicate that 600 mg of etodolac SR u.i.d. for 8 weeks is as effective as 20 mg of tenoxicam u.i.d. in the treatment of OA of the knee and/or of the hip. Both the overall and the G-I specific safety profiles were found to be more favourable in patients treated with etodolac SR. Renal function was not substantially affected in either treatment group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Evaluation of the effectiveness and safety of etodolac in prolonged treatment of active osteoarthritis.

Patients affected by osteoarthritis totalling 358 (142 males and 216 females) were recruited in an open study which lasted up to three months. All patients started treatment with etodolac 600 mg/die per os. 74 patients were treated and followed for 15 days, 94 for one month, 54 for two months, and 132 for three months. Clinical evaluations, performed at baseline and after 15, 30, 60, and 90 days of treatment were made on the following parameters: intensity of pain, index of sleep disturbance caused by symptoms related to osteoarthritis, investigator's evaluation of the global patient's condition, patient's self-evaluation about his own condition, presence and duration of morning stiffness, presence and duration of stiffness at rest, and finally the investigator's integrated evaluation about the effectiveness tolerance of etodolac during the study. All the parameters showed a noticeable and significant improvement in all groups of patients, stratified by sex, age, and duration of the disease. The younger patients and those patients with osteoarthritis of a less prolonged duration achieved the best results. Only slight differences were registered by examining the baseline values of the various parameters or the extent of the different improvements achieved, on the basis of sex, and duration of osteoarthritis and the non-steroidal anti-inflammatory drugs previously used. Among the 27 patients who withdrew, eight dropped out for clinical inefficacy and 15 for intolerance. In all these latter cases a prompt and complete resolution of the adverse reaction was achieved and maintained after the interruption of therapy. In the 49 patients who presented side-effects, these were almost always related to the gastrointestinal tract and of slight intensity. A complete resolution was promptly achieved in 25 cases, while in 17 other patients the side-effect persisted during the course of the study, but it was considered not worthy of the patient dropping out. The profile of routine laboratory parameters, measured both at inception and at the end of the study, did not show relevant changes after treatment with etodolac. In conclusion this study demonstrated that etodolac is effective and well tolerated in the prolonged treatment of patients with active osteoarthritis.

Adult↗