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One hundred patients (49 males, 51 females) with reversible neurologic deficit due to cerebral ischemia of vascular origin in the carotid artery territory were recruited for a long-term observation to follow up recurrence of ischemic events. Fifty-eight patients (mean age sixty-four years) were treated daily with 1200 mg oral pentoxifylline in addition to basic therapy (antihypertensives, antidiabetic drugs, etc), and 42 matching patients (mean age sixty-two years) of a control group had no pentoxifylline or other hemorheologic medication. The mean observation period was fifty-six months (range thirty-six to sixty). On admission patients presented with increased platelet aggregation and/or impaired red cell filterability and with enhanced red cell aggregation. Five patients in the pentoxifylline group (8.6%) and 16 control patients (38%) suffered a relapse of an ischemic episode. These data support previous reports of a beneficial effect of pentoxifylline in the prevention of cerebral ischemic events.
An 18-yer-old girl with homozygotic sickle-cell anaemia (HbSS: HbS 65% and HbF 4.9%) suffered from painful haemolytic crises since six years of age, these crises occurring almost weekly of late. Pentoxifylline (2.4 g daily in three divided doses) decreased blood viscosity in vitro from 6.7 to 4.9 (normal 4.3-5.3 at 46 s-1 shear rate) and erythrocyte filtration accelerated from 127 to 77 s (normally 30-49 s). Although pentoxifylline could not prevent haemolysis, previously necessary analgesics were no longer required, even during haemolytic crises. Thus the drug lowers viscosity also in vivo and thus improves microcirculation. It has a prophylactic effect against vaso-occlusive complications of sickle-cell anaemia.
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The difference in mean serum CRP levels of the pentoxifylline and placebo groups was not significant before study. While CRP showed showed a significant increase in the placebo group after completing the interventions (P = .01), the difference was nonsignificant in the pentoxifylline group (P = .53). The difference in the mean adequacy of dialysis was not significant before the interventions between the two groups, while there was a significant increase in the pentoxifylline group (P = .01) and a nonsignificant increase in the placebo group (P = .31) after the interventions.
This case report describes the sustained symptomatic and hematologic improvement in a 21-year-old woman with homozygous sickle cell (ss) disease during treatment with pentoxifylline, 400 mg three times daily after meals. Pain crises decreased from six to zero per year, hemoglobin level rose from 8.4 g/dL to 11.4 g/dL, hematocrit rose from 24.8% to 34.8%, lactate dehydrogenase level decreased from 375 IU/L to 322 IU/L, and total bilirubin level decreased from 1.8 mg/dL to 1.6 mg/dL. Mean corpuscular hemoglobin increased from 21.6 pg to 30 pg and mean corpuscular hemoglobin concentration increased from 24.1 g/dL to 34.5 g/dL. These changes were sustained for seven years except for a brief self-imposed hiatus in therapy during which period a pain crisis occurred. Further increase in pentoxifylline dosage to 400 mg four times daily did not result in any further improvement in these hematologic parameters. These results suggest that pentoxifylline reduces hemolysis in SS patients with a resulting improvement in anemia and a reduction in or elimination of pain crises.
TNF-alpha enhances HIV-1 replication in acutely and chronically infected cells and likely contributes to the wasting associated with the acquired immunodeficiency syndrome. Agents that inhibit TNF-alpha activity should theoretically delay the progression of disease, and several are currently in clinical trials. We hypothesized that IL-10, a cytokine that suppresses the gene expression and synthesis of TNF-alpha in monocytic cells, might inhibit HIV-1 replication. As expected, IL-10 suppressed PMA-induced TNF-alpha production in U1 cells; however, when U1 cells were cultured in the presence of PMA and increasing doses of IL-10, a dose-dependent increase in HIV-1 expression was observed. IL-10 also enhanced IL-1 beta-, TNF-alpha-, and GM-CSF-induced HIV-1 expression in U1 cells, and this occurred, at least in part, at the level of transcription. We next stimulated cells under conditions of TNF-alpha blockade. When PMA-induced TNF-alpha activity and HIV-1 replication were blocked by the presence of soluble TNF receptors, IL-10 independently enhanced HIV-1 replication. In contrast, other agents that are capable of blocking TNF-alpha synthesis or TNF-alpha activity either had no effect (IL-13 and IL-4) or inhibited HIV-1 expression (soluble TNF receptors and pentoxifylline) in U1 cells. These data suggest that IL-10, while inhibiting TNF-alpha synthesis, has an independent mechanism of action that enhances HIV-1 replication. Therefore, IL-10 may have undesirable effects in HIV-1-infected patients.
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In the second and fourth groups, the lesion surface area and average mucosal damage were fewer in comparison to the control group (p<0,03). Moreover, an histopatologically improvement in the surface epithelium was observed in these groups. The average lesion score also reduced significantly (p<0,03) only in the L-tryptophan group. On the other hand, no statistically significant improvement was observed in the pentoxifylline group.
We have identified several compounds that produce robust and effective stimulation of sperm motility and, importantly, have a positive response on patient samples.
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To investigate the protective effect of pentoxifylline on spermatogenesis following testicular torsion/detorsion in rats.
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41 nursing facilities in 6 regions of the US.
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Ongoing research evaluating potential pharmacological agents for NASH is critical, because these patients are at an increased risk for cirrhosis and hepatocellular carcinoma. The current therapies being used for the treatment of NASH include the use of vitamin E and pioglitazone, in addition to dietary counseling and regular exercise.
The possible healing effect of deferoxamine and pentoxifylline on persisting lower limb ulcers was studied in 51 patients with thalassemia major. The results indicated that the regular use of deferoxamine at an intravenous dose of 20 mg/kg did not affect the healing progress and the recurrence rate of these ulcers significantly. On the contrary, the oral administration of pentoxifylline at a dose of 1,200 mg daily during the ulcer's healing time and at a low long-term maintenance dose of 400 mg daily during the ulcer-free intervals improved their healing ability impressively and diminished their recurrence rate significantly.
The aim of this study was to assess the impact of a P-glycoprotein and CYP3A inhibitor, verapamil on the pharmacokinetics of two methylxanthines, pentoxifylline and lisofylline in male CD-1 mice. To differentiate the effects of verapamil, both methylxanthines were also given to male CF-1 mdr1a (-/-) and mdr1a (+/+) mice. CD-1 mice received a single dose (50 mg/kg) of pentoxifylline or lisofylline intravenously, whereas mutant animals were given the same dose of both compounds intravenously and orally. Blood and tissue samples were collected at different time points following drug administration and concentrations of pentoxifylline and lisofylline were measured by a chiral HPLC method. Verapamil significantly increased concentrations of both methylxanthines in murine serum and tissues. In contrast to lisofylline, pentoxifylline concentrations were also significantly higher in mutant mice 30 min following intravenous administration. Due to the fact that pentoxifylline is not a good P-glycoprotein substrate, a possible mechanism of this interaction might be that in the presence of verapamil, pentoxifylline elimination is inhibited by its metabolites that are normally eliminated through P-glycoprotein-mediated transport. This hypothesis was supported by the outcomes of pharmacokinetic analysis. In conclusion, the interaction between verapamil and pentoxifylline is, at least partially, P-glycoprotein-mediated, whereas alterations in lisofylline pharmacokinetics are caused by inhibition of drug metabolising enzymes.
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We investigated the signal transduction pathway of IL-12 and showed that lisofylline (LSF) inhibited the signal transducer and activator of transcription factor-4 (STAT4) activation. Interruption of IL-12-mediated STAT4 activation prevented autoimmune diabetes in NOD mice.
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The study included 20 metastatic solid tumor patients who showed clinical and laboratory signs of DIC. Pentoxifylline was given orally at a dose of 1200 mg/day for 28 days.
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Pharmacologic treatment showed no survival benefit, regardless of disease severity. Given the mortality risk seen in mild-moderate AH patients not receiving treatment and concern for a possible treatment ceiling effect in severe AH patients, more data are needed to adequately assess the utility of MDF in selecting appropriate candidates for AH treatment.
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Eighty-three patients receiving pentoxifylline for stable claudication were evaluated to identify factors associated with response to treatment. Patients with isolated aortoiliac occlusive disease and those with arterial occlusive disease of moderate severity were more likely to have an improvement in claudication distance.
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To assess the effects of inhibiting both tumor necrosis factor (TNF)-alpha production and xanthine oxidase activity on the inflammatory response, mitogen-activated protein kinase (MAPK) activation and mortality in necrotizing acute pancreatitis in rats.
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The combination of coronary heart disease (CHD) with increased left ventricular wall mass (LVWM) appears associated with prolonged isovolumetric relaxation (IVR) and consequently, alterations in the rapid filling phase. Methylxanthine-substances may improve relaxation through inhibition of phosphodiesterase activity. Accordingly we examined multiple indexes of left ventricular diastolic function before and after administration of 200 mg pentoxifylline (Trental) intravenously to 18 patients (51.3 +/- 9.0 years, 15 males, three females) with stable angina pectoris and positive exercise-ECG in NYHA class I or II and LVWM greater than 160 g (n = 9) and less than or equal to 160 g (n = 9). Left ventricular pressure (P) and volume (V) measurements were made with a high-fidelity-micromanometer before and twelve minutes after administration of pentoxifylline. The time constant of left ventricular isovolumic relaxation (T), usual global left ventricular volumes and derived indexes such as peak filling rate (PFR), time to peak filling rate (TPFR), segmental (relaxation and rapid filling phases) and total pressure-volume relationship before and after pentoxifylline were calculated. Significant differences between these two groups (greater than/less than or equal to 160 g LVWM) were found for end-diastolic volume (68.7 +/- 19.0 to 90.8 +/- 22.6 ml/sqm), end-systolic volume (21.7 +/- 16.0 to 36.1 +/- 14.7 ml/sqm), end-diastolic pressure (15.0 +/- 4.8 to 15.7 +/- 5.1 mm Hg), PFR (3.25 +/- 1.18 to 2.66 +/- 0.71 s-1), T (46.0 +/- 5.7 to 52.7 +/- 7.2 ms), the linear regression of lnP-V (lny = -0.117 x + 4.59 to lny = -0.091 x + 4.75) in the IVR-phase (dp/dtmin less than or equal to x less than or equal to 80 ms) (leftward shift in p-V-relationship when less than or equal to 160 g) and the complet p-V-areas. After pentoxifyl-line-administration there were significant decreases in T in patients with increased LVWM (52.7 +/- 7.2 to 47.7 +/- 5.9 ms) and the P-V-product over the time in the rapid filling phase in patients with LVWM less than or equal to 160 g. Total peripheral resistance and heart rate did not change. These changes in parameters of left ventricular diastolic function in combination with significant improvement of pump function especially in patients with LVWM greater than 160 g after administration of pentoxifylline suggest that improved diastolic function is the result of a direct myocardial effect of pentoxifylline.
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Baseline and follow-up assessments included estimated glomerular filtration rate (eGFR) and UPE. Differences in the changes in variables within the placebo and pentoxifylline treatment groups during the study period were assessed using Friedman's test.
Idiopathic Sudden Sensorineural Hearing Loss (ISSHL) is defined when a loss of at least 30 dB occurs in over 3 continuous frequencies, in up to 72 hours, of which etiology is not established, despite adequate investigation. Different types of treatment regimens have been proposed, but only glucocorticoids have shown some evidence of benefit in the literature.
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Participants (n = 39) were allocated into three groups at the termination of CPB: Group 1, (control group, n = 16); Group 2 (aprotinin group, n = 12), who received protamine + aprotinin (15,000 IU/kg); and Group 3 (Pentoxifylline group, n = 11), who received protamine + pentoxifylline (10 mg/kg). Leukocyte counts in pulmonary and radial arteries were determined after the termination of CPB and before any drug was given (t1), and 5 minutes (t2), 2 hours (t3), 6 hours (t4) and 12 hours (t5) after the administration of protamine. Alveolar-arterial O2 gradient (A-aO2) and dynamic pulmonary compliance were measured at t1, t2 and t3.
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Prostacyclin and nitric oxide donors are the best studied vasodilating agents in experimental sepsis and have shown improved tissue perfusion and oxygen extraction. In several clinical studies prostacyclin has also been shown to have such beneficial effects. Recent studies using orthogonal polarization spectral imaging have shown microcirculatory recruitment by nitric oxide donors in hemodynamically resuscitated septic patients. Whether such therapeutic modalities aimed at recruitment of the microcirculation improve outcome, however, still has to be determined.
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Male balb/c mice underwent 30% total body surface area full-thickness steam burn. Immediately after burn, animals received an intraperitoneal injection of PTX (12.5 mg/kg) in normal saline or normal saline alone. In vivo intestinal permeability to 4 kDa fluorescein isothiocyanate-dextran was measured. Intestinal extracts were obtained to measure interleukin-6 by enzyme-linked immunosorbent assay, and phosphorylated p38 MAPK, p38 MAPK, phosphorylated extracellular signal-related kinase (1/2) (ERK (1/2)), and ERK (1/2) by immunoblotting. Acute lung injury was assessed by histology at 24 hours after burn.
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The effect of pentoxifylline (Trental) on the phagocytic capacity, cAMP levels, and superoxide anion production of human peripheral blood monocytes and polymorphonuclears (PMNs) was studied. The drug inhibited the phagocytosis of latex particles by both monocytes and PMNs in a dose-dependent manner. In addition, superoxide anion production during the phagocytic process was also reduced following incubation of the cells with pentoxifylline. It is suggested that this inhibitory effect is due to the increased intracellular levels of cAMP induced by the drug.
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Peripheral facial nerve palsy (FNP) may (secondary FNP) or may not have a detectable cause (Bell's palsy). Three quarters of peripheral FNP are primary and one quarter secondary. The most prevalent causes of secondary FNP are systemic viral infections, trauma, surgery, diabetes, local infections, tumor, immunological disorders, or drugs. The diagnosis of FNP relies upon the presence of typical symptoms and signs, blood chemical investigations, cerebro-spinal-fluid-investigations, X-ray of the scull and mastoid, cerebral MRI, or nerve conduction studies. Bell's palsy may be diagnosed after exclusion of all secondary causes, but causes of secondary FNP and Bell's palsy may coexist. Treatment of secondary FNP is based on the therapy of the underlying disorder. Treatment of Bell's palsy is controversial due to the lack of large, randomized, controlled, prospective studies. There are indications that steroids or antiviral agents are beneficial but also studies, which show no beneficial effect. Additional measures include eye protection, physiotherapy, acupuncture, botulinum toxin, or possibly surgery. Prognosis of Bell's palsy is fair with complete recovery in about 80% of the cases, 15% experience some kind of permanent nerve damage and 5% remain with severe sequelae.
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Granuloma annulare is a disease characterized by granulomatous inflammation of the dermis. Localized granuloma annulare may resolve spontaneously, while generalized granuloma annulare may persist for decades. The authors present the case of a 41-year-old Hispanic man with a two-week history of periocular granuloma annulare. Due to previously reported success in the use of systemic dapsone for the treatment of granuloma annulare, and the periocular proximity of the patient's lesion, topical dapsone was used for treatment. Various additional therapies for the management of granuloma annulare have been reported, such as topical and systemic steroids, isotretinoin, pentoxifylline, cyclosporine, Interferon gamma, potassium iodide, nicotinamide, niacinamide, salicylic acid, fumaric acid ester, etanercept, infliximab, and hydroxychloroquine. Additional clinical trials are necessary to further evaluate the effectiveness of topical dapsone in the management of granuloma annulare.
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In-vitro culture of 1-cell mouse embryos was used to assess the influence of pentoxifylline or early embryonic development. If cultured in concentrations of 5, 10 or 50 microM, early embryonic development was unaffected and no differences in cell numbers were noted in embryos reaching the blastocyst stage. However, at 3.6 and 7.2 mM, pentoxifylline inhibited cleavage from the 2-cell stage onwards. If 1-cell mouse embryos were exposed for only 30 min to these concentrations, blastocyst formation was found to be morphologically normal. However, cell numbers of such blastocysts were significantly decreased after exposure to pentoxifylline. These results may indicate that exposure of gametes or zygotes to pentoxifylline should be avoided as much as possible when this drug is used in human assisted reproduction. If administered at regular therapeutic doses, it is probable that no adverse effect on early embryonic development in vivo will occur. Further research is needed to confirm and elucidate the above findings.
Heparin-anticoagulated (3 IE/ml) whole blood of healthy neonates (n = 6) and adult volunteers (n = 6) was incubated for 45 min. Spontaneous PMN-degranulation was compared with meconium-induced (3 mg/ml) and PTX-inhibited (0,025 - 0,4 mg/ml) degranulation by means of elastase (EL) and lactoferrin (LF) release from azurophilic and specific granules. EL- and LF plasma concentration was measured by immunoluminometric methods.
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The effects of pentoxifylline (PTX) on intracellular accumulation of doxorobicin (DOX), DOX cytotoxicity and expression of Pgp in multidrug resistant L1210/VCR cell line were investigated. PTX (100 mg/l) was able to enhance the DOX accumulation in resistant cells. The maximum intracellular levels of DOX were reached after treatment with PTX for 24 hours (total duration of PTX-treatment was 72 hours). The levels of mdrl mRNA (measured by RT-PCR method) were decreased 2-fold in the presence of 100 mg/l PTX (minimum reached within 48 hours) in comparison to control cells.