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Trental (Pentoxifylline)
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Trental

Generic Trental is used for treating intermittent claudication (pain, cramping, numbness, or weakness in the foot, hip, thigh, or buttocks) in certain patients. It may also be used for other conditions.

Other names for this medication:

Similar Products:
Pletal, Pentoxil

 

Also known as:  Pentoxifylline.

Description

Generic Trental is used for treating intermittent claudication (pain, cramping, numbness, or weakness in the foot, hip, thigh, or buttocks) in certain patients. It may also be used for other conditions.

Generic Trental is a xanthine derivative blood flow enhancer. It works by thinning the blood and improving red blood cell flexibility, causing the blood to flow more freely through the veins.

Trental is also known as Pentoxifylline.

Generic name of Generic Trental is Pentoxifylline.

Brand name of Generic Trental is Trental.

Dosage

Take Generic Trental by mouth with food or milk.

Swallow whole. Do not break, crush, or chew before swallowing.

If you want to achieve most effective results do not stop taking Generic Trental suddenly.

Overdose

If you overdose Generic Trental and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Trental are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Trental if you are allergic to Generic Trental components, or to methylxanthines (theophylline, caffeine, theobromine).

Be very careful with Generic Trental if you are pregnant, planning to become pregnant. Generic Trental is found in breast milk. Do not breast-feed while taking Generic Trental.

Do not take Generic Trental if you have had recent bleeding in the brain or eye.

Tell your health care provider or dentist that you take Generic Trental before you receive any medical or dental care, emergency care, or surgery.

It may take 2 to 4 weeks to notice improvement in your condition, and up to 8 weeks for maximum relief.

Use Generic Trental with caution in the elderly. They may be more sensitive to its effects.

Avoid alcohol.

Avoid machine driving.

It can be dangerous to stop Generic Trental taking suddenly.

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Systemic control mechanisms of pain are based on interplay between nervous autonomic and immune systems. The aim of this study was to examine a possible role of the vagus nerve in regulation of nocyception. Peritoneal inflammation increased vagal activity. Pretreatment of PTX had an analgesic effect confirmed by amount of WT and decreased vagal activity. The vagotomy decreased nociceptive threshold.

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To review the pharmacology and clinical utility of cilostazol, an antiplatelet and vasodilator agent approved for the management of intermittent claudication.

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Camptothecin (CAM) and cisplatin (cis-diamminedichloroplatinum(II), cis-Pt) were used as inducers of apoptosis in the mouse leukemic L1210 cells. Relatively high concentrations of 50 micromol cis-Pt and 50 micromol CAM, respectively, were used to induce the apoptotic DNA ladder. The simultaneous treatment of L1210 cells by the drug and pentoxifylline (PTX) resulted in a decrease of drug concentrations necessary for the induction of apoptosis. This study revealed that a cell cycle G2 checkpoint inhibitor PTX reduces time intervals necessary for the onset of drug-induced apoptosis in these cells. This fact might be important as the earlier onset of programmed cell death may decrease a risk of tumor cells to become resistant to drug therapy.

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We included 13 studies with a total of 445 participants. The quality of the trials was generally poor and no results could be pooled due to the treatments being so heterogeneous. Treatment with thalidomide showed a significant remission of skin lesions compared to acetylsalicylic acid (aspirin) (RR 2.43; 95% CI 1.28 to 4.59) (1 trial, 92 participants). Clofazimine treatment was superior to prednisolone (more treatment successes; RR 3.67; 95% CI 1.36 to 9.91) (1 trial, 24 participants), and thalidomide (fewer recurrences; RR 0.08; 95% CI 0.01 to 0.56) (1 trial, 72 participants). We did not find any significant benefit for intravenous betamethasone compared to dextrose (1 trial, 10 participants), pentoxifylline compared to thalidomide (1 trial, 44 participants), indomethacin compared to prednisolone, aspirin or chloroquine treatments (2 trials, 80 participants), or levamisole compared to placebo (1 trial, 12 participants). Mild to moderate adverse events were significantly lower in participants taking 100 mg thalidomide compared to 300 mg thalidomide daily (RR 0.46; 95% CI 0.23 to 0.93). Significantly more minor adverse events were reported in participants taking clofazimine compared with prednisolone (RR 1.92; 95% CI 1.10 to 3.35). None of the studies assessed quality of life or economic outcomes.

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We investigated pentoxifylline (PTF) as a pretreatment of septic syndrome in pigs with fecal peritonitis. In the untreated group there was a progressive decrease in mean arterial pressure (MAP), cardiac output, mean pulmonary artery wedge pressure (WP), and a progressive rise in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), heart rate (HR), and core temperature (T). In those pigs given PTF there was a significantly smaller increase in SVR throughout and in PVR after 270 min. No significant differences were seen in MAP, MPAP, WP, HR, and T. Neutrophil adhesiveness did not change in the untreated group. However, it decreased markedly with PTF, both before and after peritonitis induction. Electron microscopy of the lungs, liver, and spleen in the test group showed severe damage, with endothelial disruption, capillary or sinusoidal occlusion, leukostasis, and neutrophil degranulation. Pretreatment with PTF attenuated these changes.

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Acute lung inflammation is complicated by altered pulmonary surfactant phospholipid and protein composition. The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) inhibit expression of surfactant-associated proteins A and B (SP-A and SP-B), both important for normal surfactant function. The transcription factor nuclear factor-kappa B (NF-kappa B) frequently mediates regulation of gene expression by TPA and TNF-alpha. In the present study, electrophoretic mobility shift assays (EM-SAs) and pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B activation, were utilized to determine the role of NF-kappa B activation in TPA and TNF-alpha inhibition of the surfactant proteins in NCI-H441 cells. Pentoxifylline (PTX), which inhibits TNF-alpha cellular effects without preventing NF-kappa B activation, was also tested. By EMSA, TPA and TNF-alpha increased nuclear NF-kappa B binding activity in temporally distinct patterns. PDTC decreased TPA- and TNF-alpha-induced NF-kappa B binding activity but did not limit their inhibition of SP-A and SP-B mRNAs. PDTC independently decreased both SP-A and SP-B mRNAs. PTX partially reversed TNF-alpha-but not TPA-mediated inhibition of SP-A and SP-B mRNAs without altering NF-kappa B binding. The effects of PDTC and PTX on NF-kappa B and the surfactant proteins suggest that NF-kappa B activation does not mediate TPA or TNF-alpha inhibition of SP-A and SP-B mRNA accumulation.

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These studies indicate that PAF, a known stimulator of aggregation, secretory and/or contractile activity of platelets, neutrophils, smooth muscle and other cells, is produced by skeletal muscle during IRI. The maximum increase occurs at 10 to 15 minutes and continues for at least an hour. Infusions of PAF into skeletal muscle subjected to 20 minutes of ischemia and 20 hours of reperfusion resulted in tissue necrosis similar to that produced by 5 hours of ischemia and 20 hours of reperfusion. 25 mg/kg of pentoxifylline, infused immediately prior to reperfusion of ischemic skeletal muscle, decreased PAF production and muscle necrosis. It was also demonstrated that skeletal muscle necrosis can be reduced by infusion of PAF antagonists (WEB-2086) into the muscle immediately prior to reperfusion. Thus, PAF has an important role in skeletal muscle IRI and additional studies of PAF inhibition during IRI are warranted.

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40 type 2 nonhypertensive diabetic patients were randomly allocated to receive either pentoxifylline 400 mg t.i.d. or placebo daily for 16 weeks. Eligible subjects were those with urinary albumin excretion between 20 and 200 microg/min. Subjects receiving angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium antagonists, and diuretics as well as those with reduced renal function, pregnancy, urinary tract infection, and smoking were not included. A 6-month pretreatment stabilization phase aimed to reduce and stabilize fasting serum glucose levels was carried out. Urinary proteins were identified by electrophoresis, and immunodetection was identified by Western blot. Electrophoretic analysis was performed using molecular weight markers of 150, 132, 77, and 66 kDa to identify high-weight proteins, and 54, 41, 36, 27, 21, 14.3, and 12 kDa to identify low-weight proteins.

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Livedoid vasculopathy is a bilateral painful and recurrent cutaneous ulcerative disorder of the legs that leads to atrophie blanche, atrophic white-porcelain scars, and is associated with disorders of fibrinolysis and/or coagulation. We present a young boy with an association between livedoid vasculopathy in the area of a previous involuted cutaneous hemangioma. We found 4 uncommon abnormalities associated with thrombo-occlusive events: heterozygous 20210 A→G genotype of prothrombin, reduced activity of anticoagulation proteins C and S, and elevated lipoprotein (a).

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Given the high prevalence and rising incidence of non-alcoholic fatty liver disease (NAFLD), the absence of approved therapies is striking. Although the mainstay of treatment of NAFLD is weight loss, it is hard to maintain, prompting the need for pharmacotherapy as well. A greater understanding of disease pathogenesis in recent years was followed by development of new classes of medications, as well as potential repurposing of currently available agents. NAFLD therapies target four main pathways. The dominant approach is targeting hepatic fat accumulation and the resultant metabolic stress. Medications in this group include peroxisome proliferator-activator receptor agonists (eg, pioglitazone, elafibranor, saroglitazar), medications targeting the bile acid-farnesoid X receptor axis (obeticholic acid), inhibitors of de novo lipogenesis (aramchol, NDI-010976), incretins (liraglutide) and fibroblast growth factor (FGF)-21 or FGF-19 analogues. A second approach is targeting the oxidative stress, inflammation and injury that follow the metabolic stress. Medications from this group include antioxidants (vitamin E), medications with a target in the tumour necrosis factor α pathway (emricasan, pentoxifylline) and immune modulators (amlexanox, cenicriviroc). A third group has a target in the gut, including antiobesity agents such as orlistat or gut microbiome modulators (IMM-124e, faecal microbial transplant, solithromycin). Finally, as the ongoing injury leads to fibrosis, the harbinger of liver-related morbidity and mortality, antifibrotics (simtuzumab and GR-MD-02) will be an important element of therapy. It is very likely that in the next few years several medications will be available to clinicians treating patients with NAFLD across the entire spectrum of disease.

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To evaluate the influence of pentoxifylline (PTX), a phosphodiesterase inhibitor, on cytokines and inflammatory proteins in patients suffering from septic shock.

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It is recommended that the diagnosis of veno-occlusive disease (sinusoidal obstruction syndrome) [VOD (SOS)] be based primarily on established clinical criteria (modified Seattle or Baltimore criteria) (1A). Ultrasound imaging may be helpful in the exclusion of other disorders in patients with suspected VOD (SOS) (1C). It is recommended that liver biopsy be reserved for patients in whom the diagnosis of VOD (SOS) is unclear and there is a need to exclude other diagnoses (1C). It is recommended that liver biopsies are undertaken using the transjugular approach in order to reduce the risks associated with the procedure (1C). It is suggested that the role of plasminogen activator inhibitor 1 levels remains an area for further research but that these levels should not form part of the routine diagnostic work-up for VOD (SOS) at present (2C).

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Peripheral neuropathy, infection, and peripheral vascular disease can produce serious problems in diabetic patients, particularly in the lower limbs. Ulceration of the foot may progress to gangrene and ultimately necessitate amputation. Distal symmetric polyneuropathy causes sensory loss. Such loss in patients with peripheral vascular disease creates a high risk for foot ulcers, which are vulnerable to infection. Treatment includes relief of neuropathic pain and antibiotic therapy for infection. Pentoxifylline (Trental) improves microvascular flow and appears to be effective against peripheral vascular disease. Aldose reductase inhibitors are being investigated as therapy for diabetic neuropathy. Prevention is the mainstay of management in these patients. Patient education is essential to help maintain health and prevent the potential adverse effects of diabetes.

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At doses greater than 0.1 ng/Ml, TGF-beta1 increased messenger ribonucleic acid (mRNA) and protein expression of elastin in a time-dependent fashion in TADF. PTX did not interfere with TGF-beta1 mediated upregulation of elastin mRNA and protein in TADF. However, pretreatment of TADF with PTX was associated with decreased expression of AAT1, decreased activity of the Smad1/5 pathway, and enhanced phosphorylation of the inhibitory Smad6.

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Eleven studies met our inclusion criteria. Two studies did not report any outcome data relevant to the review, so the results of the review are based on nine trials that contributed data. Primary outcomes were perinatal mortality, serious maternal or infant outcomes, adverse drug reactions, birth before 48 hours of trial entry, birth before 34 weeks' gestation and preterm neonates delivered without a full course of antenatal steroids completed 24 hours before birth. The quality of evidence in included trials was mixed; only three of the trials were placebo controlled.The included trials examined seven different comparisons: intravenous (IV) ritodrine plus oral or IV magnesium (sulphate or gluconate) versus IV ritodrine alone (three trials, 231 women); IV ritodrine plus indomethacin suppositories versus IV ritodrine alone (one trial, 208 women); IV ritodrine plus vaginal progesterone versus IV ritodrine alone (one trial, 83 women); IV hexoprenaline sulphate plus IV magnesium hydrochloride versus IV hexoprenaline sulphate alone (one trial, 24 women); IV fenoterol plus oral naproxen versus IV fenoterol alone (one trial, 72 women); oral pentoxifylline plus IV magnesium sulphate plus IV fenoterol versus IV magnesium sulphate plus IV fenoterol (one trial, 125 women); and, IV terbutaline plus oral metoprolol versus IV terbutaline alone (one trial, 17 women). Few studies with small numbers of women were available for each comparison, hence very little data were pooled in meta-analysis. In all trials, not many of the primary outcomes were reported.Three trials examined intravenous (IV) ritodrine plus IV or oral magnesium (sulphate or gluconate) compared with IV ritodrine alone. One study, with 41 women, reported more adverse drug reactions in the group receiving the combined tocolytics (risk ratio (RR) 7.79, 95% confidence interval (CI) 1.11 to 54.80). Two trials reported discontinuation of therapy due to severe side effects (results were not combined due to high statistical heterogeneity, I² = 83%); one trial reported increased severe side effects in the group receiving IV ritodrine alone (RR 7.79, 95% CI 1.11 to 54.80, 41 women); in the other trial there was no clear difference between groups (RR 0.23, 95% CI 0.03 to 1.97, 107 women). Other primary outcomes were not reported.One trial assessed IV ritodrine plus indomethacin suppositories versus IV ritodrine alone. There were no significant differences between groups for perinatal mortality or serious neonatal morbidity. Results for other primary outcomes were not reported.There were no significant differences between groups receiving IV ritodrine plus vaginal progesterone compared with IV ritodrine alone for most outcomes reported, although the latency period (time from recruitment to delivery) was increased in the group receiving the combination of tocolytics.For other combinations of tocolytic agents, primary outcomes were rarely reported and for secondary outcomes results did not demonstrate differences between groups.

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A randomised, placebo-controlled, double-blind, parallel group trial was performed. Women with breast cancer were treated for 12 months with 400 mg pentoxifylline t.i.d. or placebo, in combination with 100 mg vitamin E t.i.d., starting 1-3 months after the completion of radiotherapy. The primary end-point was passive abduction of the shoulder, and the secondary end-point was difference in arm volumes. The trial is registered on the ISRCTN.org website, number ISRCTN39143623.

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Intravital microscopy was used to study changes in microvascular permeability during diabetes. The extravasation of a fluorescent macromolecular tracer (FITC-Albumin) was measured for one hour and, after computer-aided image analysis, was expressed as variations of normalized grey levels (arbitrary units).

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Currently, there are 5 million individuals with chronic heart failure (CHF) in the United States who have poor clinical outcomes, including high death rates. Observational studies have indicated a reverse epidemiology of traditional cardiovascular risk factors in CHF; in contrast to trends seen in the general population, obesity and hypercholesterolemia are associated with improved survival. The temporal discordance between the overnutrition (long-term killer) and undernutrition (short-term killer) not only can explain some of the observed paradoxes but also may indicate that malnutrition, inflammation, and oxidative stress may play a role that results in protein-energy wasting contributing to poor survival in CHF. Diminished appetite or anorexia and nutritional deficiencies may be both a cause and a consequence of this so-called malnutrition-inflammation-cachexia (MIC) or wasting syndrome in CHF. Neurohumoral activation, insulin resistance, cytokine activation, and survival selection-resultant genetic polymorphisms also may contribute to the prominent inflammatory and oxidative characteristics of this population. In patients with CHF and wasting, nutritional strategies including amino acid supplementation may represent a promising therapeutic approach, especially if the provision of additional amino acids, protein, and energy includes nutrients with anti-inflammatory and antioxidant properties. Regardless of the etiology of anorexia, appetite-stimulating agents, especially those with anti-inflammatory properties such as megesterol acetate or pentoxyphylline, may be appropriate adjuncts to dietary supplementation. Understanding the factors that modulate MIC and body wasting and their associations with clinical outcomes in CHF may lead to the development of nutritional strategies that alter the pathophysiology of CHF and improve outcomes.

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High concentrations of free human neutrophil elastase in bronchial epithelial fluid are believed to be a major factor in the evolution of pulmonary injury in cystic fibrosis (CF). To test this hypothesis, we studied pentoxifylline, a compound that inhibits tumor necrosis factor alpha transcription and its stimulatory effect on polymorphonuclear neutrophils, in patients with CF who had chronic Pseudomonas bronchitis. Subjects older than 11 years of age randomly received placebo or pentoxifylline (1600 mg/day) orally, in a double-blind fashion, for 6 months. Pulmonary function and sputum elastase concentrations were determined before therapy and bimonthly during therapy; compliance was determined by measuring serum drug concentrations. Of the 16 patients who completed the study, 9 received pentoxifylline. The sputum elastase concentrations among placebo recipients were significantly increased from baseline at 4 and 6 months (F = 3.44; p < 0.05); the values remained unchanged in the treatment group. The mean forced vital capacity for the placebo group decreased from 59.2% +/- 15.4% predicted at baseline to 52.0% +/- 12.9% predicted at 6 months; the values in the treatment group remained largely unchanged. The forced vital capacity improved between baseline and 6 months for four of nine pentoxifylline recipients and none of the seven control patients (p = 0.09). During the study, four of seven placebo recipients experienced a significant pulmonary exacerbation compared with one of nine treated patients (p = 0.077). These findings support the hypothesis that polymorphonuclear neutrophil elastase is a factor in the evolution of CF lung disease; further studies are needed to define the role of pentoxifylline in the treatment of CF.

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This randomized and blinded study was performed to determine whether pentoxifylline significantly improves tissue oxygenation after hemorrhagic shock. Hepatic surface oxygen tension was measured in anesthetized rats before and after hemorrhage. Rats were then randomly assigned to either a placebo group (n = 21) receiving 1 ml of intravenous saline solution or to a treatment group (n = 23) receiving intravenous 25 mg/kg of pentoxifylline in 1 ml of saline solution. Investigators were blinded as to which solution was injected. Five minutes after injection of pentoxifylline, there was significant increase in hepatic surface oxygen tension; this increase persisted throughout 1 hour of observation and was significantly greater than in placebo-treated animals. Further study of the effects of pentoxifylline on tissue perfusion and oxygenation after hemorrhagic shock is warranted.

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The proportions of haploid cells in the ipsilateral testes of rats undergoing torsion were significantly lower than in their contralateral testes and in the ipsilateral testes of the control groups. In group 4 (6-OHD) the proportion of haploid cells in the contralateral testes was significantly higher than those in the other groups after unilateral testicular torsion, but significantly lower than those in groups 1 and 4 after a sham operation. After unilateral testicular torsion the haploid cell proportions of the contralateral tests of groups 1-3 were not significantly different from each other.

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trental 250 mg 2015-04-30

Cachexia is a complex metabolic syndrome associated with many chronic or end-stage diseases, especially cancer, and is characterized by loss of muscle with or without loss of fat mass. The management of cachexia is a complex challenge that should address the different causes underlying this clinical event with an integrated or multimodal treatment approach targeting the different factors involved in its pathophysiology. The purpose of this article was to review the current medical treatment of cancer-related cachexia, in particular focusing on combination therapy and ongoing research. Among the treatments proposed in the literature for cancer-related cachexia, some proved to be ineffective, namely, cyproheptadine, hydrazine, metoclopramide, and pentoxifylline. Among effective treatments, progestagens are currently considered the best available treatment option for cancer-related cachexia, and they are the only drugs approved in Europe. Drugs with a strong rationale that have failed or have not shown univocal results in clinical trials so far include eicosapentaenoic acid, cannabinoids, bortezomib, and anti-TNF-alpha MoAb. Several emerging drugs have shown promising results but are still under clinical investigation (thalidomide, selective cox-2 inhibitors, ghrelin mimetics, insulin, oxandrolone, and olanzapine). To date, despite several years of coordinated efforts in basic and clinical research, practice guidelines for the prevention and treatment of cancer-related muscle wasting are lacking, mainly because of the multifactorial pathogenesis buy trental of the syndrome. From all the data presented, one can speculate that one single therapy may not be completely successful in the treatment of cachexia. From this point of view, treatments involving different combinations are more likely to be successful.

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All five of the sham rabbits were delivered at term without any evidence of infection. There were no differences in the preterm delivery rates between the placebo group (eight of 11) and the pentoxifylline-treated group (seven buy trental to 11). However, there was a trend toward prolonging time until death in the treatment group. There were no differences in intrauterine pathologic feature between the placebo and treatment groups.

trental reviews 2016-04-16

The aim of this review was to identify systematically, criteria for trismus in head and neck cancer, the evidence for risk factors for trismus buy trental and the interventions to treat trismus. Three databases were searched (time period 1966 to June 2003) for the text "trismus" or "restricted mouth opening". Included in the review were clinical studies (> or = 10 patients). Two observers independently assessed the papers identified. In 12 studies nine different criteria for trismus were found without justifying these criteria. Radiotherapy (follow-up: 6-12 months) involving the structures of the temporomandibular joint and or pterygoid muscles reduces mouth opening with 18% (sd: 17%). Exercises using a therabite device or tongue blades increase mouth opening significantly (no follow-up), effect sizes (ES) 2.6 and 1.5 respectively. Microcurrent electrotherapy (follow-up 3 months) and pentoxifylline (no follow-up) increases mouth opening significantly (ES for both: 0.3).

trental and alcohol 2015-10-28

The problem of sepsis and septic shock (SSH) is known to be very actual due to peak-shaped growth of the number of such patients and unsatisfactory results of treatment. The occurrence of SSH is different--from 10% in the structure of infectious complications after polytrauma to 50% in patients with gram-negative sepsis in patients with burn disease. An analysis of treatment of 165 patients with SSH developed against the background of peritonitis has revealed high level of lethality (64%). In the pathogenesis of SSH an important role is played by immune disorders resulting in the development of generalized inflammation and polyorganic buy trental insufficiency. Treatment of patients with SSH must be necessarily supplemented with immuno-correcting techniques: use of medicines of nonspecific anti-cytokine action (pentoxyphillin) and regulators of the immune response (ronkoleukin, blood perfusion through the donor porcine spleen). The timely performed immunomodulating therapy allowed lethality of patients with SSH to be reduced to 32%.

trental drug category 2017-10-24

Inflammation induces cardiac fibrosis and hypertrophy in multiple cardiovascular diseases, contributing to cardiac dysfunction. We tested the hypothesis that pentoxifylline (PTX), a phosphodiesterase inhibitor with anti-inflammatory property, would attenuate cardiac fibrosis and hypertrophy, and prevent cardiac dysfunction in angiotensin (ANG) II-induced hypertensive rats. Sprague-Dawley rats were divided into control and ANG II-infused groups treated with or without PTX for 2 weeks. PTX had no effect on ANG II-induced hypertension, but significantly attenuated cardiac fibrosis and hypertrophy, and ameliorated cardiac dysfunction in ANG II-induced hypertensive rats. In addition, ANG II-induced increase in circulating and cardiac proinflammatory cytokines were attenuated by PTX, which reduced cardiac nuclear factor-kappa B activity. Furthermore, PTX decreased cardiac expression of genetic buy trental markers important for fibrosis, hypertrophy, and endothelial dysfunction, and reduced migration and infiltration of macrophages. In contrast, PTX had no effects on the above parameters in control rats. The findings suggest that PTX ameliorates cardiac fibrosis, pathological hypertrophy, and cardiac dysfunction by suppressing inflammatory responses in angiotensin II-induced hypertension, and that these benefits were independent of the blood pressure lowering effect. The PTX by its anti-inflammatory property may be a potential therapeutic option for the prevention of cardiac remodeling and dysfunction in ANG II-induced hypertension.

trental 100 mg 2015-02-27

Bone fracture healing was significantly better in Group B and Group C compared buy trental to Group A (P<0.05), but Group D did not show better bone fracture healing than Group A (P>0.05).

trental medication 2017-10-29

Nonarteriitic anterior ischemic optic neuropathy (NAION) is a leading cause of sudden loss of vision, which particularly affects individuals older buy trental than 50 years. Up to now there is no treatment that is effective at reversing or limiting the course of this disease. To study the short- and long-term effects of fluocortolone (FC) on the visual outcome of patients with acute NAION compared to standard treatment with pentoxifylline (PFX).

trental pentoxifylline tablets 2016-12-01

Lisofylline (1-(5-R-hydroxyhexyl)-3,5-dimethylxanthine (LSF)) is a new methylxanthine, a stereospecific isomer which is a metabolite of pentoxifylline (1-(5-oxohexyl)-3,5-dimethylxanthine (PTX)). Alcohol dehydrogenases (E.C. 1.1.X.Y.) are enzymes that catalyze the oxidation and reduction of hydroxyl and carbonyl compounds. They may be employed either as crude or purified enzymes or as components of whole cells. The aim of this study was to explore the stereoselective bioreduction of PTX in the presence of whole cell baker's and wine yeasts, which function as biocatalysts in the production of LSF. The experiments were conducted in buy trental water and a number of organic solvents (toluene, hexane, ethyl acetate), and we obtained LSF with different yields and ee values. Our research demonstrated that the highest activity is shown when the KKPU strain is used in an aqueous medium. The biotransformation of PTX into LSF in this case was characterized by high yield and enantioselectivity: 95% and ee = 98%, respectively.

trental 20 mg 2015-09-14

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 buy trental regimens have been proposed, but only glucocorticoids have shown some evidence of benefit in the literature.

online kopen trental 2015-08-23

Tumor necrosis factor (TNF) and interleukin (IL)-6 concentrations were measured by radioimmunoassays; IL-8 concentrations by an enzyme-linked immunosorbent assay (ELISA) and pentoxifylline concentrations by high-performance liquid chromatography at 0, 3, 6, 12, 18, 24 and 48 hrs after study entry. Pulmonary artery catheter-derived hemodynamics were measured at 0, 0.75, 3, 6, 12, 18, and buy trental 24 hrs. In pentoxifylline-treated patients, at 24 hrs, serum concentrations of TNF were significantly lower compared with controls (12 +/- 2 vs. 42 +/- 12 pg/mL, respectively, p = .04). Serum concentrations of IL-6 and IL-8 did not differ between the two treatment groups. There were also no significant differences in any hemodynamic and oxygenation measurements comparing the two treatment groups. Pentoxifylline concentrations were 1,544 +/- 241 ng/mL after the initial dose, and 5,776 +/- 1,781 ng/mL at the end of the 24-hr infusion. Five patients in the pentoxifylline group and four patients in the placebo group died.

trental generic 2017-10-31

Ten couples underwent assisted reproductive technology (ART). One couple achieved pregnancy after the second cycle of electroejaculation and IUI. Seven couples underwent 8 cycles of ICSI, 4 cycles with fresh electroejaculates, 2 with cryopreserved samples, and 2 buy trental with cryopreserved samples with addition of pentoxifylline. Seven (88%) clinical pregnancies were achieved, 2 of which ended with spontaneous abortion. One couple accomplished pregnancy by ICSI with cryopreserved sperm from vasal aspiration. The percentages of fertilization and pregnancy of ICSI cycles using sperm from men with SCI were comparable to men without SCI. One couple attained pregnancy by using donor sperm. The cumulative successful pregnancy rate per couple was 80% (8/10).

trental er dosage 2017-07-22

Leukocyte adherence was studied in an original experiment that allowed study of the microcirculation in an ischemic muscle perfused by a collateral circulation. In this model, the artery feeding the cremaster muscle was ligated. Then the muscle homolateral to the ligation and its contralateral muscle were both studied by intra-vital-microscopy at 4 h, 1, 3, 7, and 21 days after the ligation. Rats were treated or not with 20 mg/kg/day pentoxifylline (PTX) i.m. In untreated rats, we found that both short-lasting and long-lasting leukocyte adherence was largely increased in the postcapillary venules of the ischemic muscle but not in its contralateral control. This dramatic increase was not limited to the hours immediately after the arterial ligation but was also found up to 3 weeks after the ligation when blood flow was almost restored to buy trental normal. This suggested that when muscle blood flow was chronically reduced, some changes promoting leukocyte adherence may occur in the endothelium. In rats treated with PTX, we found very effective inhibition of leukocyte adherence.

trental online buy 2015-05-08

The inappropriate endogenous secretion of tumour necrosis factor (TNF) could play a role in the pathogenesis of acute respiratory distress syndrome (ARDS), one of the most frequent causes of death in cancer patients. Because of its capacity to inhibit TNF secretion in vitro, pentoxifylline (PTX) Duphaston Dosage could be extremely useful in ARDS therapy. In this study 30 advanced cancer patients with ARDS were randomized to receive either the conventional care or conventional care plus PTX (100 mg i.v. twice a day for 7 days followed by an oral administration of 400 mg three times a day) to evaluate the efficacy of PTX in reducing TNF serum levels and in improving the symptoms of this syndrome. Serum levels of TNF were measured before and after 7 days of therapy. The percentage of patients alive at 7 days was significantly higher in the PTX-treated group than in the controls (12/15 versus 3/15; P < 0.001). The mean survival time was significantly higher in the PTX-treated group than in the controls. A clinical and/or radiological improvement was obtained in 11/15 patients treated with PTX and in only 2/15 patients in the conventional care group (P < 0.01). TNF mean levels significantly decrease in the PTX-treated group. These data confirm in vivo the capacity of PTX to inhibit TNF secretion in patients with ARDS. Moreover PTX therapy may improve the symptoms related to ARDS without particular toxic effects.

trental pill 2017-04-23

Nonrandomized controlled Naprosyn Gel Europe trial.

trental 500 mg 2016-11-01

This study examines the hypothesis that pentoxifylline protects splanchnic PGI2 synthesis during severe mesenteric ischemia/reperfusion injury. Anesthetized Sprague-Dawley rats (300 grams) were subjected to Lamictal Highest Dose sham or superior mesenteric artery occlusion for 20 minutes followed by 30 minutes of reperfusion. The ischemia/reperfusion groups received either enteral allopurinol (10 mg/kg) daily for 5 days prior to ischemia, PTX (50 mg/kg) 10 minutes prior to ischemia or carrier. The superior mesenteric artery was cannulated and removed with its intact intestine (SV + SI). The SV + SI was perfused in vitro with oxygenated Krebs buffer. The venous effluent was collected and assayed for release of 6-keto-PGF1 alpha, PGE2 and thromboxane B2 by enzyme immunoassay. Severe mesenteric ischemia/reperfusion decreased SV + SI 6-keto-PGF1 alpha release by 40% compared to the sham group but did not alter release of PGE2 or thromboxane B2. Pretreatment of the animals with PTX and not allopurinol preserved SV + SI 6-keto-PGF1 alpha release at all times of perfusion to a level similar to the sham group. These data showed that severe mesenteric ischemia/reperfusion injury abolished release of endogenous splanchnic PGI2. PTX exerted a protective effect against severe mesenteric ischemia/reperfusion injury by maintaining release of splanchnic PGI2, a potent endogenous splanchnic vasodilator.

trental 50 mg 2015-08-07

Consecutive patients (n = 60) with trauma or sepsis secondary to major ( Lipitor 50 Mg nontrauma) surgery. All patients received controlled mechanical ventilation.

trental renal dosing 2017-05-13

To evaluate the effects of pentoxifylline (PF) administration on liver, gut, and peripheral oxygenation during Cytoxan 25mg Tablets crystalloid resuscitation of hemorrhagic shock.

trental suspension 2015-05-31

Lipopolysaccharide (LPS, endotoxin)-induced diaphragmatic contractile dysfunction and sarcolemmal injury in animals has been identified. However, the precise nature of sepsis-related alterations in diaphragm myofiber function and the activity of Ca(2+) release from sarcoplasmic reticulum of skeletal muscle remain unclear. The present study investigated the in vivo effects of LPS on the Ca(2+)-dependent mechanical activity and ryanodine response in mouse diaphragm and Ca(2+) release from isolated sarcoplasmic reticulum membrane vesicles, and aimed to examine the role of nitric oxide (NO) in these responses. When diaphragms were bathed in a solution that was Cl(-)-free, Na(+)-free, but contained high K(+), a Ca(2+)-induced contracture was elicited. Increases in external Ca(2+) concentration produced increases in peak tension of Ca(2+)-induced contracture in control diaphragm, while a decrease was seen in endotoxemic diaphragm. Ryanodine induced a marked contracture in control diaphragms, which was diminished after endotoxemia. This finding is correlated with the decrease of ryanodine-induced Ca(2+) release and the suppression of [(3)H]ryanodine binding on the isolated SR of the skeletal muscle from LPS-treated rats. In mice treated with LPS significantly increased levels of plasma nitrite and serum TNF-alpha were observed, changes inhibited by aminoguanidine [an inhibitor of inducible NO synthase (iNOS)] and pentoxifylline (an inhibitor of tumor necrosis factor-alpha formation), respectively. Moreover, LPS treatment resulted in a significant expression of mRNA for iNOS in mouse diaphragms. The inhibitory effects on Ca(2+)- and ryanodine responses by LPS Bystolic 5mg Tablets could be prevented by treatment with polymyxin B (LPS neutralizer) and pentoxifylline, but not by treatment with dexamethasone, N(G)-nitro- L-arginine or aminoguanidine (NOS inhibitors). These results imply that the NO-related pathway may not be involved in the dysfunction of the Ca(2+) release mechanism in the sarcoplasmic reticulum of mouse diaphragm during endotoxemia.

trental dosing 2016-03-18

Red blood cell filtration test has been performed in 37 insulin dependent diabetics (IDD) and 35 controls matched for age and sex and subdivided into age groups. IDD have been classified according to the presence of vascular complications, either affecting small and/or large vessels, assessed by clinical and instrumental methods. Results evidence a close correlation between age, fibrinogen, smoking and filtration index, both in IDD and in controls. The presence and type of vascular complication in diabetics parallels the increase in the filtration index, being the blood of macroangiopathic diabetics less filtrable than that of non angiopathics and/or controls. Metabolic control, recorded as glycosylated haemoglobin shows a slight correlation with filtration index, while blood glucose of the same specimen does not. Filtration index appears to be an useful datum for assessing angiopathic risk in diabetics. Nineteen IDD have been treated with pentoxifylline, 400 mg per os 3 times daily Cymbalta High Dose for 20 days and filtration time, and other metabolic variables have been assessed. Data evidenced a marked improvement in the filtration time without any change in the other metabolic variables suggesting that the effect of this drug is mainly exerted on the RBC deformability and not on plasma viscosity. The drug has been very well tolerated and revealed itself an effective therapeutic mean for influencing RBC filtration, thus preventing angiopathic phenomena.

trental user reviews 2015-05-27

In an effort to improve the additive anti-tumor efficacy of commonly used alkylating agents, the topoisomerase-II inhibitor etoposide was used in combination with either the mitochondrial poison and energy-depleting agent lonidamine or the hemorheologic agent and tumor-blood-flow-increasing agent pentoxifylline. In the FSaIIC murine fibrosarcoma system, these modulators were evaluated for modulation of whole-tumor cell killing vs. bone-marrow CFU-GM toxicity with the alkylating drugs CDDP, CTX, L-PAM or BCNU. Etoposide alone was essentially additive with the alkylating drugs for both tumor-cell and bone-marrow killing, except for BCNU, where a substantial increase in tumor-cell killing occurred (0.5 to 2.0 logs over the dose range of BCNU tested) without a significant increase in bone-marrow toxicity. Etoposide plus lonidamine was Duphaston 10mg Reviews significantly more active than etoposide alone only with CTX and BCNU in tumor-cell vs. bone-marrow killing. Etoposide plus pentoxifylline was also most active with these two alkylating agents, where increases in tumor-cell killing of 0.5 to 1.0 log were observed. Hoechst-33342-defined tumor-cell sub-population studies revealed that etoposide significantly improved the killing of dim (putative hypoxic) cells by CDDP, but neither lonidamine nor pentoxifylline significantly improved killing of bright or dim cells together. With CTX, etoposide plus lonidamine or pentoxifylline substantially improved killing of dim cells over etoposide alone (each by about 0.8 logs). These data indicate that a therapeutic advantage may be achievable by combining etoposide with lonidamine or pentoxifylline for use with alkylating drugs.

trental dosage 2016-08-14

Treatment of patients with metastatic renal cell carcinoma with high-dose interleukin Prevacid Max Dose -2 (IL-2) administered as continuous intravenous (CIV) infusion or as bolus injection results in response rates of 15% to 30%; however, toxicities with these regimens have been severe. A trial in which CIV IL-2 was administered at high doses during days 1 to 5 and at reduced doses during days 10 to 20 reported less toxicity without a decrease in response rates. We treated a series of patients with this regimen and our experience is presented.

trental drug class 2017-04-15

Kasabach-Merritt phenomenon (KMP) can lead to life-threatening bleeding, and its optimum treatment has not been established. We review the experience of managing KMP in a single institution.

trental drug interactions 2015-01-24

This study is a retrospective review of treatment outcomes of osteoradionecrosis (ORN) of the mandible with specific reference to the evolving role of medical management with pentoxifylline, tocopherol, and doxycycline. We reviewed the presentation and management of 71 patients treated for ORN of the mandible at the regional head and neck unit during a 15-year period to January 2011, and categorised them into three grades using the Notani classification: grade I (n=28), grade II (n=16), and grade III (n=27). Twelve patients with grade I ORN, 3 with grade II, and 10 with grade III, were prescribed medical treatment. Of these, three with grade I, and two with grade II ORN were cured, and progression of the disease had halted and there was satisfactory control of symptoms in eight with grade I and four with grade III disease. Patients who failed to respond to conservative treatment were further analysed for the need for free flap reconstruction. Medical management was introduced as a standard treatment in January 2006. Of the 39 patients diagnosed before this, 20 (51%) required resection and free flap reconstruction compared with only 8/32 (25%) after it had been introduced.

trental overdose 2017-09-07

Alcoholic hepatitis (AH) remains a major cause of liver-related morbidity and mortality in the United States and is actually increasing in certain areas of Europe. Thus, there is a pressing need for new therapies/approaches. Major barriers for reducing morbidity, mortality, and costs of care include: lack of translational animal and human studies of new therapies for AH; limited trials of combination therapies in AH targeted at specific disease mechanisms (e.g., gut permeability, cytokines, oxidative stress); limited studies on non-invasive, non-mortality end points; few studies on mechanisms of steroid non-responsiveness; and inadequate prognostic indicators, to name only a few. In spite of these gaps, we have made major advances in understanding mechanisms for AH and appropriate therapies for AH. This article reviews mechanisms and rationale for use of steroids and pentoxifylline in AH and future directions in therapy.

trental 600 mg 2017-07-16

In vivo treatment of mice with anti-CD3 mAb causes polyclonal T cell activation and cytokine release. Since several cytokines are known to alter expression of MHC molecules and adhesion molecules on endothelia, we hypothesized that anti-CD3 mAb treatment should result in activation of vascular endothelia. In previous studies, we established that vascular endothelial cells in murine heterotopic cardiac grafts can develop at least 2 stable inflammatory phenotypes: cardiac allograft endothelia characteristically develop reactivity with MECA-32 mAb (undefined endothelial epitope) and M/K-2 mAb (murine vascular cell adhesion molecule-1 [VCAM-1]), whereas cardiac isografts develop reactivity with MECA-32, but not M/K-2 mAb. We now report that a single treatment of cardiac isograft recipients with the anti-CD3 mAb 145-2C11 caused expression of VCAM-1 on all cardiac isograft endothelia, including the microvascular endothelia. In contrast, expression of endothelial VCAM-1 in the native heart of the isograft recipient was limited to patchy areas of larger arteries. This patchy, arterial pattern of VCAM-1 expression was observed in lung, liver, kidney, and thymus of all mice treated with 145-2C11, whether or not they were implanted with a cardiac isograft, and was dissociated from expression of MECA-32 mAb reactivity. Hence, treatment of mice with anti-CD3 mAb causes systemic endothelial activation (VCAM-1 expression), and endothelial cells of recently implanted cardiac isografts appear to be hypersensitive to induction of VCAM-1 by anti-CD3 mAb treatment. Further studies showed that (1) treatment with 145-2C11 F(ab)'2 fragments did not induce endothelial activation, (2) intravenous pretreatment with pentoxifylline eliminated all endothelial effects of 145-2C11 treatment, (3) induction of endothelial activation by 145-2C11 mAb always paralleled the expression of adverse physiologic symptoms, and (4) mice exhibit strain-specific differences in endothelial responses to 145-2C11 treatment. We propose that anti-CD3 mAb treatment causes simultaneous activation of circulating T cells and systemic vascular endothelial cells which may facilitate systemic lymphocyte-endothelial interactions, and may explain the rapid disappearance of T cells from the circulation that is associated with anti-CD3 treatment in mouse and man.

trental 400 mg 2017-08-23

Thirty-year-old female with a previous history of a cutaneous ulcer suspicious of leishmaniasis 20 years ago presented with a new complaint of a depressed papular lesion 8 × 7 mm in the right lower extremity. The lesion was of 10-day duration. Because early cutaneous leishmaniasis (CL) lesions may have a non-ulcerated appearance, a Leishmania skin test (LST) was performed on the forearm with a strong positive result (38 × 32 mm). After 8 days, the lesion in the leg, which was diagnosed as folliculitis, completely healed. However, a typical CL ulcer (26 × 24 mm) developed at the LST site. Histopathology of the new lesion did not identifiy parasites, but the findings were consistent with a diagnosis of CL. Further analysis identified amastigotes by immunohistochemical stain. Mononuclear cells harvested from the patient were stimulated with Leishmania antigen and showed high levels of production of both tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ): 2,943 pg/mL and 2,313 pg/mL, respectively. After 40 days of treatment with antimony and pentoxifylline, the ulcer resolved. The development of CL at the LST site suggests a strong Th1 immune response, and it is an in vivo documentation of the role of the host immune response in the pathology of CL. It teaches us that LST should be cautiously, if at all, used in patients with self-healing CL ulcers.