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Voltaren (Diclofenac)

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Generic Voltaren is in a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Generic Voltaren is used to treat pain or inflammation caused by arthritis or ankylosing spondylitis. Generic Voltaren works by reducing hormones that cause inflammation and pain in the body.

Other names for this medication:

Similar Products:
Celebrex, Diclofenac Gel, Mobic, Anaprox, Naprosyn


Also known as:  Diclofenac.


Generic Voltaren is used to treat pain or inflammation caused by arthritis or ankylosing spondylitis.

Generic Voltaren is in a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Generic Voltaren works by reducing hormones that cause inflammation and pain in the body.

Voltaren is also known as Diclofenac, Voveran, Voltarol, Voltarol SR, Voltarol Retard, Voltarol Rapid, Diclomax SR, Diclomax Retard, Motifene, Defenac, Diclofex, Diclozip, Dyloject, Fenactol, Flamrase, Flamatak, Econac, Rhumalgan SR, Rhumalgan XL, Volsaid SR.

Generic name of Generic Voltaren is Diclofenac.

Brand names of Generic Voltaren are Cataflam, Voltaren, Voltaren-XR.


Take Generic Voltaren orally.

Do not crush or chew the pill. Swallow it whole.

Take Generic Voltaren with great amount of water.

Take Generic Voltaren with or without food.

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


If you overdose Generic Voltaren and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Voltaren overdosage: nausea, vomiting, stomach pain, black or bloody stool, shallow breathing, fainting, coma.


Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Voltaren 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.


Do not take Generic Voltaren if you are allergic to Generic Voltaren components or to aspirin or other NSAIDs.

Do not take Generic Voltaren if you are pregnant, planning to become pregnant. Do not breast-feed while taking Generic Voltaren.

Do not take Generic Voltaren if you just before or after having heart bypass surgery (also called coronary artery bypass graft, or CABG).

Be careful with Generic Voltaren if you use any other over-the-counter cold, allergy, or pain medicataion.

Be careful with Generic Voltaren if you had a history of heart attack, stroke or blood clot, heart disease, congestive heart failure, high blood pressure, liver or kidney diseases, asthma, polyps in the nose.

Be careful with Generic Voltaren if you smoke.

Be careful with Generic Voltaren if you take antidepressants, blood thinner (Coumadin); cyclosporine, lithium, methotrexate, you take diuretics, you take steroids.

Avoid exposure to sunlight or artificial UV rays (sunlamps or tanning beds).

Avoid alcohol.

It can be dangerous to stop Generic Voltaren taking suddenly.

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The use of chemical penetration enhancers (CPEs) is one of the most common approaches to improve the dermal and transdermal delivery of drugs. However, often, incorporation of CPEs in the formulation poses compatibility and stability challenges. Moreover, incorporation of enhancers in the formulation leads to prolonged exposure to skin increasing the concern of causing skin reactions. This study was undertaken to assess whether pretreatment with CPEs is a rational approach to enhance the permeation of diclofenac sodium. In vitro experiments were performed across porcine epidermis pretreated with propylene glycol or oleic acid or their combinations for 0.5, 2, and 4 h, respectively. Pretreatment with combination of oleic acid in propylene glycol was found to enhance the permeation of diclofenac sodium significantly only at 10% and 20% (v/v) level, and only when the pretreatment duration was 0.5 h. Longer durations of pretreatment and higher concentration of oleic acid in propylene glycol did not enhance the permeation of diclofenac sodium. In vivo dermatokinetic studies were carried out on Sprague-Dawley rats. A twofold increase in AUC and Cmax was observed in case of rats pretreated with enhancers over the group that was pretreated with buffer. In conclusion, this study showed that composition of the enhancers and duration of pretreatment are crucial in determining the efficacy of CPEs.

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Although ulcers are often associated with non-steroidal anti-inflammatory drugs (NSAIDs) little is known about the feasibility of predicting their development in patients taking NSAIDs. In addition, the ulcerogenic potentials of the newer NSAIDs, taken on long term basis, have not been compared with those of more established preparations. The aim of this study was to identify the clinical and pathological characteristics of patients at a higher risk of NSAID induced ulcers, measure the ulcerogenic potential of a variety of NSAIDs, and test the effect of these potentials on the predictability of ulceration. Altogether 190 long term NSAID users were studied. The presence of abdominal complaints, previous history of ulcers, arthritis related physical disability, anaemia, gastritis, and Helicobacter pylori status were all assessed as possible risk factors. NSAIDs were classified into established drugs (group I), and newer agents (group II). Group I included naproxen, indomethacin, diclofenac, ketoprofen, piroxicam, and flurbiprofen. Group II included fenbufen, nabumetone, ibuprofen, etodolac, azapropazone, and tiaprofenic acid. Of 63 ulcers identified in the study group, 51 (81%) were seen in group I NSAID patients (51 of 132, 39%) compared with 12 ulcers in group II (12 of 58, 21%), p < 0.02; estimated relative risk (ERR): 2.41). In group I, 25 ulcers were found in 38 patients with abdominal pain (25 of 38, 66%, p < 0.01, ERR: 5.03); 18 in 25 (72%) patients with a previous history of ulcers (p < 0.001, ERR: 5.77), 26 in 44 (59%) patients with debilitating arthritis (p < 0.001, ERR 3.64), and 35 in 73 (48%) patients with H pylori associated gastritis (p < 0.01, ERR: 2.48). The presence of these factors in group II patients did not influence the risk of ulceration. Group I NSAIDs were more likely to be associated with chemical gastritis and to intensify H pylori related damage. Although silent ulcers are not uncommon in patients taking NSAIDs, recognition of the risk factors might helps predict a significant number (up to 81%), especially in those receiving group I NSAIDs.

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We confirmed 118 cases among 16 070 cataract surgeries (incidence, 0.73%). Compared with PA alone, the OR for the relationship of macular edema with PA+NSAID was 0.45 (95% CI, 0.21-0.95) and that for TA injection was 1.21 (95% CI, 0.48-3.06). The frequency of intraocular pressure spikes of 30 mmHg or more between postoperative days 16 and 45 was 0.6% in the topical PA group, 0.3% in the topical PA+NSAID group (P = 0.13), and 0.8% for the TA group (P = 0.52). Black race was associated with a risk of macular edema (OR, 2.86; 95% CI, 1.41-5.79).

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Thirty patients undergoing laparoscopic cholecystectomy or inguinal hernioplasty under general anesthesia were studied. Half (DM) received 90 mg dextromethorphan and half received placebo 90 min before anesthesia. Intravenous Patient Controlled Aanalgesia with morphine was available for two hours within a six-hour observation period; 75 mg diclofenac i.m. prn was given later in PACU and on-ward (24 hr). Pain was assessed using the visual analogue scales. Thermal thresholds for cold and hot sensation and for pain (by limit method) were evaluated at the site of skin incision (primary-) and distantly (secondary hyperalgesia). Von Frey filaments were applied testing touch sensation. Sedation level and morphine consumption were also assessed in PACU.

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Five population-based studies were summarized to evaluate information on more than 1,000,000 patients using NSAIDs.

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Pain following embolization of the uterine arteries (UAEs) is variable and may be very severe requiring large doses of parenteral opioids for relief. The present study tested the hypothesis that the addition of ketamine to i.v. patient-controlled morphine reduces the amount of morphine required for pain-control during the first 24 h after UAE embolization.

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To evaluate the efficacy of different anesthetics and topical anti-inflammatory treatment in patients undergoing intravitreal injections (IVI).

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voltaren tablet 2017-04-19

Eyes treated with ketorolac and diclofenac demonstrated reduced aqueous leucocyte concentrations of 62% and 64% respectively, compared with untreated controls (p<0.05). Ketorolac and diclofenac reduced buy voltaren aqueous prostaglandin E2 levels by 85% (p<0.005) and 59% (p<0.005), respectively. Ketorolac and diclofenac achieved a peak vitreous concentration of 234 and 73 microg/ml, respectively. After 48 h, ketorolac was barely detectable (0.06 microg/ml) in the vitreous, and diclofenac was undetectable. The peak concentration of each drug in the retina/choroid was 201 microg/g for ketorolac and 4.1 microg/g for diclofenac. Both drugs were undetectable in the retina/choroid after 48 h.

voltaren prices 2017-06-23

Sambucus ebulus L. (S. ebulus) has had long-standing application in Traditional Persian Medicine for joint pain and for a variety of bone and joint disorders. According to traditional use of S. ebulus and its relevant pharmacologic properties, this study was designed to evaluate the efficacy and short-term safety of topical use of S. ebulus in buy voltaren patients with knee osteoarthritis (OA).

voltaren drug class 2016-11-17

To describe Ceftin Suspension Coupon the frequency and timing of intravenous patient-controlled analgesia (IV-PCA) or neuraxial morphine-induced postoperative respiratory depression.

voltaren 600 mg 2015-05-12

A series of diphenylthiazole-thiazolidinone hybrids was synthesized and evaluated in vitro and in vivo as anti-inflammatory/analgesic agents. The inhibition of cyclooxygenase (COX) enzymes was suggested as a molecular mechanism for the hybrids to exert their anti-inflammatory action. Of these compounds, 13b, 14, and 15b showed the most potent COX inhibitory activity with IC50 values between 2.03 and 12.27 µM, but with different selectivity profiles. All compounds were further evaluated in vivo for their anti-inflammatory/analgesic activities using three animal models. Interestingly, the results of the COX assay were in agreement with those of in vivo assays where the most potent COX inhibitors, 13b, 14, and 15b, exhibited the highest anti-inflammatory/analgesic activities compared to diclofenac. On the contrary, compounds 11 and 12 were the least potent ligands in vitro and in vivo as well. Mestinon Drug Class

voltaren pills dosage 2015-09-13

Non-steroidal anti-inflammatory drugs have long been known to cause gastro-duodenal damage. However, all parts of the gastrointestinal tract may be affected, including the small intestine, colon and oesophagus. Non-steroidal anti-inflammatory drugs can cause dyspeptic symptoms, erosions, ulceration, which may lead to haemorrhage or perforation, and a requirement for surgery. The purpose of this report is to assess risk factors which may lead to gastrointestinal damage and, thus, to identify those patients at greatest risk of non-steroidal anti-inflammatory drug damage. Possible risk factors include age, sex, previous ulcer history, the presence of Helicobacter pylori, the type and severity of arthritis, individual non-steroidal anti-inflammatory drugs (dose, duration Biaxin Dosage Pediatric of treatment, route of administration), other debilitating diseases, smoking, alcohol, and the use of concomitant drugs. Risk of non-steroidal anti-inflammatory drug damage is higher in older patients (RR > 60 5.52; < 60 1.65), but there is no convincing sex difference. There is increased risk in patients with a previous history of peptic ulceration (RR first gastrointestinal event 2.39; subsequent gastrointestinal event 4.76), and in the first three months of treatment. Debate continues about the relevance of Helicobacter pylori, and this will be discussed in a later report. There is no strong evidence that patients with rheumatoid arthritis are more likely to have more trouble than those with osteoarthritis, but the former are more likely to require higher doses of non-steroidal anti-inflammatory drugs. Highest risk non-steroidal anti-inflammatory drugs include azapropazone, ketoprofen and piroxicam, and those with least risk include ibuprofen, diclofenac and etodolac. There is an increased risk of gastrointestinal complications with relatively small-dose prophylactic aspirin. Other factors increasing the risk are smoking and the presence of chronic underlying respiratory and cardiovascular disease. Risk of gastrointestinal problems is increased with concomitant drugs, especially corticosteroids (RR 14.6 if given with non-steroidal anti-inflammatory drugs), but also with anticoagulants and some other drugs. The clinical importance of identifying possible risk factors lies in being aware of likely problem patients and in the use of safer non-steroidal anti-inflammatory drugs or combination therapy with protective drugs in these patients.

voltaren 100 mg 2017-07-06

These findings suggest Cleocin Dosage Forms that TDiclo represents a useful alternative to oral NSAID therapy in the management of OA, with a more favorable safety profile.

voltaren arthritis medication 2015-04-04

We sought to evaluate the efficacy of topical 3% diclofenac gel in the management of periocular actinic keratosis. Viagra Purchase Uk

voltaren 75mg reviews 2016-11-23

Fibromyalgia is a prevalent and burdensome disorder characterized by chronic widespread pain and complex comorbid symptoms. To develop better treatments for pain-centered fibromyalgia symptoms, there is still a need for animal models which mimic the features of fibromyalgia patients. In the present study, we have established a fibromyalgia animal model by utilizing a never-before-published pharmacological effect of reserpine. Repeated administration of reserpine (1mg/kg s.c., once daily, for three consecutive days) causes a significant decrease in the muscle pressure threshold and tactile allodynia, which are sustained for 1week or more in both male and female Glucophage 850 Mg rats. This treatment regimen decreases the amount of biogenic amines (dopamine, norepinephrine, and 5-hydroxytryptamine) in the spinal cord, thalamus, and prefrontal cortex, which are deeply involved in pain signal processing. It also significantly increases immobility time in the forced swim test, which is indicative of depression, a common comorbid symptom of fibromyalgia. Pregabalin, duloxetine, and pramipexole significantly attenuated the reserpine-induced decrease in muscle pressure threshold, but diclofenac did not. The validity of the use of this reserpinized animal as a fibromyalgia model is demonstrated from three different aspects, i.e., face validity (manifestation of chronic pain and comorbid symptoms), construct validity (dysfunction of biogenic amine-mediated central nervous system pain control is involved), and predictive validity (similar responses to treatments used in fibromyalgia patients). This animal model is expected to contribute to the better understanding of fibromyalgia pathophysiology and the evaluation of drugs, especially those which would activate biogenic amine system.