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Indocin (Indomethacin)

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Also known as:  Indomethacin.


Indocin is a perfect remedy, which helps to fight against pain or inflammation caused by many conditions such as gout, ankylosing spondylitis, arthritis, bursitis, or tendinitis.

Indocin acts by reducing hormones that cause inflammation and pain in the body.

Indocin is also known as Indometacin, Indocid, Inmecin, Indochron E-R, Indocin-SR, Flexin Continus, Indolar, Indomax, Indomod, Pardelprin, Rheumacin, Rimacid, Slo-Indo.

It is nonsteroidal anti-inflammatory drug.


Shake the liquid form of Indocin before using.

Take Indocin tablets and liquid form orally with water.

Take Indocin once or twice a day at the same time.

Do not crush or chew it.

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


If you overdose Indocin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Indocin overdosage: vomiting, migraine, lightheadedness, confusion, extreme tiredness, feeling of numbness, pricking, burning, creeping on the skin, convulsions, dyspepsia.


Store at room temperature between 15 and 30 degrees C (59 and 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 Indocin 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 Indocin if you are allergic to Indocin components.

Do not take Indocin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Indocin if you are taking angiotensin ii receptor antagonists such as candesartan (atacand), eprosartan (teveten), irbesartan (avapro), losartan (cozaar), olmesartan (benicar), telmisartan (micardis), and valsartan (diovan); beta blockers such as atenolol (tenormin), labetalol (normodyne), metoprolol (lopressor, toprol xl), nadolol (corgard), and propranolol (inderal); cyclosporine (neoral, sandimmune); digoxin (lanoxin); diuretics ('water pills') such as triamterene (dyrenium, in dyazide); lithium (eskalith, lithobid); methotrexate (rheumatrex); phenytoin (dilantin); and probenecid (benemid), angiotensin-converting enzyme (ace) inhibitors such as benazepril (lotensin), captopril (capoten), enalapril (vasotec), fosinopril (monopril), lisinopril (prinivil, zestril), moexipril (univasc), perindopril (aceon), quinapril (accupril), ramipril (altace), and trandolapril (mavik).

It can be dangerous to use Indocin if you suffer from or have a history of seizures, parkinson's disease, depression or mental illness, or liver or kidney disease.

Be careful with Indocin if you are planning to use indomethacin suppositories.

Be careful with Indocin if you had proctitis (inflammation of the rectum) or have recently had rectal bleeding, asthma, frequent stuffed or runny nose or nasal polyps (swelling of the lining of the nose).

Avoid alcohol.

Be careful with Indocin if you are going to have a surgery.

Avoid driving machine.

Do not stop take it suddenly.

indocin preterm labor dosage

All trials 1) using randomized or quasi-randomized patient allocation, 2) in preterm infants < 37 weeks gestational age or low-birth-weight infants (< 2500 grams) with symptomatic PDA in the neonatal period (< 28 days) and 3) comparing surgical ligation with medical treatment with cyclooxygenase inhibitors, each used as the initial treatment for closure of PDA.

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 Twelve phenolic metabolites including three phenolic acids, namely caffeic acid 1, rosmarinic acid 2 and methyl rosmarinate 3; four flavone glycosides viz the new compound luteolin 7-O-(4″,6″-di-O-α-L-rhamnopyranosyl)-β-D-glucopyranoside 4, apigenin 7-O-β-D-rutinoside 5, cosmosiin 6 and cinaroside 7, together with four flavones aglycone, luteolin 8, apigenin 9, pedalitin 10 and crisiliol 11 in addition to one coumarin, 6,7-dihydroxycoumarin 12 were isolated from the leaves of S. splendens Sellow ex Roem & Schult. The AME of S. splendens was non toxic to mice up to 5 g/kg b.wt. it exhibited a significant hypoglycemic activity at 250 and 500 mg/kg as compared with control pre-drug (zero time) for each group as well as the diabetic control. Moreover, AME exhibited a significant antiinflammatory activity only at 1000 mg/kg in comparison to indomethacin. Finally, AME exhibited a marked significant scavenging activity against DPPH; the maximum reactive reaction rate after 5 min was 62.9, 82.5, 83.7, 84.3 and 85.1% for the concentrations 10, 20, 30, 40 and 50 mg/ml, respectively in comparison to L-ascorbic acid (86.8%).

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A series of 5-Aryl-6-(4-methylsulfonyl)-3-(metylthio)-1,2,4-triazine derivatives were synthesized and their COX-1/COX-2 inhibitory activity as well as in vivo anti-inflammatory and analgesic effects were evaluated. All of compounds showed strong inhibition of COX-2 with IC50 values in the range of 0.1-0.2μM and in most cases had stronger anti-inflammatory and analgesic effects than indomethacin at doses 3 and 6mg/kg. Among them, 5-(4-chlorophenyl)-6-(4-(methylsulfonyl) phenyl)-3-(methylthio)-1,2,4-triazine (9c) was the most potent and selective COX-2 compound; its selectivity index of 395 was comparable to celecoxib (SI=405). Evaluation of anti-inflammatory and analgesic effects of 9c showed its higher potency than indomethacin and hence could be considered as a promising lead candidate for further drug development. Furthermore, the affinity data of these compounds were rationalized through enzyme docking simulation and 3D-QSAR study by k-Nearest Neighbour Molecular Field Analysis.

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The current study was planned to explore the therapeutic potency of M2000 (beta-D-mannuronic acid), a novel designed non-steroidal anti-inflammatory drug (NSAID) in adjuvant-induced arthritis model. Arthritis was induced in Lewis rats by a single intradermal injection (0.1 ml) of heat-killed Mycobacterium tuberculosis (0.3 mg) in Freund's incomplete adjuvant into the right footpad. Fourteen days after injection of adjuvant, the contralateral left footpad volume was measured. The animals with paw volumes 0.37 ml greater than normal paws were then randomized into treatment groups. Orally and intraperitoneally administrations of test drugs (M2000, 40/mg/kg/day and indomethacin, 2/mg/kg/day) were started on day 15 post-adjuvant injection and continued until final assessment on day 25. The left hind limb was removed for histological evaluation. The WEHI-164 cell line was used for assaying tolerability and matrix metalloproteinase type 2 (MMP-2) activity. MMP-2 activity was assessed using zymography. Pharmacotoxicology study was carried out on animal models based on the evaluation of serum and urine determinants, histology of kidney, gastrointestinal tolerability and body temperature. Results showed that the orally administration as well as intraperitoneally injection of M2000 to arthritic rats induced a significant reduction in paw oedema. Histopathological assessment showed a reduced inflammatory cells infiltrate in joints of treated rats, as well as the number of osteoclasts present in the subchondral bone, tissue oedema and bone erosion in the paws were markedly reduced following M2000 therapy. Cytotoxicity analysis of M2000 showed a much higher tolerability compared with other tested drugs (diclofenac, piroxicam and dexamethasone). The inhibitory effect of M2000 in MMP-2 activity was significantly greater than that of dexamethasone and of piroxicam at a concentration of 200 microg/ml. Moreover, the toxicological study revealed that M2000 had no influence on serum (blood urea nitrogen, creatinine, triglyceride and cholesterol) and urine (urea and urinary protein excretion) determinants, glomerular histology and body temperature in normothermic rats and had no ulcerogenic effects on rats' stomach. Our data show that M2000, as a novel NSAID, could be strongly suggested as the safest anti-inflammatory drug for long-term administration.

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There was a significant difference in favor of LADG for postoperative use of analgesics (P = 0.022). Unexpectedly, there was no significant difference in degree of pain in the immediate postoperative period, putatively due to the optimal use of analgesics. Of the secondary outcomes, residual pain at postoperative day 7 (P = 0.003) and days to first flatus (P = 0.001) were significantly better with LADG. Postoperative complications, number of days hospitalized, and number of days with fever were also better with LADG, but the differences were not significant. Blood data representing inflammation (WBC and CRP) showed marked differences, especially on postoperative day 7 (P = 0.0016 and P = 0.0061, respectively).

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In this study, goat fat (Capra hircus) and melon oil were extracted and used to formulate self-nanoemulsifying drug delivery systems (SNEDDS) based on either goat fat alone or its admixture with melon oil by employing escalating ratios of oil(s), surfactant blend (1 : 1 Tween 60 and Tween 80), and cosurfactant (Span 85), with or without carbosil, a glidant, for the delivery of indomethacin. The formulations were encapsulated in hard gelatin capsules and then assessed using isotropicity test, aqueous dilution stability and precipitation propensity, absolute drug content, emulsification time, in vitro drug release, and anti-inflammatory activity. The SNEDDS exhibited low precipitation propensity and excellent stability on copious dilution, as well as high drug release in vitro and in vivo. The inhibition produced by the SNEDDS was comparable to that of indomethacin injection (positive control) for much of the 5 h test period, indicating a high degree of bioavailability of the administered SNEDDS. The absolute drug contents and emulsification times fell within narrow limits. This study has shown that a 1 : 1 ratio of melon oil and goat fat could confer favourable properties with respect to drug release and anti-inflammatory activity on SNEDDS for the delivery of indomethacin, thus encouraging further development of the formulations.

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Neurogenic differentiation of bone marrow (BM) mesenchymal stem cells (MSCs) offers a new hope for patients with many neurological disorders. Several chemical inducers are employed to induce BMMSCs differentiation into nerve cells. In the present study, we compared different inducers [2-mercaptoethanol (BME), tretinoin (ATRA), dimethyl sulfoxide/butylated hydroxyanisole (DMSO/BHA), and indomethacin/3-isobutyl-1-methylxanthine (indomethacin/IBMX)] on the neurogenic differentiation of BMMSCs and aimed to identify a more efficient and safer method. The MSCs were first identified by their ability to adhere to plastic and by the expression of positive (CD44, CD90, and CD105) and negative (CD34) markers assessed by flow cytometry. The efficiency of the neurogenic differentiation was determined by assessing the mRNA and protein expression of nestin, microtubule-associated protein-2 (MAP2), neuron specific enolase (NSE), and glial fibrillary acidic protein (GFAP) by reverse transcription-polymerase chain reaction and western-blot, respectively. The effect of these inducers on cell viability was also evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. This comprehensive study shows that indomethacin/IBMX is better than BME, DMSO/BHA, and ATRA both in terms of efficiency and safety, while BME suppressed the growth and proliferation of MSCs.

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Nitric oxide (NO) and prostaglandins (PG) together play a role in regulating blood flow during exercise. NO also regulates mitochondrial oxygen consumption through competitive binding to cytochrome-c oxidase. Indomethacin uncouples and inhibits the electron transport chain in a concentration-dependent manner, and thus, inhibition of NO and PG synthesis may regulate both muscle oxygen delivery and utilization. The purpose of this study was to examine the independent and combined effects of NO and PG synthesis blockade (L-NMMA and indomethacin, respectively) on mitochondrial respiration in human muscle following knee extension exercise (KEE). Specifically, this study examined the physiological effect of NO, and the pharmacological effect of indomethacin, on muscle mitochondrial function. Consistent with their mechanism of action, we hypothesized that inhibition of nitric oxide synthase (NOS) and PG synthesis would have opposite effects on muscle mitochondrial respiration. Mitochondrial respiration was measured ex vivo by high-resolution respirometry in saponin-permeabilized fibers following 6 min KEE in control (CON; n = 8), arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA; n = 4) and Indo (n = 4) followed by combined inhibition of NOS and PG synthesis (L-NMMA + Indo, n = 8). ADP-stimulated state 3 respiration (OXPHOS) with substrates for complex I (glutamate, malate) was reduced 50% by Indo. State 3 O(2) flux with complex I and II substrates was reduced less with both Indo (20%) and L-NMMA + Indo (15%) compared with CON. The results indicate that indomethacin reduces state 3 mitochondrial respiration primarily at complex I of the respiratory chain, while blockade of NOS by L-NMMA counteracts the inhibition by Indo. This effect on muscle mitochondria, in concert with a reduction of blood flow accounts for in vivo changes in muscle O(2) consumption during combined blockade of NOS and PG synthesis.

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Heme oxygenase-1 can play a protective role against cellular stress. In colon cancer cells, these effects would be relevant to oncogenesis and resistance to chemotherapy. The aim of the study was to examine the effects of heme oxygenase-1 induction on cell survival in a human colon cancer cell line, Caco-2. Serum deprivation induced apoptosis, reduced Akt and p38 phosphorylation, and increased p21(Cip/WAF1) levels. Heme oxygenase-1 induction by treatment with cobalt protoporphyrin IX resulted in resistance to apoptosis, activation of Akt, reduction in p21(Cip/WAF1) levels and modification of bcl2/bax ratio towards survival. Indomethacin reduced apoptosis but in contrast to heme oxygenase-1, arrested cells in G0/G1. Apoptosis was also inhibited by the heme oxygenase metabolites bilirubin and biliverdin but the CO donor tricarbonyldichlororuthenium(II) dimer did not exert significant effects. Protection against apoptosis in cells treated with cobalt protoporphyrin IX was reverted by incubation with heme oxygenase-1 small interfering RNA. This study shows an antiapoptotic effect of heme oxygenase-1 in colon cancer cells which could be mediated by the formation of bilirubin and biliverdin. Our results support an antiapoptotic role for HO-1 in these cells and provide a mechanism by which overexpression of HO-1 may promote tumor resistance to stress in conditions of limited nutrient supply. We have extended these observations by demonstrating that these effects are independent of p38 but are mediated via Akt pathway.

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Primary care acute gout management is suboptimal. Education of general practitioners about acute gout management and cardiovascular risk is a priority.

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This single-centre double-blind randomized controlled trial was undertaken in patients who underwent primary total knee arthroplasty. All subjects received acetaminophen 1,000 mg and ketorolac 15 mg po preoperatively. Postoperatively, subjects received PCA morphine, acetaminophen 1,000 mg every six hours, and ketorolac 15 mg po every six hours. Subjects received either gabapentin 600 mg po preoperatively followed by 200 mg po every eight hours for two days or matching placebo. The primary outcome was cumulative morphine consumption at 72 hr following surgery. Secondary outcome measures included pain scores and patient satisfaction.

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Little information on the management and long-term follow-up of patients with biallelic mutations in the chloride channel gene CLCNKB is available.

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The amplitude of the contractions was not changed following indomethacin administration but was significantly increased 15 min after washout of the drug. Diazoxide pretreatment inhibited the stimulatory post-washout response of both strips. Glybenclamide pretreatment showed different results depending on the type of strip. In the transverse strips the drug showed no effect while in the longitudinal strips it decreased the post-washout response.

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The objective of this study was to determine whether the incidence of emergence agitation (EA) can be reduced by adding an additional, faster onset, non-IV analgesic, intranasal fentanyl or intramuscular (im) ketorolac to rectal acetaminophen.

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indocin and alcohol 2016-01-26

It is established that the molecular chaperone, chaperonin 60, from various bacteria and from Homo sapiens has cell-cell signalling activity and is able to induce proinflammatory cytokine synthesis. We previously reported that chaperonin 60 proteins from Gram-negative bacteria, but not mycobacteria, have the capacity to resorb cultured murine calvarial bone. We now report that lipopolysaccharide-low human recombinant chaperonin 60 (Hsp60) is a relatively weak cytokine-inducing Missed 2 Alesse Pills agonist but is a potent stimulator of murine calvarial bone resorption. The osteolytic activity of Hsp60 was significantly inhibited by indomethacin, interleukin-1 receptor antagonist, and osteoprotegerin, but 5-lipoxygenase inhibitors were less effective. Analysis of Hsp60 truncation mutants revealed that N-terminal mutants (Delta1-137, Delta1-358, and Delta1-465) retained bone resorbing activity. In contrast, a C-terminal truncation mutant (Delta1-26 + Delta466-573) was inactive. This suggests that the active domain in this protein is found within residues 466-573. It is now established that Hsp60 is present in the blood of the majority of the population with the normal range encompassing levels able to activate bone cells. The possibility exists that this protein could play a role in bone remodelling.

indocin gout dose 2015-05-18

There were 90 patients randomized: 46 patients to the indomethacin group and 44 patients to the prednisolone group. Baseline characteristics, including pain scores, were similar in the 2 groups. Both treatment groups had a similar decrease in pain score in the ED. The mean rate of decrease in pain score with activity for indomethacin was -1.7+/-1.6 (SD) mm per day and for prednisolone was -2.9+/-2.0 (SD) mm per day (mean difference 1.2 mm/day; 95% confidence interval 0.4 to 2.0 mm/day; P=.0026). Although these differences were statistically significant, at no time was the difference in mean pain score greater than 13 mm. Therefore, it is unclear whether these differences are clinically significant. The mean total dose Clomid Fertility Drug Cost of acetaminophen consumed by the prednisolone group was significantly more than in the indomethacin group (mean 10.3 g, range 1 to 21 g versus mean 6.4 g, range 1 to 21 g). Twenty-nine patients in the indomethacin group and 12 patients in the prednisolone group experienced adverse effects (P<.05). The commonest adverse effects in the indomethacin group were nausea, indigestion, epigastric pain, dizziness, and gastrointestinal bleeding (N=5; 11%). None of the patients in the prednisolone group developed gastrointestinal bleeding. The relapse rate for both groups was similar.

indocin preterm labor dosage 2015-05-20

Ibuprofen suppressed somatic growth in the sucking rats, but the effect was transient, resolving by P14. Indomethacin had an opposite, latent effect on body weight and liver to body weight ratios Levaquin 750 Mg Levofloxacin in weanling rats. Both indomethacin and ibuprofen had profound hormonal effects that differed in magnitude and timing. Indomethacin resulted in a sustained elevation in corticosterone levels at P21, while ibuprofen increased serum and hepatic GH levels. Both drugs suppressed GHBP in serum at P7 and P14; and liver at P4 and P7, but a rebound increase in serum GHBP was noted at P21 with Ibuprofen only. Both drugs increased serum IGF-I at P7. The effect remained sustained with indomethacin.

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Renal dysfunction and/or failure are common diagnoses, especially in extremely premature neonates and there are potentially Zoloft 150 Mg modifiable factors that increase the risk of renal problems.

indocin tab 25 mg 2016-08-11

First, the effects of DRSP on the activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT) and fibrinogen (FIB) were measured. Then, the effects of DRSP on platelet activation were investigated in response to low levels of Kapikachhu Capsules collagen, adenosine 5'-diphosphate (ADP), thrombin, U46619, adrenaline and botrocetin/von Willebrand factor (VWF).

indocin dose 2016-07-06

The cultured cells displayed adipocyte but not chondrogenic lineage under these conditions. Considering the possibility that some differentiation potential may be lost with in vitro culture but maintained using another chondrogenic differentiation medium Accutane Off Brand containing TGF-beta1, it is possible that cultured cells may have multilineage potential, including chondrogenic differentiation ability.

indocin in pregnancy dose 2016-07-11

Both increased glutathione content and GST Neem Pills activity are significant in the cisplatin resistance of human bladder tumour cells. Because BSO, ethacrynic acid and indomethacin caused a partial recovery of resistance in the cisplatin-resistant cell line, further studies are needed to investigate their efficacy for treating patients with metastatic bladder carcinoma resistant to cisplatin.

indocin 50 mg cost 2017-08-02

Tumor necrosis factor (TNF)-alpha is a potent inflammatory cytokine implicated in the exacerbation of asthma. Chronic exposure to TNF-alpha has been reported to induce G protein-coupled receptor desensitization, but adenylyl cyclase sensitization, in airway smooth muscle cells by an unknown mechanism. Cyclic AMP, which is synthesized by adenylyl cyclases in response to G protein-coupled receptor signals, is an important second messenger involved in the regulation of the airway muscle proliferation, migration, and tone. In other cell types, TNF-alpha receptors transactivate the EGF receptor, which activates raf-1 kinase. Further studies in transfected cells show that raf-1 kinase can phosphorylate and activate some isoforms of Moduretic Buy adenylyl cyclase. Cultured human airway smooth muscle cells were treated with TNF-alpha in the presence or absence of inhibitors of prostaglandin signaling, protein kinases, or G(i) proteins. TNF-alpha caused a significant dose- (1-10 ng/ml) and time-dependent (24 and 48 h) increase in forskolin-stimulated adenylyl cyclase activity, which was abrogated by pretreatment with GW5074 (a raf-1 kinase inhibitor), was partially inhibited by an EGF receptor inhibitor, but was unaffected by pertussis toxin. TNF-alpha also increased phosphorylation of Ser(338) on raf-1 kinase, indicative of activation. IL-1beta and EGF sensitization of adenylyl cyclase activity was also sensitive to raf-1 kinase inhibition by GW5074. Taken together, these studies link two signaling pathways not previously characterized in human airway smooth muscle cells: TNF-alpha transactivation of the EGF receptor, with subsequent raf-1 kinase-mediated activation of adenylyl cyclase.

indocin 25mg suspension 2017-02-09

The primary objective of this review is to verify if there are differences in the diagnostic and therapeutic strategies in cases of PDA employed in different NICUs that might help explain the different percentages of duct closure, surgical ligation and outcome in these vulnerable patients. The secondary objective is to document if the selection of a specific NSAID and/or the way of administration are based on factors such as costs and local availability of drugs, as well as influenced by clinical and haemodynamic parameters, potential risks, local experience and the existing literature. Data Sources were MEDLINE, EMBASE, Cochrane Library and analysis of the most important papers were performed. We examined a total of 89 trials including 15, Buy Clomid Online Safely Uk 657 neonates (with gestational ages between 22 and 35 weeks and study weights between 380 and 2500 g), due to the lack of homogeneity of case studies it was not possible to standardize for gestational age and weight. To simplify, the studies we considered were subdivided into 5 groups corresponding to 5 tables: 1- INDO-prophylaxis (15 trials); 2- IBU-prophylaxis (11 trials); 3- INDO-therapy (18 trials); 4- IBU-therapy (16 trials); 5- IBU vs INDO therapy (29 trials). Each table reports the journal, the reference, the type of study, the number of neonates enrolled, the drugs used, management after failure of the first cycle, percentage of duct closure and adverse effects. Treatment with indomethacin is prescribed prevalently in the United States and Canada. According to the data collected, prolonged treatment and administration of high doses would appear to be more effective. The early administration of indometacin has been associated with gastrointestinal bleeding, renal insufficiency, altered cerebral self-regulation and, especially when administered together with postnatal steroids, it has been correlated with isolated intestinal perforation. Ibuprofen treatment is preferred in Europe but it may be associated with nephrotoxicity and an increase in BDP and ROP, although less frequently compared to indometacin. Indometacin is associated with major nephrotoxicity, as well as with a higher incidence of NEC, intestinal perforations and a reduced cerebral blood flow. Despite this, the administration of ibuprofen does not appear to be without short- and long-term renal adverse effects.

indocin renal dosing 2016-03-11

Indomethacin is commonly used for Moduretic Tablets Dose the treatment of patent ductus arteriosus (PDA) but has renal failure as a main side-effect. Ibuprofen seems to be efficient in closing the ductus with less side-effects, but few studies are available in literature as regards its use in preterm infants. This study is a retrospective analysis of clinical data in order to compare the efficacy and the renal tolerability of ibuprofen and indomethacin administered to preterm infants with gestational age (GA) < or = 30 weeks for the treatment of PDA. From our data, ibuprofen results pharmacologically as efficient as indomethacin and could be an alternative in prematures. About renal tolerability, our data confirm that non-steroidal anti-inflammatory drugs treatment could affect at least transiently renal function. Moreover, indomethacin could be more nephrotoxic compared with ibuprofen, as creatinine concentrations normalize more slowly in this group, although the mean difference between the two drugs was not significant as our population sample was small. Further studies are needed to assess whether ibuprofen is really less nephrotoxic than indomethacin, in particular by examining carefully the correlation between GA and ibuprofen administration.