Diclofenac

Diclofenac · Diciofenac · DICLOFENAC FREE ACID · dichlofenac · Pennsaid · Dichlofenac acid · Diclofenac (Aceclofenac EP Impurity A) · [2-(2,6-Dichloroanilino)phenyl]-acetic acid

https://huagongshe.com/de/chemical/3033

Identifikatoren & physikalische Daten

CAS No.	15307-86-5
Summenformel	C14H11Cl2NO2
Durchschnittliche Molmasse	296,1 g/mol
Monoisotopische Masse	295,01668395 g/mol
SMILES	O=C(O)Cc1ccccc1Nc1c(Cl)cccc1Cl
InChIKey	DCOPUUMXTXDBNB-UHFFFAOYSA-N
PubChem CID	3033
ChEMBL	CHEMBL139
ChEBI	CHEBI:47381
EC No.	239-348-5
DTXSID	DTXSID6022923
Lokaler Name	Diclofenac

Chemische & physikalische Eigenschaften

XLogP	4,4
Polarare Oberfläche (TPSA)	49,3
H-Brücken-Donoren	2
H-Brücken-Akzeptoren	3
Frei drehbare Bindungen	4
Schwere Atome	19
Formalladung	0
Komplexität	304
Arzneimittel	Pharmaceuticals -> NSAIDsPharmaceuticals -> Used in SwitzerlandPharmaceuticals -> Listed in ZINC15
LogP (Verteilungskoeffizient)	log Kow = 4.513.9
Color/Form	Crystals from ether-petroleum ether
Löslichkeit	In water, 2.37 mg/L at 25 °C4.47e-03 g/Lsoluble in Methanol1.278mg/L(30 ºC)
Human Drugs	Breast FeedingLactationMilk, HumanAnalgesic AgentsAnti-inflammatory Agents, NonsteroidalFDA approved drugs -> Active ingredientPharmaceuticals
Schmelzpunkt	283-285 °C156-158 °C283 - 285 °C156-158°
Physical Description	Solid
Ionization Efficiency	Positive1.782.7Agilent XCTElectrospray ionizationformic acid (5.3nM)
Dissociation Constants	3.994.24.34.15pKa = 4.15
Collision Cross Section	166.4 Å² [M+Na]+ [CCS Type: DTBuffer gas: N2Ionization: ESI+Dataset: TOXCASTSource Identifier: DTXSID6022923]157.7 Å² [M+H]+ [CCS Type: TWMethod: Major Mix IMS/Tof Calibration Kit (Waters)]157.2 Å² [M+H]+ [CCS Type: TW]155.98 Å² [M+H]+ [CCS Type: TWMethod: calibrated with polyalanine and drug standards]163.79 Å² [M+Na]+
Other Experimental Properties	MW 334.24 /Diclofenac potassium salt/Crystals from watermp 283-285 °C. UV max (methanol) 283 nm (epsilon 1.01X10+5)(phosphate buffer, pH 7.2) 276 nm (epsilon 1.01X10+5). Solubility at 25 °C (mg/mL): deionized water (pH 5.2) >0methanol >24acetone 6acetonitrile <1cyclohexane <1HCl (pH 1.1) <1phosphate buffer (pH 7.2) 6. pKa 4. Partition coefficient (N-octanol/aqueous buffer): 13.4 /Diclofenac sodium salt/MW: 411.3MF: C20H24Cl2N2O3. log Kow = 8 at pH 8.5 /Diclofenac epolamine/
Siedepunkt	412.0±45.0 °C(Predicted)
Dichte	1.431±0.06 g/cm3(Predicted)
Lagerbedingungen	Sealed in dry,Room Temperature
Aggregatzustand	powder to crystal
pKa (Säurekonstante)	pKa 4 (Uncertain)
Farbe	White to Almost white
Merck	14,3081
InChI	InChI=1S/C14H11Cl2NO2/c15-10-5-3-6-11(16)14(10)17-12-7-2-1-4-9(12)8-13(18)19/h1-7,17H,8H2,(H,18,19)
InChIKey	DCOPUUMXTXDBNB-UHFFFAOYSA-N
SMILES	C1(CC(O)=O)=CC=CC=C1NC1=C(Cl)C=CC=C1Cl
CAS Datenbank	15307-86-5(CAS DataBase Reference)
NIST chemische Informationen	Benzeneacetic acid, 2-[(2,6-dichlorophenyl)amino]-(15307-86-5)
EPA chemische Informationen	Benzeneacetic acid, 2-[(2,6-dichlorophenyl)amino]- (15307-86-5)

Sicherheit & Vorschriften

GHS-Einstufung	This chemical does not meet GHS hazard criteria for 29.2% (52 of 178) of reports.DangerH301 (30.3%): Toxic if swallowed [Danger Acute toxicity, oral]P203, P260, P264, P270, P273, P280, P301+P316, P301+P317, P318, P319, P321, P330, P391, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 178 reports by companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Regulatorische Informationen	Status: Active Update: 17-05-2018 https://echa.europa.eu/registration-dossier/-/registered-dossier/13096
Weitere Sicherheitsinformationen	IMAP assessments - Benzeneacetic acid, 2-[(2,6-dichlorophenyl)amino]-: Human health tier I assessment
FDA-Anforderungen	Indications for use in horses: For the control of pain and inflammation associated with osteoarthritis in tarsal, carpal, metacarpophalangeal, metatarsophalangeal, and proximal interphalangeal (hock, knee, fetlock and pastern) joints. ... Limitations: Do not use in horses intended for human consumption. Federal law restricts this drug to use by or on the order of a licensed veterinarian.The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including diclofenac sodium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Diclofenac sodium/The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including diclofenac potassium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Diclofenac potassium/The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including diclofenac epolamine, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Diclofenac epolamine/The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Diclofenac sodium is included on this list. /Diclofenac sodium/
Hazard Classes and Categories	Acute Tox. 3 (30.3%)
Lagerbedingungen	Diclofenac sodium 1% gel and diclofenac epolamine transdermal system should be stored at 25 °C but may be exposed to temperatures ranging from 15-30 °C. Diclofenac gel should not be frozen.Diclofenac sodium delayed-release (enteric-coated) tablets, diclofenac sodium extended-release tablets, and diclofenac potassium tablets should be protected from moisture and stored in tight containers at a temperature not exceeding 30 °C. Commercially available diclofenac sodium and misoprostol tablets should be stored in a dry area at a temperature not exceeding 25 °C.
Entsorgungsverfahren	SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.
Wechselwirkungen	Concomitant use of aspirin and a nonsteroidal anti-inflammatory agent (NSAIA) increases the risk for serious GI events. Because of the potential for increased adverse effects, patients receiving diclofenac should be advised not to take aspirin. There is no consistent evidence that use of low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs.Concurrent use /of alcohol or glucocorticoid corticosteroids or chronic therapeutic use of corticotropin or potassium supplements/ with an nonsteroidal anti-inflammatory drug may increase the risk of gastrointestinal side effects, including ulceration or hemorrhagehowever, concurrent use with a glucocorticoid or corticotropin in the treatment of arthritis may provide additional therapeutic benefit and permit reduction of glucocorticoid or corticotropin dosage. /Nonsteroidal anti-inflammatory drugs/Nonsteroidal anti-inflammatory drugs may increase the hypoglycemic effect of these medications /oral antidiabetic agents or insulin/ because prostaglandins are directly involved in regulatory mechanisms of glucose metabolism and possibly because of displacement of the oral antidiabetics from serum proteinsdosage adjustments of the antidiabetic agent may be necessary... caution with concurrent use is recommended. /Nonsteroidal anti-inflammatory drugs/These medications /cefamandole or cefoperazone or cefotetan or plicamycin or valproic acid/ may cause hypoprothrombinemiain addition, plicamycin or valproic acid may inhibit platelet aggregationconcurrent use with an nonsteroidal anti-inflammatory drug may increase the risk of bleeding because of additive interferences with platelet function and/or the potential occurrence of nonsteroidal anti-inflammatory drug-induced gastrointestinal ulceration or hemorrhage. /Nonsteroidal anti-inflammatory drugs/For more Interactions (Complete) data for DICLOFENAC (16 total), please visit the HSDB record page.
Hepatotoxicity	Elevated serum aminotransferase levels have been reported in up to 15% of patients taking oral diclofenac chronically, but are greater than 3 times the upper limit of normal in only 2% to 4% (Cases 1 and 2). Clinically apparent and symptomatic liver disease with jaundice due to diclofenac is rare (1 to 5 cases per 100,000 prescriptions, occurring in 1 to 5 persons per 10,000 exposed). Nevertheless, more than a hundred instances of clinically apparent liver injury due to diclofenac have been reported in the literature and, in most case series, diclofenac ranks in the top 10 causes of drug induced liver injury. The time to onset of liver injury varies from within a week to over a year after starting. The majority of cases present within 2 to 6 months (Cases 3 and 4), and the more severe cases tend to present earlier. The pattern of injury is almost exclusively hepatocellular, although cases presenting with mixed patterns have been reported. The clinical picture is that of jaundice preceded by anorexia, nausea, vomiting and malaise. Fever and rash occur in 25% of cases and some cases have immunoallergic features, while others resemble chronic hepatitis and have autoimmune features. In most cases, liver histology reveals an acute lobular hepatitis. However, a cases with prolonged latency diclofenac hepatotoxicity can have clinical and histologic features of chronic hepatitis (Case 2). There seems to be greater susceptibility for diclofenac liver injury among women than men. The injury can be severe, and several cases of acute liver failure have been attributed to diclofenac.
Umweltverhalten	TERRESTRIAL FATE: Based on a classification scheme(1), a Koc value of 245(SRC), from a log Koc of 2.39(2), indicates that diclofenac is expected to have moderate mobility in soil(SRC). The pKa of diclofenac is 4.15(3), indicating that this compound will exist almost entirely in the dissociated form in the environment and anions generally do not adsorb more strongly to organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as an anion and anions do not volatilize. Diclofenac is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.1X10-8 mm Hg(SRC), determined from a fragment constant method(5). Little or no biodegradation using a freshwater inoculum(6) suggests that biodegradation is not an important environmental fate process in soil(SRC).AQUATIC FATE: Based on a classification scheme(1), a Koc value of 245(SRC), from a log Koc of 2.39(2), indicates that diclofenac is expected to adsorb to suspended solids and sediment(SRC). The pKa is 4.15(3), indicating that diclofenac will exist almost entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process. According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of 4.51(5) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Little or no biodegradation using a freshwater inoculum(7) suggests that biodegradation is not an important environmental fate process in water. Direct photolysis is the predominant removal process in freshwater, exhibiting a half-life of 8 days(8).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), diclofenac, which has an estimated vapor pressure of 6.1X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase diclofenac is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC)the half-life for this reaction in air is estimated to be 0.8 hours(SRC), calculated from its rate constant of 1.6X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase Diclofenac may be removed from the air by wet or dry deposition(SRC).
Unerwünschte Wirkungen	Diclofenac has many similar adverse effects shared with the NSAID family of drugs due to the inhibition of COX enzymes. Because diclofenac appears to act more selectively on COX-2 inhibition, it has an increased associated risk of cardiovascular events and less risk for gastrointestinal events, but this article will also examine the gastrointestinal risk for completeness. The following side effects involve systemic effects that arise from systemic exposure to diclofenac. These are less likely to be involved in the topical application of the medication, as there is less risk of systemic exposure to the drug.
Expositionspfade	Completely absorbed from the gastrointestinal tract.
Milk Concentrations	Diclofenac is distributed into breast milk. In one study, long-term use of 150 mg per day produced concentrations of 100 ng/g in the breast milk. An infant of 4 to 5 kg consuming one liter per day would therefore ingest approximately 0.03 mg/kg/day.
Toxizitätsübersicht	Diclofenac’s potential for toxicity is associated with polymorphisms of the cytochrome P450 gene family, which affects the patient’s potential for drug metabolism. OTC NSAID toxicity is not uncommon but is generally limited to mild symptoms with a low risk of serious effects. These effects are usually limited to GI upset, nausea, and dizziness. Severe overdose may lead to more serious symptoms involving seizure, coma, cardiovascular events, and metabolic acidosis.The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (COX-1 and COX-2), leading to the peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, inhibition of their synthesis is responsible for the analgesic effects of diclofenac. Antipyretic effects may be due to action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat dissipation.
Ökotoxizitätsauszüge	/BIRDS and MAMMALS/ The nonsteroidal anti-inflammatory drug diclofenac is extremely toxic to Old World Gyps vultures (median lethal dose ~0.1-0.2 mg/kg), evoking visceral gout, renal necrosis, and mortality within a few days of exposure. Unintentional secondary poisoning of vultures that fed upon carcasses of diclofenac-treated livestock decimated populations in the Indian subcontinent. Because of the widespread use of diclofenac and other cyclooxygenase-2 inhibiting drugs, a toxicological study was undertaken in turkey vultures (Cathartes aura) as an initial step in examining sensitivity of New World scavenging birds. Two trials were conducted entailing oral gavage of diclofenac at doses ranging from 0.08 to 25 mg/kg body weight. Birds were observed for 7 days, blood samples were collected for plasma chemistry (predose and 12, 24, and 48 hr and 7 days postdose), and select individuals were necropsied. Diclofenac failed to evoke overt signs of toxicity, visceral gout, renal necrosis, or elevate plasma uric acid at concentrations greater than 100 times the estimated median lethal dose reported for Gyps vultures. For turkey vultures receiving 8 or 25 mg/kg, the plasma half-life of diclofenac was estimated to be 6 hr, and it was apparently cleared after several days as no residues were detectable in liver or kidney at necropsy. Differential sensitivity among avian species is a hallmark of cyclooxygenase-2 inhibitors, and despite the tolerance of turkey vultures to diclofenac, additional studies in related scavenging species seem warranted./AQUATIC SPECIES/ One of the most frequently detected pharmaceuticals in environmental water samples is the anti-rheumatic drug, diclofenac. Despite its increasing environmental significance, investigations concerning the effects of this drug on the early developmental stages of aquatic species are lacking up to now. To determine the developmental toxicity and proteotoxicity of this drug on the growing fish embryos, eggs of zebrafish were exposed to six concentrations of diclofenac (0, 1, 20, 100, 500, 1000, and 2000 microgl(-1)) using DMSO as solvent. Early life stage parameters such as egg and embryo mortality, gastrulation, somite formation, movement and tail detachment, pigmentation, heart beat, and hatching success were noted and described within 48- and 96-h of exposure. After the 96-h exposure, the levels of stress proteins (hsp 70) were determined in both the diclofenac-treated and respective DMSO controls. Results showed no significant inhibition in the normal development until the end of 96 h for all exposure groups. However, there was a delay in the hatching time among embryos exposed to 1000 and 2000 microgl(-1). Late-hatched embryos (108 h) did not differ morphologically from normally hatched embryos. The mortality and average heart rate data did not show significant differences for all embryos in both diclofenac-treated and DMSO control groups. No significant malformations were likewise noted among all developing embryos throughout the exposure period. The levels of heat shock proteins in diclofenac-treated and control embryos did not differ significantly. DMSO control embryos, on the other hand, showed a concentration-dependent increase in hsp 70 levels. We suggest possible modulating effect of diclofenac in DMSO-triggered expression of stress proteins and this might have a possible repercussion on the use of DMSO as solvent in any toxicity assay. Since the present data indicate no significant embryotoxicity and proteotoxicity induced by diclofenac and due to the fact that the concentrations of diclofenac used in the present study is up to 2000-fold higher than the concentrations detected in the environment, it is unlikely that this drug would pose a hazard to early-life stages of zebrafish./AQUATIC SPECIES/ In the present study, cytopathology was investigated in the liver, kidney, gills and gut of rainbow trout (Oncorhynchus mykiss) exposed to five different concentrations (1, 5, 20, 100 and 500 ug/L) of the anti-inflammatory drug diclofenac under laboratory conditions. The lowest observed effect concentration (LOEC) for cytological alterations in liver, kidney and gills was 1 ug/L. In the gut, however, no diclofenac-induced cytopathology occurred. As the most prominent reactions induced by diclofenac (1) in the kidney, a severe accumulation of protein in the tubular cells (so called hyaline droplet degeneration), macrophage infiltration and structural alterations (dilation, vesiculation) of the endoplasmic reticulum (ER) in the proximal and distal renal tubules were observed. Furthermore, shortening of podocytes and their retraction from the basal lamina, a thickening of the basal lamina, the formation of desmosomes, and necrosis of endothelial cells in the renal corpuscles occurred(2) in the liver, the most striking reactions were the collapse of the cellular compartmentation as well as the glycogen depletion of hepatocytes(3) in the gills, pillar cell necrosis, hypertrophy of chloride cells, and epithelium lifting became evident in the secondary lamellae./AQUATIC SPECIES/ ...The impact of diclofenac on river biofilm communities was investigated at exposures of 10 and 100 ug/L of diclofenac or its molar equivalent in carbon and nutrients. Experiments were carried out with river water during spring and summer using rotating annular reactors as model systems. Diclofenac or nutrients at 10 ug/L were observed to have no significant effect on algal, bacterial, and cyanobacterial biomass in spring, whereas in the summer the nutrient equivalent reduced algal biomass and diclofenac reduced cyanobacterial biomass relative to control biofilms (p<0.05). In contrast, at 100 ug/L diclofenac or nutrients, the result was increased cyanobacterial and bacterial biomass, respectively, relative to control biofilms in spring. In summer, 100 ug/L diclofenac significantly increased bacterial biomass and the nutrient treatment had no significant effect (p<0.05)both treatments resulted in increased biofilm thickness. The glycoconjugate composition of the exopolysaccharide matrix was influenced differentially by the treatments in both seasons. Biolog assessments of carbon use indicated that 100 ug/L diclofenac or nutrients resulted in significant depressions in the use of carbon sources in summer and significant increases in spring. Impacts on protozoan and micrometazoan populations also were assessed. Denaturing gradient gel electrophoresis analyses of community DNA and fluorescent in situ hybridization studies indicated that diclofenac had significant effects on the nature of the bacterial community in comparison with control and nutrient-treated river biofilm communities.For more Ecotoxicity Excerpts (Complete) data for DICLOFENAC (7 total), please visit the HSDB record page.
Signs and Symptoms	Symptoms of overdose include loss of consciousness, increased intracranial pressure, and aspiration pneumonitis.
Effluent Concentrations	Samples of effluent from 18 sewage treatment plants in 14 municipalities in Canada were analyzed for the presence of neutral and acidic drugs over the period from September 1998 to February 1999(1). The median diclofenac influent concentration was 1.3 ug/Lthe compound was not detected in any of the effluent samples, detection limit of 0.25 ug/L(1). Diclofenac was detected in effluents of three wastewater treatment plant samples collected in the region of Lake Greifensee, Switzerland between August 16, 1999 and October 22, 1999 at a maximum concentration of 0.99 ug/L(2). The compound was detected in 49 of 49 treatment plant effluents in Germany at a median concentration of 0.81 ug/L, detection limit = 0.05 ug/L(3). The compound was detected in wastewater treatment plant effluents in France, Greece, and Switzerland at a range of 0.25-5.45 ug/L, median of 0.47 ug/Lsampling conducted from February to March 2001(4). Diclofenac removal efficiencies from wastewater treatment plants ranges from 0 to 80% but fall mainly in the range of 21-40%. Average diclofenac concentrations in wastewater treatment plant effluents worldwide were as follows (ng/L): Austria, 1750Denmark 950Finland, 1000France, 750Germany, 3250Greece, 750Italy, 700Spain, 600Sweden, 800Switzerland, 100UK, not reportedCanada, 1400USA, 200Brazil, not reported, Japan, 50, Korea, 400(5). The estimated total discharge in 2002 from riverine, sewage treatment plants, and industrial sources in the Netherlands was 4.075 tons/year(6). Influent and effluent concentrations ranged from 112-438 ng/L (mean 286 ng/L) and 35.3 to 463 ng/L (mean 185 ng/L), respectively, in samples from 2 sewage treatment plants in Beijing, China, sampled monthly from February 2009-January 2010(7).
Soil Adsorption/Mobility	Using an agricultural soil from Corrstown, County Dublin, Ireland a log Koc of 2.39 was measured(1), corresponding to a Koc of 245(SRC). According to a classification scheme(2), this estimated Koc value suggests that diclofenac is expected to have moderate mobility in soil. The pKa of diclofenac is 4.15(3), indicating that this compound will exist almost entirely in the dissociated form in the environment and anions generally do not adsorb more strongly to organic carbon and clay than their neutral counterparts(4). Adsorption to sediments from Lake Greifensee, Switzerland was found to be negligible(5). When 500 ng/L diclofenac was mixed with one liter of lake water and 1 g sediment/L water, the aqueous phase showed no decrease in concentration following centrifugation and removal of sediment particles(5).
Human Toxicity Excerpts	/CASE REPORTS/ No signs or symptoms of toxicity were observed in a few patients who ingested 3.75-4 g of diclofenac. However, vomiting and drowsiness occurred in an adolescent who ingested 2.37 g of the drug./CASE REPORTS/ Acute diclofenac overdosage produces manifestations that are mainly extension of adverse effects of the drug. Loss of consciousness, increased intracranial pressure, and aspiration pneumonitis were reported in a 17 year old male who died 2 days after ingestion 5 g of diclofenac./CASE REPORTS/ A case of hypoxic brain damage that occurred after intramuscular injection of diclofenac due to a severe anaphylactic reaction /is presented/. A 38-year-old nurse treated herself for acute lower back pain with 100 mg diclofenac intramuscularly. Five minutes later, she collapsed and developed coma and respiratory arrest. After cardiopulmonary resuscitation she was transferred to hospital. On admission she was comatose and received controlled ventilation of the lungs. Magnetic resonance imaging and computerized tomography showed signs of hypoxic brain injury and the patient died from central cardiopulmonary failure 7 days later. Intramuscular treatment with non-steroidal anti-inflammatory drugs such as diclofenac has rare but potentially severe side-effects./CASE REPORTS/ Upper gastrointestinal tract complications due to non-steroidal anti-inflammatory drugs are well recognised. However, adverse effects on large intestinal mucosa are less common and less well recognised, even though they carry a significant morbidity and mortality. Here we report a case of colonic perforation in a healthy woman without any underlying colonic pathology associated with ingestion of slow release diclofenac sodium. /Diclofenac sodium/For more Human Toxicity Excerpts (Complete) data for DICLOFENAC (13 total), please visit the HSDB record page.
Wassergefährdungsklasse (WGK)	WGK 3
UN-Transportnummer	3249
Zollcode	2922.49.2600
RTECS-Nr.	AG6310000
Gefahrenklasse	6.1(b)Acute Tox. 3 OralAquatic Chronic 2Repr. 2STOT RE 1 Oral
Verpackungsgruppe	III
Lagerklasse	6.1C - Combustible acute toxic Cat.3toxic compounds or compounds which causing chronic effects
Gefahrstoffdaten	15307-86-5(Hazardous Substances Data)

Anwendungen & Verwendung

Verwenden

prostaglandin synthetic inhibitor