EDITORIAL ESPANOL:

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PAÍSES QUE RECIBEN EL DERMAGIC/EXPRESS: Venezuela, Brasil, Chile, Colombia, Argentina, Paraguay, Perú, Panamá, Estados Unidos de América, España, Italia, Portugal, Turquía, Holanda, Marruecos, Egipto, Israel, India, Bélgica, Dinamarca, Nueva Zelanda, Baharian, Inglaterra, Kuwait, México, Grecia y Alemania.

Saludos,,,          

Dr. José Lapenta R.

 EDITORIAL ENGLISH:

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COUNTRIES THAT DERMAGIC/EXPRESS RECEIVES: Venezuela, Brasil, Chile, Colombia, Argentina, Paraguay, Perú, Panamá, United States of América, Spain, Italy, Portugal, Turkey, Holland, Morocco, Egypt, Israel, The India, Belgium, Danmark, New Zealand, Baharian, England, Kuwait, México, Greece, and Germany.

Greetings,,, 

Dr. José Lapenta R. 

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DERMAGIC/EXPRESS(27)

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NIMESULIDE EFECTOS ADVERSOS II / NIMESULIDE ADVERSE EFFECTS II          

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REFERENCIAS BIBLIOGRAFICAS / BIBLIOGRAPHICAL REFERENCES

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1.) Hepatitis.

2.) Increased hepatic enzyme levels.

3.) Hepatocellular necrosis.

4.) Cholestasis.

5.) Fatal liver damage./ Fulminant hepatic failure.

6.) Gastrointestinal tract ulcers. /Bleeding gastric ulcers.

7.) Hepatic insufficiency.

8.) Renal failure./ Renal impairment.

9.) Urticaria.

10.) Jaundice.

11.) Neonatal chronic kidney failure./Neonatal end-stage renal failure./ Perinatal vasoconstrictive renal insufficiency.

12.) Purpura.

13.) Synergistic effect with use of cetirizine with nimesulide.

14.) Fixed drug eruptions.

15.) Toxic hepatitis in pregnancy.

16.) Hypothermia.

17.) [Toxic hepatitis caused by nimesulide, presentation of a new case and review of the literature].

18.) [Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case].

19.) Nimesulide-induced acute hepatitis: evidence from six cases.

20.) Nimesulide-induced purpura.

21.) Modification of antihistaminic activity of cetirizine by nimesulide.

22.) Perinatal vasoconstrictive renal insufficiency associated with maternal nimesulide use.

23.) Acute renal failure induced by nimesulide in a patient suffering from temporal arteritis.

24.) Drug-induced cholestasis.

25.) Adverse drug reactions postal survey-bronchial asthma and angioedema with nimesulide.

26.) Hypothermia with nimesulide.

27.) [Nimesulide-induced acute hepatitis].

28.) [Nimesulide toxic hepatitis in pregnancy]. 2

29.) Positive lesional patch tests in fixed drug eruptions from nimesulide.

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1.) Nimesulide

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SOURCE: THE WHO. /Organizacion Mundial de la SALUD WHO PHARMACEUTICALS NEWSLETTER

Nimesulide

A total of 17 of the reports on adverse effects on the liver were linked with the use of nimesulide. Eight of these cases involved hepatitis and 9 increased hepatic enzyme levels. The majority of patients (14) were women. The average age was 61 years (ranging between 23 and 88 years), and 9 of the patients were over 60 years of age. The symptoms or findings of liver effects usually appeared after 1-6 weeks of treatment. In 11 patients the laboratory values had returned to normal at the follow-up after nimesulide was stopped. Six patients had still not recovered 2-8 weeks after withdrawal of medication, when the report on the adverse effect was made. Five patients were using concomitant drugs which have been reported to have hepatic reactions. According to published case reports, nimesulide can cause both hepatocellular necrosis and pure cholestasis. Individual cases of fatal liver damage have also been reported.

Nimesulide is a relatively new drug, introduced on the Finnish market in January 1998. However, it is widely used and the number of daily doses (0.2 g) by September 2000 totalled over 14 million. One reason for the popularity of nimesulide is probably its selectivity – which, as a COX-2 inhibitor, is claimed to be higher than that of older anti-inflammatory analgesics – and the fewer cases of gastrointestinal tract ulcers it causes.

Due to its adverse effects on the liver, the product information on nimesulide was updated at the beginning of 2000. Hepatic insufficiency was added to the contraindications and additional text was included in the section on warnings according to which patients with abnormal values in their liver function tests and/or patients with symptoms indicative of liver damage (anorexia, nausea, vomiting, jaundice) during nimesulide therapy must be closely monitored and medication stopped. These patients should not be re-exposed to nimesulide. Increased hepatic enzyme values were included in the section on rare adverse effects in the SPC, and cholestasis and rapidly developing hepatitis were included in the list of very rare adverse effects.

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2.) COX 2 inhibitor and fulminant hepatic failure.

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McCormick PA, Kennedy F, Curry M, Traynor O. Lancet. 1999 Jan 2;353(9146):40-1.

This article reports on the case of a patient who developed fulminant hepatic failure from treatment with the selective COX2 inhibitor Nimesulide.

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3.) CASE REPORT Fatal hepatitis and renal failure during treatment with nimesulide

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A. Schattner1, 3, N. Sokolovskaya2 & J. Cohen2, 3

Schattner A, Sokolovskaya N, Cohen J (Kaplan Medical Center, Rehovot, and the Hebrew University-Hadassah School of Medicine, Jerusalem, Israel). Fatal hepatitis and renal failure during treatment with nimesulide (Case Report). J Intern Med 2000; 247: 153–155.

A healthy 70-year-old woman who took nimesulide for 5 days, presented 2 weeks later with jaundice for which no other cause was found. Laboratory evidence of coagulopathy, hypoalbuminaemia and hypoglycaemia were present on admission, and liver biopsy showed massive necrosis of hepatocytes and severe inflammatory infiltrate. Despite supportive and corticosteroid treatment, her jaundice deepened and progressive acute renal failure developed, characterized by a ‘prerenal’ profile changing into irreversible acute tubular necrosis pattern, coma, occult Gram-negative sepsis and death. Although rare, nimesulide-associated hepatotoxicity and nephrotoxicity may occur and should be recognized as early as possible, to ensure immediate drug withdrawal and treatment.

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4.) Nimesulide and renal impairment.

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Eur J Clin Pharmacol 1999 Apr;55(2):151-4 Related Articles, Books, LinkOut

Leone R, Conforti A, Ghiotto E, Moretti U, Valvo E, Velo GP.

Clinical Pharmacology Unit, Institute of Pharmacology, Policlinico B.go Roma, University of Verona, Italy. leone@farma.univr.it

OBJECTIVES: To analyse from spontaneous reporting data the renal adverse reactions associated with the use of nimesulide. METHODS: Case reports were obtained from a Northern Italian Regional database (Veneto Pharmacovigilance System), containing all the spontaneous reports filed between 1988 and 1997. The Veneto Region is the principal contributor to the Italian spontaneous reporting system, with an annual report rate of approximately 17 per 100,000 inhabitants. The clinical records of hospitalized patients were also analysed. RESULTS: Of the 120 reports associated with oral nimesulide, 11 referred to suspected renal adverse reactions. The drug was taken by ten patients for a short period. All the patients discontinued the therapy and hospitalization was required in six cases. Other risk factors were identified in six cases. DISCUSSION: Together with the new insights into the possible consequences of renal cyclooxygenase-2 (COX-2) inhibition, the reported cases should draw the attention of doctors and patients to the importance of recognizing any possible signs of renal impairment during nimesulide therapy, although only extensive epidemiological data can define the real impact of its renal toxicity.

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5.) Aspirin and paracetamol tolerance in patients with nimesulide-induced urticaria.

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Ann Allergy Asthma Immunol 1998 Sep;81(3):237-8 Related Articles, Books, LinkOut

Asero R.

Ambulatorio di Allergologia, Ospedale Caduti Bollatesi, Bollate (MI), Italy.

BACKGROUND: The administration of aspirin and other nonsteroidal anti-inflammatory drugs in patients sensitive to nimesulide might be hazardous. OBJECTIVE: To assess the tolerance to both acetaminophen (paracetamol) and aspirin in patients with a history of urticaria induced by nimesulide. METHODS: Nine patients with a history of nimesulide intolerance were submitted to single-blind, placebo-controlled peroral challenges with increasing doses of acetaminophen and aspirin. RESULTS: Acetaminophen was tolerated by all patients, whereas two experienced immediate systemic urticaria after the administration of 125 mg of aspirin. CONCLUSION: Acetaminophen and aspirin are well tolerated by most nimesulide-sensitive patients. Since a minority of patients show aspirin sensitivity, tolerance of this agent should always be ascertained by properly performed peroral challenges.

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6.) Risk factors for acetaminophen and nimesulide intolerance in patients with NSAID-induced skin disorders.

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Ann Allergy Asthma Immunol 1999 Jun;82(6):554-8 Related Articles, Books, LinkOut

Asero R.

Allergy Clinic, Caduti Bollatesi Hospital, Bollate, Italy.

BACKGROUND: Previous studies show skin reactions after exposure to acetaminophen and/or nimesulide to occur in about 10% of patients with a history of urticaria induced by aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). This fact is surprising since cross-reactivity among different NSAIDs should not occur among subjects without a history of chronic urticaria. OBJECTIVE: To detect risk factors for intolerance to alternative drugs such as acetaminophen and nimesulide in different groups of patients with a history of adverse skin reactions (urticaria/angioedema, or anaphylaxis) after the ingestion of aspirin and other NSAIDs. METHODS: Two hundred fifty-six patients with a history of recent pseudoallergic skin reactions caused by NSAIDs underwent elective oral challenges with increasing doses of both acetaminophen and nimesulide. Patients were divided into three groups: A = 69 subjects with chronic urticaria, B = 163 otherwise normal subjects with a history of urticaria after the ingestion of aspirin, and C = 24 otherwise normal subjects with a history of urticaria after the ingestion of pyrazolones but aspirin-tolerant. RESULTS: Forty-eight (19%) patients reacted to acetaminophen and/or nimesulide. Similar numbers of patients with chronic urticaria (23%) and of normal subjects with a history of aspirin-induced urticaria (19%) did not tolerate one of the alternative drugs challenged. Pyrazolones-intolerant patients showed the lowest number of reactors (4%). Aspirin intolerance represented a risk factor for acetaminophen- and/or nimesulide-induced urticaria (RR = 5.4). A history of anaphylactoid reactions induced by NSAID represented a risk factor for urticaria after the ingestion of the alternative study drugs (RR = 5.7). Atopic status was associated with a higher risk of reactivity to nimesulide: this drug induced urticaria in 11/47 (23%) atopics versus 18/209 (9%) non-atopics (P < .005; RR = 3.2). A history of intolerance to antibacterial drugs was not associated with a higher prevalence of reactivity against acetaminophen and/or nimesulide. CONCLUSIONS: In at least 20% of patients with a history of urticaria/angioedema or anaphylaxis induced by aspirin or other NSAIDs, but without a history of chronic urticaria, cross-reactivity with other NSAIDs occurs. Atopy as well as a history of aspirin-induced anapylactoid reactions seem to represent relevant risk factors for intolerance to alternative NSAIDs. In view of these findings, aspirin-intolerant patients with such clinical features should be submitted to peroral tolerance tests with at least two alternative substances in order to avoid potentially severe reactions.

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7.) Neonatal chronic kidney failure associated to cyclo-oxygenase inhibitors administered during pregnancy.

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Minerva Urol Nefrol 2001 Jun;53(2):113-6

Peruzzi L, Gianoglio B, Porcellini G, Conti G, Amore A, Coppo R.

Nefrologia e Dialisi, Ospedale Infantile Regina Margherita, Turin, Italy.

Non-steroidal anti-inflammatory drugs (NSAID) are used since years as tocolytic due to their capacity to inhibit cyclo-oxygenase (COX) expressed in uterus and fetal membranes, fundamental for labour initiation and maintenance. The use of nimesulide, a COX-2 selective NSAID, has been recently proposed due to its capacity to selectively inhibit the enzyme expressed in the myometrium and endometrium. A case of neonatal irreversible end stage renal failure after maternal assumption of nimesulide as tocolytic for 6 week is reported. Cesarean section at the 32nd week due to oligohydramnios gave birth to a baby girl of 2090 g, in good general conditions, without signs of respiratory distress and of visible abnormalities. From birth she displayed oligo-anuria which required dialytic substitutive therapy from the second day of life. At US scan both kidneys had normal diameters for gestational age slightly increased echogenicity and a reduced cortico-medullary differentiation. On the 20th day of life she had a surgical renal biopsy for the persistence of oligo-anuria, showing fetal glomeruli, without lymphocytic interstitial infiltrate, and normal tubuli without evidence of necrosis. She is now 16 months old and under automated peritoneal dialysis on a home dialysis program. The occurrence of chronic renal failure in strict relationship with maternal nimesulide assumption in this case is strongly suggestive for a pharmacological damage, either direct or mediated by renin angiotensin inhibition, and possibly modulated by genetic factors, likely to account for the different outcome of similarly treated patients. A cautious use of this drug as long term tocolytic should be recommended while waiting for ad hoc experimental and clinical evidences of safeness.

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8.) Nimesulide aggravates kainic acid-induced seizures in the rat.

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Pharmacol Toxicol 2001 May;88(5):271-6

Kunz T, Oliw EH.

Department of Pharmaceutical Biosciences, Uppsala University, Uppsala Biomedical Centre, Sweden. Tina.Kunz@farmbio.uu.se

Treatment of rats with kainic acid (10 mg/kg, intraperitoneally) triggers limbic seizures. Cyclooxygenase-2 mRNA is expressed in the hippocampus and cortex after 8 hr and marked cell loss occurs after 72 hr in the CA1-CA3 areas of the hippocampus. We examined the effect of the cyclooxygenase-2 inhibitor, nimesulide (N-(4-nitro-2-phenoxyphenyl)-methanesulfonamide), on kainate-induced seizures and delayed neurotoxicity. Nimesulide (10 mg/kg, intraperitoneally) was well tolerated given alone or 6-8 hr after kainate. However, pretreatment with nimesulide augmented seizures and increased the mortality rate from approximately 10% to 69%. We examined the effect of nimesulide on delayed cell loss after 72 hr in the surviving animals with histological staining. Cell loss did not seem to be reduced in animals treated with nimesulide 6-8 hr after kainate, but in the surviving animals pretreated with nimesulide less cell loss occurred. We conclude that nimesulide should be used with caution as an antiinflammatory drug in patients with convulsive disorders.

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9.) Nimesulide-induced hepatitis and acute liver failure.

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Isr Med Assoc J 1999 Oct;1(2):89-91

Weiss P, Mouallem M, Bruck R, Hassin D, Tanay A, Brickman CM, Farfel Z, Bar-Meir S.

Department of Gastroenterology, Sheba Medical Center, Tel-Hashomer, Israel.

BACKGROUND: Nimesulide is a relatively new non-steroidal anti-inflammatory drug that is gaining popularity in many countries because it is a selective cyclooxygenase 2 inhibitor. Occasionally, treatment is associated with mild elevation of liver enzymes, which return to normal upon discontinuation of the drug. Several cases of nimesulide-induced symptomatic hepatitis were also recently reported, but these patients all recovered. OBJECTIVES: To report the characteristics of liver injury induced by nimesulide. PATIENTS AND METHODS: We report retrospectively six patients, five of them females with a median age of 59 years, whose aminotransferase levels rose after they took nimesulide for joint pains. In all patients nimesulide was discontinued, laboratory tests for viral and autoimmune causes of hepatitis were performed, and sufficient follow-up was available. RESULTS: One patient remained asymptomatic. Four patients presented with symptoms, including fatigue, nausea and vomiting, which had developed several weeks after they began taking nimesulide (median 10 weeks, range 2-13). Hepatocellular injury was observed with median peak serum alanine aminotransferase 15 times the upper limit of normal (range 4-35), reversing to normal 2-4 months after discontinuation of the drug. The remaining patient developed symptoms, but continued taking the drug for another 2 weeks. She subsequently developed acute hepatic failure with encephalopathy and hepatorenal syndrome and died 6 weeks after hospitalization. In none of the cases did serological tests for hepatitis A, B and C viruses, Epstein-Barr virus and cytomegalovirus, as well as autoimmune hepatitis reveal findings. CONCLUSIONS: Nimesulide may cause liver damage. The clinical presentation may vary from abnormal liver enzyme levels with no symptoms, to fatal hepatic failure. Therefore, monitoring liver enzymes after initiating therapy with nimesulide seems prudent.

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10.) Nimeulide and neonatal renal failure.

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Lancet 2000 Feb 12;355(9203):575

Balasubramaniam J.

Publication Types: Comment, Letter

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11.) Fatal hepatitis associated with nimesulide.

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J Hepatol 2000 Jan;32(1):174

Andrade RJ, Lucena MI, Fernandez MC, Gonzalez M.

Publication Types: Comment, Letter

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12.) Neonatal end-stage renal failure associated with maternal ingestion of cyclo-oxygenase-type-1 selective inhibitor nimesulide as tocolytic.

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Lancet 1999 Nov 6;354(9190):1615

Peruzzi L, Gianoglio B, Porcellini MG, Coppo R.

Cyclo-oxygenase-type-2 (COX-2) enzyme is fundamental for nephrogenesis, upregulated on fetal membranes and myometrium at parturition. Fetal COX-2 inhibition, due to maternal nimesulide assumption, can be responsible for neonatal chronic renal failure.

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13.) [Nimesulide acute hepatitis: description of 3 cases].

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Med Clin (Barc) 1999 Sep 25;113(9):357-8

Romero Gomez M, Nevado Santos M, Fobelo MJ, Castro Fernandez M.

Publication Types: Letter

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14.) Analgesics for pediatric use.

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Indian J Pediatr 2000 Aug;67(8):589-90

Malhotra S, Pandhi P.

Department of Clinical Pharmacology, PGIMER, Chandigarh.

The use of nimesulide is increasing and recently, concerns have been raised regarding its hepatotoxicity, especially in children. At least two deaths due to fulminant hepatic failure have been attributed to nimesulide. In India, nimesulide has been approved and about twelve pediatric preparations are available. Lack of effective postmarketing surveillance means that adverse drug reactions may not be picked or reported. Therefore, quick approval of those drugs for which substitutes are available may not be desirable in India and in other developing countries.

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15.) Nimesulide, clavulanic acid and hepatitis.

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J Intern Med 2000 Aug;248(2):168-9

Elmalem E.

Publication Types: Comment, Letter

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16.) Nimesulide-induced hepatitis and acute liver failure.

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Isr Med Assoc J 1999 Nov;1(3):221

Weiss P.

Publication Types: Comment, Letter

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17.) [Toxic hepatitis caused by nimesulide, presentation of a new case and review of the literature].

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Gastroenterol Hepatol 2000 Nov;23(9):428-30

Ferreiro C, Vivas S, Jorquera F, Dominguez AB, Espinel J, Munoz F, Herrera A, Fernandez MJ, Olcoz JL, Ortiz de Urbina J.

Seccion de Aparato Digestivo y Servicio de Farmacia, Hospital de Leon, Leon.

Nimesulide is a potent non-steroidal anti-inflammatory drug. It is a new, selective cyclooxygenase-2 inhibitor with few adverse effects on the gastrointestinal system. We present a case of hepatotoxicity in which other possible causes of liver damage were excluded. A biochemical pattern of cholestasis was predominant. Evolution was favorable after the drug was stopped and enzymatic alterations progressively returned to normal. The cases reported to date are reviewed. The precise mechanism by which nimesulide produces liver damage is not known but it is probably caused by an idiosyncratic reaction. Because of the severity of the hepatitis described in some cases, treatment should be stopped when liver dysfunction is detected and the patients should be closely monitored.

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18.) [Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case].

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Rev Med Chil 2000 Dec;128(12):1349-53

Tejos S, Torrejon N, Reyes H, Meneses M.

Servicios de Medicina y de Anatomia Patologica, Hospital del Salvador, Departamento de Medicina (Campus Oriente), Facultad de Medicina, Universidad de Chile, Santiago, Chile. stejos@alfared.cl

A 66 year-old obese woman with arthrosis, self-medicated with oral nimesulide, 200 mg daily. After 6 weeks she developed nausea, jaundice and dark urine. Two weeks later she had recurrent hematemesis and was hospitalized. Besides obesity and anemia her physical examination was unremarkable. An upper GI endoscopy revealed 3 acute gastric ulcers and a 4th one in the pyloric channel. Abdominal ultrasonogram showed a slightly enlarged liver with diffuse reduction in ecogenicity; the gallbladder and biliary tract were normal. Blood tests demonstrated a conjugated hyperbilirubinemia (maximal total value: 18.4 mg/dl), ALAT 960 U/l, ASAT 850 U/l, GGT 420 U/l, alkaline phosphatases mildly elevated, pro-time 49% and albumin 2.7 mg/dl. Serum markers for hepatitis A, B and C viruses were negative. ANA, AMA, anti-SmA, were negative. Ceruloplasmin was normal. A liver biopsy showed bridging necrosis and other signs of acute toxic liver damage. Gastric ulcers healed after conventional treatment and hepatitis subsided after 2 months leaving no signs of chronic liver damage. The diagnosis of toxic hepatitis due to nimesulide was supported by the time-course of drug usage, sex, age, absence of other causes of liver disease, a compatible liver biopsy and the improvement after drug withdrawal. Peptic ulcers or toxic hepatitis have been previously described as independent adverse reactions in patients taking nimesulide or other NSAIDs but their simultaneous occurrence in a single patient is a unique event that deserves to be reported.

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19.) Nimesulide-induced acute hepatitis: evidence from six cases.

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J Hepatol 1998 Jul;29(1):135-41

Van Steenbergen W, Peeters P, De Bondt J, Staessen D, Buscher H, Laporta T, Roskams T, Desmet V.

Department of Internal Medicine, University Hospital Gasthuisberg-St Rafael, Catholic University of Leuven, Belgium.

BACKGROUND/AIMS: A number of nonsteroidal anti-inflammatory drugs have been reported to provoke hepatic injury. Nimesulide is a new agent of the sulfonanilide class, and is a more selective inhibitor of cyclooxygenase type 2 than of type 1. Well-documented cases of acute hepatitis have not yet been reported with this drug. We report on six patients who developed acute liver damage after initiation of nimesulide. METHODS: Between April 1996 and January 1997, six patients with apparent nimesulide-induced liver injury were admitted. Clinical, laboratory, serologic, radiological, and histologic data of all six cases were extensively analyzed. The causal relationship between nimesulide and liver injury was assessed, using a scoring system elaborated by the French and International consensus meeting group. RESULTS: Four women developed a centrilobular (three) or panlobular (one) bridging necrosis, whereas two men showed a bland intrahepatic cholestasis. Jaundice was the presenting symptom in five of the six cases. One patient with hepatocellular necrosis and one with cholestasis had hallmarks of hypersensitivity with an increased blood and tissue eosinophilia. The causal relationship could be designated as "highly probable" in one, "probable" in four, and "possible" in one patient. One patient died from a pancreatic tumor 5 months after the diagnosis of toxic liver injury. In all other patients, liver tests returned to completely normal values within a late follow-up period of 6 to 17 months. CONCLUSIONS: Nimesulide-induced liver injury can present with hepatocellular necrosis or with pure cholestasis. From clinical and histologic data, it appears that both immunologic and metabolic idiosyncratic reactions can be invoked as the pathogenic mechanisms of nimesulide-induced liver disease.

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20.) Nimesulide-induced purpura.

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Dermatology 2000;201(4):376

Kanwar AJ, Kaur S, Thami GP.

Publication Types: Letter

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21.) Modification of antihistaminic activity of cetirizine by nimesulide.

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J Assoc Physicians India 1999 Apr;47(4):389-92

Rewari S, Gupta U.

Dept of Pharmacology, Maulana Azad Medical College and Associated Hospitals, New Delhi.

OBJECTIVE: To study the effect of nimesulide (4-nitro-2-phenoxymethane sulfonanilide) a non-steroidal anti-inflammatory drug, on antihistaminic activity of cetirizine. METHOD: A randomized, double blind, cross over study was conducted in ten healthy male volunteers. Wheal and flare responses to histamine were measured by performing intradermal injection of histamine (2 micrograms base) diluted in 100 microliters volume of saline on the volar surface of forearm, on four occasions (0, 2, 4, and 6 hrs. post-dosing). Each volunteer was randomized to receive either treatment A (cetirizine 10 mg + placebo) or treatment B (cetirizine 100 mg + nimesulide 100 mg), with one week wash out period in between each administration. Wheal and flare responses were measured ten minutes after each histamine injection. RESULTS: Both cetirizine 10 mg alone and cetirizine 10 mg + nimesulide 100 mg, decreased wheal and flare responses significantly at 2 hrs. and this continued till 6 hrs. post-dosing. This decrease was highly significant when cetirizine was given along with nimesulide. CONCLUSION: The results suggest a synergistic effect exhibited by the combined use of cetirizine with nimesulide.

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22.) Perinatal vasoconstrictive renal insufficiency associated with maternal nimesulide use.

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Am J Perinatol 1999;16(9):441-4

Landau D, Shelef I, Polacheck H, Marks K, Holcberg G.

Department of Pediatrics, Soroka Medical Center and Ben Gurion University of the Negev, Beer Sheva, Israel.

A full-term newborn developed oliguric renal failure at 24 hr of life, which persisted for several days. Her mother ingested therapeutic doses of nimesulide, a non-steroidal anti-inflammatory (cyclo-oxygenase-2 inhibitor) drug, during the last 2 weeks of pregnancy. She was found at delivery to have developed oligohydramnion, esophagitis, and a bleeding peptic ulcer. The infant's fractional excretion of sodium was very low (0.5%) pointing for a severe vasoconstrictive mechanism involved. Renal sonogram showed hyperechogenic medullary papillae, which resolved during convalescence. This case emphasizes the importance of renal prostagandins in the control of vascular tone and sodium homeostasis. This is the first report of an adverse effect of fetal renal circulation by maternal ingestion of nimesulide.

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23.) Acute renal failure induced by nimesulide in a patient suffering from temporal arteritis.

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Nephrol Dial Transplant 1997 Jul;12(7):1493-6

Apostolou T, Sotsiou F, Yfanti G, Andreadis E, Nikolopoulou N, Diamantopoulos E, Billis A.

Department of Medicine, Evangelismos Hospital, Athens, Greece.

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24.) Drug-induced cholestasis.

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Semin Gastrointest Dis 2001 Apr;12(2):113-24

Chitturi S, Farrell GC.

Storr Liver Unit, Westmead Millennium Institute, University of Sydney, Westmead Hospital, New South Wales, Australia.

The spectrum of drug-induced cholestasis ranges from 'bland' reversible cholestasis to chronic forms due to the vanishing bile duct syndrome. Agents known for many years to cause cholestasis include estrogens and anabolic steroids, chlorpromazine, erythromycin, and the oxypenicillins; structurally similar congeners of these drugs (tamoxifen, newer macrolides) may also cause cholestasis. Contemporary drugs linked to cholestastic liver injury include ticlopidine, terfenadine, terbinafine, nimesulide, irbesartan, fluoroquinolones, cholesterol-lowering 'statins,' and some herbal remedies (greater celandine, glycyrrhizin, chaparral). Amoxillin-clavulanate, ibuprofen, and pediatric cases of the vanishing bile duct syndrome are recent additions to a long list of drugs associated with the vanishing bile duct syndrome. Particular human leukocyte antigen profiles have recently been identified among those who have developed cholestasis with specific drugs (tiopronin and amoxicillin-clavulanate), and the mechanistic relevance of these genetic associations is being explored. The treatment of drug-induced cholestasis is largely supportive. The offending drug should be withdrawn immediately. Cholestyramine or ursodeoxycholic acid are used to alleviate pruritus, with rifampicin and opioid antagonists being reserved for those who fail first line therapy. Nutritional support is essential for those with prolonged cholestasis, a subgroup who are at risk of developing biliary cirrhosis and liver failure. Timely referral for liver transplant assessment is crucial in these patients.

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25.) Adverse drug reactions postal survey-bronchial asthma and angioedema with nimesulide.

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J Assoc Physicians India 2000 May;48(5):548

Mangalvedhekar SS, Gogtay NJ, Phadke AV, Gore S, Shah JM, Shah SM, Kshirsagar NA.

Publication Types: Letter

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26.) Hypothermia with nimesulide.

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Indian Pediatr 2001 Jul;38(7):799-800

Sharma S.

Professor, Department of Pediatrics, Medical College, Amritsar, Punjab, India.

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27.) [Nimesulide-induced acute hepatitis].

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Gastroenterol Hepatol 2001 Apr;24(4):219-20

Montesinos S, Hallal H, Rausell V, Conesa F, Lopez A.

Servicio de Farmacia y aSeccion de Aparato Digestivo. Hospital Santa Maria del Rosell. Cartagena. Murcia.

Publication Types: Letter

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28.) [Nimesulide toxic hepatitis in pregnancy].

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Gastroenterol Hepatol 2000 Dec;23(10):498-9

Perez-Moreno J, Llerena Guerrero RM, Puertas Montenegro M, Jimenez Arjona MJ.

Publication Types: Letter

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29.) Positive lesional patch tests in fixed drug eruptions from nimesulide.

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Contact Dermatitis 2000 Nov;43(5):307

Cordeiro MR, Goncalo M, Fernandes B, Oliveira H, Figueiredo A.

Clínica de Dermatología, Hospitais da Universidade, Coímbra, Portugal.

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DATA-MÉDICOS/DERMAGIC-EXPRESS No 3-(103) 12/08/2.001 DR. JOSÉ LAPENTA R.

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    Produced by Dr. José Lapenta R. Dermatologist  

Maracay Estado Aragua Venezuela 2.001-2025  

     Telf.: 04142976087 - 04127766810

 

   

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DATA-MÉDICOS/DERMAGIC-EXPRESS No (27) 06/01/99 DR. JOSE LAPENTA R. 

UPDATED 07/12/2025

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Produced by Dr. José Lapenta R. Dermatologist

Venezuela 1.998-2.026

Producido por Dr. José Lapenta R. Dermatólogo
Venezuela 1.998-2.026

Tlf: 0414-2976087 - 04127766810

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