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                                                ENERO 2.004

                                              JANUARY 2.004

  THE BEXTRA (VALDECOXIB) 250 SIDE EFFECTS !!!!, CELEBREX,  CIPROFLOXACIN, LAMOTRIGINE, TOXIC EPIDERMAL NECROLYSIS

 

 1.) THE BEXTRA (VALDECOXIB) SIDE EFFECTS.

 2.) Valdecoxib-induced toxic epidermal necrolysis in a patient allergic to sulfa.

3.) New Warnings for Bextra (Valdedcoxib).

4.) Toxic Epidermal Necrolysis due to administration of Celecoxib (CELEBREX).

5.) Ciprofloxacin-induced toxic epidermal necrolysis in a patient with systemic lupus erythematosus.

6.) Lupus-associated toxic epidermal necrolysis: a novel manifestation of lupus?.

7.) Suspected lamotrigine-induced toxic epidermal necrolysis.

8.) A study of the efficacy of plasmapheresis for the treatment of drug induced toxic epidermal necrolysis.

9.) Treatment of toxic epidermal necrolysis with intravenous immunoglobulin.

10.) High-dose intravenous immunoglobulin for severe drug reactions: efficacy in toxic epidermal necrolysis.

 

1.)  THE BEXTRA (VALDECOXIB) SIDE EFFECTS
 

Source: Http://www.rxlist.com/

Of the patients treated with BEXTRA Tablets in controlled arthritis trials,2665 were patients with OA,and 2684 were patients with RA.More than 4000 patients have received a chronic total daily dose of BEXTRA 10 mg or more.More than 2800 patients have received BEXTRA 10 mg/day,or more,for at least 6 months and 988 of these have received BEXTRA for at least 1 year.

Osteoarthritis and Rheumatoid Arthritis

Table 4 lists all adverse events,regardless of causality,that occurred in ³ 2.0% of patients receiving BEXTRA 10 and 20mg/day in studies of three months or longer from 7 controlled studies conducted in patients with OA or RA that included a placebo and/or a positive control group.

In these placebo- and active-controlled clinical trials, the discontinuation rate due to adverse events was 7.5% for arthritis patients receiving valdecoxib 10 mg daily, 7.9% for arthritis patients receiving valdecoxib 20 mg daily and 6.0% for patients receiving placebo.

In the seven controlled OA and RA studies, the following adverse events occurred in 0.1–1.9% of patients treated with BEXTRA 10 –20 mg daily, regardless of causality.

Application site disorders: Cellulitis, dermatitis contact

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Cardiovascular:Aggravated hypertension, aneurysm, anginapectoris, arrhythmia, cardiomyopathy, congestive heart failure, coronary artery disorder, heart murmur, hypotension

Central, peripheral nervous system: Cerebrovascular disorder, hypertonia, hypoesthesia, migraine, neuralgia, neuropathy, pares-thesia, tremor, twitching, vertigo

Endocrine: Goiter

Female reproductive: Amenorrhea, dysmenorrhea, leukorrhea, mastitis, menstrual disorder, menorrhagia, menstrual bloating, vaginal hemorrhage

Gastrointestinal:
Abnormal stools, constipation, diverticulosis, dry mouth, duodenal ulcer, duodenitis, eructation, esophagitis, fecal incontinence, gastric ulcer, gastritis, gastroenteritis, gastroe-sophageal reflux, hematemesis, hematochezia, hemorrhoids, hemorrhoids bleeding, hiatal hernia, melena, stomatitis, stool frequency increased, tenesmus, tooth disorder, vomiting

General: Allergy aggravated, allergic reaction, asthenia, chest pain, chills, cyst NOS, edema generalized, face edema, fatigue, fever, hot flushes, halitosis, malaise, pain, periorbital swelling, peripheral pain Hearing and vestibular: Ear abnormality, earache, tinnitus

Heart rate and rhythm: Bradycardia, palpitation, tachycardia

Hemic: Anemia

Liver and biliary system: Hepatic function abnormal, hepatitis, ALT increased, AST increased

Male reproductive: Impotence, prostatic disorder

Metabolic and nutritional: Alkaline phosphatase increased, BUN increased, CPK increased, creatinine increased, diabetes mellitus, glycosuria, gout, hypercholesterolemia, hyperglycemia, hyperkalemia, hyperlipemia, hyperuricemia, hypocalcemia, hypokalemia, LDH increased, thirst increased, weight decrease, weight increase, xerophthalmia

Musculoskeletal: Arthralgia, fracture accidental, neck stiffness, osteoporosis, synovitis, tendonitis

Neoplasm: Breast neoplasm, lipoma, malignant ovarian cyst

Platelets (bleeding or clotting): Ecchymosis, epistaxis, hematoma NOS, thrombocytopenia

Psychiatric: Anorexia, anxiety, appetite increased, confusion, depression, depression aggravated, insomnia, nervousness, morbid dreaming, somnolence

Resistance mechanism disorders: Herpes simplex, herpes zoster, infection fungal,infection soft tissue, infection viral, moniliasis, moniliasis genital, otitis media

Respiratory: Abnormal breath sounds, bronchitis, bronchospasm, coughing, dyspnea, emphysema, laryngitis, pneumonia, pharyngitis, pleurisy, rhinitis

Skin and appendages: Acne, alopecia, dermatitis, dermatitis fungal, eczema, photosensitivity allergic reaction, pruritus, rash erythematous, rash maculopapular, rash psoriaform, skin dry, skin hypertrophy, skin ulceration, sweating increased, urticaria

Special senses:
Taste perversion


Urinary system: Albuminuria, cystitis, dysuria, hematuria, micturition frequency increased, pyuria, urinary incontinence, urinary tract infection

Vascular: Claudication intermittent, hemangioma acquired, varicose vein

Vision: Blurred vision, cataract, conjunctival hemorrhage, conjunctivitis, eye pain, keratitis, vision abnormal

White cell and RES disorders: Eosinophilia, leukopenia, leukocytosis, lymphadenopathy, lymphangitis, lymphopenia

Other serious adverse events that were reported rarely (estimated <0.1%) in clinical trials, regardless of causality, in patients taking BEXTRA:

Autonomic nervous system disorders: Hypertensive encephalopathy, vasospasm

Cardiovascular: Abnormal ECG,aortic stenosis, atrial fibrillation, carotid stenosis, coronary thrombosis, heart block,heart valve disorders, mitral insufficiency, myocardial infarction, myocardial ischemia, pericarditis, syncope, thrombophlebitis, unstable angina, ventricular fibrillation

Central, peripheral nervous system: Convulsions

Endocrine: Hyperparathyroidism

Female reproductive: Cervical dysplasia

Gastrointestinal: Appendicitis, colitis with bleeding, dysphagia, esophageal perforation, gastrointestinal bleeding, ileus, intestinal obstruction, peritonitis

Hemic: Lymphoma-like disorder, pancytopenia

Liver and biliary system: Cholelithiasis

Metabolic: Dehydration

Musculoskeletal: Pathological fracture, osteomyelitis

Neoplasm: Benign brain neoplasm, bladder carcinoma, carcinoma, gastric carcinoma, prostate carcinoma, pulmonary carcinoma

Platelets (bleeding or clotting): Embolism, pulmonary embolism, thrombosis

Psychiatric: Manic reaction, psychosis

Renal: Acute renal failure

Resistance mechanism disorders: Sepsis

Respiratory: Apnea, pleural effusion, pulmonary edema, pulmonary fibrosis, pulmonary infarction, pulmonary hemorrhage, respiratory insufficiency

Skin: Basal cell carcinoma, malignant melanoma

Urinary system: Pyelonephritis, renal calculus

Vision: Retinal detachment

Postmarketing Experience

The following reactions have been identified during postmarketing use of BEXTRA. These reactions have been chosen for inclusion either due to their seriousness, reporting frequency, possible causal relationship to BEXTRA, or a combination of these factors. Because these reactions were reported voluntarily from a population of uncertain size, it is not possible to reliably estimate their frequency or establish a causal relationship to drug exposure.

General: Hypersensitivity reactions (including anaphylactic reactions and angioedema)

Skin and appendages: Erythema multiforme, exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis


DRUG INTERACTIONS
The drug interaction studies with valdecoxib were performed both with valdecoxib and a rapidly hydrolyzed intravenous prodrug form. The results from trials using the intravenous prodrug are reported in this section as they relate to the role of valdecoxib in drug interactions.

General: In humans,valdecoxib metabolism is predominantly mediated via CYP 3A4 and 2C9 with glucuronidation being a further (20%) route of metabolism.In vitrostudies indicate that valdecoxib is a moderate inhibitor of CYP 2C19 (IC50 = 6 µg/mL),and a weak inhibitor of both 3A4 (IC50 = 44µg/mL) and 2C9 (IC50 = 13 µg/mL).In view of the limitations of in vitrostudies and the high valdecoxib IC50 values,the potential for such metabolic inhibitory effects in vivoat therapeutic doses of valdecoxib is low.

Aspirin: Concomitant administration of aspirin with valdecoxib may result in an increased risk of GI ulceration and complications compared to valdecoxib alone.Because of its lack of anti-platelet effect valdecoxib is not a substitute for aspirin for cardiovascular prophylaxis.

In a parallel group drug interaction study comparing the intravenous prodrug form of valdecoxib at 40 mg BID (n=10) vs placebo (n=9),valdecoxib had no effect on in vitroaspirin-mediated inhibition of arachidonate- or collagen-stimulated platelet aggregation.

Methotrexate: Valdecoxib 10 mg BID did not show a significant effect on the plasma exposure or renal clearance of methotrexate.

ACE-inhibitors: Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE-inhibitors.This interaction should be given consideration in patients taking BEXTRA concomitantly with ACE-inhibitors.

Furosemide: Clinical studies,as well as post-marketing observations, have shown that NSAIDs can reduce the natriuretic effect of furosemide and thiazides in some patients.This response has been attributed to inhibition of renal prostaglandin synthesis.

Anticonvulsants: Anticonvulsant drug interaction studies with val-decoxib have not been conducted.As with other drugs,routine monitoring should be performed when therapy with BEXTRA is either initiated or discontinued in patients on anticonvulsant therapy.

Dextromethorphan: Dextromethorphan is primarily metabolized by CYP 2D6 and to a lesser extent by 3A4.Coadministration with val-decoxib (40 mg BID for 7 days) resulted in a significant increase in dextromethorphan plasma levels suggesting that,at these doses,val-decoxib is a weak inhibitor of 2D6.Dextromethorphan plasma concentrations in the presence of high doses of valdecoxib were almost 5-fold lower than those seen in CYP 2D6 poor metabolizers.

Lithium: Valdecoxib 40 mg BID for 7 days produced significant decreases in lithium serum clearance (25%) and renal clearance (30%) with a 34% higher serum exposure compared to lithium alone. Lithium serum concentrations should be monitored closely when initiating or changing therapy with BEXTRA in patients receiving lithium.Lithium carbonate (450mg BID for 7 days) had no effect on valdecoxib pharmacokinetics.

Warfarin: The effect of valdecoxib on the anticoagulant effect of warfarin (1 – 8 mg/day) was studied in healthy subjects by coadminis-tration of BEXTRA 40 mg BID for 7 days.Valdecoxib caused a statistically significant increase in plasma exposures of R-warfarin and S-warfarin (12% and 15%,respectively),and in the pharmacodynamic effects (prothrombin time,measured as INR) of warfarin.While mean INR values were only slightly increased with coadministration of valdecoxib,the day-to-day variability in individual INR values was increased.Anticoagulant therapy should be monitored,particularly during the first few weeks,after initiating therapy with BEXTRA in patients receiving warfarin or similar agents.

Fluconazole and Ketoconazole: Ketoconazole and fluconazole are predominantly CYP 3A4 and 2C9 inhibitors, respectively. Concomitant single dose administration of valdecoxib 20 mg with multiple doses of ketoconazole and fluconazole produced a significant increase in exposure of valdecoxib.Plasma exposure (AUC) to valdecoxib was increased 62% when coadministered with flucona-zole and 38% when coadministered with ketoconazole.

Glyburide: Glyburide is a CYP 3A4 substrate.Coadministration of valdecoxib (10 mg BID for 7 days) with glyburide (5 mg QD or 10 mg BID) did not affect the pharmacokinetics (exposure) of glyburide.

Carcinogenesis, Mutagenesis, Impairment of Fertility

Valdecoxib was not carcinogenic in rats given oral doses up to 7.5mg/kg/day for males and 1.5mg/kg/day for females (equivalent to approximately 2- to 6-fold human exposure at 20 mg QD as measured by the AUC(0-24hr)) or in mice given oral doses up to 25mg/kg/day for males and 50mg/kg/day for females (equivalent to approximately 0.6- to 2.4-fold human exposure at 20 mg QD as measured by the AUC(0-24hr)) for two years..

Valdecoxib was not mutagenic in an Ames test or a mutation assay in Chinese hamster ovary (CHO) cells,nor was it clastogenic in a chromosome aberration assay in CHO cells or in an in vivomicronucleus test in rat bone marrow.

Valdecoxib did not impair male rat fertility at oral doses up to 9.0mg/kg/day (equivalent to approximately 3- to 6-fold human exposure at 20 mg QD as measured by the AUC (0-24hr)).In female rats,a decrease in ovulation with increased pre- and post-implantation loss resulted in decreased live embryos/fetuses at doses ³ 2 mg/kg/day (equivalent to approximately 2-fold human exposure at 20mg QD as measured by the AUC (0-24hr) for valdecoxib).The effects on female fertility were reversible.This effect is expected with inhibition of prostaglandin synthesis and is not the result of irreversible alteration of female reproductive function.

Pregnancy

Teratogenic Effects: Pregnancy Category C.

The incidence of fetuses with skeletal anomalies such as semi-bipartite thoracic vertebra centra and fused sternebrae was slightly higher in rabbits at an oral dose of 40 mg/kg/day (equivalent to approximately 72-fold human exposures at 20mg QD as measured by the AUC(0-24hr)) throughout organogenesis.Valdecoxib was not teratogenic in rabbits up to an oral dose of 10 mg/kg/day (equivalent to approximately 8-fold human exposures at 20 mg QD as measured by the AUC(0-24hr)).

Valdecoxib was not teratogenic in rats up to an oral dose of 10mg/kg/day (equivalent to approximately 19-fold human exposure at 20 mg QD as measured by the AUC (0-24hr)).There are no studies in pregnant women.However,valdecoxib crosses the placenta in rats and rabbits.BEXTRA should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Non-teratogenic Effects: Valdecoxib caused increased pre-and post-implantation loss with reduced live fetuses at oral doses

³ 10mg/kg/day (equivalent to approximately 19-fold human exposure at 20 mg QD as measured by the AUC (0-24hr)) in rats and an oral dose of 40 mg/kg/day (equivalent to approximately 72-fold human exposure at 20 mg QD as measured by the AUC (0-24hr)) in rabbits throughout organogenesis.In addition,reduced neonatal survival and decreased neonatal body weight when rats were treated with valdecoxib at oral doses ³ 6 mg/kg/day (equivalent to approximately 7-fold human exposure at 20 mg QD as measured by the AUC(0-24hr)) throughout organogenesis and lactation period.No studies have been conducted to evaluate the effect of valdecoxib on the closure of the ductus arteriosus in humans.Therefore,as with other drugs known to inhibit prostaglandin synthesis,use of BEXTRA during the third trimester of pregnancy should be avoided.

Labor and Delivery

Valdecoxib produced no evidence of delayed labor or parturition at oral doses up to 10 mg/kg/day in rats (equivalent to approximately 19-fold human exposure at 20 mg QD as measured by the AUC (0-24hr)). The effects of BEXTRA on labor and delivery in pregnant women are unknown.

Nursing Mothers

Valdecoxib and its active metabolite are excreted in the milk of lactating rats.It is not known whether this drug is excreted in human milk.Because many drugs are excreted in human milk,and because of the potential for adverse reactions in nursing infants from BEXTRA,a decision should be made whether to discontinue nursing or to discontinue the drug,taking into account the importance of the drug to the mother and the importance of nursing to the infant.

Pediatric Use

Safety and effectiveness of BEXTRA in pediatric patients below the age of 18 years have not been evaluated.

Geriatric Use

Of the patients who received BEXTRA in arthritis clinical trials of three months duration,or greater,approximately 2100 were 65 years of age or older,including 570 patients who were 75 years or older.No overall differences in effectiveness were observed between these patients and younger patients.




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2.) Valdecoxib-induced toxic epidermal necrolysis in a patient allergic to sulfa drugs.

Pharmacotherapy. 2003 Apr; 23(4): 551-3.

Glasser DL, Burroughs SH.

Department of Pharmacy Practice, Bernard J. Dunn School of Pharmacy, Shenandoah University, 1460 University Drive, Winchester, VA 22601, USA. [email protected]

A 55-year-old Caucasian woman with a previously documented sulfa allergy was admitted to the hospital after she developed toxic epidermal necrolysis; she had been taking valdecoxib for 8 days for knee pain. Four days later, her bullous lesions had progressed to 45-50% of her body surface area. She was transferred to a burn unit for aggressive wound care and fluid hydration. Valdecoxib, a cyclooxygenase-2 inhibitor, is a benzenesulfonamide prescribed for arthritis pain and inflammation, and dysmenorrhea. Clinicians should exercise caution when prescribing valdecoxib to patients who are allergic to sulfa drugs.



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3.) New Warnings for Bextra (VALDECOXIB).

Source: Http://www.fda.gov/

The FDA and Pharmacia Corporation are advising health-care professionals about new warnings and information in the product labeling of Bextra (valdecoxib), a drug approved for treatment of osteoarthritis, rheumatoid arthritis and menstrual pain (dysmenorrhea). The labeling is being updated with new warnings following postmarketing reports of serious adverse effects, including serious allergic reactions (anaphylactoid reactions). As these reactions can be life-threatening, people who start Bextra and experience a rash should discontinue the drug immediately. In addition, the labeling will state that the drug is contraindicated--not to be used--in patients allergic to sulfa-containing products.

Health-care professionals are encouraged to report any unexpected adverse or serious events associated with the use of Bextra directly to Pharmacia Corporation, Peapack, N.J. at 1-800-323-4204 or to the FDA MedWatch program at 1-800-FDA-1088.




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4.)  Toxic epidermal necrolysis due to administration of celecoxib (Celebrex).

South Med J. 2002 Oct; 95(10): 1213-4.

Comment in:
South Med J. 2003 Mar;96(3):320-1.

Friedman B, Orlet HK, Still JM, Law E.

Joseph M. Still Burn Center, Doctor's Hospital, Augusta, GA, USA.

A 41-year-old woman was given celecoxib (Celebrex) for the treatment of carpal tunnel syndrome. An erythematous rash developed that progressed to exfoliative dermatitis, and the patient was diagnosed with toxic epidermal necrolysis. After transfer to the burn unit, she was treated with topical mupirocin calcium cream and bismuth tribromophenatein petrolatum gauze dressings. Her wounds healed well. This is the first case report of toxic epidermal necrolysis due to treatment with celecoxib of which we are aware.


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5.) Ciprofloxacin-induced toxic epidermal necrolysis in a patient with systemic lupus erythematosus.

Infection. 2003 Dec;31(6):428-9.

Jongen-Lavrencic M, Schneeberger PM, van der Hoeven JG.

Dept. of Internal Medicine, Jeroen Bosch Ziekenhuis, 's-Hertogenbosch, The Netherlands.

Toxic epidermal necrolysis (TEN), or Lyell's syndrome, is a fulminant bullous dermatitis. TEN is often a drug-induced reaction and virtually any drug class appears capable of provoking it. We report here a case of TEN after administration of ciprofloxacin. Systemic lupus erythematosus (SLE) was suspected as a possible etiologic or modifying cofactor in TEN in this case.



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6.) Lupus-associated toxic epidermal necrolysis: a novel manifestation of lupus?
 

J Am Acad Dermatol. 2003 Apr;48(4):525-9.

Mandelcorn R, Shear NH.

Division of Dermatology, Department of Medicine, University of Toronto.

BACKGROUND: Toxic epidermal necrolysis is an acute mucocutaneous reaction characterized by extensive cutaneous and mucosal sloughing and systemic involvement. It is generally associated with drug ingestion. OBJECTIVE AND METHODS: We describe 2 patients who developed typical clinical and histopathologic features of toxic epidermal necrolysis with unusual subacute progression, absence of systemic involvement or high-risk drug ingestion, and features of lupus erythematosus. CONCLUSION: We propose that this constellation of features represents a new entity not previously described. This entity may represent a more severe variant of Rowell's syndrome or, alternatively, a novel manifestation of lupus erythematosus



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 7.) Suspected lamotrigine-induced toxic epidermal necrolysis.
 

Acta Neurol Belg. 2003 Jun;103(2):95-8.

Sogut A, Yilmaz A, Kilinc M, Sogut AG, Demiralay E, Uzar H.

Baskent University Faculty of Medicine, Neurology Department.

Toxic epidermal necrolysis and Stevens-Johnson syndrome are rare, life treating cutaneous reactions. Most cases of toxic epidermal necrolysis are drug induced. The drugs with the highest estimated incidence include co-trimoxazloe (trimethoprim-sulfamethoxazole), sulfadoxine-pyrethamine, and carbamazepine. Among other drugs, the reported reaction rates are relatively low for lamotrigine and sulbactam-ampicillin. We describe a patient who developed toxic epidermal necrolysis after either administration of lamotrigine or of ampicillin.



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8.) A study of the efficacy of plasmapheresis for the treatment of drug induced toxic epidermal necrolysis.

Ther Apher. 1998 May;2(2):153-6.

Yamada H, Takamori K, Yaguchi H, Ogawa H.

Department of Dermatology, International Goodwill Hospital, Yokohama, Japan.

The efficacy of plasmapheresis for the treatment of toxic epidermal necrolysis (TEN) in our patient and related reports in the literature were examined. The patient, a 41-year-old female, was diagnosed as having drug (Sedes-G [isopropylantipyrin, arylisopropylacetoureid, and phenacetinum]) induced TEN. Upon admission to our hospital, extensive corticostroid therapy was initiated. After 6 days, because more than 90% of the patient's body surface was affected by TEN, it was concluded that the patient was unresponsive to corticosteroid therapy. Double filtration plasmapheresis (DFPP) was therefore begun. After 2 sessions of DFPP, extensive reepithelialization rapidly occurred, and after 3 sessions of DFPP, the improvement was dramatic. The patient's condition had almost healed during 1 month's hospitalization. It has been reported in the literature that 22 patients with drug induced TEN have been treated with plasmapheresis. The mortality rate of 23 patients, including our patient, was 17.4%. The rate of effectiveness of plasmapheresis on drug induced TEN is 82.6%. It appears that some kind of necrolytic factors were removed by the plasmapheresis. This suggests that plasmapheresis may be an effective treatment for drug induced TEN.


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9.) Treatment of toxic epidermal necrolysis with intravenous immunoglobulin.

J La State Med Soc. 2003 Sep-Oct;155(5):266-9.

Simeone F, Rubio ER.

Department of Medicine, Tulane University Health Sciences Center, New Orleans, USA.

Toxic epidermal necrolysis is a severe adverse drug reaction that produces extensive mucocutaneous damage, with full-thickness epidermal detachment, and has many clinical similarities to severe burn injuries. The treatment is mainly supportive and aimed at preventing complications while the disease takes its natural course, and the skin reepithelializes. Much interest exists in the development of a specific therapy targeted at the disease process itself. Because the diagnosis has an incidence of only 0.5-1 case/million/year, large controlled studies are lacking, but a recent, better understanding of this disease has provided the rationale for the use of intravenous immunoglobulin. We present a case of toxic epidermal necrolysis that showed a good response to intravenous immunoglobulin G and review the recent literature condition and its management.



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10.) High-dose intravenous immunoglobulin for severe drug reactions: efficacy in toxic epidermal necrolysis.
.

Acta Derm Venereol. 2003;83(6):430-2.

Campione E, Marulli GC, Carrozzo AM, Chimenti MS, Costanzo A, Bianchi L.

Department of Dermatology, Tor Vergata University of Rome, Policlinico di Tor Vergata, Rome, Italy.

High-dose intravenous immunoglobulin has been proposed as an alternative treatment for several immuno-mediated inflammatory skin diseases, usually at a dosage of 1 - 2 g/kg. We describe the treatment of 10 patients affected by toxic epidermal necrolysis using 400 mg/kg per day on 5 consecutive days--a schedule that is lower than previously reported schedules. According to the SCORTEN, the earlier predicted mortality rate was 35%. After high-dose intravenous immunoglobulin therapy, a mortality rate of 10% and a survival rate of 90% were reached. In particular, nine patients showed a dramatic improvement already after one course of infusion started at an early stage of the disease. It is our experience, and that of others, that high-dose intravenous immunoglobulin can be considered the drug of first choice for toxic epidermal necrolysis, one of the most severe life-threatening dermatological conditions, and a valid alternative therapy for different long-standing chronic dermatological diseases. This therapy can also be effective in avoiding high steroid dosages and consequently steroid-related or immunosuppressive-related side effects. It is therefore reasonable to propose high-dose intravenous immunoglobulin treatment as a valuable therapeutic tool for dermatologists.
 



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DATA-MEDICOS/DERMAGIC-EXPRESS /JANUARY JOURNAL 2.004/ DR. JOSE LAPENTA R. 
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Maracay Estado Aragua Venezuela 2.004  
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