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
From Our Sponsors
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.
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.
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.
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.
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.
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
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.
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.
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.
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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