Case Of Stevens-Johnson Syndrome Research Articles

Fluconazole-induced Stevens-Johnson Syndrome in a HIV-negative Patient

Sir, Stevens-Johnson syndrome (SJS) is a rare and severe mucocutaneous disorder, most frequently caused by systemic drugs, with an incidence of 1–6 cases per million person-years (1). It is characterized clinically by a maculopapular and bullous eruption with epidermal necrosis and detachment, mucosal ulcers and erosions and constitutional signs and symptoms. SJS and toxic epidermal necrolysis (TEN) are presently regarded as clinical forms of the same disorder that share common aetiopathogenetic factors but mainly differ in: (i) the extent of epidermal detachment (SJS 30%); (ii) the prognosis (SJS = good; TEN = poor); and (iii) the mortality rate (SJS < 5% vs. TEN = 30–40%) (2, 3). Although the exact pathogenetic mechanisms of SJS and TEN at the molecular and cellular level remain to be elucidated, there is evidence suggesting a cytotoxic cell immune response against keratinocytes that is induced by various drugs, mostly sulphonamides, allopurinol, phenytoine, phenobarbital, carbamazepine, lamotrigine, non-steroidal anti-inflammatory drugs and nevirapine (4). Since it is of essential importance to recognize and report drugs capable of inducing severe adverse reactions, we describe herein the first case of SJS occurring in a HIVnegative patient during oral fluconazole treatment. CASE REPORT A 50-year-old Caucasian woman was admitted to the Department of Dermatology at the University of Patras Medical Center with a 3-day history of skin and mucosal lesions accompanied by high fever and malaise. The cutaneous manifestations had developed one week after the onset of treatment of vaginal candidiasis with 200 mg/day oral fluconazole (Flucodrug caps; Med-One, Athens, Greece). Apart from fluconazole, the patient had received no other medication and had no history or evidence of infectious, autoimmune or neoplastic disorders. Physical examination of the patient on admission revealed a confluent erythematoviolaceous, maculopapular and focally bullous pruritic skin rash with large numbers of targeted lesions over her face, upper trunk and the extremities. In a small area on her back, epidermal detachment was clearly seen (Fig. 1A). There were superficial ulcers and erosions in the oral mucosae, erosions and crusts on her oedematous lips (Fig. 1B) and a severe conjunctivitis. Blisters and epidermal detachment affected about 9% of the patient’s body surface. Apart from a vaginal culture positive for Candida albicans, all haematological, biochemical, immunological and serological investigations (including tests for HSV, HIV 1 & 2, hepatitis A, B and C, Toxoplasma, Epstein Barr virus, Fluconazole-induced Stevens-Johnson Syndrome in a HIV-negative Patient

A Case of Stevens-Johnson Syndrome Associated with Mycoplasma pneumoniae Pneumonia in an Adult Patient

Stevens-Johnson syndrome is an acute mucocutaneous syndrome that is related to drugs and infections. Mycoplasma pneumoniae infection is known as one of the causes of Stevens-Johnson syndrome in children and young adults. In Korea, Mycoplasma pneumoniae infection is rarely reported as a cause of Stevens-Johnson syndrome in adults. We report a case of StevensJohnson syndrome associated with Mycoplasma pneumoniae pneumonia in an adult patient. A 34-years old woman was admitted to our hospital and was diagnosed with mycoplasma pneumonia. At the time of admission, she had hemorrhagic crusts on her lips. On the 2nd day of admission, target lesions also developed on her skin. We diagnosed her disease as StevensJohnson syndrome associated with Mycoplasma pneumoniae pneumonia. She completely recovered from pneumonia and Stevens-Johnson syndrome after treatment with antibiotics and conservative management.

Syndrome de Stevens-Johnson à la lymécycline (Tétralysal ®)

Reports of severe drug-induced bullous reactions to tetracyclines are rare. A case of Stevens-Johnson syndrome in a patient treated with lymecycline is reported herein. A 22 year-old woman with acne was referred for Stevens-Johnson syndrome occurring ten days after starting lymecycline. The patient was initially treated with high doses of corticosteroid. She presented with severe oral and vulvar erosions and erosive cutaneous lesions involving 5 to 7% of the body surface area. Erosive cutaneous lesions progressively extended to 20-30% of the body surface area for a 27-day period. Histological analysis of a skin biopsy showed epidermal necrolysis typical of toxic epidermal necrolysis. Epithelialization of mucosal and cutaneous lesions was achieved 34 days after lymecycline withdrawal. Stevens-Johnson syndrome is an extremely rare reaction to lymecycline. The prolonged development of skin lesions seen here after lymecycline withdrawal despite the short half life of the drug is surprising. It could have been due to use of strong systemic corticosteroids, as described in certain other case reports.

Stevens-Johnson Syndrome From Oral Acetazolamide In A 19-Year Old Male

RATIONALE: Stevens-Johnson Syndrome (SJS) is described as a systemic adverse reaction to drugs with severe cutaneous manifestations. This reaction is particular to certain classes of drugs such as nonsteroidal anti-inflammatory drugs, allopurinol, anticonvulsants, antibacterial sulfonamides and chlormezanone. Carbonic anhydrase inhibitors are rarely associated with SJS and there has been no previously reported case of SJS from oral acetazolamide.

Betahistine

Betahistine is a structural analogue of histamine that is prescribed for the treatment of vestibular disorders such as Ménière's disease and the symptomatic treatment of vertigo. It is estimated from sales information that >130 million patients have been exposed to the drug since its registration in 1968. In this review we analyse the safety profile of betahistine based on data obtained during >35 years of worldwide postmarketing surveillance. Until 31 December 2005, 554 adverse drug reaction (ADR) reports with 994 individual signs and symptoms were received by the marketing authorisation holder from worldwide sources and were reviewed and evaluated. Signs and symptoms of cutaneous hypersensitivity reactions during betahistine therapy were the most frequently reported complaints. They consisted of usually mild and self-limiting rash, pruritus and urticaria, and all symptoms were reversible after drug discontinuation. Betahistine was reported to be involved in one anaphylactoid reaction and one case of Stevens-Johnson syndrome. Anaphylactic reactions with fatal outcome were not reported. The reports that describe gastrointestinal complaints mostly concern nausea and vomiting or unspecific abdominal pain. These were typically non-serious complaints. Hepatobiliary involvement was reported 25 times, including increases in alkaline phosphatase, gamma-glutamyltransferase, and alanine and aspartate aminotransferase levels. None of the patients concerned developed severe liver failure or died. ADRs related to the nervous system predominantly reveal heterogeneous events that are not suggestive of a specific adverse reaction profile for betahistine. A clinical intolerance to betahistine that gave rise to asthma or bronchospasm was only reported in eight ADRs. A total of three cases of neoplasm have been reported. One case concerned a male patient of unknown age who experienced weight loss, insomnia, impatience and irritability soon after the start of betahistine therapy. An undiagnosed phaeochromocytoma was suspected. The remaining two cases were assessed as being unrelated to betahistine by the reporter. Finally, four deaths have been reported during the course of postmarketing surveillance for betahistine. The reporter assessed the causal relationship to betahistine in two as unrelated, in one as unlikely and the other as unassessable. In summary, clinical and postmarketing studies have revealed a good safety profile of betahistine that was confirmed by the safety surveillance data presented.

Chlordiazepoxide-induced Stevens-Johnson Syndrome

The causes of Stevens-Johnson syndrome (SJS) can be categorized as iatrogenic, infectious or idiopathic. Drug-induced SJS is associated with various antibiotics, anticonvulsants, and other drugs. However, no previous reports have mentioned an association between chlordiazepoxide, a benzodiazepine sedative, and SJS. Here, we present a case of SJS induced by chlordiazepoxide overdose. This case reminds us that SJS may be an adverse effect of chlordiazepoxide. Further, overdosage with benzodiazepine sedatives should be added to the list of potential causes of SJS.

Síndrome de Stevens-Johnson probablemente asociado a tratamiento con amifostina durante la radioterapia

The Stevens-Johnson syndrome is a muco-cutaneous disorder related to pharmacological agents. The most frequent cause is sulphonamides in 30% of cases. The incidence rate of severe cutaneous reactions secondary to amifostine is <1%; Stevens-Johnson syndrome being one of them. We report a case of Stevens-Johnson syndrome probably related to amifostine administration during radiation therapy.

Stevens-Johnson Syndrome Secondary to Vancomycin Exposure

A case of Stevens-Johnson syndrome (SJS) is reported in a 64- year-old woman following 8 days of vancomycin for the treatment of a urinary tract infection with methicillin-resistant Staphylococcus aureus. Diffuse erythematous plaques with dusky centers confluent over the trunk, arms, and axillae, lesions of the oral mucosa, and conjunctiva involvement were present. Beta-lactam antibiotics, sulfa drugs, and anticonvulsants have the highest incidences of SJS. Cases of vancomycin-induced SJS have been reported in the literature. This patient received supportive care and systemic and topical corticosteroids. However, the efficacy and safety associated with the use of corticosteroids in the treatment of SJS remain controversial. Vancomycin has been associated with the development of SJS and the ability of corticosteroids to decrease morbidity, and slow the progression of lesions associated with SJS remains unclear.

Stevens-Johnson Syndrome Associated with Codeine in a Child

Stevens-Johnson syndrome and toxic epidermal necrolysis (TEN) are part of a spectrum of mucocutaneous disorders with similar clinical features. The incidence of TEN and StevensJohnson syndrome has been estimated at 0.4 to 1.2 and 1 to 6 cases per million person-years, respectively.[1-3] Factors such as race, age, gender and socioeconomic status do not appear to affect the epidemiology of the two disorders. The pathophysiology of these skin syndromes remains unknown. Stevens-Johnson syndrome is considered to be a milder form of TEN. StevensJohnson syndrome typically presents as small blisters on dusky pruritic macules on the face and upper trunk, occurring 1 to 3 weeks after drug exposure. The rash progresses rapidly to include the epithelium of the gastrointestinal and respiratory tracts and eyes, and it usually reaches its maximum within hours to days.[4] Detachment of less than 10% of the epidermis is considered StevensJohnson syndrome, while involvement of greater than 30% of the body surface is diagnosed as TEN. Fever is usually higher in TEN than in StevensJohnson syndrome. Mortality depends upon the extent of skin necrosis and damage to other systems and is usually below 5% for Stevens-Johnson syndrome and as high as 30% in cases of TEN.[1,5] Patients may be severely dehydrated with electrolyte abnormalities, and anaemia, lymphopenia and pre-renal azotemia are common. Bacterial colonisation of the skin and decreased immune response increases the likelihood of sepsis, the major cause of death.[4] Thirty-five percent of patients with TEN and fewer with Stevens-Johnson syndrome experience ocular sequelae including formation of synechiae between the eyelids and the conjunctiva, corneal erosions and scarring, and punctate keratitis.[6] Neutropenia, visceral involvement and high blood urea nitrogen levels are associated with a poorer prognosis. While both are primarily associated with drug use, infections, including mycoplasma pneumonia and viruses, are also implicated in the Stevens-Johnson syndrome. The drugs most often causing Stevens-Johnson syndrome and TEN include sulfonamides, aminopenicillins, phenytoin and nonsteroidal anti-inflammatory drugs (NSAIDs). Despite its wide clinical use for cough suppression and pain control, codeine has not been implicated as a cause of Stevens-Johnson syndrome. We report a paediatric case of Stevens-Johnson syndrome associated with codeine phosphate.

Bupropion-Induced Erythema Multiforme

Bupropion-Induced Erythema Multiforme

Stevens-Johnson Syndrome with Ginkgo Biloba

Gingko biloba is a popular herbal remedy for improving memory. Its side effects include headaches, stomach upset, bleeding complications and dermatitis. We report another adverse reaction, a case of Stevens-Johnson syndrome (SJS), which appears to be associated with use of gingko biloba. Ingestion by our patient of two doses of a ginkgo-containing preparation resulted in exfoliative rash, blistering and other symptoms consistent with SJS. Upon aggressive treatment with corticosteroids, her rash improved, however, she still had residual symptoms five months after treatment. It is important for clinicians to be aware of this possible side effect related to use of ginkgo preparations.

Intravenous Immunoglobulin Therapy for Stevens-Johnson Syndrome

Stevens-Johnson syndrome (SJS) is an acute mucocutaneous disorder that can be associated with considerable morbidity. Several previous reports, all involving either adults with acquired immunodeficiency syndrome or children, suggest that intravenous immunoglobulin may be an effective treatment for SJS. We report a case of SJS in an immunocompetent adult whose condition improved dramatically after therapy with intravenous immunoglobulin.

Stevens-Johnson Syndrome with Ginkgo Biloba

Gingko biloba is a popular herbal remedy for improving memory. Its side effects include headaches, stomach upset, bleeding complications and dermatitis. We report another adverse reaction, a case of Stevens-Johnson syndrome (SJS), which appears to be associated with use of gingko biloba. Ingestion by our patient of two doses of a ginkgo-containing preparation resulted in exfoliative rash, blistering and other symptoms consistent with SJS. Upon aggressive treatment with corticosteroids, her rash improved, however, she still had residual symptoms five months after treatment. It is important for clinicians to be aware of this possible side effect related to use of ginkgo preparations.

Stevens-Johnson syndrome associated with concomitant use of lamotrigine and valproic acid

<h2>Abstract</h2> Lamotrigine (LTG) is a novel antiepileptic drug effective in partial and generalized seizures. Recently, this drug has started being used for mood stabilization in psychiatric patients. Cutaneous side effects of this drug are mostly maculopapular eruptions that have been seen in 3% to 10% of patients. We describe a 33-year-old female patient in whom Stevens-Johnson syndrome (SJS) developed because of LTG. The drug was discontinued, and patient's signs and symptoms progressively resolved in 10 days after oral prednisolone therapy. The case is relevant because this is the first case of SJS as a result of LTG, probably associated with concomitant use of valproic acid and neuroleptic drugs. (J Am Acad Dermatol 2000;43:898-9.)

Stevens-Johnson syndrome associated with concomitant use of lamotrigine and valproic acid

Lamotrigine (LTG) is a novel antiepileptic drug effective in partial and generalized seizures. Recently, this drug has started being used for mood stabilization in psychiatric patients. Cutaneous side effects of this drug are mostly maculopapular eruptions that have been seen in 3% to 10% of patients. We describe a 33-year-old female patient in whom Stevens-Johnson syndrome (SJS) developed because of LTG. The drug was discontinued, and patient's signs and symptoms progressively resolved in 10 days after oral prednisolone therapy. The case is relevant because this is the first case of SJS as a result of LTG, probably associated with concomitant use of valproic acid and neuroleptic drugs. (J Am Acad Dermatol 2000;43:898-9.)

Stevens-Johnson Syndrome after Erythromycin Therapy While Deployed at Sea

Stevens-Johnson syndrome is a cutaneous reaction pattern that represents the progression of symptoms of erythema multiforme. These reactions can range from mild (EM minor) to severe (EM major) and even life-threatening (Stevens-Johnson syndrome or toxic epidermal necrolysis). The difference between Stevens-Johnson syndrome and toxic epidermal necrolysis is the percentage of body surface area involved; toxic epidermal necrolysis involves widespread skin necrosis and bullous formation with epidermal detachment resembling scalded skin. The three most common triggers for Stevens-Johnson syndrome are herpes simplex infection, Mycoplasma infection, and drug reactions. This is a case of Stevens-Johnson syndrome occurring after erythromycin treatment aboard an aircraft carrier while deployed at sea in the Persian Gulf.

Stevens-Johnson syndrome limited to multiple sites of radiation therapy in a patient receiving phenobarbital

Stevens-Johnson syndrome (SJS) is a severe cutaneous eruption that most often appears as an adverse reaction to a medication. There have been 21 reported cases of atypical erythema multiforme, toxic epidermal necrolysis, and SJS arising in patients receiving radiation therapy in addition to phenytoin, phenobarbital, or carbamazepine. We report the second case of SJS resulting from concomitant phenobarbital and radiation therapy, in which the eruption was limited to the sites of radiation, which were multiple.(J Am Acad Dermatol 1999;40:493-6.)

Diaminopyrimidines and Severe Cutaneous Adverse Reactions

The occurrence of cutaneous adverse reactions with the use of lamotrigine (Lamictal, Glaxo-Wellcome Inc, Research Triangle Park, NC) should prompt a reevaluation of rashes seen with the use of drugs of similar structure, specifically diaminopyrimidines. Trimethoprim and pyrimethamine both contain diaminopyrimidine ring structures. Lamotrigine has a triazine ring structure but is strikingly similar in other respects (Figure). Lamotrigine is currently marketed as an anticonvulsant in the United States and in more than 67 countries worldwide. During premarketing clinical trials of lamotrigine in 3400 subjects, one case of Stevens-Johnson syndrome and one case of toxic epidermal necrolysis were reported.1This incidence rate of 2 per 3400 individuals exposed is comparable to (if not greater than) the risks of severe cutaneous adverse reactions reported for the combination products trimethoprim-sulfamethoxazole (1-3 per 100 000 exposed) and pyrimethamine-sulfadoxine (10-20 per 100 000 exposed).2,3Pyrimethamine-sulfadoxine is marketed in the United States (Fansidar, Roche

スルピリンによると思われたＳｔｅｖｅｎｓ‐Ｊｏｈｎｓｏｎ症候群の１例

スルピリンによると思われたＳｔｅｖｅｎｓ‐Ｊｏｈｎｓｏｎ症候群の１例

Adverse Reactions to Dapsone in Persons Infected with Human Immunodeficiency Virus

Dapsone is used in prophylaxis for and treatment of Pneumocystis carinii pneumonia. We present a case of Stevens-Johnson syndrome that was likely induced by administration of dapsone. A review of charts at the HIV Treatment Center of Northwestern University (Chicago) revealed that 40.3% of patients treated with trimethoprim-sulfamethoxazole could not tolerate the medication, while 25.2% of those treated with dapsone were intolerant of the drug. We also found a higher rate of adverse reactions to dapsone among patients with prior intolerance to trimethoprim-sulfamethoxazole than among patients without such a history; however, the difference was not significant.