Symmetrical drug-related intertriginous and flexural erythema is characterized by a diffuse symmetric rash of the gluteal and intertriginous areas with only one published report of association with tamoxifen. It is imperative for clinicians to recognize tamoxifen-induced SDRIFE to avoid life-threatening dermatologic complications, which can be resolved with discontinuation of tamoxifen.

Symmetrical drug-related intertriginous and flexural exanthema, commonly known as \"baboon syndrome\" due to its typical involvement of the gluteal area, is an erythematous symmetrical rash associated with systemic drug administration.

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BACKGROUND: Symmetrical drug-related intertriginous and flexural exanthema (SDRIFE), formerly also called baboon syndrome, is characterized by symmetrical erythematous rash with typical localization in the gluteal and intertriginous areas. A type IV delayed hypersensitivity immune response is thought to be responsible for its development. CGRP monoclonal antibodies (CGRP mAbs) are a new class of drugs for the prevention of migraine. We present the first case of SDRIFE occurring in temporal relation to the use of erenumab for migraine prevention.
METHODS: A 48-year-old female patient with migraine received erenumab 140 mg subcutaneously in the thigh area for the prevention of migraine in repetitive cycles, each 1 month apart. Initially, the patient experienced no side effects. After the third cycle, a masseuse incidentally noticed a reddish, circular rash in the buttock area during a back massage. There were no other symptoms. The skin changes resolved spontaneously. Two years later, approximately 40 h after reapplication of erenumab 140 mg, the patient experienced a severe pain in the buttock area centered over the anal crease. The area of pain extended in a circular pattern with approximately 20 cm in diameter. The pain started abruptly and reached a severe intensity within about 30 min. Sitting on the buttocks was no longer possible for the patient. There was marked allodynia and hyperpathia in the entire buttocks region. A flat, broad-based blister-like skin swelling developed in this region. The blisters began opening up on the fourth day after the onset of the skin reaction. In addition, there was a pronounced redness in the entire buttock area. Here, the patient felt a strong burning pain, similar to a scald.
RESULTS: The symptoms lasted for a period of 10 days. From this point on, they fully subsided under concomitant therapy with prednisolone.
CONCLUSIONS: SDRIFE as a rare dermatological side effect should be considered in the monitoring of skin lesions during migraine prophylaxis. In view of the high migraine prevalence, knowledge of this uncommon syndrome is important. It is crucial to recognize the relationship between the medication and the circumscribed exanthema occurring distant from the injection site.

Herein, we present a case of baboon syndrome/SDRIFE that occurred after intake of valsartan/hydrochlorothiazide for several years. The patient falls within the five diagnostic criteria and to the best of our knowledge, there have been no previous reports associating valsartan/hydrochlorothiazide with baboon syndrome/SDRIFE. Withdrawal of the anti-hypertensive drugs and initiation of topical and systemic steroids provided symptomatic relief and follow-up showed favourable results with complete remission of the cutaneous eruptions.

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Baboon syndrome, also called symmetrical drug-related intertriginous and flexural exanthema (SDRIFE), is an erythematous maculopapular rash that presents in skin folds in a symmetrical pattern. This condition may develop after the patient starts a particular agent. Treatment consists of stopping the associated trigger and medicating with topical or systemic corticosteroids. A 30-year-old man with odynophagia, otalgia and fever was prescribed amoxicillin. He developed erythematous and pruriginous lesions in the cubital fossa and inguinal regions. He attended the emergency department (ED) where he was prescribed penicillin. Lesions continued to progressively worsen with a bilateral symmetrical pattern in the axillary region and later in the nape folds, popliteal regions, and on the perineum and buttocks. The patient presented to the ED for a second time, where he was diagnosed with baboon syndrome and prescribed topical steroids with clear improvement.
CONCLUSIONS: It is important to identify adverse drug effects.Baboon syndrome is rare and secondary to the use of particular drugs.The diagnosis is based mainly on the patient\'s clinical presentation.

The literature on systemic allergic dermatitis (SAD; synonym: systemic contact dermatitis) is reviewed. Both topical drugs (from absorption through mucosae or skin) and systemic drugs (oral, parenteral, rectal) may be responsible. The topical route appears to be rare with 41 culprit topical drugs found causing SAD in 95 patients. Most reactions are caused by budesonide (especially from inhalation), bufexamac and dibucaine. SAD from systemic drugs is infrequent with 95 culprit drugs identified causing SAD in 240 patients. The drugs most frequently implicated are mitomycin C, methylprednisolone (salt, ester) and hydrocortisone (salt). The largest group of drugs consisted of corticosteroids (19%), being responsible for >30% of the reactions, of which nearly 40% were not caused by therapeutic drugs, but by drug provocation tests. The most frequent manifestations of SAD from drugs are eczematous eruptions (scattered, widespread, generalized, worsening, reactivation), maculopapular eruptions, symmetrical drug-related intertriginous and flexural exanthema (SDRIFE, baboon syndrome) and widespread erythema or erythroderma. Therapeutic systemic drugs hardly ever cause reactivation of previously positive patch tests and infrequently of previous allergic contact dermatitis. The pathophysiology of SAD has received very little attention. Explanations for the rarity of SAD are suggested. All data in this article are fully referenced (n=272). This article is protected by copyright. All rights reserved.

Systemic contact dermatitis (SCD) is a generalized reactivation of type IV hypersensitivity skin diseases in individuals with previous sensitization after a contact allergen is administered systemically. Patients with SCD may consider their dermatitis unpredictable and recalcitrant since the causative allergens are difficult to find. If a patient has a pattern of dermatitis suggestive of SCD but fails to improve with conventional treatment, SCD should be taken into consideration. If doctors are not familiar with the presentations of SCD and the possible routes of allergen sensitization and exposure, the diagnosis of SCD may be delayed. In this work, we summarized all of the routes through which allergens can enter the body and cause SCD, including oral intake, local contact (through skin, inhalation, nasal spray and anal application), implants, and other iatrogenic or invasive routes (intravenous, intramuscular, intraarticular, and intravesicular). This will provide a comprehensive reference for the clinicians to identify the culprit of SCD.