Acute generalized exanthematous pustulosis (AGEP) is a rare, severe type IV hypersensitivity reaction, most commonly triggered by antibiotics, calcium channel blockers, or antifungal agents, while fluconazole-induced AGEP is exceptionally reported. Early recognition and prompt management are essential to prevent complications. We report the case of a 21-year-old female with no personal or family history of psoriasis who developed a sudden-onset, pruritic, erythematous pustular rash six days after a single 150 mg dose of fluconazole prescribed for vaginal candidiasis. On examination, she was febrile (39°C) and asthenic, with widespread non-follicular pustules initially involving intertriginous areas and subsequently extending to the trunk and limbs. The Nikolsky sign was negative, and mucosal surfaces were spared. Laboratory investigations revealed leukocytosis (10,400/mm[3]) with neutrophilia (7,800/mm[3]), and pustular cultures were sterile. Histopathological examination showed intraepidermal pustules associated with dermal neutrophilic and eosinophilic infiltrates. The European Study of Severe Cutaneous Adverse Reactions (EuroSCAR) score was 11, confirming the diagnosis of fluconazole-induced AGEP. Rapid clinical improvement was observed following discontinuation of fluconazole and supportive treatment with antihistamines and emollients; desquamation occurred within four days, and no systemic complications were noted. Although rare, fluconazole should be considered a potential cause of AGEP, and early diagnosis with prompt withdrawal of the offending drug remains essential to ensure a favorable prognosis.

Paraphenylenediamine (PPD) is an aromatic amine that was first manufactured in Germany by Hofmann in 1833. It is primarily employed for its antioxidant and staining properties and is found in rubber goods, printer ink, photographic supplies, textiles and footwear, henna tattoos, and hair dyes. As it is a prehapten that can cross the skin barrier easily, it can be detected in plasma, urine, and faeces after application of hair dye within half an hour. The molecular properties of PPD allow hair dye to effectively permeate the skin, resulting in sensitisation and the eventual development of allergic contact dermatitis. Redness, pain, pruritus, dryness, prickling sensation, burning or tingling sensation, and discomfort are some of the symptoms of hair dye dermatitis. Clinically, allergic reactions to PPD may vary from localised lesions, such as eyelid eczema, nummular eczema, or hand eczema, to disseminated forms, such as airborne contact dermatitis, prurigo-nodularis-like, or erythroderma-like. Systemic contact dermatitis (SCD) is a severe, delayed immune-mediated reaction (type IV hypersensitivity reaction) to PPD, a common ingredient in hair dyes and temporary "black henna" tattoos, causing widespread eczema, intense itching, redness, swelling, and sometimes even asthma-like symptoms or lymph node swelling, occurring far beyond the direct contact area after initial sensitization, and requires strict avoidance of PPD in all forms. This is a case of a woman who presented with symmetrical drug-related intertriginous and flexural exanthema (SDRIFE)-like features, a type of SCD post hairdye application, but without any history of drug intake that is relevant for Baboon syndrome (synonymous with SDRIFE).

Symmetrical drug-related intertriginous and flexural exanthema (SDRIFE) is a symmetrical erythematous rash on the gluteal and intertriginous areas observed after exposure to systemic drugs.[1] Previously, in 1984, it was referred as baboon syndrome, due to the distribution of the lesions which localized to the buttocks and inner thighs (resembling the red rump of baboons), and observed as a response to systemic or local administration of contact allergens and drugs.[2] Hausermann proposed the term SDRIFE in 2004 as more appropriate for those reactions occurring after exposure to systemic drugs, regardless of prior sensitization.[3] SDRIFE is distinct from other cutaneous drug reactions due to its typical morphology, distribution, and the absence of systemic findings.

This case report describes a rare instance of symmetrical drug-related intertriginous and flexural exanthema (SDRIFE) following the first administration of intravenous immunoglobulin (Ig) in a woman in her 30s with secondary immunodeficiency from rituximab treatment for multiple sclerosis. 3 days after receiving her first dose of intravenous Ig, she developed a pruritic rash in her intertriginous regions of the body. Laboratory and dermatologic evaluation confirmed the SDRIFE diagnosis. Treatment with systemic and topical steroids led to the resolution of her symptoms and rash. This case represents one of the few reported cases of SDRIFE resulting from intravenous Ig treatment and the first to demonstrate successful continuation of immunoglobulin therapy with a change in intravenous Ig formulation. The patient has tolerated multiple subsequent infusions well, with no further rash, and with improvement in her frequency and severity of infections. This case highlights a rare complication of intravenous Ig therapy and describes a successful management to continue this critical therapy.

Symmetrical drug-related intertriginous and flexural exanthema (SDRIFE) is an uncommon, symmetrical drug rash that impacts intertriginous areas without exhibiting systemic symptoms. Its occurrence in a patient with pre-existing flexural dermatoses such as inverse psoriasis can complicate diagnosis, as in our case, where the eruption was initially suspected to represent a psoriatic flare. We present a 53-year-old female with biopsy-proven inverse psoriasis who experienced a broad symmetrical erythematous rash in flexural areas after receiving amoxicillin-clavulanate treatment. Clinical assessment, histopathological results, and Naranjo scoring supported a diagnosis of SDRIFE. The case emphasizes diagnostic challenges arising from shared characteristics with conditions like candidiasis, acute generalised exanthematous pustulosis (AGEP), and inverse psoriasis. SDRIFE was preferred over the flare of inverse psoriasis due to lesion appearance, temporal correlation with drug exposure, and absence of systemic symptoms. Interestingly, previous flexural psoriasis might have contributed as a risk factor via barrier impairment or recall phenomenon. This case emphasizes the importance of increased clinical awareness and histological assessment in flexural lesions, particularly in individuals with pre-existing dermatoses.

We present a case of a 2-month-old female with an acute onset and rapidly progressing diffuse erythroderma involving the scalp, face, neck folds, torso, and groin. She had a history of seborrheic and diaper dermatitis and developed a worsening rash that initially appeared as a "blister-like" lesion on the cheek. Examination revealed greasy yellow scaling and intertriginous erythema. Workup ruled out herpes simplex virus/varicella-zoster virus, and blood cultures grew presumed contaminant Staphylococcus epidermidis. She was treated empirically with antibiotics, antivirals, anti-fungals, and topical steroids. Dermatology suspected inverse psoriasis. The patient improved within 48 h of treatment. Diagnoses included inverse psoriasis, fungal diaper dermatitis with secondary bacterial infection, and possible early staphylococcal scalded skin syndrome. This case emphasizes the diagnostic complexity of infantile erythroderma and the importance of a broad differential and multidisciplinary approach. Recognition of inverse psoriasis in this age group is crucial, especially in the setting of superimposed fungal and bacterial infections.

Symmetrical Drug-Related Intertriginous and Flexural Exanthema is a rare and often overlooked cutaneous drug reaction. Prompt recognition of its symmetrical, flexural distribution and association with systemic drugs like amoxicillin-clavulanate can prevent misdiagnosis and ensure timely management.

Acute generalized exanthematous pustulosis (AGEP) is a rare, potentially severe cutaneous adverse reaction characterized by the rapid onset of numerous small, sterile pustules on edematous erythema, commonly accompanied by systemic symptoms such as high-grade fever and neutrophilic leukocytosis. AGEP is most frequently triggered by medications, especially antibiotics, though infections and other exposures can also be causative. We report the case of a previously healthy 27-year-old male patient who developed a febrile pustular eruption with systemic involvement. Initial symptoms included sore throat, malaise, and a progressing maculopapular rash evolving into pustular plaques. The patient had previously taken oral ibuprofen without any adverse reactions; therefore, a drug-related trigger was considered unlikely, and an infectious etiology was suspected. Diagnosis of definite AGEP was established through clinical evaluation, laboratory findings showing leukocytosis with neutrophilia, and histopathology revealing subcorneal neutrophilic pustules with dermal edema and eosinophilic infiltrate. This case underscores the importance of early recognition of AGEP in febrile pustular eruptions, even without clear drug exposure.