T-cell engager therapies, including bispecific T-cell engagers and the immune-mobilizing monoclonal T-cell receptor against cancer tebentafusp, are an emerging class of anticancer immunotherapy, with rapid expansion of the class since initial approval of blinatumomab in 2014 and with distinct dermatologic adverse events increasingly recognized across agents. Tebentafusp and talquetamab demonstrate highest rates of notable dermatologic toxicity reflecting on-target off-tumor cutaneous effects. Tebentafusp produces dermatologic adverse events in the majority of treated patients, characterized by diffuse erythematous and frequently photodistributed eruptions. Talquetamab is notable for a characteristic constellation of cutaneous, nail, and oral toxicities linked to target G protein-coupled receptor class C group 5 member D expression in keratinized tissues. Subcutaneous cluster of differentiation (CD)20- and B-cell maturation antigen-targeted agents frequently cause injection-site reactions, generally low-grade and self-limited. Blinatumomab and other CD19- and CD20-directed agents have been associated with a spectrum of heterogeneous rashes. Across agents, most dermatologic adverse events can be managed with topical corticosteroids, emollients, antihistamines, or brief courses of systemic corticosteroids without requiring treatment discontinuation. Recognition of these agent-specific and mechanistically linked patterns is essential for dermatologists as T-cell engager therapies become increasingly integrated into oncology practice.

Phototoxic drug eruptions are well-recognized adverse reactions to several classes of medications, including fluoroquinolones, sulfonamides, and antifungals. However, sequential photosensitization following exposure to multiple agents is rarely described. We present the case of a 44-year-old Hispanic male commercial driver who developed a severe, vesiculobullous, photo-distributed rash following sequential exposure to terbinafine, ciprofloxacin, and trimethoprim-sulfamethoxazole (Bactrim). The patient initially presented with ringworm of the lower extremity and was started on topical and oral terbinafine. When the rash worsened approximately one week later, he was sequentially prescribed ciprofloxacin and then Bactrim for suspected cellulitis. Each new medication was associated with progressive worsening of the rash, which was confined to sun-exposed areas (distal arms, distal legs, neck) and characterized by erythema, pruritus, pain, clear fluid-filled vesicles, and superficial skin peeling. There was no mucosal involvement, no Nikolsky sign, and no systemic symptoms. Laboratory evaluation revealed elevated C-reactive protein (2.7 mg/dL) with normal complete blood count, comprehensive metabolic panel, erythrocyte sedimentation rate, and negative autoimmune serologies (antinuclear antibody, anti-SSA, anti-SSB). Infectious workup, including HIV, syphilis, hepatitis panel, and blood cultures, was negative. An infectious disease consultant ruled out onychomycosis and cellulitis. All suspected offending medications were discontinued on admission. The patient was treated with intravenous methylprednisolone (40 mg every eight hours for three days), topical clobetasol, and supportive care. By hospital day three, the erythema had resolved completely, the vesicles had substantially decreased, and the pain had resolved. The patient was discharged home on a prednisone taper. This case highlights the importance of recognizing phototoxic drug eruptions in patients presenting with photo-distributed vesiculobullous rashes, particularly when multiple photosensitizing medications have been prescribed sequentially. A systematic approach to excluding infectious, autoimmune, and other drug-induced conditions is essential for diagnosis when a biopsy is not available.

While topical steroids are an invaluable tool used for the treatment of pruritic rashes, they can also complicate attempts at a definitive diagnosis. The temporal association between steroid use and biopsy must be taken into account when investigating the underlying etiology of such rashes. In patients with a history of dermatologic disease with the onset of a new rash, management should include a biopsy, if deemed necessary for diagnosis, followed by a prescription of topical steroids for symptomatic treatment. A 63-year-old male with a history of psoriasis presented with a new-onset pruritic, erythematous-to-violaceous rash on sun-exposed areas. The final diagnosis of subacute cutaneous lupus erythematosus (SCLE) was delayed due to the use of topical steroids on cutaneous eruptions before presentation in the clinic for biopsy. Diagnosis of SCLE can be difficult, especially for primary care providers who do not see the initial presentation regularly, as cutaneous findings can be variable in presentation. However, recurrent eruptions in similar photo-distributed locations should alert providers of a potential underlying diagnosis and prompt referral for dermatologic evaluation should be suggested. Thorough personal and family history should be taken and photographs of the rash should be documented in the patient's chart for future reference. Ultimately, biopsy is the gold standard diagnostic method for evaluating the etiology of new-onset rash. When there is suspicion of an underlying disease beyond idiopathic contact or irritant dermatitis, a biopsy should be considered as the next best step in management.

Drug-induced photodistributed telangiectasia (PT) is a cutaneous adverse effect (AE) resulting from the interaction of ultraviolet radiation with pharmacotherapy. Reports of PT in the literature are scarce. We report 25 cases of drug-induced PT highlighting the potential relationship between the onset of skin lesions, drug intake and photo exposure. We alert practitioners that PT is a possible dermatological phototoxic AE of many drugs.

A 27-year-old woman presented with persistent dryness of the mouth and eyes. She presented with permanent photodistributed rash involving the face and distal extremities. Laboratory tests showed positive Sjögren's syndrome (SS)-A and SS-B antibodies. Histological examination of minor salivary gland biopsy revealed inflammatory infiltration grade 4 according to Chisholm's classification. Skin biopsy showed acanthosis, hyperkeratosis in the epidermis and little inflammatory infiltrate in the dermis. There was an infiltration of CD4 T lymphocytes in the dermis. Based on the characteristics of the dermatitis and on a rapid response to niacin replacement, the diagnosis of pellagra was carried out. A complete resolution of the dermatological signs was obtained within 2 months. To the best of our knowledge, the association between primary SS and pellagra has never been reported. We emphasise the possible mechanisms of this association.

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening dermatological conditions that are characterized by mucositis, epidermal detachment and erosions. The underlying etiology in SJS and TEN is almost invariably secondary to drugs. Rarely, other causes such as systemic lupus erythematosus (SLE), infections and vaccinations have been implicated. This report describes three patients with SLE who presented with manifestations of SJS/TEN without a clear drug causality. All three patients presented with photodistributed macular exanthema, which evolved to target lesions, bullae, erosions or sheet-like detachment. This was associated with oral mucositis and conjunctivitis. The onset of the rash was insidious with a protracted clinical course. Ultraviolet exposure and steroid tapering appear to be precipitating factors. In two of the patients, SJS and TEN were the initial presentation of lupus. Although SJS and TEN are almost invariably due to medications, they may, rarely, be an initial presentation of lupus, particularly when associated with an initial photodistribution, absence of genital involvement and a prolonged clinical course.