Importance: Dermatologic and psychotropic therapies intersect frequently in patients with bipolar disorder, in whom systemic dermatologic medications may affect mood stability and mood stabilizers or antipsychotics may produce clinically important cutaneous adverse reactions. Because several medications discussed in this review are also used for psychotic disorders, severe or treatment-resistant major depressive disorder, suicidality, and other psychiatric conditions, this article distinguishes medication-related risks from considerations specific to bipolar disorder.

Treatment options remain limited for unresectable or advanced lung squamous cell carcinoma (LSqCC) that progresses after immune checkpoint inhibitor (ICI)-based therapy. Although combination therapy with cisplatin, gemcitabine, and necitumumab (CGN) represents a potential second-line regimen, no prospective data in a post-ICI setting have been reported. This open-label, multicenter single-arm Phase II study enrolled patients with LSqCC after platinum-based chemotherapy plus ICI, including concurrent chemoradiotherapy. The primary endpoint was objective response rate (ORR), with the null and alternative hypotheses set at 23% and 40%, respectively. Secondary endpoints included the disease-control rate (DCR), progression-free survival (PFS), overall survival (OS), the impact of platinum-free interval (PFI), eligibility for anti-angiogenic therapies, and safety. Forty-six patients were evaluable for efficacy. ORR was 26.1% (80% CI, 17.7-36.2) and DCR was 87.0% (95% CI, 73.7-95.1). Median PFS and OS were 4.4 months (95% CI, 4.1-5.5) and 12.2 months (95% CI, 9.4-15.2), respectively. Common adverse events included hematological toxicities, acneiform rash, and hypomagnesemia. No pneumonitis or treatment-related deaths were observed. The safety profile was consistent across prior treatment types and anti-angiogenic therapies eligibility. PFI analysis showed that longer PFI durations were associated with improvements in PFS and OS, and the optimal PFI cutoff value was approximately 4 months. Although the predefined response threshold was not met, CGN demonstrated modest antitumor activity with a high DCR and a manageable toxicity after ICI-based therapy. CGN may be a feasible treatment option for second-line after ICI-based therapy, including for patients unsuitable for anti-angiogenic therapies, although further validation is warranted. Trial Registration: jRCTs051200138.

Chronic non-bacterial osteitis (CNO) is an autoinflammatory bone disorder with an evolving classification and limited treatment options. It encompasses conditions like SAPHO (Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis) syndrome and chronic recurrent multifocal osteomyelitis, which share overlapping clinical and radiological features. While nonsteroidal anti-inflammatory drugs (NSAIDs) serve as first-line therapy, refractory cases require second-line options such as tumor necrosis factor (TNF) inhibitors or bisphosphonates. Emerging evidence suggests Janus kinase inhibitors (JAKis), including tofacitinib, as a viable third-line alternative, though data remains limited. We describe a 16-year-old adolescent male presenting with multifocal osteitis and acneiform lesions, initially classified as SAPHO syndrome but later redefined as CNO based on "2024 recommendations published in Annals of the Rheumatic Diseases." The patient had an inadequate response to NSAIDs, and financial constraints precluded the use of TNF inhibitors or bisphosphonates. Tofacitinib (5 mg twice daily) was introduced as a third-line therapy. Within 8 weeks, the patient showed significant symptom resolution, and magnetic resonance imaging confirmed a reduction in STIR (Short-Tau Inversion Recovery) hyperintense signals. By 6 months, there was complete clinical and radiological remission. This case underscores the reclassification of SAPHO within the broader CNO spectrum and highlights the potential role of tofacitinib as a third-line treatment for refractory CNO. The rapid and sustained response observed suggests that JAKis could be considered in select cases where second-line options are inaccessible. Further research is warranted to establish optimal treatment strategies for this complex condition.

Eczema molluscatum refers to widespread molluscum contagiosum (MC) infection occurring in patients with atopic dermatitis (AD), a setting in which impaired skin barrier function and immune dysregulation both promote viral spread. We report the case of a 29-year-old man with longstanding, treatment-refractory AD who was well controlled on upadacitinib, a selective Janus kinase 1 (JAK1) inhibitor, and methotrexate when he developed multiple pink, dome-shaped papules with central umbilication across the cheeks and forehead over a six-month period. The lesions were unresponsive to topical clindamycin-benzoyl peroxide gel. The differential diagnosis included eczema coxsackium, eczema herpeticum, eruptive syringomas, and a refractory JAK inhibitor-associated acneiform eruption, but the absence of pain, systemic symptoms, vesiculation, and follicular morphology supported a diagnosis of eczema molluscatum. The patient was treated with cryotherapy for each lesion, with marked improvement at one-month follow-up. AD itself is a recognized risk factor for MC, reflecting the disease's inherent Th2-skewed, barrier-disrupted immune environment. However, this case raises the possibility that systemic immunosuppression with JAK1 inhibitors, particularly in combination with methotrexate, may further impair type I interferon-mediated antiviral defense and compound susceptibility to MC in patients with AD. Nonetheless, clinicians should maintain a high index of suspicion for eczema molluscatum in patients with AD on JAK inhibitor therapy who develop new facial papules, as these lesions are readily mistaken for a JAK inhibitor-associated acneiform eruption, potentially delaying appropriate treatment.

Atopic dermatitis (AD) is a chronic inflammatory skin disease that may require systemic therapy in patients with moderate-to-severe or refractory disease. Tofacitinib, a Janus kinase (JAK) inhibitor, has demonstrated efficacy in the treatment of severe inflammatory dermatoses, including refractory AD. However, its use may be associated with various adverse events, and acneiform eruptions have increasingly been reported with JAK inhibitor therapy. We report the case of an 18-year-old female patient with severe AD who was treated with tofacitinib, resulting in marked improvement of her eczematous lesions and pruritus. After several weeks of treatment, she developed inflammatory facial acne without a history of severe acne or any other identified precipitating factor. Clinical examination revealed multiple inflammatory papules and pustules predominantly involving the centrofacial region, associated with comedones and microcysts. Laboratory investigations were unremarkable. The acne was successfully managed with appropriate topical therapy while tofacitinib was continued. This case highlights acne as a potentially emerging cutaneous adverse event associated with JAK inhibitor therapy. Early recognition and appropriate management may help prevent impairment of quality of life and treatment adherence while allowing continuation of effective systemic therapy for severe AD.

A middle-aged man presented with asymptomatic multiple grouped papules present bilaterally symmetrically on the face. Histopathology revealed peri-follicular, predominantly B-cell lymphoid aggregates with germinal center formation and occasional tingible body macrophages. Immunohistochemistry for Bcl-2 was positive in the peripheral mantle zone while sparing the follicle center, suggesting a reactive lymphoid follicle. Clinical differential diagnosis of facial papules can be broad, encompassing sarcoidosis, granulomatous rosacea, lupus miliaris disseminatus faciei, acneiform eruption, and eruptive benign appendageal tumors, among others. We report a rare case of pseudolymphoma clinically presenting as multiple facial papules, diagnosed through combined histopathological and immunohistochemical evaluation.

Epidermal growth factor receptor (EGFR) inhibitors commonly cause papulopustular eruptions that may significantly impair quality of life and interfere with continuation of effective oncologic therapy. Oral tetracyclines remain the cornerstone of treatment because of their anti-inflammatory properties; however, prolonged therapy, particularly with minocycline, carries a risk of cumulative adverse effects, including drug-induced hyperpigmentation. We report the case of a 40-year-old man with hereditary leiomyomatosis and renal cell carcinoma (HLRCC) who developed an EGFR inhibitor-associated papulopustular eruption shortly after initiating erlotinib and bevacizumab. Persistent disease despite doxycycline therapy and concern for doxycycline-associated photosensitivity prompted a transition to long-term minocycline. After approximately 29 months of treatment, the patient developed symmetric slate-blue macules on the bilateral shins consistent with type II minocycline-induced hyperpigmentation. Reduction of the minocycline dose resulted in gradual improvement of the pigmentation while maintaining adequate control of the eruption. This case highlights the importance of longitudinal dermatologic follow-up in patients receiving prolonged tetracycline therapy for EGFR inhibitor-associated cutaneous toxicities. Periodic reassessment of treatment necessity, dose optimization, and early recognition of delayed medication-related adverse effects may minimize cumulative toxicity while preserving effective oncologic therapy.