Localized cutaneous squamous cell carcinoma (cSCC) has a favorable prognosis, unlike advanced disease, especially with clinical perineural invasion (PNI), which poses substantial management challenges due to aggressivity and higher recurrence, metastasis, and mortality risks. PNI, a high-risk staging feature, has worse outcomes, particularly when clinically evident rather than incidental. Clinical PNI (cPNI) is evident by clinical symptoms (such as pain, paresthesia, or motor deficits) or radiologic findings, whereas incidental PNI (iPNI) is identified only histologically without associated symptoms or radiologic evidence. PNI remains a novel area with varying practice patterns across institutions. Improving risk stratification and tailoring multidisciplinary approaches are critical for optimizing outcomes. Our review outlines clinical practice patterns at our institution, providing insights into managing cSCC with PNI, focusing on diagnosis, imaging, staging, and emerging immunotherapies. A structured search was conducted using the terms “perineural invasion,” “cutaneous squamous cell carcinoma,” and “immunotherapy.” cPNI has a poor prognosis and requires nuanced clinical decision-making. Surgery and radiation remain central to management. Adjuvant therapy offers substantial survival benefit in cSCC with PNI, with improved disease-free and overall survival compared with surgery alone, supporting its use in appropriately selected high-risk patients. Traditional systemic therapies, including cisplatin and cetuximab, remain foundational but have shown only moderate response rates and limited durability in advanced or neurotropic cSCC. In contrast, immunotherapy—now preferred for advanced or unresectable cases—has transformed management, with programmed cell death protein-1 (PD-1) inhibitors showing promising results (up to 69% response rate) and disease stabilization. Neoadjuvant immunotherapy may enable tumor downstaging, improve radiation planning, and reduce surgical morbidity. Imaging for squamous cell carcinoma (SCC) with PNI aids staging and surveillance, but symptoms remain key for detecting recurrence. Our multidisciplinary approach emphasizes personalized care. Larger trials are needed to define the optimal role and sequencing of immunotherapy in this high-risk patient population.

Catastrophic antiphospholipid syndrome (CAPS) is a rare, life‐threatening variant of antiphospholipid syndrome (APS) characterized by rapid, widespread thrombosis leading to multiorgan failure. Affecting less than 1% of APS patients, CAPS is associated with a high mortality rate of 30%–50%, necessitating prompt diagnosis and aggressive treatment. The mainstay of management includes anticoagulation, high‐dose glucocorticoids, and plasma exchange or intravenous immunoglobulins, with biologic therapies such as rituximab and eculizumab reserved for refractory cases. We report a case of a 60‐year‐old male with a history of triple‐antibody–positive APS complicated by recurrent diffuse alveolar hemorrhage (DAH), adrenal hemorrhage, chronic kidney disease, and superficial vein thrombosis. His condition progressed to CAPS approximately 5 years prior with a course complicated by heparin‐induced thrombocytopenia. His condition stabilized with high‐dose corticosteroids and rituximab therapy with sustained symptomatic improvement after 10 months of rituximab. This case highlights the complexity of CAPS diagnosis and management, in the context of DAH, emphasizing the importance of early recognition, multidisciplinary care, and individualized treatment strategies. Our patient’s prolonged disease stabilization with rituximab underscores its potential role in long‐term CAPS management. Further research is needed to refine treatment protocols and improve outcomes for this rare but life‐threatening condition.

An 85‐year‐old man developed acute neurologic dysfunction, severe thrombocytopenia, microangiopathic hemolytic anemia, and ADAMTS13 activity of 4.6% after TMP‐SMX reexposure. Seven plasma‐exchange sessions plus corticosteroids produced rapid recovery. This case highlights the diagnostic challenge of possible TMP‐SMX–associated iTTP and the importance of prompt treatment.

Cutaneous T-cell lymphomas (CTCL) are rare, heterogeneous non-Hodgkin lymphomas primarily involving the skin and are associated with poor outcomes in advanced disease. CD30 expression varies across CTCL subtypes and serves as the therapeutic target for brentuximab vedotin (BV), an antibody-drug conjugate with established efficacy in CD30-positive CTCL. To review the clinical evidence supporting BV use in CTCL, with emphasis on CD30-low (<10%) and CD30-negative disease, and to contextualize its role relative to standard therapies. A comprehensive literature review was conducted, including prospective clinical trials, retrospective analyses, and real-world studies. Key areas of focus included BV's mechanism of action, predictors of response, safety profile, and guideline recommendations across levels of CD30 expression, particularly in CD30-negative CTCL. BV demonstrates robust efficacy in CD30-positive CTCL, with the phase III ALCANZA trial showing superior response rates, progression-free survival, and quality-of-life outcomes compared with standard therapies. In contrast, responses among CD30-negative patients included in clinical trials were limited and inconsistent. However, emerging real-world data describe clinically meaningful responses in CD30-negative and CD30-low disease, potentially mediated by bystander cytotoxicity or heterogeneous, low-level CD30 expression, particularly in transformed mycosis fungoides. BV is guideline-endorsed for relapsed or refractory CD30-positive CTCL, and ongoing studies are exploring combination strategies and next-generation antibody-drug conjugates. BV is a key therapy for CD30-positive CTCL. While real-world experience suggests potential activity in CD30-negative or low disease, prospective trials are needed to define its role in this challenging subgroup.

Introduction: T‐cell lymphomas are rare, comprising 10%–15% of non‐Hodgkin lymphomas (NHLs). Their etiology remains unclear, and pathophysiology varies widely among subtypes. Sarcoid‐like reactions (SLRs) have been reported in approximately 7.3% of NHLs, including T‐cell lymphomas, and can closely resemble sarcoidosis clinically/histologically. This overlap complicates diagnosis, particularly when secondary myelofibrosis—a rare and poorly understood complication—arises. Myelofibrosis has also been observed in sarcoidosis, further blurring the distinction between these entities. Treatment for T‐cell lymphoma‐associated secondary myelofibrosis is not standardized, with predominantly CHOP‐based regimens showing variable efficacy. This warrants further research to guide diagnostic and management frameworks. Case Description: We report the case of a 57‐year‐old male with known systemic sarcoidosis who developed recurrent symptomatic hypercalcemia and new‐onset transfusion‐dependent pancytopenia. Initial evaluation revealed bone marrow fibrosis with noncaseating granulomas, raising concern for sarcoidosis‐driven secondary myelofibrosis. However, repeat bone marrow biopsy demonstrated T‐cell lymphoma with a SLR. Primary myelofibrosis was excluded, supporting a secondary lymphoma‐driven process. The patient is currently undergoing treatment with BV‐CHP with close hematologic monitoring. Conclusion: T‐cell lymphoma‐associated SLR can closely mimic sarcoidosis and should be considered in the differential, particularly in patients with atypical presentations or cytopenias. Despite similar clinical and histological features, the underlying pathophysiology differs, necessitating thorough molecular and immunophenotypic evaluation. Though rare, this entity can lead to secondary myelofibrosis, underscoring the importance of excluding a primary myeloproliferative process. Further research is needed to define optimal therapy, with BV‐CHP representing a promising option in the evolving landscape of T‐cell lymphoma management.