Splenosis is defined as the autotransplantation of splenic tissue to abnormal locations after splenic injury. Although abdominal splenosis is the most common form and is usually discovered at laparotomy, thoracic splenosis is less common and occurs as an asymptomatic peripheral pulmonary nodule, incidentally discovered on a routine chest radiograph. Given the long interval between the initial trauma and its discovery, thoracic splenosis is rarely considered in the differential diagnosis of left-sided, pleural-based pulmonary nodules or masses. The diagnosis is often a result of surgery. The authors report an additional case of thoracic splenosis, review the literature, and discuss nonsurgical diagnostic methods.

Splenosis is defined as the autotransplantation of splenic tissue to abnormal locations after splenic injury. Although abdominal splenosis is the most common form and is usually discovered at laparotomy, thoracic splenosis is less common and occurs as an asymptomatic peripheral pulmonary nodule, incidentally discovered on a routine chest radiograph. Given the long interval between the initial trauma and its discovery, thoracic splenosis is rarely considered in the differential diagnosis of left-sided, pleural-based pulmonary nodules or masses. The diagnosis is often a result of surgery. The authors report an additional case of thoracic splenosis, review the literature, and discuss nonsurgical diagnostic methods.

A 64-year-old patient developed a widespread autoimmune mucocutaneous blistering disease 3 weeks after the initiation of the anti-programmed death-1 (anti-PD-1) pembrolizumab therapy administered for a locally advanced cutaneous squamous cell carcinoma (SCC) of the buttocks arising from hidradenitis suppurativa. A diagnosis of paraneoplastic pemphigus (PNP) was made based on the presence of a suprabasal acantholysis associated with intercellular deposits of immunoglobulin G and C3 on basement membrane zone. Analysis of the patient's sera was positive on monkey bladder and detected circulating antibodies against desmoglein 3 and desmoplakin I prior to the initiation of pembrolizumab. At that time, the patient had few localized blisters limited to the peri-tumoral skin of the buttocks with acantholysis but without in vivo immune deposits. Pembrolizumab therapy was discontinued and a complete remission of PNP was obtained using oral steroids. Reintroduction of pembrolizumab resulted in flare of PNP. Given the close temporal relation between pembrolizumab initiation and the subsequent clinical expression of a widespread PNP, the patient was diagnosed with pre-existing subclinical PNP exacerbated by PD-1 inhibitor. The extreme rarity of PNP in the setting of cutaneous SCC and the effects of challenge, dechallenge, and rechallenge of pembrolizumab argue in favor of a checkpoint inhibitor related adverse effect. Our case is the first PNP associated with anti-PD-1 therapy and serological follow-up suggest that one infusion of pembrolizumab is sufficient to allow clinical expression of underlying pemphigus auto-immunity.

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