BACKGROUND: Cutaneous granulomatous inflammation can occur in patients with T-cell lymphoma and Hodgkin disease. We describe the unusual microscopic pattern of a granuloma annulare (GA)-like eruption co-existing with B-cell chronic lymphocytic leukemia (B-CLL). METHODS: We reviewed the histopathology and immunophenotype of skin biopsies from two patients with B-CLL and cutaneous lesions resembling GA. RESULTS: Both patients had symptomatic cutaneous lesions clinically resembling GA; one had lesions refractory to standard dermatologic therapy. Histopathology showed GA-like palisaded histiocytic infiltration, with subtle collections of lymphocytes interspersed among the granulomatous inflammation. Immunohistochemistry showed strong expression of CD20 and CD79a, with aberrant CD5 co-expression, confirming cutaneous involvement by B-CLL. CONCLUSIONS: Co-existence of a GA-like infiltrate and cutaneous B-CLL raises the possibility that granulomatous inflammation occurs as a secondary response to dermal infiltration by leukemic cells. Because histopathologic findings can be subtle, knowledge of this association is essential to avoid overlooking the diagnosis. Regardless of whether histopathology reflects a reactive or primary phenomenon, documentation of cutaneous involvement by B-CLL may serve as a rationale for specific treatment of the underlying B-CLL in patients with skin lesions unresponsive to dermatologic therapy and for whom there is no other justification for leukemia-targeted therapy.
BACKGROUND:Cutaneous granulomatous inflammation can occur in patients with T-cell lymphoma and Hodgkin disease. We describe the unusual microscopic pattern of a granuloma annulare (GA)-like eruption co-existing with B-cell chronic lymphocytic leukemia (B-CLL). METHODS: We reviewed the histopathology and immunophenotype of skin biopsies from two patients with B-CLL and cutaneous lesions resembling GA. RESULTS: Both patients had symptomatic cutaneous lesions clinically resembling GA; one had lesions refractory to standard dermatologic therapy. Histopathology showed GA-like palisaded histiocytic infiltration, with subtle collections of lymphocytes interspersed among the granulomatous inflammation. Immunohistochemistry showed strong expression of CD20 and CD79a, with aberrant CD5 co-expression, confirming cutaneous involvement by B-CLL. CONCLUSIONS: Co-existence of a GA-like infiltrate and cutaneous B-CLL raises the possibility that granulomatous inflammation occurs as a secondary response to dermal infiltration by leukemic cells. Because histopathologic findings can be subtle, knowledge of this association is essential to avoid overlooking the diagnosis. Regardless of whether histopathology reflects a reactive or primary phenomenon, documentation of cutaneous involvement by B-CLL may serve as a rationale for specific treatment of the underlying B-CLL in patients with skin lesions unresponsive to dermatologic therapy and for whom there is no other justification for leukemia-targeted therapy.