Clinico-Pathologic Evaluation of 18 Cases of Lymphomatoid Papulosis

ABSTRACT

Lymphomatoid papulosis is an enigmatic disease entity which is clinically benign and histologically malignant. Although sporadic cases have been reported, we could not find any comprehensive report on the combined clinical and histologic features of lymphomatoid papulosis in the literature. Perhaps the most controversial aspect of lymphomatoid papulosis is its pathogenesis and categorization as a benign versus a malignant entity. To date, there are no reports on p53 and bcl-2 protein expression in lymphomatoid papulosis. We analysed the clinico-pathological findings of 18 cases with lymphomatoid papulosis during the 10 year period from 1984 to 1995 and examined the prevalence of immunoreactivity for CD30(DAKO, Ber-H2), p53(DAKO, DO-7), and bcl-2(DAKO, 124) using an immunohistochemical(ABC) method. The results obtained are summarized as follows. 1) Age distribution ranged from 20 to 65, with a mean age of 45 years and a sex distribution which showed a male predominence(81). The lesions were located on the trunk and extremities(8cases), extremities (7cases), and trunk(3 cases). The morphology of the lesions were papules or plaques(12 cases), and nodules(6 cases). 2) Histopathologic types were classified into 3 types type A(4 cases), type B(8 cases) and mixed type (6 cases). 3) Positive immunoreactivity for CD30 was seen in 17%(3 of 18cases) type A(2 of 3) and mixed type(1 of 3). 4) The positive immunoreactivity for p53 and bcl-2 was observed in 29%(5 of 18) and 11%(2 of 18), respectively. 5) Cases showing positive immunoreactivity for P53 were type A(1 of 5), type B(1 of 5), and mixed type(3 of 5). 6) Cases showing positive immunoreactivity for bcl-2 were mixed type(2 of 2). One case developed into Ki-1 lymphoma. These results support the idea that lymphomatoid papulosis and Ki-1 lymphoma represent a continuum. The role of p53 gene mutation and bcl-2 activation in the development of lymphomatoid papulosis is currently unknown. But, our results suggest that p53 gene mutation and bcl-2 activation are not a critical step in the development of lymphomatoid papulosis. Further studies are needed to elucidate the role of p53 gene mutation and bcl-2 activation in the development and progression of lymphomatoid papulosis.