Intranodal palisaded myofibroblastoma; a case report and review of the literature.

Intranodal palisaded myofibroblastoma (IPM) also called as intranodal hemorrhagic spindle cell tumor with amianthoid fibers is a distinctive and rare mesenchymal neoplasm of lymph nodes. This entity generally misdiagnosed as intranodal Kaposi's sarcoma or schwannoma in past. In contrast to Kaposi's sarcoma, it behaves in a benign fashion and does not need any further therapy except total surgical resection of the mass. This neoplasm has a great predilection for the inguinal region. The lesion presents typically as a unilateral, painless, solitary mass. To our knowledge, approximately 53 cases of IPM have been reported in the English-language literature. We present a 43-year-old-male patient with IPM and discuss histological, immunohistochemical features and pathogenesis of this rare benign neoplasm.

Fournier's gangrene: is it scrotal gangrene?

INTRODUCTION: Fournier's gangrene was originally described as scrotal gangrene in young males. Today, it is generally accepted as synergistic necrotizing fasciitis of perineal, genital, or perianal regions, and the epidemiologic data have changed. However, there are still limited data about females due to the lack of female patients, even in large case series. METHODS: A retrospective review of the medical records of all patients who received surgery for emergency conditions over the past 22 years was performed to identify patients with Fournier's gangrene. Data from these patients were then reviewed to determine the age, gender, etiology, causative bacteria, predisposing factors, treatment modalities, length of hospital stay, and morbidity and mortality rates associated with Fournier's gangrene. Data were evaluated using multivariate analyses. RESULTS: Sixty-five patients (20 female) were identified with the diagnosis of Fournier's gangrene. The mean age was 50.8 years. The most common etiology was hemorrhoidectomy in male and perianal abscess in female patients. The most commonly isolated microorganism in both male and female patients was Escherichia coli. Twenty-nine patients had diabetes mellitus, which was the most common predisposing factor. Mean hospitalization time was 24.4 days and the overall mortality was 27.70%. CONCLUSION: Fournier's gangrene is still an important disease with high mortality rates in spite of the developments in intensive care units and new-generation antibiotics. It seems that there are no major differences between male and female patients in the characteristics of the condition.

Developmental exposure to noninherited maternal antigens induces CD4+ T regulatory cells: relevance to mechanism of heart allograft tolerance.

We hypothesize that developmental exposure to noninherited maternal Ags (NIMA) results in alloantigen-specific natural and adaptive T regulatory (T(R)) cells. We compared offspring exposed to maternal H-2(d) (NIMA(d)) with nonexposed controls. In vitro assays did not reveal any differences in T cell responses pretransplant. Adoptive transfer assays revealed lower lymphoproliferation and greater cell surface TGF-beta expression on CD4(+) T cells of NIMA(d)-exposed vs control splenocytes. NIMA(d)-exposed splenocytes exhibited bystander suppression of tetanus-specific delayed-type hypersensitivity responses, which was reversed with Abs to TGF-beta and IL-10. Allospecific T effector cells were induced in all mice upon i.v. challenge with B6D2F1 splenocytes or a DBA/2 heart transplant, but were controlled in NIMA(d)-exposed mice by T(R) cells to varying degrees. Some (40%) NIMA(d)-exposed mice accepted a DBA/2 allograft while others (60%) rejected in delayed fashion. Rejector and acceptor NIMA(d)-exposed mice had reduced T effector responses and increased Foxp3(+) T(R) cells (CD4(+)CD25(+)Foxp3(+) T(R)) in spleen and lymph nodes compared with controls. The key features distinguishing NIMA(d)-exposed acceptors from all other mice were: 1) higher frequency of IL-10- and TGF-beta-producing cells primarily in the CD4(+)CD25(+) T cell subset within lymph nodes and allografts, 2) a suppressed delayed-type hypersensitivity response to B6D2F1 Ags, and 3) allografts enriched in LAP(+), Foxp3(+), and CD4(+) T cells, with few CD8(+) T cells. We conclude that the beneficial NIMA effect is due to induction of NIMA-specific T(R) cells during ontogeny. Their persistence in the adult, and the ability of the host to mobilize them to the graft, may determine whether NIMA-specific tolerance is achieved.