Placenta accreta: an association with fibroids and Asherman syndrome.

OBJECTIVE: Placenta accreta is a life-threatening problem that is rising in incidence in the developed world. The increased risk of placenta accreta in women with placenta previa and 1 or more prior cesarean deliveries is well established and prompts careful sonographic evaluation. Our objective was to emphasize that accreta is also identified at sites other than cesarean scars. METHODS: Two cases of placenta accreta without placenta previa seen in association with uterine scarring from myomectomy and uterine fibroids are described. RESULTS: The sonographic and magnetic resonance imaging findings of accreta are reviewed in the classic setting of prior cesarean deliveries as well as myomectomy and uterine fibroids. CONCLUSIONS: We suggest that when the placenta overlies any uterine abnormality, a careful search for invasive placentation is warranted.

Predominant expression of Th2 cytokines and interferon-gamma in xenogeneic cardiac grafts undergoing acute vascular rejection.

BACKGROUND: The Th1 response has been shown to play a role in acute allograft rejection, whereas the Th2 response has been implicated in the protection of allografts. Unlike allografts, the pattern of cytokines in response to solid-organ xenografts has been the subject of limited studies. We investigated intragraft cytokine expression in a concordant cardiac xenograft model (rat-to-mouse) to test if a particular cytokine profile predominates. METHODS: Intra-abdominal cardiac transplantation was performed using C57BL/10 mice as recipients of PVG.R8 rat hearts. Syngeneic grafts (C57BL/10-to-C75BL/10) served as controls. Cardiac grafts harvested on various days posttransplantation were analyzed for histology and intragraft cytokine expression using reverse-transcriptase polymerase chain reaction. RESULTS: The grafts in this model were rejected with a mean survival time of 7+/-1 days and showed extensive evidence of acute vascular rejection, consisting of global distortion of myocardial architecture, fewer cellular infiltrates, interstitial hemorrhage with myocyte necrosis thrombosis, and vasculitis with neutrophils and lymphocytes infiltrating vessel walls. Cardiac xenografts predominantly expressed Th2 cytokines, interleukin (IL)-4, IL-10, and transforming growth factor-beta with various kinetics. IL-10 was detectable on day 1 and reached its peak level of expression on day 6 posttransplantation. IL-4 showed minimal and undetectable expression on days 1 and 3 and significant expression on day 6 posttransplantation. Transforming growth factor-beta was expressed moderately on all days examined. The expression of interferon (IFN)-gamma, a Th1 cytokine, was specific to xenografts and showed a gradual increase from days 3 to 6 posttransplantation. In marked contrast, IL-2 showed complete lack of expression. CONCLUSIONS: Our data demonstrate predominant expression of Th2 cytokines and IFN-gamma in cardiac xenografts undergoing acute vascular rejection. The Th2 cytokines may promote acute vascular rejection by regulating the humoral response, and IFN-gamma may delay, but not prevent, this response.

Chronic cardiac allograft rejection in a rat model disparate for one single class I MHC molecule is associated with indirect recognition by CD4(+) T cells.

T-cell mediated immune responses play a critical role in chronic allograft dysfunction. The complex nature of allograft rejection, particularly with respect to the vast repertoire of alloantigens and their mode of recognition by T cells, presents a major challenge for the design of well-controlled studies into the immunobiology of chronic rejection. The purpose of this study was to develop a rat model with restricted antigenic specificity that develops chronic rejection without any immunologic manipulation to study the T-cell response. PVG.1U allogeneic hearts disparate for one single class I antigen, RT.1A(u), were transplanted into PVG.R8 rat recipients. Grafts from PVG.R8 were used as syngeneic controls. Chronic rejection was studied by histological analysis of the grafted hearts at various time points posttransplantation (20-100 days). Donor specific alloreactive response was studied in a mixed lymphocyte reaction assay. All allografts survived more than 90 days and showed extensive evidence of chronic rejection, which was characterized by interstitial fibrosis, vasculitis, and occlusive myointimal thickening. Chronic rejection was evident by day 20 and most extensive by day 100 posttransplantation. In marked contrast, syngeneic grafts remained free of chronic lesions. Lymphocytes harvested from graft recipients showed a more vigorous proliferative response to allogeneic splenocytes as compared with that of lymphocytes from nai;ve animals. The proliferative response was primarily mediated by CD4(+) T cells recognizing the RT1.A(a) molecule via the indirect pathway. A single class I disparity in this model generates chronic rejection associated with potent CD4(+) T-cell responses induced by the indirect recognition pathway. The use of this antigenically restricted model may facilitate the design of well-controlled studies for the characterization of immune mechanisms responsible for chronic rejection.

Epithelioid hemangioendothelioma of the lung diagnosed by transesophageal endoscopic ultrasound-guided fine needle aspiration: a case report.

BACKGROUND: Epithelioid hemangioendothelioma is a rare vascular tumor of the lung and is also known as intravascular sclerosing bronchoalveolar tumor. Although it has relatively low malignant potential, extensive pulmonary involvement and systemic metastasis have been described. The cytologic features of these tumors are not very well defined, with only few case reports describing the cytologic findings of epithelioid hemangioendothelioma of the lung on fine needle aspiration. CASE: Endoscopic ultrasound-guided fine needle aspiration of a hilar mass was performed on a 25-year-old female. The cytology showed loosely cohesive sheets and clusters of epithelioid cells. The cellular features included large, irregular nuclei with nucleoli and a moderate amount of vacuolated cytoplasm. Rare cells had a suggestion of cytoplasmic lumen formation. Histologic examination of tissue fragments on the cell block revealed a tumor composed of rounded to spindled epithelioid cells in a background of light blue stroma. The endothelial differentiation was evidenced by cytoplasmic vacuoles and lumens, some of which contained erythrocytes. The endothelial nature of these cells was confirmed by positive staining with factor VIII and CD34. CONCLUSION: The cytomorphologic features of epithelioid hemangioendothelioma described in the literature and observed in our case are distinctive and can help with the interpretation of cytologic smears and prevent misdiagnosis.

Delayed death in sudden infant death syndrome: a San Diego SIDS/SUDC Research Project 15-year population-based report.

A fraction of SIDS cases have death delayed by successful CPR, yet they have not been compared to SIDS cases which were found dead or not successfully resuscitated. Our aims were to: (1) determine the percent of SIDS cases in the San Diego SIDS Research Project database for whom death was delayed by CPR and subsequent life support; (2) compare demographics, circumstances of death and autopsy findings of delayed death SIDS cases (delayed SIDS) with those whose deaths were not delayed (non-delayed SIDS); (3) examine the evolution of pathologic changes in delayed SIDS as a function of survival interval. A retrospective 15-year population-based study of 454 infant deaths attributed to SIDS revealed 29 delayed SIDS cases (Group I) and 425 non-delayed SIDS cases (Group II). Group I cases were significantly older than Group II cases (mean age 132 days vs. 102 days and p<0.0001). Eighty-nine percent of the Group I cases were discovered between 08.00 and 19.59 h; none were found between 00.00 and 07.59 h, compared to 38% of the Group II cases. Group I infants were found significantly more often away from home (at daycare, or at the home of a relative, friend, or baby sitter) than Group II infants (45% vs. 25%, p<0.05). There were no differences between groups with regard to gender, gestational age, type of delivery, bed sharing, URI within 48 h of death, ALTEs, a history of referral to child protective services, body position when placed or found, or face position when found. Pathologic changes were semiquantitatively evaluated; findings were characteristic of anoxic-ischemic injury that generally became more severe with increasing survival intervals. Anoxic-ischemic brain injury was the immediate cause of death in all delayed SIDS cases. Aspiration of gastric contents was identified in Group I cases surviving less than 48 h and was the likely etiology of acute bronchopneumonia occurring in 83% of the Group I cases. We did not identify factors that would reliably predict which SIDS cases might be discovered soon enough to allow earlier and more effective CPR and survival without permanent brain injury.

Prevention of chronic rejection with immunoregulatory cells induced by intrathymic immune modulation with class I allopeptides.

Intrathymic immune modulation with RT1.Aa allopeptides in the PVG.R8-to-PVG.1 U rat strain combination leads to long-term survival of cardiac allografts. This regimen, however, does not induce transplantation tolerance, since most long-surviving allografts undergo chronic rejection. We investigated recipients with chronic rejection for donor-specific immune nonresponsiveness and immunoregulatory cells as possible mechanisms responsible for long-term graft survival. There was a significant reduction in the proliferative response of T cells from long-term allograft recipients to donor alloantigens as compared with that of naïve T cells. Adoptive transfer of splenocytes from intrathymically manipulated primary long-term graft survivors into minimally irradiated secondary hosts resulted in indefinite survival of > 80% of allografts, providing evidence for immunoregulatory cells. Secondary recipients had total absence of donor-reactive cellular and humoral responses. Immunoregulation was also transferable from secondary to tertiary graft recipients. More importantly, there was a significant reduction in the incidence of chronic rejection in secondary hosts (> 85%) and complete prevention of acute and chronic rejection in tertiary hosts. This study demonstrates that intrathymic immunomodulation with class I allopeptides results in the generation of immunoregulatory cells that do not block chronic rejection in primary hosts where they develop, but prevent both acute and chronic allograft rejection when adoptively transferred into secondary and tertiary recipients.

Predominant expression of the Th2 response in chronic cardiac allograft rejection.

Chronic rejection is the main cause of late allograft failure in patients. CD4+ T cells activated by indirect recognition of alloantigens are implicated in this rejection reaction. However, the type of T cell response (Th1 vs Th2) that contributes to chronic rejection has not been fully investigated. The purpose of this study is to examine whether chronic rejection is associated with a polarized T-cell response in a rat cardiac allograft model, where long-term graft survival is achieved by intrathymic immunomodulation with donor class I, RT1.Aa, allopeptides. All long-surviving allografts showed histological evidence of chronic rejection. Chronic rejection was associated with high levels of intragraft Th2 cytokines and the Th2-regulated alloantibodies. The Th2 response was systemic, since long-surviving allografts with chronic rejection had high levels of serum IL-10. The predominance of the Th2 cytokines demonstrates that the Th2 response was not sufficient for the prevention of chronic rejection in this model. The predominant expression of Th2 cytokines, together with the presence of Th2-regulated alloantibodies, suggests that the Th2 response may play a role in the development of chronic rejection.