Pseudo-Meigs' syndrome associated with hydropic degenerating uterine leiomyoma: a case report.

Pseudo-Meigs' syndrome secondary to uterine leiomyoma is a rare entity. A 50-year-old Japanese woman presented with a 3-month history of shortness of breath. Chest X-ray and magnetic resonance imaging revealed massive right pleural effusion, ascites and a large subserosal uterine myoma. She underwent a total abdominal hysterectomy with bilateral salpingo-oophorectomy. The pathology was consistent with a benign leiomyoma. The ascites and pleural effusion rapidly disappeared postoperatively. The serum interleukin-6 level was 3.9 pg/mL before surgery and declined to 1.6 pg/mL postoperatively. Previous published work has demonstrated that vascular endothelial growth factor and interleukin-6 may play a role in the pathogenesis of Meigs' syndrome and that vascular endothelial growth factor may contribute to the development of pseudo-Meigs' syndrome due to metastatic ovarian cancer. This is the first English-language study showing the possibility that interleukin-6 is relevant to the pathogenesis of pseudo-Meigs' syndrome caused by degenerating uterine leiomyoma.

[Successful treatment with the combination of recombinant human soluble thrombomodulin and gabexate mesilate in three patients with obstetric disseminated intravascular coagulation].

Recombinant human soluble thrombomodulin (rTM) is a new drug for the treatment of disseminated intravascular coagulation (DIC), although the effects on obstetric DIC have not yet been fully elucidated. We report herein three patients with obstetric DIC caused by placental abruption, hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome, and atonic bleeding, respectively. In all three cases, treatment with rTM proved successful, suggesting that rTM is an efficient method for treating obstetric DIC.

Essential role of IkappaB kinase alpha in thymic organogenesis required for the establishment of self-tolerance.

IkappaB kinase (IKK) alpha exhibits diverse biological activities through protein kinase-dependent and -independent functions, the former mediated predominantly through a noncanonical NF-kappaB activation pathway. The in vivo function of IKKalpha, however, still remains elusive. Because a natural strain of mice with mutant NF-kappaB-inducing kinase (NIK) manifests autoimmunity as a result of disorganized thymic structure with abnormal expression of Rel proteins in the thymic stroma, we speculated that the NIK-IKKalpha axis might constitute an essential step in the thymic organogenesis that is required for the establishment of self-tolerance. An autoimmune disease phenotype was induced in athymic nude mice by grafting embryonic thymus from IKKalpha-deficient mice. The thymic microenvironment that caused autoimmunity in an IKKalpha-dependent manner was associated with defective processing of NF-kappaB2, resulting in the impaired development of thymic epithelial cells. Thus, our results demonstrate a novel function for IKKalpha in thymic organogenesis for the establishment of central tolerance that depends on its protein kinase activity in cooperation with NIK.