Delayed onset septic pelvic thrombophlebitis treated by tissue-plasminogen activator following initial treatment for massive right ovarian vein thrombosis and methicillin-resistant Staphylococcus aureus bacteremia: A case report.

Septic pelvic thrombophlebitis (SPT) is a rare condition that forms thrombosis in the pelvic veins, typically the ovarian veins, with subsequent infection and inflammation. We present a case of right ovarian vein thrombosis (ROVT), methicillin-resistant Staphylococcus aureus (MRSA) bacteremia, and delayed onset of SPT symptoms, requiring tissue-plasminogen activator. A 40-year-old woman, G3P2, at 38 weeks' gestation, was admitted with a fever of 39°C. She had cervical insufficiency and had been often on bed rest. Blood culture revealed MRSA and computed tomography revealed a large ROVT. She received vancomycin and direct oral anticoagulant, and her fever resolved by day 3. On day 16, fever recurred with severe pain over the ROVT. Second computed tomography showed thickening of venous wall with enhancement around ROVT, consistent with SPT. Since pain and fever gradually exacerbated despite treatment with DOAC and antimicrobials, she was started on heparin and tissue plasminogen activator on days 23 and 25, respectively. Along with recanalization on the thrombosis by day 29, fever and abdominal pain resolved. We experienced a case of delayed onset SPT associated with MRSA bacteremia and a large ROVT. MRSA bacteremia might cause the originally existing ROVT to become an infection source, resulting in SPT with recurrent symptoms and long-term treatment. Early and strict anticoagulation is crucial in cases with a large thrombosis and bacteremia, due to the high risk of progression to SPT. This case highlights the importance of recanalization for the treatment of SPT and usefulness of administration of tissue-plasminogen activator for the massive thrombosis.

A case of coexistent poorly differentiated adenosquamous carcinoma (glassy cell carcinoma), usual-type adenocarcinoma, and squamous cell carcinoma in situ of the cervix.

Poorly differentiated adenosquamous carcinoma (glassy cell carcinoma) of the cervix is extremely rare, accounting for 1-2% of all cervical cancers. Herein, we report a case with coexistent poorly differentiated adenosquamous carcinoma (glassy cell carcinoma), "usual-type" adenocarcinoma, and squamous cell carcinoma in situ of the cervix. A female patient in her 60 s was referred to our hospital and diagnosed with poorly differentiated adenosquamous carcinoma based on cervical cytology and biopsy. The tumor was classified as clinical stage IB1 cervical cancer following magnetic resonance imaging; radical hysterectomy was performed. Histopathological examination revealed poorly differentiated adenosquamous carcinoma (glassy cell carcinoma), usual-type adenocarcinoma, and squamous cell carcinoma in situ, all coexisting. All carcinoma regions showed identical sizes to high-risk human papillomavirus (HPV) in fragment analysis. The patient is currently alive, without evidence of recurrence, 31 months post surgery. In this case, three different carcinomas coexisted. Fragment analysis of the patient's HPV status suggested that all carcinomas were related to an infection with the same high-risk HPV type. To determine the precise mechanism of tumor development, i.e., whether the tumors were of the mixed or collision type, further studies are needed, including clonal analysis for the loss of heterozygosity pattern.

Circulating endothelial progenitor cells and placental abruption in women with preeclampsia.

OBJECTIVE: Abnormalities in circulating angiogenic factors and endothelial progenitor cells (EPCs) have been reported in patients with preeclampsia and placental abruption. The objective of this study was to determine whether the number of EPCs is altered in patients with placental abruption. DESIGN: A case control study. SETTING: Hiroshima University Hospital in Japan. SAMPLE: Pregnant Japanese women with preeclampsia (n=27) and those without any complications (n=15). METHOD: The EPC (CD45(low)CD34(+)CD133(+) cells) counts were examined using flow cytometry in peripheral blood collected from 27 women with preeclampsia and 15 normal pregnant women. Among the 27 women with preeclampsia, five subsequently developed placental abruption. All subjects were divided into three groups: normal pregnancy (NP, n=15), preeclampsia without placenta abruption (PE, n=22) and preeclampsia with placental abruption (PA, n=5). MAIN OUTCOME MEASURES: The EPC counts were measured in pregnant women with preeclampsia who subsequently developed placental abruption. RESULTS: The EPC count in the PE group significantly decreased in comparison to that observed in the NP group (620cells/ml versus 1918 cells/ml, P<0.01). In the PA group, the EPC count was found to markedly decrease in comparison to that observed in the PE group (221cells/ml, P<0.05). CONCLUSIONS: The number of EPCs was found to significantly decrease in preeclamptic women who subsequently developed placental abruption.

Effects of menopause and hormone therapy on erythrocyte deformability.

OBJECTIVE: The climacteric disturbance seen among perimenopausal women often includes symptoms related to poor microcirculation. This hemorheological condition plays an important role in the hemodynamism of microcirculation. Specifically, erythrocyte deformability is considered to be one of the most significant factors in determining this hemorheological condition. METHODS: The present study investigated the level of erythrocyte deformability in four groups of women: namely, 10 healthy premenopausal women (PRE group), 25 postmenopausal women (POST group), 20 postmenopausal women on estrogen therapy (ET group) who received conjugated equine estrogens 0.625 mg/day, and 20 postmenopausal women on estrogen plus progestogen therapy (EPT group) who received conjugated equine estrogens 0.625 mg/day plus medroxyprogesterone acetate 2.5 mg/day. The erythrocyte deformability score (EDS), measured by the Micro Channel Array Flow Analyzer, was determined as an index of erythrocyte deformability. RESULTS: The mean EDS for the POST group was significantly higher (mean +/- SE, 1.02 +/- 0.04) (P < 0.01) than that for the PRE group (0.78 +/- 0.05). The mean EDS for the ET group (0.88 +/- 0.03) was significantly lower than that for the POST group and close to that of the PRE group. There was no difference in the EDS values between the ET group and the EPT group (0.87 +/- 0.03). CONCLUSIONS: These results indicate that erythrocyte deformability may worsen with the decrease in the estrogen level because of the onset of menopause, and also suggest that ET and EPT may allow it to recover.

Substitution of transdermal estradiol during oral estrogen-progestin therapy in postmenopausal women: effects on hypertriglyceridemia.

OBJECTIVE: We investigated effects of changing from oral estrogen to transdermal estradiol on the lipid and lipoprotein profile of postmenopausal women who developed hypertriglyceridemia (serum concentrations exceeding 150 mg/dL) during estrogen-progestin therapy. DESIGN: Sixty-one postmenopausal Japanese women receiving 0.625 mg of conjugated equine estrogen plus 2.5 mg of medroxyprogesterone acetate daily for 12 months had developed serum triglyceride concentrations exceeding 150 mg/dL after 12 months of treatment. Thirty-six of them, chosen randomly for study, were assigned at random to either a group that continued this oral regimen or another that changed to transdermal estradiol while continuing 2.5 mg of oral medroxyprogesterone acetate for the next 3 months (n = 18 for each). Blood lipids were compared between groups. RESULTS: Serum concentrations of triglyceride and very-low-density lipoprotein triglyceride decreased significantly after changing to transdermal estradiol (triglyceride, from 226.0 +/- 43.9 to 110.5 +/- 44.1 mg/dL, P < 0.01). No changes were seen in concentrations of low-density lipoprotein cholesterol or high-density lipoprotein cholesterol. CONCLUSION: Changing to transdermal estradiol may improve triglyceride metabolism in women who developed hypertriglyceridemia during oral estrogen-progestin therapy, with minimal effect on cholesterol profiles.

[Recurrent ovarian cancer with cancer peritonitis treated with weekly paclitaxel infusion--a clinicopharmacological study].

We treated a patient with recurrent ovarian cancer with cancerous peritonitis by weekly paclitaxel (w-TXL) therapy (65 mg/m2). Abdominocentesis was not performed to eliminate ascites, in order to maintain higher quality of life (QOL), and critical adverse reaction was not seen for 12 months. We measured the TXL concentration in blood plasma and ascites after TXL infusion by HPLC method. The TXL titer in plasma was 427 ng/ml after infusion, 23 ng/ml after 24 hours and under 10 ng/ml after 48 hours. The TXL titer in ascites was 41 ng/ml after infusion, 37 ng/ml after 6 hours, 18 ng/ml after 12 hours, 10 ng/ml after 24 hours and under 10 ng/ml after 48 hours. TXL transportation from blood to ascites was good. This result suggested that intravenous infusion of TXL was effective for cancerous peritonitis treatment.

[A case of ovarian cancer with Parkinson's disease treated by combined chemotherapy with paclitaxel and carboplatin followed by surgery].

It is well known that neuropathy, myelopathy, and arthropathy are specific adverse effects induced by paclitaxel administration. Parkinson's disease is neural degenerative disease, and the influence of paclitaxel administration on patients with Parkinson's disease is unknown. We have successfully treated an ovarian cancer patient with Parkinson's disease by paclitaxel/CBDCA combined chemotherapy after surgery. The patient was a 57-year-old woman with solid and cystic ovarian tumor. Among the tumor markers CA125, CA19-9, and SLX, only SLX was elevated. We operated and made a pathological diagnosis of the ovarian tumor as clear cell adenocarcinoma (FIGO stage Ic). After surgery, the patient was treated with paclitaxel (260 mg [175 mg/m2]) and CBDCA (600 mg [AUC = 5]) combined chemotherapy for 5 courses. Her status is complete remission. During chemotherapy, she had felt the decreased efficacy of her Parkinson's disease medication. We could continue chemotherapy by increasing the dose of the Parkinson's drug. There is only one case report on the influence of paclitaxel on Parkinson's disease, in which the course was similar to the present case.