Factor V G1691A (FV-Leiden) and prothrombin G20210A mutations are major inherited risk factors for venous thrombosis. Recently, it was suggested that both mutations, through stimulation of venous and placental thrombosis events, were strongly associated with recurrent idiopathic miscarriages, although other studies disputed such a link. The aim of this study was to determine the prevalence of prothrombin G20210A and factor V G1691A (R506Q, FV-Leiden) mutations in women with recurrent idiopathic abortions and to recommend management for high-risk mutation carriers. One hundred ten women with two or more consecutive unexplained first-trimester miscarriages (mean age ± SD, 32.3 ± 5.3) were compared to 67 parous women with uncomplicated pregnancies (mean age ± SD, 33.9 ±7.3) (P = 0.134) from the same ethnic background. The presence or absence of the prothrombin G20210A and FV-Leiden mutations was assessed by PCR and RFLP analysis, using HindIII and MnlI digestion, respectively. In women with primary habitual abortion, 45 (40.91%) carried the FV-Leiden mutation, of whom 7 were in the homozygote and 38 were in the heterozygote states, and 15 (13.64%) carried the prothrombin G20210A mutation all as heterozygotes, compared to 16.42% and 2.99% carrier rates among controls, respectively, all of whom were heterozygote carriers. Of the other risk factors analyzed, smoking (OR 1.76; 95% CI = 0.79-3.94) was more prevalent in habitual aborters compared to controls. Both FV-Leiden and factor II G20210A mutations are major inherited risk factor associated with primary recurrent miscarriages. Women with a family or personal history of thrombosis should be screened before or early in the pregnancy for FV-Leiden and factor II G20210A mutations. Am. J. Hematol. 71:300-305, 2002.

Introduction. Nonpuerperal uterine inversion (NPUI) is a rare clinical problem with diagnostic and surgical challenges. The objective of our study was to review the literature on NPUI and describe causative pathologies, diagnosis, and different surgical options available for treatment. Materials and Methods. A comprehensive literature review was carried out on MEDLINE and Google Scholar databases to look for NPUI using the term “non-puerperal uterine inversion,” and further went through the cross-references of the published articles. Data are published case reports from 1911 to September 2018. Of the 153 published cases, 133 reports had adequate details of surgery for analysis. These reports were analyzed, concerning the clinical presentation, methods of diagnosis, and surgical treatment. Results. Mean age of the women was 46.3 years (standard deviation: 18, N = 153). Leiomyoma remained the commonest (56.2%) aetiology. While malignancies contributed to 32.02% of cases, 9.2% were idiopathic. High degree of clinical suspicion and identification of unique features on ultrasonography and magnetic resonance imaging enable prompt diagnosis. In cases of uncertainty, laparoscopy or biopsy of the mass was used to confirm the diagnosis. Hysterectomy or repositioning and repair of the uterus are the only treatment options available. The surgical methods implemented were analyzed in three aspects: route of surgical access, method of repositioning, and final surgical procedure undertaken. The majority (48.8%) had only abdominal access, while 27.1% had both abdominal and vaginal access. Haultain procedure was the most useful procedure for reposition (18.0%) of the uterus. The majority (39.7%) required abdominal hysterectomy with or without debulking of the tumour abdominally, while 15.0% had uterine repair after repositioning. We reviewed the different surgical techniques and described and proposed a treatment algorithm. Conclusions. Fibroids were the commonest cause for NPUI. Malignancies accounted for one-third of cases. A combined abdominal and vaginal approach, followed by hysterectomy or repair after repositioning, seems to be better for nonmalignant cases.

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Immunohistochemistry increases accuracy of BP diagnosis in CNB specimens. Benign papillary lesions diagnosed on CNB do not require excision in the absence of suspicious clinical/radiological findings.

A 60-year old woman presented with features of Cushing's syndrome (CS) secondary to an ectopic adrenocorticotropic hormone (ACTH) secreting metastatic parotid tumour 3 years after excision of the original tumour. She subsequently developed fatal intestinal perforation and unfortunately died despite best possible medical measures. Ectopic ACTH secretion accounts for 5–10% of all patients presenting with ACTH dependent hypercortisolism; small cell carcinoma of lung (SCLC) and neuroendocrine tumours (NET) account for the majority of such cases. Although there are 4 previous case reports of ectopic ACTH secreting salivary tumours in literature, to our knowledge this is the first published case report in which the CS developed after 3 years of what was deemed as a successful surgical excision of primary salivary tumour. Our patient initially had nonspecific symptoms which may have contributed to a delay in diagnosis. Perforation of sigmoid colon is a recognised though underdiagnosed complication associated with steroid therapy and hypercortisolism. This case demonstrates the challenges faced in diagnosis as well as management of patients with CS apart from the practical difficulties faced while trying to identify source of ectopic ACTH.