Abstractj og_1856 1125..1136Aim: Despite tuberculosis (TB) being a global problem, maternal TB remains an unrecognized and underestimated tragedy, especially in South Asian countries. Therefore, we performed a non-systematic review regarding implications of maternal TB on obstetric and perinatal outcomes in the South Asian context. Material and Methods:We reviewed original studies, both descriptive and analytical, that originated from South Asian countries following an electronic search supplemented by a manual search. Although relevant studies from developed countries were reviewed, they were not included in the tabulation process because those studies had different socioeconomic/epidemiological background. Results: Diagnosis of TB is often delayed during pregnancy, because of its non-specific symptoms, and overlapping presentation with other infectious diseases. Poverty, undernutrition, lack of social support and poor health infrastructure along with complications of TB and need for prolonged medications lead to increased maternal morbidity and mortality. Maternal TB in general (except lymphadenitis), is associated with an increased risk of small-for-gestational age, preterm and low-birthweight neonates, and high perinatal mortality. These adverse perinatal outcomes are even more pronounced in women with advanced disease, late diagnosis, and incomplete or irregular drug treatment. There could be a synergy of TB, socioeconomic and nutritional factors, which might have contributed to adverse perinatal effects, especially in low-income countries. Conclusions: As active TB poses grave maternal and perinatal risks, early, appropriate and adequate anti-TB treatment is a mainstay for successful pregnancy outcome. The current knowledge gaps in perinatal implications of maternal TB can be addressed by a multicenter comparative cohort study.

Pregnancy-related acute renal failure is potentially fatal but largely preventable. Universal prenatal care and greater access to emergency obstetric services, especially in rural India, could avert PRARF and its consequences.

ObjectivesAmong women with epithelial ovarian cancer (EOC), histotype is one of the major prognostic factors. However, few data are available on histotype- specific survival and mortality estimates among these patients. We therefore examined survival and causes of death among women with EOC by histotype.MethodsA population- based cohort including all ovarian cancer patients diagnosed in British Columbia (BC) between 1990 and 2014 was built using population-based administrative datasets. We compared causes of death within histotypes, by age at diagnosis, BRCA status, and time since diagnosis.ResultsA total of 6975 women were identified as having been diagnosed with EOC between 1990 and 2014 in BC. The most common cause of death among these women was ovarian cancer until 10 years post diagnosis when other causes surpassed ovarian cancer as the leading cause of death. Among women with serous EOCs, ovarian cancer was the leading cause of death 12 years after diagnosis, whereas ovarian cancer was the leading cause of death for 8 years among women with non- serous EOCs. Among women with serous EOCs, ovarian cancer was the leading cause of death for 12 years among younger women (< 60 years of age) compared to 8 years among women > = 60 years of age, and those with BRCA mutations were more likely to die from ovarian cancer than those without a BRCA mutation.ConclusionsWithin 10 years from diagnosis, ovarian cancer is the leading cause of death among women diagnosed with EOC.Electronic supplementary materialThe online version of this article (10.1186/s12885-018-4970-9) contains supplementary material, which is available to authorized users.

BackgroundAlthough eponyms are widely used in medicine, they arbitrarily alternate between the possessive and nonpossessive forms. As very little is known regarding extent and distribution of this variation, the present study was planned to assess current use of eponymous term taking "Down syndrome" and "Down's syndrome" as an example.MethodsThis study was carried out in two phases – first phase in 1998 and second phase in 2008. In the first phase, we manually searched the terms "Down syndrome" and "Down's syndrome" in the indexes of 70 medical books, and 46 medical journals. In second phase, we performed PubMed search with both the terms, followed by text-word search for the same.ResultsIn the first phase, there was an overall tilt towards possessive form – 62(53.4%) "Down's syndrome" versus 54(46.6%) "Down syndrome." However, the American publications preferred the nonpossesive form when compared with their European counterpart (40/50 versus 14/66; P < 0.001). In the second phase, PubMed search showed, compared to "Down syndrome," term "Down's syndrome" yielded approximately 5% more articles. The text-word search of both forms between January 1970 and June 2008 showed a gradual shift from "Down's syndrome" to "Down syndrome," and over the last 20 years, the frequency of the former was approximately halved (33.7% versus 16.5%; P < 0.001). The abstracts having possessive form were mostly published from the European countries, while most American publications used nonpossesive form consistently.ConclusionInconsistency in the use of medical eponyms remains a major problem in literature search. Because of linguistic simplicity and technical advantages, the nonpossessive form should be used uniformly worldwide.

Congenital fibrinogen deficiency is an extremely rare (1:1 000 000) hereditary bleeding disorder caused by defects in genes coding for fibrinogen Aα-, Bβ- and γ-chains, respectively. We report here the molecular basis of fibrinogen deficiency in a large series of patients from India. Twenty-seven patients with clinical features suggestive of fibrinogen deficiency and with prolonged plasma clotting times and low fibrinogen levels were studied. Genomic DNA was screened for mutations in the fibrinogen alpha (FGA), beta (FGB), gamma (FGG) genes by PCR and conformation sensitive gel electrophoresis. Fourteen different disease-causing mutations including frameshifts (51.9%), splice site (22.2%), missense (18.5%) and nonsense mutation (7.4%) were identified in 27 patients. Thirteen of them were novel, including seven frameshifts (fibrinogen Aα: p.Asp296 fs*59, p.Thr466 fs*17 and p.Lys575 fs*74; fibrinogen Bβ: p.Gly414 fs*2 and fibrinogen γ: p.Ser81 fs*5, p.Lys185 fs*13 and p.Asp278_279 fs*17), three splice site mutations (FGA gene c.364+1G>A; c.510+2 T>G; FGB gene c.851+1G>A), two missense substitutions (fibrinogen Bβ: p.Gly288Ser; p.Arg445Thr) and a nonsense mutation in fibrinogen Aα (p.Tyr127*). Two common mutations (FGA: c.364+1G>A, n = 6, FGG: p.Lys185 fs*13, n = 7) affecting 13 patients were identified in this series, suggesting that these mutations could be screened first in Indian patients with fibrinogen deficiency. The molecular data presented here is the largest series of patients with fibrinogen deficiency reported so far, adding significantly to the mutation database of this condition. It also helps create an algorithm for its genetic diagnosis in India.