The aim of this study is to evaluate the folate, vitamin B12, fluoride and homocysteine levels in newborns with neural tube defect (NTD) and their parents. The study included 35 neonates with NTD and their parents, 31 neonates with congenital anomalies other than NTD formed control 1, 24 neonates with no anomalies, with the highest birth order and normal siblings formed control 2. These groups matched for socio-economic and nutritional status. Demographic, antenatal history, parental habits, folate (RBC, whole blood and serum), serum vitamin B12 and homocysteine levels were estimated using chemiluminescence technology. Chi-square test was used to assess association between factors and the outcome. One-way ANOVA was used to compare means in the three groups. To determine the risk factors for NTD, odds ratios (95% CI) was computed using bivariate and multivariate logistic regression analysis (STATA 9.0). No difference was found between NTD group and 'control 1' group. The fathers in NTD group had significantly lower folate and vitamin B12 and a higher homocysteine, in comparison to 'control 2' group (i.e. with normal babies). The babies with NTD had higher homocysteine while their mothers had significantly low folate levels in comparison to 'control 2' mothers. Low RBC folate, low serum vitamin B12 and high plasma homocysteine in both the parents had an association with NTD. Multivariate logistic regression revealed high homocysteine of father as the only independent significant risk factor [OR(95% CI):2.6(2.6, 226)] for NTD and also for other anomalies. NTD (and other congenital anomalies) may not only be due to nutritional deficiency in the mothers but also due to more intricate gene-nutrient interaction defects in the affected families, probably some abnormal folate-homocysteine metabolism. These defects seem to be affect the fathers more severely and in all likelihood, get transmitted to the babies from either or both the parents. The emergence of father's serum homocysteine levels as an independent risk factor for NTD and also other congenital anomalies calls for further studies to evaluate if this can be taken as a marker for congenital anomalies in the fetus during antenatal screening.

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Background: To assess the role of the surged faradic stimulation to the pelvic floor muscles as an adjunct to the conservative management in the children of idiopathic rectal prolapse

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Superior mesenteric artery (SMA) syndrome is also known as Wilkie's syndrome. Sometimes it is the cause of obstruction in the duodenum. In SMA syndrome, the acute angulation of the SMA against the abdominal aorta can prevent duodenal contents from draining into the jejunum (upper small intestine); hence inadequate intake of nutrition leads to weight loss and malnutrition. This is primarily attributed to the loss of intervening pad of mesenteric fat tissue due to various debilitating conditions.Abnormal connections between the intra-abdominal gastrointestinal tracts and skin over the abdomen are known as enterocutaneous fistulas (ECF).In this case report, a 37-year-old woman with a history of chronic dull pain in the upper abdominal region over the last seven months, who also complained of bloating, infrequent vomiting, nausea, and upper abdominal fullness for the same amount of time, was seen in the emergency room. Her symptoms had deteriorated by the time she approached the hospital. Additionally, she reports having had a foulsmelling, purulent discharge for the past five years right below the umbilicus. Upon close investigation, it was determined to be feces, and it was later discovered to be a low-output enterocutaneous fistula. She describes having an exploratory laparotomy and adhesiolysis for an intra-abdominal abscess and an acute intestinal obstruction caused by adhesions. This case emphasizes the provocation given a diagnosis of SMA syndrome with enterocutaneous fistula and demands increased awareness of this entity. This will ameliorate early identification to reduce immaterial tests and irrelevant treatments.