Pattern of upper gastrointestinal haemorrhage in northern India—An endoscopic study of 316 patients

Three hundred and sixteen patients with acute upper gastrointestinal haemorrhage were studied prospectively and consecutively. The most frequent cause was variceal bleeding due to portal hypertension (36%), followed by peptic ulceration (24%) and gastric erosions (19%). Variceal haemorrhage tended to be severe and had a high individual mortality rate. Associated acute mucosal lesions with portal hypertension were strikingly less frequent when compared with the experience from the West. Seven per cent of patients died of bleeding alone and an equal number of an associated systemic disorder or complication. Splenomegaly was present in all patients with a variceal haemorrhage due to non-cirrhotic portal hypertension. However, in patients with portal hypertension due to cirrhosis splenomegaly was present in 63%. Endoscopy altered the clinical diagnosis in 13.2% of patients. Based on previous experience oesophago-gastro-duodenal endoscopy has been a useful tool in the management of acute upper gastrointestinal haemorrhage.     

Congenital Narrowing of a Pulmonary Vein: Slit‐like Pulmonary Vein Ostium

We report the case of a 60‐year‐old female with a history of refractory paroxysmal atrial fibrillation. Preablation contrast enhanced pulmonary vein computed tomography (CT) scan demonstrated a slit‐like narrowing of the left inferior pulmonary vein ostium. The narrowing measured approximately 3 mm, with poststenotic dilation. The patient had no prior history of ablation. The patient subsequently underwent segmental antral isolation of all four pulmonary veins and cavo‐tricuspid isthmus ablation with bidirectional block. The diagnosis of preexisting congenital pulmonary vein stenosis had an impact on the type of ablation procedure performed (antral rather than ostial) and will affect the interpretation of postablation CT scans. (PACE 2013; 36:e150–e152)     

Statin-mediated cytoprotection of human vascular endothelial cells: a role for Kruppel-like factor 2-dependent induction of heme oxygenase-1

BACKGROUND: Heme oxygenase-1 (HO-1), by exerting anti-inflammatory, antiproliferative, antiapoptotic and antioxidant effects in the vasculature, protects against atherosclerosis and post-transplant vasculopathy. We noted the overlap between the effects of HO-1 and those attributed to 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins). This led to an investigation of the role of HO-1 in statin-mediated cytoprotection in primary human endothelial cells (ECs), and the ability of Kruppel-like factor 2 (KLF2) to regulate HO-1 function. METHODS/RESULTS: Treatment of human umbilical vein and aortic ECs with atorvastatin significantly upregulated HO-1 promoter activity, mRNA expression and protein expression, increasing HO-1 enzymatic activity as shown by raised intracellular bilirubin IXalpha. This effect was indirect, dependent upon inhibition of HMG-CoA reductase and geranylgeranylation, and independent of nitric oxide or changes in mRNA stability. Atorvastatin protected ECs against the generation of reactive oxygen species and H(2)O(2)-induced injury. HO-1 inhibition, with small interfering RNA (siRNA) or zinc protoporphyrin IX, abrogated atorvastatin-mediated cytoprotection. Atorvastatin upregulated KLF2 expression, whereas KLF2 siRNA attenuated statin-induced HO-1 and its associated antioxidant cytoprotective effects. Iron chelation, adenoviral-mediated overexpression of ferritin or supplementation of culture media with biliverdin reversed the inhibitory effects of HO-1 and KLF2 siRNA, suggesting that bile pigments and ferritin mediate the antioxidant actions of statin-induced HO-1. CONCLUSIONS: We have identified a novel link between KLF2 and HO-1 in human vascular ECs, demonstrating that atorvastatin-mediated HO-1 upregulation, and its associated antioxidant effect, is KLF2-dependent. The relationship between KLF2 and HO-1 is likely to represent an important component of the vasculoprotective profile of statins.     

Can mothers identify malnutrition in their children?

To assess mothers' perceptions about malnutrition and theirability to identify malnutrition in their own children, 339children aged 3–35 months and their mothers were studiedin two urban hospitals in Dhaka, Bangladesh, and in a communityclinic. The weight, height, and mid-upper arm circumferenceof the children were measured, and their mothers were interviewed.Child nutritional status according to their mother's statementand anthropometrically assessed nutritional status were compared.Sixty per cent of the mothers correctly identified better nutritionalstatus (weight/age >75% of NCHS median) and 67% mothers correctlyidentified malnutrition (weight/age < 75% of NCHS median)in their children. Sixty-one per cent of mothers with less than5 years of formal education correctly identified better nutrition(weight/age >75%) whereas 38% mothers with more than 5 yearsof education correctly identified better nutrition. Correctidentification of malnutrition was made by 70% of mothers withless than 5 years of formal education, and 74% of educated mothersdid the same. As regards causes of malnutrition, 33% of mothers stated thatlack of food at home resulted in undernutri-tion in their children(mean weight-for-age of these children was 65% of the NCHS median).Mothers' suggestions for improving child health were: betterfood in 31% cases; treatment of illnesses in 22% cases; andboth in 42% cases. The results suggest that most of the mothersare able to identify malnutrition in their children, and 95%of them are aware of ways to improve it, and that the provisionof adequate food and health care may improve child nutritionalstatus.     

Spontaneous expulsion of a bullet via the urethra

The rare clinical occurrence of the spontaneous passage of bullet which was not found during an operation after a gunshot wound to the bladder in a 28-year-old man is described.     

Case report: Liver function abnormalities in a severe case of hyperreactio luteinalis

Rare causes of liver dysfunction in pregnancy may pose a challenge to the consulting gastroenterologist or hepatologist from both the diagnostic and therapeutic standpoints. We describe here liver function abnormalities in a case of hyperreactio luteinalis with light and electron microscopic findings.     

Evidence for a Leukocyte Adhesion Factor Produced by the Early Embryo

PROBLEM : To determine if the embryo may induce adhesive molecules needed for implantation. METHOD : Determination of whether platelet rosetting around lymphocytes might occur when exposed to sera from pregnant, but not nonpregnant patients and from culture fluid from embryos but not oocytes. RESULTS : 90.2% of women with positive sera beta human chorionic gonadotropin (P-hCG) levels taken at least 12 days postovulation demonstrated platelet rosette factor (PRF) vs only 18.7% when β-hCG was negative. Using mid-luteal phase sera in women receiving hCG injection 1 wk before, 64.7% had positive PRF when serial β-hCG levels were positive as did 100% of samples taken from in vitro fertilization (IVF) patients; however, only 15.3% were positive with negative serial hCG levels. Culture media from fertilized oocytes and embryos tested positive for PRF, but follicular fluid and media from unfertilized oocytes were negative. CONCLUSION : The early embryo secretes a factor(s) that gains access to maternal serum and promotes increased lymphocyte/platelet adhesiveness.     

Histopathological Changes of the Placenta in Diabetes Induced by Maternal Administration of Streptozotocin during Pregnancy in the Rat

Abstract The objective of this investigation was to find out the histopathological changes of the placenta and to correlate them with fetal malformations and growth retardation in experimental diabetes. Diabetes was induced in Wistar rats at different stages of gestation by intraperitoneal injection of streptozotocin (STZ). The controls were either buffer treated or injected with STZ followed by 2–6 IU insulin until term. All fetuses and placentae were collected on day 20 of gestation. Fetuses of diabetic rats were significantly growth retarded. Maxillary hypoplasia, edema, gastroschisis, exencephaly and septal defects of the heart were the major malformations. Most of the experimental placentae weighed heavier relative to their body mass. Toluidine blue stained sections of the placentae revealed severe histological abnormalities. The unusually large sized placentae had extensive cystic degeneration, often with an increased population of leucocytes. Giant cells were very numerous. Perivascular fibrosis, persistence of fetal mesenchyme, edema, infarcts and vacuolisation were observed in the labyrinths. In the small placentae, the glycogen cells were fewer and the glycogen in them remained unutilized. Reduction of labyrinthine zone, hypovascularity, constriction of vessels, perivascular edema and platelet aggregation characterized these placentae. The placentae of externally malformed fetuses showed cystic degeneration; their labyrinths contained constricted and less extensive vascular network. Phagocytic giant cells, polymorphs and platelet aggregation were also marked. Placentae of externally normal looking fetuses also presented cystic degeneration, reduction in fetal vasculature, dilated maternal sinusoids and giant cell proliferation. Insulin treatment resulted in the preservation of most of the normal histology of the placenta which correlated well with the reduced fetal malformations.