Showing papers by "Pramod Kumar Garg published in 2009"

Association of SPINK1 gene mutation and CFTR gene polymorphisms in patients with pancreas divisum presenting with idiopathic pancreatitis.

Abstract: BackgroundPancreas divisum has been associated with idiopathic pancreatitis. However, the causal association remains controversial.ObjectiveTo study the gene mutations in patients with pancreas divisum presenting with idiopathic pancreatitis.MethodsAll consecutive patients with pancreas divisum pres

Acute pancreatitis with CMV papillitis and cholangiopathy in a renal transplant recipient.

Abstract: Acute pancreatitis with cholangiopathy is an uncommon complication in renal transplant patients. Further, a combination of pancreatitis and cholangiopathy due to CMV disease in renal allograft recipient is further uncommon. We report a renal transplant recipient who developed acute pancreatitis and cholangiopathy with CMV papillitis of the Ampulla of Vater.

Spontaneous fracture of an uncovered enteral stent with proximal migration of fractured segment into cervical esophagus: first report.

Abstract: scopic placement of a biliary self-expandable metallic stent (SEMS) and a 22 ” 90 mm WallFlex duodenal stent (Boston Scientific, Natick, Massachusetts, USA) across an inoperable periampullary adenocarcinoma. Eighteen months later, the patient presented with nonbilious vomiting. A clinical diagnosis of gastric outlet obstruction due to disease progression was made. Endoscopy revealed a normal esophagus, dilated stomach, and narrowing between the first and second parts of the duodenum, but the stent was not clearly visualized. One week later, the patient underwent a water-soluble contrast study for assessment of the gastric outlet obstruction. Preliminary fluoroscopy revealed a radiopaque foreign body in the cervical esophagus, which was presumed to be the displaced fragment of the stent (l\" Fig. 1 a). There was free flow of contrast across the fragment (l\" Fig. 1 b). Luminal obstruction was apparent at the proximal end of the fractured stent in the second part of the duodenum with abrupt cutoff and prestenotic dilatation of the proximal duodenum and stomach (l\" Fig. 2). At endoscopy, the stent fragment, with a partially disrupted mesh, was seen just below the cricopharynx (l\" Fig. 3 a). It was retrieved by grasping it by its sides with two forceps, using a double-channel endoscope (Fujinon, Tokyo, Japan) (l\" Fig. 3 b). Migration is a known complication of enteral SEMS with reported rates of up to 5 % [1]. Distal migration is the norm and proximal migration is an exceptional event. The incidence of SEMS fracture and the exact reasons for this complication are elusive. Acid corrosion, thermal overstrain induced by laser application, and defective material at the time of deployment are some of the proposed explanations [2, 3]. However, there was no obvious reason for the cervical esophageal migration of the fractured segment in our patient, and we hypothesize that the reverse peristalsis accompanying the frequent episodes of vomiting was responsible for this unusual presentation. Endoscopic removal of stents that have migrated into the esophagus should be considered after ruling out potential complications with a water-soluble contrast study.

Water Area Extraction Using Geocoded High Resolution Imagery of TerraSAR-X Radar Satellite in Cloud Prone Brahmaputra River Valley

Abstract: In this study, supervised pixel based maximum likelyhood classifier (MLC) was evaluated for differentiating water area from non-water area in a cloud prone river valley region using images obtained from German TerraSAR-X radar satellite. TerraSAR-X satellite microwave data acquired on 8th May 2008 was used for a test site in Brahmputra river valley, India. The performance of traditional supervised (MLC) classification method was evaluated on TerraSAR's X band strip geo coded high resolution (6 meter) images in VV polarization channel. The 42 training sites for water area and 40 training sites for non-water areas were carefully selected over the entire image where optical Resourcesat - 1 LISS IV multi-spectral image and pre- classification ground truth were used as apriori knowledge. The calculated backscatter coefficient ranges from approximately - 24.1 to 6.5 dB where water areas usually have low dB value around -20 dB. Overall classification accuracy was 94.92 %. This study shows that high resolution TerraSAR-X radar satellite image have advantage of weather independence over optical data. Furthermore, the supervised (MLC) classification can be used for extraction of water area from single band high resolution radar images where traditional water area extraction methods i.e., NDVI, NDWI etc., can not be used on radar images.

The role of leptin in idiopathic chronic pancreatitis

Abstract: To the Editor: We read, with great interest, the article entitled BSerum Adiponectin and Leptin Concentrations in Patients With Chronic Pancreatitis of Alcoholic and NonalcoholicOrigin[byAdrychet al, published recently in the March issue of the Journal. We have previously published our study regarding leptin in patients with chronic pancreatitis (CP). In our study on patients with idiopathic CP (ICP), we did not find any difference in the unadjusted and the fatmass (FM) Yadjusted plasma leptin levels between patients with ICP and healthy controls (median, 4.0 ng/mL [range, 2.0Y 62.5 ng/mL] vs median, 5.0 ng/mL [range, 2.0Y63.0 ng/mL]; adjusted mean, 11.6 vs 11.4 ng/mL). There was also no difference in leptin levels among ICP patients with diabetes as compared with those without diabetes (median, 4.5 ng/mL [range, 2.0Y 62.5 ng/mL] vs median, 4.0 ng/mL [range, 2.0Y26.0 ng/mL]). As expected, we found significantly lower values of measures of FM, that is, body mass index (BMI), triceps skin-fold thickness, waist-hip circumference, FM, and %FM, among our patients with ICP as compared with healthy controls. Pancreatic exocrine and endocrine functions, as measured by fecal chymotrypsin and serum C-peptide levels, respectively, were also significantly lower among patients with ICP as compared with healthy controls. We found that leptin was significantly and positively correlated with BMI, FM, %FM, waist-hip circumferences, all skin-fold thicknesses, and midYupper arm circumference in ICP patients. Based on these findings, we suggested that leptin did not have a significant role in the pathogenesis of ICP and consequent pancreatic dysfunction. Furthermore, the normal physiological effects of leptin in the pancreas, which may be hormonal or paracrine in nature, are not affected by pancreatic ductal obstruction and fibrosis, and the adipocyte response to malnutrition remains intact independent of CP and pancreatic dysfunction. Interestingly, despite being the first and the only study on this subject outside the authors’ own previous study, they have not discussed our study in their article. The results of the study by Adrych et al are in contrast to our results. They found significantly lower serum leptin levels in patients with alcoholic pancreatitis and ICP. The single most factor leading to their results of lower leptin levels in patients with CP seems to be nonadjustment of leptin levels for the body FM. The authors found that patients with CP had lower BMI compared with controls, yet they did not adjust the leptin levels for the body FM. Leptin is produced primarily by adipocytes in response to the fat content of the body and the state of nutrition. We have shown that patients with CP have generally depleted fat stores.Hence,while interpreting any data involving leptin, it is important to adjust the leptin level for the body FM. It is pertinent that measures of leptin correlations should be carried out after fat-mass adjustment. This would allow a better interpretation of its role in CP. Another reason for altered leptin levels could be alcohol consumption. The data regarding active alcohol consumption by patients and by controls are not available in their study. Alcohol has been shown to increase serum leptin levels in a dosedependent manner, regardless of the nutritional status. Also, in alcohol-drinking normal rats, serumleptinconcentrationwas found to be augmented despite reduced blood insulin, suggesting that, after alcohol consumption, the physiological mechanisms regulating leptin secretion are disturbed. Based on this, it would be difficult to interpret the implication of serum leptin on patients with alcohol-induced CP who continue to consume alcohol. In our study, we had specifically excluded patients with alcoholic CP or patients with continued alcohol usage. Adrych et al have studied only 4 patients with ICP, and hence, any interpretation made for the role of leptin in patients with ICP is approximate at best. The authors also measured serum insulin levels for assessment of pancreatic endocrine function. The use of serum insulin measurements in patients with diabetes (17 patients had diabetes) is not advised because patients may be taking exogenous insulin or may be on insulin sensitizers. For this reason, serum C-peptide level, which is representative of endogenous insulin, is a better marker of body insulin production, and one should be cautious in interpreting the data regarding serum insulin levels. They found a significant correlation between serum leptin and serum insulin in patients with CP and suggested that the low serum insulin could result in low serum leptin because insulin stimulates leptin gene expression. It iswell known that circulating glucose and insulin levels seem to have a stimulatory effect on leptin secretion. On the other hand, increased plasma leptin levels act to increase peripheral insulin sensitivity while reducing insulin release from pancreatic beta cells. This bidirectional feedbackloopbetweenadipose tissue and pancreatic islets is called adipoinsular axis.10 The existence of an adipoinsular axis, wherein each of leptin and insulin affects each other’s level, makes it difficult to attribute a low serum leptin level to a low serum insulin level. The authors’suggestion in their study that leptin could be used to differentiate between acute pancreatitis and CP is premature because the picture is still not clear with regard to leptin levels in acute pancreatitis and CP. Similarly, their interpretation that a low level of leptin would be protective in CP is purely conjectural and wishful. We suggest therefore that the results of the study by Adrych et al should be interpreted in light of these observations.

Genome wide association studies: way forward or work backwards?

Abstract: Deciphering the 3 billion nucleotides long human genome through direct sequencing that culminated in 2001, in fact ahead of schedule, was a jewel in the crown of human geneticists.1 And the hallowed yet seemingly imponderable precincts of genetics were conquered but only to further incite the insatiable human curiosity. The marvellous insight into the hidden truths of nature revealed that there are about 25,000 genes in the human genome. As we know these genes are embedded long stretches of DNA which rearrange into a pair of 23 chromosomes during the cell cycle for even distribution of the genome to daughter cells. These genes are interspersed within a large non-coding DNA sometimes referred to as ‘junk’ DNA (more out of ignorance than otherwise). The human race is relatively of recent origin being the last during the 3.5 billion or more of evolution of life on earth attesting to the complexity or the superiority of being a human (at least humans tend to believe that!). Evolutionary changes in the human genome are relatively rare events to the tune of one nucleotide change in 108 nucleotides per generation.2 Thus, there are remarkable similarities in the human genome across different populations despite obvious phenotypic differences. There are however, recombination events in the genome during the meiosis between different segments of 2 chromosomes so that the offspring inherits a mixture of information from both the paternal and maternal genes. For distantly located genes on different chromosomes, the frequency of a genotype will depend on the frequencies of alleles (alternate forms of a gene; Figure 1) in a large random mating population. For example, for 2 different genes (e.g. A and B) having 2 alleles each (A1, A2 and B1, B2), the chance of an individual possessing a particular genotype (A1B1, A1B2, A2B1, A2B2) depends on the frequency of the alleles in the population e.g. for frequencies of A1 90%, A2 10%, B1 95%, B2 5%, the chances of genotypes A1B1, A1B2, A2B1, A2B2 will be 85.5%, 4.5%, 9.5%, and 5% respectively. This is known as linkage equilibrium where the frequencies of genotype at one locus are independent of the frequencies at another locus. However, closer loci on one chromosome are in what is known as linkage disequilibrium (LD).3 Linkage disequilibrium is a result of recent mutations or polymorphisms in that particular area that have not been subjected to meiotic recombination events over a long period of time and thus the chances of 2 neighbouring alleles inherited together are more than that in linkage equilibrium. The recombination events occur at certain spots separated by relatively long distance in the chromosome. Thus, the part of the chromosome in between the recombination sites is passed on to the next generation en bloc. The genomic elements e.g. genes or short tandem repeats (microsatellites) within such a block are linked physically and are in LD. Linkage disequilibrium is the basis of genetic association studies. Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, India.