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Showing papers by "Pramod Kumar Garg published in 2007"


Journal ArticleDOI
TL;DR: Predictors of mortality were development and early onset of organ failure, and newer subgroups of patients with fulminant and subfulminant AP with important prognostic and management implications are characterized.

84 citations


Journal ArticleDOI
TL;DR: The aim of the present paper was to study the profile of anti‐ and proinflammatory cytokines in AP and to determine their predictive value for severity of AP, organ failure and mortality.
Abstract: Background and aim Cytokines play an important role in the pathogenesis of acute pancreatitis (AP). The aim of the present paper was to study the profile of anti- and proinflammatory cytokines in AP and to determine their predictive value for severity of AP, organ failure and mortality. Methods Consecutive patients with AP were included in the study. Cytokines were measured in those patients who presented within the first 72 h of the onset of AP. Plasma levels of proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-Ibeta, IL-6 and anti-inflammatory cytokine IL-10 were measured on days 1, 3, 7 and 14 of AP. Results Of 108 patients, 30 presented within 72 h of the onset (mean age 40.27 +/- 13.89 years; 22 males). Of the 30 patients, 13 (43.3%) had severe and 17 (56.7%) had mild pancreatitis. Eleven (36.7%) patients developed organ failure and three died. The level of IL-6 on day 3 was significantly higher in severe pancreatitis than in mild pancreatitis (146.29 +/- 57.53 pg/mL vs 91.42 +/- 71.65 pg/mL; P = 0.04) and was significantly higher in patients who developed organ failure compared with those who did not (161.59 +/- 53.46 pg/mL vs 88.16 +/- 65.50 pg/mL; P = 0.004). At a cut-off value of 122 pg/mL on day 3, IL-6 predicted organ failure and severe pancreatitis with a sensitivity and specificity of 81.8% and 77.7%, respectively. TNF-alpha and IL-10 were detectable only in one-third of patients and were not related to the severity of pancreatitis, while Il-1beta was not detectable. Conclusion Elevated levels of IL-6 predicted organ failure and severe pancreatitis and suggested its pathophysiological significance in AP.

82 citations


Journal ArticleDOI
TL;DR: Microlithiasis was not a significant cause of idiopathic RAP in the authors' patients, and about one half of the patients with RAP developed chronic pancreatitis during the follow-up period.

82 citations


Journal ArticleDOI
TL;DR: The diagnostic yield was higher in patients with overt, obscureGI bleeding than in those with occult obscure GI bleeding, and the success rate in detection of the cause of bleeding using CT enteroclysis was 47.6%.

38 citations



Journal ArticleDOI
TL;DR: Strongyloides stercoralis, a nematode endemic in the tropics, was the cause of chronic diarrhea in this 50-year-old farmer with seropositive rheumatoid arthritis on corticosteroid therapy for the past 15 years.
Abstract: sulfosalazine. Corticosteroids affect immunity by increasing the apoptosis of Th2 cells and accelerating the conversion of free-living rhabditiform larva into tissue-penetrating filariform larvae, completing the autoinfection cycle. Rogers et al and Cruz et al first described the occurrence of fatal disseminated strongyloidiasis in immunosuppressed patients in 1966. Therefore, physicians prescribing immunosuppressive therapy in endemic areas need to pay special attention to this fact. Hyperinfection syndrome or infiltration of crypts by filariform larvae is estimated to happen in 1.5% to 2.5% of patients with strongyloidiasis. The steroids precipitated the hyperinfection and chronic diarrhea in this patient who was probably harboring Strongyloides in the small intestine (Figures 2, 3). The mortality in disseminated infection nears 87% to 100% because of difficulty in diagnosis and high potential for fatal complications. Strongyloides stercoralis, a nematode endemic in the tropics, was the cause of chronic diarrhea in this 50-year-old farmer with seropositive rheumatoid arthritis on corticosteroid therapy for the past 15 years. HIV enzyme-linked immunosorbent assay (ELISA) was negative. Duodenal biopsy, done for the evaluation of chronic diarrhea revealed Strongyloides larvae in the duodenal crypts (Figures 1-3). Subsequently, the patient received oral ivermectin (200 μg/kg). His appetite returned, the diarrhea decreased, and the patient was discharged on

10 citations


Journal ArticleDOI
01 Aug 2007-Pancreas
TL;DR: Leptin does not seem to have a pathophysiological role in either ICP or the development of diabetes in ICP.
Abstract: OBJECTIVES Leptin alters pancreatic exocrine and beta-cell secretion in animal studies. We hypothesized that leptin might be important in the pathogenesis of idiopathic chronic pancreatitis (ICP) and/or the development of diabetes in ICP. METHODS Fifty patients with ICP (25 with diabetes, 25 without diabetes) and 25 healthy controls were included in a prospective, case-control study. Fasting plasma leptin concentration was measured by enzyme-linked immunosorbent assay. Exocrine and endocrine pancreatic functions were assessed by fecal chymotrypsin and serum C-peptide, respectively. Anthropometric parameters and body fat mass (FM) were measured. RESULTS Patients with ICP (mean age, 30 years; 33 men) had significantly lower body mass index (19.5 +/- 2.6 kg/m2) and FM (10.6 +/- 4.2 kg) as compared with controls (body mass index, 21.7 +/- 4.1 kg/m2; FM, 19.0 +/- 16.6 kg; P < 0.01). Fecal chymotrypsin (median, 5.2 [range, 0.3-42.6] U/kg) and C-peptide (median, 1.7 [range, 0.2-9.5] ng/mL) were significantly lower in patients than in controls (12.9 [range, 2.5-33.0] U/kg and 3.5 [range, 0.3-10.3] ng/mL; P < 0.01). Plasma leptin concentration was slightly lower but statistically insignificant in patients with ICP (median, 4.0 [range, 2.0-62.5] ng/mL) as compared with controls (median, 5.0 [range, 2.0-63.0] ng/mL). Patients with and those without diabetes were also comparable with regard to their leptin concentration, pancreatic functions, and anthropometric parameters. CONCLUSIONS Leptin does not seem to have a pathophysiological role in either ICP or the development of diabetes in ICP.

6 citations