Aim: To unravel the differences between systematic inflammatory response syndrome (SIRS) of acute pancreatitis compared to the same syndrome in sepsis.
Methods: Twenty-five patients were enrolled, 12 with sepsis and 13 acute pancreatitis. After diagnosis 20 mL blood was sampled. Half were assayed for isolation of monocytes and 10 mL was centrifuged for serum test of tumor necrosis factor alpha (TNFalpha and interleukin-6 (IL-6). Half of monocytes were incubated in the presence of patients' serum and supernatants were collected. The other half was treated for estimation of optical photometry under caspase-3 inhibition. TNFalpha and IL-6 were estimated by an enzyme immunoassay.
Results: median+/-SE of serum IL-6 in septic patients and acute pancreatitis patients was 192.30+/-35.40 ng/L and 21.00+/-16.05 ng/L, respectively (P<0.01). Respective values of caspase-3 were 0.94+/-0.17 pmol/min 10(4) cells and 0.34+/-0.09 pmol/min 10(4) cells (P<0.05). IL-6 of monocyte supernatants of patients with sepsis was significantly increased after addition of patients' serum, while that of patients with acute pancreatitis did not show significant difference.
Conclusion: The data have shown that monocyte activity is different between acute pancreatitis and sepsis. This phenomenon might be explained as a different pathway to the pro-inflammatory cytokines release or could be a novel anti-inflammatory response in acute pancreatitis.
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http://dx.doi.org/10.3748/wjg.v12.i41.6711 | DOI Listing |
Front Microbiol
December 2024
Department of Laboratory Medicine, Shengjing Hospital of China Medical University, Shenyang, China.
Aim: The current study aims to delineate subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), the sacrospinalis muscle, and all abdominal musculature at the L3-L5 vertebral level from non-contrast computed tomography (CT) imagery using deep learning algorithms. Subsequently, radiomic features are collected from these segmented images and subjected to medical interpretation.
Materials And Methods: This retrospective analysis includes a cohort of 315 patients diagnosed with acute necrotizing pancreatitis (ANP) who had undergone comprehensive whole-abdomen CT scans.
Cureus
November 2024
Radiology, Government Medical College & Hospital, Jammu, Jammu, IND.
Introduction: Obstructive jaundice resulting from a duodenal diverticulum is known as Lemmel syndrome. Lemmel syndrome should be included in the differential diagnosis in patients presenting with obstructive jaundice in the absence of choledocholithiasis, mass, or a stricture.
Aims And Objectives: To describe the computed tomography (CT) findings in patients with Lemmel syndrome.
AACE Clin Case Rep
August 2024
Department of Endocrinology, Endocrine Associates of West Village, New York City, New York.
Background/objective: Genetic causes of hypertriglyceridemia like familial chylomicronemia syndrome can be overlooked in everyday practice. We report a patient with a rare genetic mutation, highlighting the importance of genetic testing for timely diagnosis and prevention of complications.
Case Report: A 45-year-old Hispanic female presented with serum triglyceride levels of 749 mg/dL, refractory to rosuvastatin 10 mg daily and omega-3 ethyl esters 2 g daily.
AACE Clin Case Rep
July 2024
Department of Endocrinology, University of Maryland School of Medicine, Baltimore, Maryland.
Background/objective: Diabetic ketoacidosis (DKA) is typically but not exclusively seen in patients with a history of diabetes mellitus.
Case Report: This is a case of 39 year-old male who was diagnosed with acute pancreatitis based on characteristic symptoms and positive CT findings on presentation. Laboratory testing revealed elevated serum glucose 251 mg/dL, low serum bicarbonate 8 mmol/L, increased anion gap 21, and elevated serum beta-hydroxybutyrate 9.
Pancreatology
December 2024
Department of Surgery, University of California Los Angeles, Los Angeles, CA, USA. Electronic address:
Background/objectives: Genetic variants in PRSS1 encoding human cationic trypsinogen are associated with hereditary pancreatitis. The clinically frequent variants exert their pathogenic effect by increasing intrapancreatic trypsin activity, while a distinct subset of variants causes disease via mutation-induced trypsinogen misfolding and endoplasmic reticulum (ER) stress. Here, we report a novel misfolding PRSS1 variant.
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