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Incomplete small bowel obstruction in a patient with ankylosing spondylitis.

ABSTRACT: Small bowel obstruction is a blockage in the small intestine, which is usually caused by adhesion scar tissue, hernia, medication, or malignancy. The symptoms of small bowel obstruction include nausea and vomiting of bile, abdominal distention and obstipation. We present a case of a 61-year-old man with ankylosing spondylitis and scoliosis, who suffered from incomplete small bowel obstruction due to unusual direction of duodenum and externally compressed by liver, gallbladder and pancreas. We gave conservative treatment and inserted a nasojejunal tube for enteral feeding, and the duodenum broke free from the grip of liver, gallbladder and pancreas to its normal anatomical direction. Besides common etiology of small bowel obstruction, unusual body shape and smaller abdominal cavity may cause obstruction due to external compression of neighbor organs. Conservative treatments include gastrointestinal decompression, correction of electrolytes abnormality and nutrition support, while surgical intervention is suggested for the patient without improvement on conservative management.

SUBMITTER: Chiang HC

PROVIDER: S-EPMC8259219 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature

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Incomplete small bowel obstruction in a patient with ankylosing spondylitis.

Chiang Hsueh-Chien HC Chen Chiung-Yu CY Chuang Chiao-Hsiung CH Hsu Hung-Lung HL

Radiology case reports 20210703 9

Small bowel obstruction is a blockage in the small intestine, which is usually caused by adhesion scar tissue, hernia, medication, or malignancy. The symptoms of small bowel obstruction include nausea and vomiting of bile, abdominal distention and obstipation. We present a case of a 61-year-old man with ankylosing spondylitis and scoliosis, who suffered from incomplete small bowel obstruction due to unusual direction of duodenum and externally compressed by liver, gallbladder and pancreas. We ga ...[more]

PMID: 34257789

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Project description:IntroductionDisulfidptosis is a recently identified form of cell death that contributes to maintaining the internal environment balance of an organism. However, the molecular basis of disulfidptosis in ulcerative colitis (UC), ankylosing spondylitis (AS), and Crohn's disease (CD) has not been thoroughly explored.MethodsFirstly, the differentially expressed genes (DEGs) and disulfidptosis-associated genes (DAGs) were obtained through differential analysis between diseases (AS, CD, and UC) and control groups. After the disulfidptosis score was acquired using the single-sample gene set enrichment analysis (ssGSEA) algorithm, the DE-DAGs were screened by overlapping DAGs and DEGs of the three diseases. Next, the feature genes were selected through a combination of machine learning algorithms, receiver operating characteristic (ROC) curves, and expression analysis. Based on these feature genes, nomograms were created for AS, CD and UC. The co-feature genes were then identified by taking the intersections of the genes featured in all three diseases. Meanwhile, single-gene set enrichment analysis (GSEA) and the TF-mRNA-miRNA network were utilized to investigate the molecular mechanisms of the co-feature genes. To validate the expression differences of the co-feature genes between healthy controls and patients (AS and IBD), RT-PCR was performed. Lastly, mendelian randomization (MR) analysis was utilized to explore the causality between genetic variants of S100A12 with AS, UC and CD.ResultsIn this study, 11 DE-DAGs were obtained. Functional enrichment analysis revealed their involvement in cytokine production and fatty acid biosynthesis. Latterly, AS/CD/UC -feature genes were derived, and they all had decent diagnostic performance. Through evaluation, the performance of the nomogram was decent for three diseases. Then, 2 co-feature genes (S100A12 and LILRA5) were obtained. The GSEA enrichment results indicated that the co-feature genes were mainly enriched in the cytokine-cytokine receptor interaction and drug metabolism cytochrome P450. As shown by functional experiments, there was a correlation between the mRNA expression of S100A12 with AS, UC and CD. Additionally, a causal connection between S100A12 and IBD was detected through MR analysis.DiscussionIn this study, 2 co-feature genes (S100A12 and LILRA5) were screened, and their functions were investigated in AS, CD and UC, providing a basis for further research into diagnosis and treatment.

Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling. Fifteen knee synovial biopsy tissue samples consisting of six seronegative spondyloarthropy (SpA), two ankylosing spondylitis (AS), three osteoarthritis (OA) and four normal control biopsies were obtained from the Synovial Tissue Bank at the Repatriation General Hospital in Adelaide, South Australia with the appropriate ethical approval (Supplementary Table 1). All patients provided informed written consent.

Dataset Information

Incomplete small bowel obstruction in a patient with ankylosing spondylitis.

Publications

Incomplete small bowel obstruction in a patient with ankylosing spondylitis.

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