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The endoscopically normal colon: when is mapping biopsy histopathologically justifiable?

ABSTRACT: Mapping biopsy of endoscopically normal colon is a contentious area and generates considerable work for histopathology services. Managing demand for pathological testing is a current healthcare priority. In this retrospective audit, the authors aimed to establish diagnostic yield of mapping biopsy in this specific subgroup and identify situations where practice could be safely streamlined.Cases were retrieved over a 10-month period. Histopathology results were correlated with relevant endoscopy reports. The data were anonymised and analysed.Department of Cellular Pathology, Southampton General Hospital, UK.717 cases were retrieved. 308 (43%) cases were reported as endoscopically normal. 278 (90%) cases with endoscopically normal/near normal mucosa showed normal/near normal histology. 30/308 (9.7%) endoscopically normal cases showed pathological abnormalities. 9/308 (2.9%) cases of microscopic colitis were detected. Of the 30 cases with pathological abnormalities, 20 (66.7%) presented with change in bowel habit and 6 (20%) had a pre-existing diagnosis of inflammatory bowel disease.Pathological abnormalities in endoscopically normal colon are found most frequently in those who present with change in bowel habit or a known history of inflammatory bowel disease. The authors support biopsy in these individuals and believe that mapping biopsy of endoscopically normal colon in patients referred for other reasons (eg, bright red rectal bleeding or iron deficiency anaemia) should not be performed routinely as diagnostic yields are very low. Guidelines on appropriate use of mapping biopsy in this setting are limited. Streamlining patients based on reason for referral or presenting symptoms may be a useful step towards more effective management of histopathological demand.

SUBMITTER: Elliot VJ

PROVIDER: S-EPMC5517258 | biostudies-other | 2012 Apr

REPOSITORIES: biostudies-other

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Project description:Observational studies indicate that calcium supplementation may protect against colorectal cancer. Stratified analyses suggest that this protective effect may differ based on anatomic subsite and sex, but these hypotheses have been difficult to test experimentally. Here, we exposed 36 patient-derived organoid lines derived from normal colon biopsies (21 right colons, 15 left colons) of unrelated subjects (18 female, 18 male) to moderate (1.66 mmol/L) or high (5.0 mmol/L) concentrations of calcium for 72 hours. We performed bulk RNA-sequencing to measure gene expression, and cell composition was inferred using single-cell deconvolution in CIBERSORTx. We tested for significant differences in gene expression using generalized linear models in DESeq2. Exposure to higher levels of calcium was associated with changes in cell composition (P < 0.05), most notably increased goblet and reduced stem cell populations, and differential expression of 485 genes (FDR < 0.05). We found that 40 of these differentially expressed genes mapped to genomic loci identified through colorectal cancer genome-wide association studies, suggesting a potential biologic overlap between calcium supplementation and inherited colorectal cancer risk. Stratified analyses identified more differentially expressed genes in colon organoids derived from right sided colon and male subjects than those derived from left sided colon and female subjects. We confirmed the presence of a stronger right-sided effect for one of these genes, HSD17B2 using qPCR in a subset of matched right and left colon organoids (n = 4). By relating our findings to genetic data, we provide new insights into how nutritional and genetic factors may interact to influence colorectal cancer risk.Prevention relevanceA chemopreventive role for calcium in colorectal cancer is still unclear. Here, we identify mechanisms through which calcium supplementation may reduce risk. Calcium supplementation increased differentiation and altered expression of colorectal cancer-related genes in a large study of patient-derived colon organoids. These findings were influenced by colon location and sex.

Project description:BackgroundThe significance of amyloid precursor protein (APP) and neuroinflammation in idiopathic normal pressure hydrocephalus (iNPH) and Alzheimer's disease (AD) is unknown.ObjectiveTo investigate the role of soluble APP (sAPP) and amyloid beta (A?) isoforms, proinflammatory cytokines, and biomarkers of neuronal damage in the cerebrospinal fluid (CSF) in relation to brain biopsy A? and hyperphosphorylated tau (HP?) findings.MethodsThe study population comprised 102 patients with possible NPH with cortical brain biopsies, ventricular and lumbar CSF samples, and DNA available. The final clinical diagnoses were: 53 iNPH (91% shunt-responders), 26 AD (10 mixed iNPH+AD), and 23 others. Biopsy samples were immunostained against A? and HP?. CSF levels of AD-related biomarkers (A?42, p-tau, total tau), non-AD-related A? isoforms (A?38, A?40), sAPP isoforms (sAPP?, sAPP?), proinflammatory cytokines (several interleukins (IL), interferon-gamma, monocyte chemoattractant protein-1, tumor necrosis factor-alpha) and biomarkers of neuronal damage (neurofilament light and myelin basic protein) were measured. All patients were genotyped for APOE.ResultsLumbar CSF levels of sAPP? were lower (p<0.05) in patients with shunt-responsive iNPH compared to non-iNPH patients. sAPP? showed a similar trend (p?=?0.06). CSF sAPP isoform levels showed no association to A? or HP? in the brain biopsy. Quantified A? load in the brain biopsy showed a negative correlation with CSF levels of A?42 in ventricular (r?=?-0.295, p?=?0.003) and lumbar (r?=?-0.356, p?=?0.01) samples, while the levels of A?38 and A?40 showed no correlation. CSF levels of proinflammatory cytokines and biomarkers of neuronal damage did not associate to the brain biopsy findings, diagnosis, or shunt response. Higher lumbar/ventricular CSF IL-8 ratios (p<0.001) were seen in lumbar samples collected after ventriculostomy compared to the samples collected before the procedure.ConclusionsThe role of sAPP isoforms in iNPH seems to be independent from the amyloid cascade. No neuroinflammatory background was observed in iNPH or AD.

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The endoscopically normal colon: when is mapping biopsy histopathologically justifiable?

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