Anatomical study of the length of the human intestine

Hounnou, G.M.; Destrieux, Christophe; Desme, J.; Bertrand, P; Velut, Stéphane

doi:10.1007/s00276-002-0057-y

Cited by 160 publications

(33 citation statements)

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“…In the standard diagram shown in Figure 15, the total length of the lower gastrointestinal tract is represented as 150 cm, with the colon (from the cecum to the rectosigmoid junction) being 130 cm. This is consistent with the lengths of colon measured in living individuals (reviewed in [36]). From our observations of 32 resected colon segments, with 12 in the ascending colon, 6 in the transverse colon and 14 in the descending/sigmoid colon (Table 2) and taking an average of the inner circumferences of the three regions, we determined that 6.2 cm is the average inner circumference of the colon (see Figure 13 for how inner circumferences were measured, after colon segments were opened longitudinally).…”

Section: Resultssupporting

confidence: 90%

“…The inner longitudinal dimension of the freshly obtained, non-fixed human colon (from 100 male and 100 female cadavers, measured a few hours after being brought to the laboratory, or after the intestinal tracts were preserved in a refrigerator at 3°C for 24-72 hours) is, on average, 160.5 cm (measured from the bottom of the cecum to the colorectal junction) with a range of 80 cm to 313 cm [36]. The intestine lengthens after death, possibly because of loss of intestinal muscular tone (reviewed in [36]). Thus, a 160.5 cm length is consistent with the length shown in Figure 15, representing the living colon.…”

Section: Resultsmentioning

confidence: 99%

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Deficient expression of DNA repair enzymes in early progression to sporadic colon cancer

et al. 2012

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BackgroundCancers often arise within an area of cells (e.g. an epithelial patch) that is predisposed to the development of cancer, i.e. a "field of cancerization" or "field defect." Sporadic colon cancer is characterized by an elevated mutation rate and genomic instability. If a field defect were deficient in DNA repair, DNA damages would tend to escape repair and give rise to carcinogenic mutations.PurposeTo determine whether reduced expression of DNA repair proteins Pms2, Ercc1 and Xpf (pairing partner of Ercc1) are early steps in progression to colon cancer.ResultsTissue biopsies were taken during colonoscopies of 77 patients at 4 different risk levels for colon cancer, including 19 patients who had never had colonic neoplasia (who served as controls). In addition, 158 tissue samples were taken from tissues near or within colon cancers removed by resection and 16 tissue samples were taken near tubulovillous adenomas (TVAs) removed by resection. 568 triplicate tissue sections (a total of 1,704 tissue sections) from these tissue samples were evaluated by immunohistochemistry for 4 DNA repair proteins. Substantially reduced protein expression of Pms2, Ercc1 and Xpf occurred in field defects of up to 10 cm longitudinally distant from colon cancers or TVAs and within colon cancers. Expression of another DNA repair protein, Ku86, was infrequently reduced in these areas. When Pms2, Ercc1 or Xpf were reduced in protein expression, then either one or both of the other two proteins most often had reduced protein expression as well. The mean inner colon circumferences, from 32 resections, of the ascending, transverse and descending/sigmoid areas were measured as 6.6 cm, 5.8 cm and 6.3 cm, respectively. When combined with other measurements in the literature, this indicates the approximate mean number of colonic crypts in humans is 10 million.ConclusionsThe substantial deficiencies in protein expression of DNA repair proteins Pms2, Ercc1 and Xpf in about 1 million crypts near cancers and TVAs suggests that the tumors arose in field defects that were deficient in DNA repair and that deficiencies in Pms2, Ercc1 and Xpf are early steps, often occurring together, in progression to colon cancer.

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Section: Resultssupporting

confidence: 90%

Section: Resultsmentioning

confidence: 99%

Deficient expression of DNA repair enzymes in early progression to sporadic colon cancer

et al. 2012

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“…Colon lengths may vary over 2-fold [16], allowing for the variation predicted with the equation. This example indicates how a small biological feature ( m or the number of crypts) is interrelated with cancer risks and can be indirectly measured from cancer epidemiology.…”

Section: Resultsmentioning

confidence: 99%

A simple algebraic cancer equation: calculating how cancers may arise with normal mutation rates

Calabrese

Shibata

2010

BMC Cancer

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BackgroundThe purpose of this article is to present a relatively easy to understand cancer model where transformation occurs when the first cell, among many at risk within a colon, accumulates a set of driver mutations. The analysis of this model yields a simple algebraic equation, which takes as inputs the number of stem cells, mutation and division rates, and the number of driver mutations, and makes predictions about cancer epidemiology.MethodsThe equation [p = 1 - (1 - (1 - (1 - u)d)k)Nm ] calculates the probability of cancer (p) and contains five parameters: the number of divisions (d), the number of stem cells (N × m), the number of critical rate-limiting pathway driver mutations (k), and the mutation rate (u). In this model progression to cancer "starts" at conception and mutations accumulate with cell division. Transformation occurs when a critical number of rate-limiting pathway mutations first accumulates within a single stem cell.ResultsWhen applied to several colorectal cancer data sets, parameter values consistent with crypt stem cell biology and normal mutation rates were able to match the increase in cancer with aging, and the mutation frequencies found in cancer genomes. The equation can help explain how cancer risks may vary with age, height, germline mutations, and aspirin use. APC mutations may shorten pathways to cancer by effectively increasing the numbers of stem cells at risk.ConclusionsThe equation illustrates that age-related increases in cancer frequencies may result from relatively normal division and mutation rates. Although this equation does not encompass all of the known complexity of cancer, it may be useful, especially in a teaching setting, to help illustrate relationships between small and large cancer features.

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“…Khashab et al 8. measured CT regional volumes of an insufflated bowel and found an increase in the length of transverse colon with age and female gender, Postmortem studies are hard to interpret5 while measurements from barium enema7 are likely to be influenced by the volume infused which depends on patient tolerance. This study found that the total length of colon was longer in females (and female colon lengths tended to increase with height and weight), and tendency to increase with age for both genders.…”

Section: Discussionmentioning

confidence: 99%

“…To date, measurements of regional colon dimensions have mainly been obtained from resected cadaver specimens,4,5 interoperative measurements6 or from radiological assessments of the prepared, distended colon during barium examination7 or CT colonoscopy 8. All these methods disturb the natural morphology of the bowel.…”

Section: Introductionmentioning

confidence: 99%

Fasting and postprandial volumes of the undisturbed colon: normal values and changes in diarrhea‐predominant irritable bowel syndrome measured using serial MRI

Pritchard

Marciani

Garsed

et al. 2013

Neurogastroenterology Motil

124

153

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Key Messages• Previous measurements of regional colonic volume have used invasive methods that could disturb natural morphology.• Using MRI, volume measurement of the undisturbed colon was achieved in 75 healthy volunteers and 25 IBS-D patients. Normal volume ranges were defined.• IBS-D patients showed less ability to accommodate post-prandial inflow in the ascending colon. AbstractBackground Previous assessments of colon morphology have relied on tests which were either invasive or used ionizing radiation. We aimed to measure regional volumes of the undisturbed colon in healthy volunteers (HV) and patients with diarrhea-predominant irritable bowel syndrome (IBS-D). Methods 3D regional (ascending, transverse, and descending) colon volumes were measured in fasting abdominal magnetic resonance (MR) images of 75 HVs and 25 IBS-D patients. Thirty-five of the HV and all 25 IBS-D subjects were fed a standard meal and postprandial MRI data obtained over 225 min. Key Results Colonic regions were identified and 3D maps from cecum to sigmoid flexure were defined. Fasted regional volumes showed wide variation in both HVs being (mean AE SD) ascending colon (AC) 203 AE 75 mL, transverse (TC) 198 AE 79 mL, and descending (DC) 160 AE 86 mL with no difference from IBS-D subjects (AC 205 AE 69 mL, TC 232 AE 100 mL, and DC 151 AE 71 mL, respectively). The AC volume expanded by 10% after feeding (p = 0.007) in the 35 HV possibly due to increased ileo-colonic inflow. A later rise in AC volume occurred from t = 90 to t = 240 min as the meal residue entered the cecum. In contrast, IBS-D subjects showed a much reduced postprandial response of the AC (p < 0.0001) and a greater increase in TC volume after 90 min (p = 0.0244) compared to HV. Conclusions & Inferences We have defined a normal range of the regional volumes of the undisturbed colon in fasted and fed states. The AC in IBS-D appeared less able to accommodate postprandial inflow which may account for faster colonic transit.

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Anatomical study of the length of the human intestine

Cited by 160 publications

References 0 publications

Deficient expression of DNA repair enzymes in early progression to sporadic colon cancer

Deficient expression of DNA repair enzymes in early progression to sporadic colon cancer

A simple algebraic cancer equation: calculating how cancers may arise with normal mutation rates

Fasting and postprandial volumes of the undisturbed colon: normal values and changes in diarrhea‐predominant irritable bowel syndrome measured using serial MRI

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