An inflammatory disorder of the colon known as ulcerative colitis causes superficial erosions and widespread friability on the colonic wall accompanied by bleeding. Typically, it only affects the colon’s submucosa and mucosa, causing localized inflammation.
The disease often begins in the rectum and progresses upward. A quarter of a million doctor visits are attributed to the disease each year in the US, and its direct medical expenses are thought to total more than $4 billion.
Epidemiology
North America and Northern Europe have the most significant prevalence of inflammatory bowel disorders globally. A western-influenced environment and lifestyle are strongly associated with inflammatory bowel disease. 9 to 20 instances of ulcerative colitis occur per 100,000 individuals each year. Adults are more likely to have ulcerative colitis than Crohn’s disease.
However, Crohn’s disease and ulcerative colitis are less common compared to the pediatric population. The incidence of ulcerative colitis follows a bimodal distribution between the ages of 15 and 30, and the primary onset peaks. Between the ages of 50 and 70, the incidence reaches a second. Although some research indicates minor precedence for males, most studies reveal no sex preference.
Ulcerative colitis is common in nonsmokers or individuals who have quit smoking. Additionally, smokers with ulcerative colitis frequently experience a milder illness, require fewer hospital stays, and require less medication. Although limited, there is evidence connecting the use of non-steroidal anti-inflammatory drugs to the development or recurrence of ulcerative colitis.
Additionally, removing an infected appendix is associated with inflammatory bowel disease. In contrast to Crohn’s disease, ulcerative colitis is related to a lower appendectomy incidence before the age of twenty. It has been demonstrated that having an appendectomy lowers the likelihood of developing ulcerative colitis by 69%.
Anatomy
Pathophysiology
Defects in the immunological response, epithelial barrier, leukocyte recruitment, and colonic microbiota play a role in the pathophysiology of ulcerative colitis. Colonic mucin and tight junctions are defective in the epithelial barrier, which causes more luminal antigens to be absorbed. Additionally, there are more mature, activated dendritic cells with many toll-like receptors (TLR), mainly TLR4 and TLR2, in the lamina propria of the mucosa.
Additionally, ulcerative colitis patients appear to have an abnormal T-helper (Th) cell response, particularly Th2, which has cytotoxic effects on epithelial cells. TNF-alpha, IL-13, and natural killer T-cells are additional immune-related components that contribute to the pathophysiology of ulcerative colitis. Inflammatory bowel disease increases IgA, IgG, and IgM levels; however, individuals with ulcerative colitis have disproportionately high IgG1 antibodies.
There are two methods by which leukocyte recruitment is impacted. Leukocytes from the systemic circulation are drawn to the mucosa in ulcerative colitis due to increased production of the chemoattractant CXCL8. The endothelium of mucosal blood vessels also exhibits an elevation of mucosal addressin cellular adhesion molecule-1 (Mad-CAM1), which facilitates leukocyte extravasation and adherence into mucosal tissue.
According to studies, intestinal microflora has a significant role in disease development, severity, and manifestation. The host’s mucosal immunology and intestinal bacteria appear to be in a homeostatic equilibrium, which may contribute to ulcerative colitis. As a result, non-pathogenic bacteria are encountered with an abnormal reaction.
Etiology
Inflammatory bowel disease has an unknown etiology. Since a family history of the disease occurs in 8% to 14% of individuals, it appears that there is a fundamental genetic component. There is a four-fold increased likelihood of acquiring ulcerative colitis in a first-degree relative of a patient.
Additionally, compared to other ethnic groups, Jewish communities have a greater frequency of ulcerative colitis. It has been hypothesized that changes in the gut microbiota’s composition and inadequate mucosal immunity may cause ulcerative colitis, although there is little evidence to back this up.
Autoimmune conditions may significantly influence the etiology of ulcerative colitis. According to some studies, smoking may be protective, but there is no definitive link between the two.
Genetics
Prognostic Factors
Despite being a lifelong condition, ulcerative colitis does not have a higher overall death rate than the general population. However, individuals with shock or surgical complications have a higher death rate. When the muscularis propria is involved, it may damage the nerves and cause dilatation, ischemia, and peristalsis.
The most frequent cause of mortality in ulcerative colitis is toxic megacolon. Colon cancer affects at least 5% of patients, and the risk rises with the severity of the condition. Stricture development is less common than Crohn’s disease.
Initial: 3-4 g/day orally divided three times a day
Do not exceed more than 4g a day leads to increased risk of toxicity
Maintenance: 2 g/day in divided doses every 8 hours
160mg subcutaneously as four injections in 40mg each on day 1 or 80mg subcutaneously two weeks later
Maintenance dose:2 weeks later-40mg subcutaneously every two weeks
Take maintenance dose of 1 g orally daily in couple of divided doses
Administration.
Consume with meal Dosing Modifications
Renal impairment
If renal function diminishes while taking medication, stop taking it.
<5 years: Safety and efficacy not established
>5 years (20 to <40kgs):
Days 1-15:
Day 1:80 mg subcutaneous
Day 8: 40mg subcutaneous
Day 15: 40mg subcutaneous
Maintenance dose: From week 4
80mg subcutaneous every two weeks
20mg subcutaneously every week
Future Trends
Media Gallary
References
www.ncbi.nlm.nih.gov/books/NBK459282
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An inflammatory disorder of the colon known as ulcerative colitis causes superficial erosions and widespread friability on the colonic wall accompanied by bleeding. Typically, it only affects the colon’s submucosa and mucosa, causing localized inflammation.
The disease often begins in the rectum and progresses upward. A quarter of a million doctor visits are attributed to the disease each year in the US, and its direct medical expenses are thought to total more than $4 billion.
North America and Northern Europe have the most significant prevalence of inflammatory bowel disorders globally. A western-influenced environment and lifestyle are strongly associated with inflammatory bowel disease. 9 to 20 instances of ulcerative colitis occur per 100,000 individuals each year. Adults are more likely to have ulcerative colitis than Crohn’s disease.
However, Crohn’s disease and ulcerative colitis are less common compared to the pediatric population. The incidence of ulcerative colitis follows a bimodal distribution between the ages of 15 and 30, and the primary onset peaks. Between the ages of 50 and 70, the incidence reaches a second. Although some research indicates minor precedence for males, most studies reveal no sex preference.
Ulcerative colitis is common in nonsmokers or individuals who have quit smoking. Additionally, smokers with ulcerative colitis frequently experience a milder illness, require fewer hospital stays, and require less medication. Although limited, there is evidence connecting the use of non-steroidal anti-inflammatory drugs to the development or recurrence of ulcerative colitis.
Additionally, removing an infected appendix is associated with inflammatory bowel disease. In contrast to Crohn’s disease, ulcerative colitis is related to a lower appendectomy incidence before the age of twenty. It has been demonstrated that having an appendectomy lowers the likelihood of developing ulcerative colitis by 69%.
Defects in the immunological response, epithelial barrier, leukocyte recruitment, and colonic microbiota play a role in the pathophysiology of ulcerative colitis. Colonic mucin and tight junctions are defective in the epithelial barrier, which causes more luminal antigens to be absorbed. Additionally, there are more mature, activated dendritic cells with many toll-like receptors (TLR), mainly TLR4 and TLR2, in the lamina propria of the mucosa.
Additionally, ulcerative colitis patients appear to have an abnormal T-helper (Th) cell response, particularly Th2, which has cytotoxic effects on epithelial cells. TNF-alpha, IL-13, and natural killer T-cells are additional immune-related components that contribute to the pathophysiology of ulcerative colitis. Inflammatory bowel disease increases IgA, IgG, and IgM levels; however, individuals with ulcerative colitis have disproportionately high IgG1 antibodies.
There are two methods by which leukocyte recruitment is impacted. Leukocytes from the systemic circulation are drawn to the mucosa in ulcerative colitis due to increased production of the chemoattractant CXCL8. The endothelium of mucosal blood vessels also exhibits an elevation of mucosal addressin cellular adhesion molecule-1 (Mad-CAM1), which facilitates leukocyte extravasation and adherence into mucosal tissue.
According to studies, intestinal microflora has a significant role in disease development, severity, and manifestation. The host’s mucosal immunology and intestinal bacteria appear to be in a homeostatic equilibrium, which may contribute to ulcerative colitis. As a result, non-pathogenic bacteria are encountered with an abnormal reaction.
Inflammatory bowel disease has an unknown etiology. Since a family history of the disease occurs in 8% to 14% of individuals, it appears that there is a fundamental genetic component. There is a four-fold increased likelihood of acquiring ulcerative colitis in a first-degree relative of a patient.
Additionally, compared to other ethnic groups, Jewish communities have a greater frequency of ulcerative colitis. It has been hypothesized that changes in the gut microbiota’s composition and inadequate mucosal immunity may cause ulcerative colitis, although there is little evidence to back this up.
Autoimmune conditions may significantly influence the etiology of ulcerative colitis. According to some studies, smoking may be protective, but there is no definitive link between the two.
Despite being a lifelong condition, ulcerative colitis does not have a higher overall death rate than the general population. However, individuals with shock or surgical complications have a higher death rate. When the muscularis propria is involved, it may damage the nerves and cause dilatation, ischemia, and peristalsis.
The most frequent cause of mortality in ulcerative colitis is toxic megacolon. Colon cancer affects at least 5% of patients, and the risk rises with the severity of the condition. Stricture development is less common than Crohn’s disease.
Initial: 3-4 g/day orally divided three times a day
Do not exceed more than 4g a day leads to increased risk of toxicity
Maintenance: 2 g/day in divided doses every 8 hours
160mg subcutaneously as four injections in 40mg each on day 1 or 80mg subcutaneously two weeks later
Maintenance dose:2 weeks later-40mg subcutaneously every two weeks
Take maintenance dose of 1 g orally daily in couple of divided doses
Administration.
Consume with meal Dosing Modifications
Renal impairment
If renal function diminishes while taking medication, stop taking it.
<5 years: Safety and efficacy not established
>5 years (20 to <40kgs):
Days 1-15:
Day 1:80 mg subcutaneous
Day 8: 40mg subcutaneous
Day 15: 40mg subcutaneous
Maintenance dose: From week 4
80mg subcutaneous every two weeks
20mg subcutaneously every week
www.ncbi.nlm.nih.gov/books/NBK459282
medtigo
Ulcerative Colitis
Updated :
December 7, 2022
An inflammatory disorder of the colon known as ulcerative colitis causes superficial erosions and widespread friability on the colonic wall accompanied by bleeding. Typically, it only affects the colon’s submucosa and mucosa, causing localized inflammation.
The disease often begins in the rectum and progresses upward. A quarter of a million doctor visits are attributed to the disease each year in the US, and its direct medical expenses are thought to total more than $4 billion.
North America and Northern Europe have the most significant prevalence of inflammatory bowel disorders globally. A western-influenced environment and lifestyle are strongly associated with inflammatory bowel disease. 9 to 20 instances of ulcerative colitis occur per 100,000 individuals each year. Adults are more likely to have ulcerative colitis than Crohn’s disease.
However, Crohn’s disease and ulcerative colitis are less common compared to the pediatric population. The incidence of ulcerative colitis follows a bimodal distribution between the ages of 15 and 30, and the primary onset peaks. Between the ages of 50 and 70, the incidence reaches a second. Although some research indicates minor precedence for males, most studies reveal no sex preference.
Ulcerative colitis is common in nonsmokers or individuals who have quit smoking. Additionally, smokers with ulcerative colitis frequently experience a milder illness, require fewer hospital stays, and require less medication. Although limited, there is evidence connecting the use of non-steroidal anti-inflammatory drugs to the development or recurrence of ulcerative colitis.
Additionally, removing an infected appendix is associated with inflammatory bowel disease. In contrast to Crohn’s disease, ulcerative colitis is related to a lower appendectomy incidence before the age of twenty. It has been demonstrated that having an appendectomy lowers the likelihood of developing ulcerative colitis by 69%.
Defects in the immunological response, epithelial barrier, leukocyte recruitment, and colonic microbiota play a role in the pathophysiology of ulcerative colitis. Colonic mucin and tight junctions are defective in the epithelial barrier, which causes more luminal antigens to be absorbed. Additionally, there are more mature, activated dendritic cells with many toll-like receptors (TLR), mainly TLR4 and TLR2, in the lamina propria of the mucosa.
Additionally, ulcerative colitis patients appear to have an abnormal T-helper (Th) cell response, particularly Th2, which has cytotoxic effects on epithelial cells. TNF-alpha, IL-13, and natural killer T-cells are additional immune-related components that contribute to the pathophysiology of ulcerative colitis. Inflammatory bowel disease increases IgA, IgG, and IgM levels; however, individuals with ulcerative colitis have disproportionately high IgG1 antibodies.
There are two methods by which leukocyte recruitment is impacted. Leukocytes from the systemic circulation are drawn to the mucosa in ulcerative colitis due to increased production of the chemoattractant CXCL8. The endothelium of mucosal blood vessels also exhibits an elevation of mucosal addressin cellular adhesion molecule-1 (Mad-CAM1), which facilitates leukocyte extravasation and adherence into mucosal tissue.
According to studies, intestinal microflora has a significant role in disease development, severity, and manifestation. The host’s mucosal immunology and intestinal bacteria appear to be in a homeostatic equilibrium, which may contribute to ulcerative colitis. As a result, non-pathogenic bacteria are encountered with an abnormal reaction.
Inflammatory bowel disease has an unknown etiology. Since a family history of the disease occurs in 8% to 14% of individuals, it appears that there is a fundamental genetic component. There is a four-fold increased likelihood of acquiring ulcerative colitis in a first-degree relative of a patient.
Additionally, compared to other ethnic groups, Jewish communities have a greater frequency of ulcerative colitis. It has been hypothesized that changes in the gut microbiota’s composition and inadequate mucosal immunity may cause ulcerative colitis, although there is little evidence to back this up.
Autoimmune conditions may significantly influence the etiology of ulcerative colitis. According to some studies, smoking may be protective, but there is no definitive link between the two.
Despite being a lifelong condition, ulcerative colitis does not have a higher overall death rate than the general population. However, individuals with shock or surgical complications have a higher death rate. When the muscularis propria is involved, it may damage the nerves and cause dilatation, ischemia, and peristalsis.
The most frequent cause of mortality in ulcerative colitis is toxic megacolon. Colon cancer affects at least 5% of patients, and the risk rises with the severity of the condition. Stricture development is less common than Crohn’s disease.
www.ncbi.nlm.nih.gov/books/NBK459282
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