Inflammatory bowel disease in the elderly

Introduction to inflammatory bowel disease in the elderly Senile inflammatory bowel disease (IBD) in the elderly generally refers to the age of patients with inflammatory bowel disease when the age of onset is greater than 60 or 65 years old. In addition, some patients with inflammatory bowel disease in the elderly are ill at a young age, and the course continues to 60. Or 65 years of age or older. Due to the special age of the elderly, the etiology, differential diagnosis and treatment of enteropathy are more complicated than for young people, such as ischemic bowel disease, infectious bowel disease and drug-related enteritis. basic knowledge The proportion of illness: 0.03% - 0.09% Susceptible people: the elderly Mode of infection: non-infectious Complications: ulcerative colitis Crohn's disease

The cause of inflammatory bowel disease in the elderly

Environmental factors (40%):

Epidemiological studies have found that the incidence of IBD varies greatly in different geographical locations and in different periods; Asian immigrants and their offspring migrate to Europe and the United States, the susceptibility of IBD increases, the incidence of black American IBD is close to that of white Americans, and Africa Blacks rarely suffer from IBD; the incidence of IBD in urban residents is higher than that in surrounding villages, suggesting that the environment or lifestyle is closely related to IBD, and many environmental factors related to IBD such as smoking, oral contraceptives, incidents occurring in childhood, infections Among the dietary factors, it is now clear that smoking increases the risk of Crohn's disease (CD) and protects against ulcerative enteritis (UC).

Genetic factors (20%):

The incidence of IBD is significantly different between races; there is family aggregation; the incidence of IBD in monozygotic twins is higher than that in twins; some patients with IBD are often associated with genetic diseases and immune susceptibility to genetic susceptibility. It is suggested that genetic factors play an important role in the pathogenesis of IBD. Early genetic studies found that HLA gene is associated with IBD, but the results are not consistent, and the HLA-DR2, DR9 and DRB1*0103 alleles and UC are more certain. Relatedly, the HLA-DR7 and DRB3*0301 alleles are associated with CD. In recent years, some cytokine genes have been found to be associated with IBD, such as the tumor necrosis factor gene (TNF--1031CD) associated with CD, interleukin-1 receptor. The antagonist gene is associated with UC, and the susceptibility gene of IBD is found on chromosomes 3, 7, 12, and 16, and in recent years, the NOD2/CARD15 gene located at the IBD1 locus of chromosome 16 is more frequently studied. Gene mutations can increase the susceptibility of CD. The genetic study of IBD is not only crucial for elucidating the pathogenesis, but also has a direct impact on the diagnosis and treatment of this disease. The existing research shows that IBD is Polygenic genetic disease heterogeneity (different people caused by different genes).

Infection factor (15%):

Because UC is similar to infectious colitis such as Salmonella, Shigella or amoeba, CD is similar to intestinal tuberculosis, prompting people to search for infectious pathogens such as intestinal bacteria or other microorganisms for many years. The cellular and humoral immune responses against bacterial antigens are enhanced, bacterial retention is beneficial to the development of IBD, and fecal bypass can prevent CD recurrence. Antibiotics and eco-promoting agents are beneficial to some IBD patients, especially in recent years, using transgenic methods to cause immunodeficiency. Animal models can not induce intestinal lesions similar to IBD in sterilized state, suggesting that bacteria are involved in the development of IBD, but so far there has not been a constant relationship between the specific microbial pathogens and IBD in bacteria, viruses, fungi, etc. It is believed that pathogenic microorganisms may be a non-specific triggering factor for this disease. It is also believed that IBD is caused by an abnormal immune response against its normal intestinal flora. As for whether or not the disease has specific pathogenic microorganisms and its effects, For further study.

Immunity factor (15%):

The immune mechanism of IBD is the most active field in recent years. The research progress has enabled us to have a deeper understanding of the immune inflammatory process of IBD. The immune mechanism is based on the fact that the disease often shows immune abnormalities, such as an increase in the number of intestinal mucosal immune cells. Intestinal local body fluid or cellular immune activity is enhanced, patients can have a variety of parenteral manifestations, and the use of glucocorticoids or immunosuppressive agents can alleviate the disease. It is generally believed that IBD acts as a triggering factor for susceptible individuals, stimulating genetically related Induced by the immune inflammatory response of intestinal mucosa, the intestinal mucosal immune system plays an important role in the development, progression and outcome of intestinal inflammation of IBD. Immunoinflammatory cells such as neutrophils, which are involved in intestinal immune inflammatory reactions, Macrophages, mast cells, lymphocytes, natural killer cells, etc. release antibodies, cytokines (interleukins, -interferons, TNF, TGF, etc.) and inflammatory mediators cause inflammatory lesions and tissue damage, which are produced during inflammation. A large number of oxygen free radicals also have damage to the intestinal mucosa. In addition, the non-immune cells of the intestine are epithelial cells, vascular endothelium. The cytoplasm also participates in the inflammatory reaction, interacts with local immunoinflammatory cells, and has many cytokines and mediators involved in the immune inflammatory response. The interaction mechanism between them is very complicated, some are still unclear, and the expression of tissue damage is different. Depending on the release of expression of different cytokines, the synthesis of cytokines is mainly regulated by gene transcription factors expressed by mucosal immune cells.

The immune response of UC and CD is different. CD has the characteristics of TH1 cell-mediated immune response (cellular immunity), which is a TH1 type reaction, while UC has the characteristics of antibody-mediated immune response (humoral immunity). A type TH2 reaction.

There are different opinions on the causes of the immune inflammatory response of this disease. Some people think that it may be a food antigen or an intestinal symbiotic bacteria that usually has no pathogenic effect. Some studies have found that there may be genetically related epithelial cell structure in the colonic mucosa of patients with this disease. The function and abnormality of the mucous layer of the intestinal mucosa improve the permeability of the normal colonic mucosa, so that it is generally difficult to pass through the normal intestinal mucosa. Intestinal commensal bacteria and food antigens that are harmless to normal people can also enter the intestinal mucosa, thereby exciting a series of Antigen-specific immune response; the role of microbial pathogens has not been fully confirmed; some people believe that this disease is an autoimmune disease, found in the serum of IBD patients against colonic epithelial cells, endothelial cells, neutrophils, etc. A series of autoantibodies and some anti-bacterial, viral and anti-food antigen antibodies have been found, but no direct evidence of autoimmune response has been found so far. In recent years, more autoantibodies have been reported - nuclear para-anti-neutrophils The detection rate of antibody (perinuclear antineutrophil cytoplasmic antibody, pANCA) in sera of UC patients is about 70%. CD and normal people are more than 20%, but they have not been able to find the exact evidence of their disease. Therefore, it is believed that pANCA may not participate in the disease, which may be the result of enteritis or a marker of genetic susceptibility. To be clarified.

Pathogenesis

The etiology and pathogenesis of IBD have not yet been fully clarified. It is currently believed that this disease is an intestinal immune inflammatory disease caused by multi-factor interaction. The pathogenesis hypothesis is that environmental factors act on susceptible populations, and the intestinal immune inflammatory response is excessive. Hyperactivity leads to inflammatory lesions and tissue destruction.

Both UC and CD have extraintestinal manifestations, and the population distribution and epidemiological manifestations of the disease are similar, suggesting that they may be different manifestations of the same disease, but there are both pathological histology and immunological manifestations in the lesions. Differences may indicate that the body has different specific pathogenesis caused by different pathogenic factors, and ultimately the performance of tissue damage is different.

Elderly inflammatory bowel disease prevention

1. Patients should have adequate rest during the active period.

2. Give a low-nutrition high-nutrition diet, appropriate supplementation of folic acid, vitamin B12 and other vitamins and trace elements, severely fasted.

3. Infected patients, active anti-infective treatment.

Elderly inflammatory bowel disease complications Complications ulcerative colitis Crohn's disease

1. Ulcerative colitis, severe delayed onset of ulcerative colitis in the elderly is easy to be complicated by toxic megacolon, Greenstein et al found that the toxic megacolon mortality rate of 40 years and older is 30%, while the toxic giant under 40 years old The mortality rate of colon is 5%. Regarding other parenteral complications, there is no significant difference in joint and eye diseases and delayed ulcerative colitis in patients with early-onset ulcerative colitis in the elderly, but the oral and skin ulcers of the former. More common.

In addition to proctitis, the risk of colon cancer is generally related to the course of colitis. The longer the course of disease, the higher the risk of concurrent tumors. For the risk of cancerous ulcerative colitis in the elderly, it is necessary to distinguish between delayed ulcers. Colitis and early onset ulcerative colitis, the longer the history of early onset ulcerative colitis, the higher the risk of colon cancer, but the relative risk of colon cancer (referring to age-matched non-ulcerative colitis) Compared with younger patients with ulcerative colitis, the age-specific risk of patients with delayed ulcerative colitis is high, but the relative risk of colon cancer is small, for example, young people with severe colitis for 10 years The relative risk of canceration is 20:1; in patients with colitis who have been ill for 10 years after age 45, the relative risk of canceration is small, about 2:1.

2. The complications and extraintestinal complications of Crohn's disease in Crohn's disease are not significantly different from those in young people. However, the incidence of intestinal perforation in Crohn's disease is higher than that in young adults. Human Crohn's disease, and the incidence of abscesses and fistulas may also be high, the incidence of diverticulitis in the elderly is high, and often occurs in the intestinal lesions of Crohn's disease, which may be more likely to cause complications.

The incidence of colon cancer in patients with Crohn's disease colitis is slightly higher, but in general, its relative risk is less.

Symptoms of inflammatory bowel disease in the elderly Common symptoms Abdominal pain, diarrhea, intestinal bleeding, constipation, abscess, blood in the stool

Ulcerative colitis

Most scholars believe that the main clinical manifestations and course of ulcerative colitis in the elderly are similar to those of young people, but diarrhea and weight loss are more prominent, while abdominal pain and rectal bleeding are rare. Zimmermann et al reported that middle-aged patients over the age of 51 are 21 to 30 years old. The number of patients with diarrhea is high, the clinical symptoms last for a long time, and the incidence of delayed ulcerative colitis in the elderly is high. It also includes some cases before the age of 60 and delayed treatment to delay the treatment. The lesions of colitis are mostly distributed in the distal rectum.

2. Crohn's disease

The clinical manifestations of late-onset Crohn's disease in the elderly are not much different from those in young people. The most common symptoms are diarrhea, weight loss, abdominal pain, other rectal bleeding, fever, abdominal mass, perianal pain, and constipation. Woolrich and Korelitz believe that the most common clinical symptoms of Crohn's disease in the elderly are diarrhea, abdominal pain and weight loss. Harper grouped them according to their gender and duration of disease, and found that early bloody stools in elderly Crohn's disease The rate is high, the abdominal mass, the incidence of abdominal pain is low, blood in the stool and constipation are related to the lesion in the colon. Stalinikowicz found that the diagnosis time of Crohn's disease was prolonged, the rate of misdiagnosis increased, diarrhea, blood in the stool, the formation of abscess and the incidence of complications increased.

Compared with young people, elderly Crohn's disease is common in colon lesions and is more common in women. For example, older people have more than 50% Crohn's disease proctitis.

Examination of inflammatory bowel disease in the elderly

The liver function of the elderly with ulcerative colitis is more common than that of young people, and it mainly occurs in elderly women, such as AST, ALT, ALP, GGTP, etc. Older colitis is also prone to anemia, ESR increases. , leukocytosis and hypoproteinemia.

The elderly Crohn's disease is not much different from that of young people. Common findings include anemia, leukocytosis, hypoproteinemia, and increased erythrocyte sedimentation rate.

1. X-ray abdominal flattening: For patients with severe activity, X-ray abdominal plain film examination should be performed. In patients with toxic megacolon, mucosal edema (indentation), signs of intestinal dilatation or intestinal perforation, and small bowel CD patients can be found. It can be found that intestinal obstruction or intestinal fistula is displaced by the mass of the mass.

2. Colonoscopy: one of the most important means for the diagnosis and differential diagnosis of this disease, not only can directly observe the mucosal lesions, the extent of the lesion, but also biopsy to obtain histological diagnosis, UC lesions often retrograde upward from the rectum, continuous Sexual, diffuse distribution, endoscopic features are: 1 diffuse mucosal congestion, edema, vascular texture blur, disorder, mucosal roughness is fine granular, brittle and easy to hemorrhage and pus and bloody secretions attached; 2 lesions are clearly visible diffuse Sexual or multiple ulcers with different sizes and shapes can be fused; 3 chronic lesions can be seen as shallow, dull or disappeared colonic pouch, pseudopolyps and bridge-like mucosa, and the active period of colonoscopy under mucosal histology Diffuse chronic and acute inflammatory cell infiltration, cryptitis, crypt abscess, erosion, ulcer, remission period manifested as glandular deformation, disordered arrangement, goblet cell reduction and other mucosal atrophy changes.

CD lesions are segmental distribution, seeing a thrush-like or longitudinal or lame ulcer, the mucosa around the ulcer is normal or proliferative cobblestone-like, the intestinal lumen is narrow, the intestinal wall is stiff, there may be inflammatory polyps, between the diseased intestines The appearance of the mucosa is normal, and deep biopsy of the lesion may reveal non-cheese necrotizing granuloma or lymphocyte aggregation in the lamina propria.

3. X-ray angiography: according to the clinical manifestations of sputum small bowel angiography or barium enema examination, if necessary, combined with sensitivity, not as good as colonoscopy, and can not be biopsy, heavy or violent UC is generally not suitable for barium enema examination, The X-ray features of UC are mainly:

1 mucosal coarse and/or granular changes;

2 The edge of the intestine is burr-like or jagged, and the intestinal wall sees multiple small shadows and filling defects;

3 The colonic bag disappears and the intestine is shortened, which can be lead-tube-like.

The X-ray of CD showed multiple, segmental intestinal inflammatory lesions, showing lesions of mucosal folds, longitudinal fissure ulcers, pebbles, stenosis, fistulas, and formation of pseudopolyps.

4. B-mode ultrasound, CT, magnetic resonance (MRI) can show thickening of the intestinal wall, abdominal mass or abscess.

Diagnosis and diagnosis of inflammatory bowel disease in the elderly

Diagnostic criteria

The clinical manifestations of inflammatory bowel disease in the elderly are similar to those of other elderly people with intestinal diseases, so early diagnosis is difficult. Harper et al observed that the time from onset to diagnosis of Crohn's disease in the elderly was 6.4 years, while the young group For 2.4 years, Foxwolthy and Wilson's study also showed that in addition to the time delay of diagnosis, 60% of elderly patients were initially misdiagnosed, compared with 15% in the younger group.

Inflammatory bowel disease in the elderly needs to be differentiated from ischemic enteritis. Although the clinical manifestations of ischemic enteritis are similar to inflammatory bowel disease, the history and pathological changes of ischemic diseases are characterized by self-limiting and low recurrence rate. The acute attack of inflammatory bowel disease is similar to that of intestinal diverticulitis. The diagnosis can be diagnosed according to X-ray examination, endoscopy, and histological examination.

Differential diagnosis

Because some elderly people suffer from diverticulosis, attention should be paid to the coexistence of the two. Inflammatory bowel disease needs to be differentiated from infectious enteritis, autoimmune enteritis, radiation enteritis, and intestinal tumor.

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