Effects Of Diabetes On Digestive System
 |
According to 2013 data, there are approximately 380 million diabetic patients in the world, and this number is increasing due to obesity and sedentary lifestyles. The findings of the digestive system (Gastrointestinal system) in diabetes develop due to poor blood sugar control (glycemic control) and chronic degenerative effects of diabetes and usually occur in the advanced stages of the disease.
[Chronic degenerative effects of diabetes; diabetic neuropathy (degeneration in the body, especially in the autonomic nerves in diabetes) and vasculopathy (the occlusive vascular disease caused by diabetes)].
Gastrointestinal symptoms usually occur as a result of motor dysfunction (dysmotility) caused by neuropathy in these organs. Nausea in sudden complications of diabetes such as diabetic ketoacidosis and non-ketotic hyperosmolar coma, While temporary complaints such as abdominal pain and vomiting may occur, permanent findings develop in long-term disease.
In diabetes, changes may occur in all parts of the digestive system and may lead to the emergence of different clinical symptoms. The main gastrointestinal complications of diabetes are gastroparesis (stomach paralysis), intestinal enteropathy (diarrhea, constipation, and fecal incontinence -fecal incontinence), and fatty liver.
Oral problems (Oral problems)
Poor glycemic control can lead to dental and gum problems in diabetics. Tooth decay, tooth decay, and infection that may occur during caries treatment or preparation for prosthesis, etc. Complications are more common in diabetics. The increase in the amount of sugar in the saliva due to poor glycemic control causes the proliferation of different bacteria in the mouth, leading to gingivitis and bad breath, especially in patients who do not pay attention to oral hygiene.
The increase in saliva sugar can cause the development of fungal infection in the mouth by disrupting the balance in the oral flora (Candida infection). Decreased salivary secretion due to diabetes itself or coexisting diseases such as Sjögren's syndrome may cause difficulty in chewing, grinding, and swallowing.
Difficulty swallowing (dysphagia) and other problems with the esophagus
Pharyngoesophageal dysfunction, which may develop due to autonomic neuropathy, myopathy, or previous central nervous system diseases (stroke, etc.) caused by diabetes may cause difficulty in swallowing. In this type of swallowing difficulty, there is difficulty in the passage of chewed food in the mouth to the esophagus after swallowing. During swallowing of liquid substances, the swallowed food may escape into the trachea and cause coughing and, rarely, choking.
Diabetic neuropathy can cause irregularity (dysmotility) and weaken the contractions of the esophagus (lazy esophagus, lazy esophagus) by affecting the nerves that stimulate the esophagus (esophagus) and the esophagus and stomach junction (lower esophageal sphincter). These patients have difficulty swallowing solid foods.
As a result of the lowering of the lower esophageal sphincter pressure, the escape of gastric contents into the esophagus becomes easier and gastroesophageal reflux occurs (see Reflux). 40% of patients with diabetic neuropathy have reflux complaints. Both the restriction in the movements of the esophagus and the low pressure in the lower esophageal sphincter cause more severe reflux in diabetics.
The narrowing of the lower end of the esophagus (peptic stricture) after chronic reflux may create a mechanical barrier in this region and cause aggravated swallowing difficulties. Although studies with manometry, pH monitoring, and barium radiographs show that 63% of diabetics have dysfunction in the esophagus, only a small proportion of patients describe swallowing difficulties.
Candidiasis (a fungal infection), which is a common esophageal infection especially in diabetics with poor glycemic control, can cause pain when swallowing (odynophagia) and difficulty in swallowing.
Gastroparesis
Gastroparesis is the slowing and delay of gastric emptying, although there is no mechanical obstruction to delay gastric emptying (see Gastroparesis, gastric paralysis). Particularly, the discharge of solid foods from the stomach is delayed. Decreased vagal tone (vagus; the main nerve branch that innervates the stomach) due to diabetic neuropathy is considered the most important reason for the development of gastroparesis.
Degeneration of inhibitory neurons containing nitric oxide and natural pacemaker cells (Cajal cells) and smooth muscle dysfunction are other mechanisms thought to have an effect on the development of gastroparesis. 5 to 15% of diabetic patients have complaints that can be attributed to delayed gastric emptying.
Studies have shown that 65% of type 1 diabetics and 30% of type 2 diabetics have a delay in gastric emptying. Diabetic gastroparesis is more common in women. The risk of developing gastroparesis is higher in patients with poor glycemic control (high HbA1c level, >7 g/dl), vascular complications (vasculopathy), and a history of diabetes for more than 10 years. Symptoms such as early satiety, bloating in the upper abdomen, nausea, vomiting and abdominal pain can be seen.
Vomiting may be gushing, and food that has been eaten 12-24 hours ago is usually removed. Impaired gastric emptying can make blood sugar control difficult. In diabetic patients who are thought to develop gastroparesis, thyroid function tests and other metabolic parameters (urea, electrolytes, etc.) should be checked, and pancreatic enzymes (amylase and lipase) should be measured, especially in patients with abdominal pain, and biliary tract and pancreas should be checked by ultrasonography. A pregnancy test should not be neglected in female patients in the productive period.
Other causes that may delay gastric emptyings, such as a chronic peptic ulcer or tumor of the stomach/duodenum or pancreas, should not be ignored in these patients. Some psychiatric drugs with anticholinergic effects (antidepressants, sedatives, etc.), aluminum-containing antacids, beta-adrenergic receptor agonists, calcium channel blockers, antiallergic drugs, sucralfate, and proton pump inhibitors, which can be used in diabetic patients, may cause symptoms similar to gastroparesis.
The appearance of the food remaining in the stomach in the endoscopy of the gastroparesis patient
Many tests have been developed to be used in the diagnosis of gastroparesis, and these include gastric emptying scintigraphy, barium gastric-duodenal radiography, gastroduodenal manometry, MRI (magnetic resonance imaging), ultrasonography, smart pill cam., electrogastrography, and C13 respiratory test.
The most frequently preferred method in practice is gastric emptying scintigraphy. In this method, after the patient is fed an egg marked with technetium, measurements are made at 15-minute intervals and gastric emptying is evaluated for 4 hours. At the end of the 4th hour, retention of more than 10% in the stomach is considered compatible with gastroparesis.
In the treatment of gastroparesis, besides providing good blood sugar regulation, dietary changes, and some drugs (prokinetic agents) help. Good glycemic control is required in patients with gastroparesis, as elevations in blood sugar impair gastric motility and delay emptying. Since the discharge of liquid foods from the stomach is generally preserved in gastroparesis, it may be recommended that patients prefer liquid foods and feed with frequent and small meals.
Smoking must be stopped. Foods containing high amounts of fiber (fiber), fatty foods, and alcohol should not be consumed if possible as they delay gastric emptying. Prokinetic agents (drugs that stimulate motility in the stomach and intestines) may be helpful in relieving symptoms. The most widely used medication for this purpose is 'domperidone,' a dopamine receptor antagonist. Another agent that can be used is 'itoprid'. The drug exerts prokinetic effects by two different mechanisms (dopamine receptor antagonist + acetylcholinesterase inhibitor).
Both domperidone and itopride are medications that are favored in practice because of their minimal side-effect profiles; nevertheless, they must be administered under the guidance of a doctor. Because of their side effects, 'metoclopramide' and 'tegaserod' should not be preferred unless absolutely necessary.
Erythromycin, which is also an antibiotic, may be beneficial in some patients. Beta-adrenergic receptor blockers (beta-blockers), cholinergic agents (bethanechol) can be tried. In patients with severe nausea, anti-nausea drugs (anti-emetics) such as promethazine and ondansetron may need to be added to the treatment.
The drug exerts prokinetic effects by two different mechanisms (dopamine receptor antagonist + acetylcholinesterase inhibitor). Both domperidone and itopride are drugs that are preferred in practice due to their low side-effect profiles and they must be used under the supervision of a doctor.
Because of their side effects, 'metoclopramide' and 'tegaserod' should not be preferred unless absolutely necessary. Erythromycin, which is also an antibiotic, may be beneficial in some patients. Beta-adrenergic receptor blockers (beta-blockers), cholinergic agents (betanechol) can be tried.
In patients with severe nausea, anti-nausea drugs (anti-emetics) such as promethazine and ondansetron may need to be added to the treatment. The drug exerts prokinetic effects by two different mechanisms (dopamine receptor antagonist + acetylcholinesterase inhibitor).
Both domperidone and itopride are drugs that are preferred in practice due to their low side-effect profiles and they must be used under the supervision of a doctor. Because of their side effects, 'metoclopramide' and 'tegaserod' should not be preferred unless absolutely necessary.
Erythromycin, which is also an antibiotic, may be beneficial in some patients. Beta-adrenergic receptor blockers (beta-blockers), cholinergic agents (betanechol) can be tried. In patients with severe nausea, anti-nausea drugs (anti-emetics) such as promethazine and ondansetron may need to be added to the treatment. and itopride is the drugs preferred in practice due to its low side-effect profiles and they must be used under the supervision of a doctor. Because of their side effects, 'metoclopramide' and 'tegaserod' should not be preferred unless absolutely necessary.
Placing electrical stimulators in the stomach in cases resistant to medical treatment has emerged as a method that has been used in recent years and reported good results (Gastric pacing, gastric neurostimulation, Enterra, Medtronic incorp.).
The electrodes of the device are implanted in the stomach with a minor surgical intervention, and a 5-6 cm in diameter programmable neurostimulator placed under the skin sends an electrical impulse at regular intervals and provides contraction in the stomach.
Gastric neurostimulation (Enterra) is an FDA-approved method and can be tried in cases resistant to medical treatment (FDA; American Food and Drug Administration). Complications such as gastric erosion and infection can be seen in 5-10% of patients.
Botulinum toxin injection into the gastric outlet (pylorus) during endoscopy is another interventional method that can be tried in persistent gastroparesis cases.
In patients who are resistant to treatment and develop malnutrition, feeding may be required by inserting a gastrostomy or jejunostomy tube with the endoscopic method. In stubborn cases, an application such as connecting the stomach to the intestines surgically can be considered (gastroenterostomy).
Intestinal enteropathy is a picture that manifests itself with one or more of the symptoms such as diarrhea, constipation or fecal incontinence (fecal incontinence). Diabetic diarrhea is chronic and usually recurrent. It usually occurs in poorly controlled and prolonged diabetes. It is more common in men.
Abdominal pain may be present but is usually mild or absent. In cases where abdominal pain is prominent, other pathologies that may cause diarrhea such as chronic pancreatitis or intestinal ischemia (see vascular diseases of the intestines) should be considered.
Although the pathophysiology (formation mechanism) of diabetic diarrhea is not known exactly, it is thought that the movement disorder in bowel movements due to autonomic neuropathy is responsible (dysmotility). Bacterial overgrowth caused by stagnation in the intestine due to the severe slowing of bowel movements due to diabetic neuropathy is the main mechanism responsible for diarrhea.
Bile acid deconjugation and fat malabsorption in bacterial overgrowth lead to diarrhea. In these cases, it is observed that diarrhea improves with antibiotic treatment. In addition to stasis in the intestines, diarrhea may also develop with different mechanisms due to increased bowel movements and secretion due to decreased sympathetic activity in some cases.
Excessive consumption of low-calorie sweeteners such as sorbitol and some artificial sweeteners can also cause osmotic diarrhea in diabetics. Metformin, a drug frequently used in the treatment of diabetes, can also cause diarrhea when taken in high doses, and this is a common situation in practice.
Discontinuation of diarrhea with drug discontinuation or dose reduction confirms the diagnosis. Drugs such as 'orlistat', which are given to obese diabetics to lose weight and act by reducing the absorption of fat from the intestines, may cause fatty diarrhea.
Since diabetes can also be a complication that can occur in the late phase of chronic pancreatitis (Type-3 diabetes), diarrhea in such cases usually progresses as fatty diarrhea (steatorrhea) due to chronic pancreatitis.
In cases with diarrhea and abdominal pain, the pancreas should be checked for chronic pancreatitis by measuring pancreatic enzymes in the blood and performing abdominal ultrasonography. Oral administration of pancreatic enzyme preparations in these cases reduces diarrhea (see Chronic pancreatitis).
Another disease that can be seen in diabetics and cause recurrent chronic diarrhea is microscopic colitis. In microscopic colitis, excretion of inflammatory markers such as calprotectin is increased, and the diagnosis is confirmed by biopsy taken during colonoscopy.
In diabetic patients who are examined for diarrhea, a biopsy should be taken even if the colonic mucosa appears normal when colonoscopy is performed. Diarrhea that comes at night and awakens sleep may be seen in some patients as a result of colonic dysfunction (dysfunction in the large intestines) due to diabetes (nocturnal diarrhea).
Diarrhea in diabetics may be accompanied by stool incontinence (anal incontinence, fecal incontinence). Anorectal dysfunction is common in patients with fecal incontinence, and 20% of long-standing diabetic patients have fecal incontinence. In the tests performed in these patients, decreased rectal sensation and hypotonia in the anal canal due to autonomic dysfunction of the internal anal sphincter were observed.
In the treatment of diabetic diarrhea, first of all, other diseases that may cause diarrhea and the drugs used should be investigated. Blood sugar regulation helps reduce diarrhea. Oral antibiotics may be beneficial in cases where excessive bacterial growth due to stasis is thought.
In cases with severe diarrhea, antidiarrheal drugs (opiate derivatives, atropine sulfate + diphenoxylate, lopermide, etc.) can be used, provided that they are under the control of a doctor. Such drugs work especially well in cases with fecal incontinence. Such drugs should be used with caution, as they may cause toxic megacolon in patients with pronounced neuropathy (Toxic megacolon; a type of colon paralysis).
Constipation
In the studies, it has been observed that the gastrocolic reflex is greatly reduced or lost in diabetic patients with severe constipation. In diabetic constipation, the use of drugs that can cause hypothyroidism and constipation should be investigated. Measures such as blood sugar regulation, increasing oral fluid intake, regular physical activity, and feeding with fiber foods can alleviate complaints. In persistent cases, prokinetics, sorbitol, and lactulose can be tried.
Non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) (see Fatty liver) is a disease characterized by the appearance of pathological findings that may be caused by alcohol use in the liver of a person who does not have a history of alcohol use. Although the cause of NAFLD is not known exactly, the disease is frequently associated with type-2 diabetes (the incidence of NAFLD is 4-17% in type-1 diabetes and 21-78% in type-2 diabetes).
In some cases, as a result of the progression of NAFLD, inflammatory activity in the liver may develop (non-alcoholic steatohepatitis), and, although rarely, liver cirrhosis may develop in the progressive process. Almost all severely obese diabetics have varying amounts of fatty liver, and almost half of them have steatohepatitis. Most diabetics with fatty liver are asymptomatic. Some patients may experience right upper quadrant pain and fatigue in the abdomen.
Most patients have a mild liver enlargement that they are unaware of. Liver function tests are usually normal or there may be slight increases in ALT and AST levels. Mild increases in serum ALP and GGT levels may be observed in 15-20% of patients (see Liver function tests).
When steatohepatitis develops, more significant deterioration in liver function tests begins. In patients with impaired liver function tests, viral and autoimmune hepatitis tests, thyroid function tests, and transferrin saturation measurement should be performed and abdominal ultrasonography should be performed.
Liver function tests are usually normal or there may be slight increases in ALT and AST levels. Mild increases in serum ALP and GGT levels may be observed in 15-20% of patients (see Liver function tests). When steatohepatitis develops, more significant deterioration in liver function tests begins.
In patients with impaired liver function tests, viral and autoimmune hepatitis tests, thyroid function tests, and transferrin saturation measurement should be performed and abdominal ultrasonography should be performed.
Liver function tests are usually normal or there may be slight increases in ALT and AST levels. Mild increases in serum ALP and GGT levels may be observed in 15-20% of patients (see Liver function tests). When steatohepatitis develops, more significant deterioration in liver function tests begins.
In patients with impaired liver function tests, viral and autoimmune hepatitis tests, thyroid function tests, and transferrin saturation measurement should be performed and abdominal ultrasonography should be performed.
NAFLD prognosis can be variable. When patients with NAFLD were followed up for a long time with repeated liver biopsies in terms of liver damage, there was no change in histological findings in 1/3 of the cases, worsening in 1/3 and improvement in 1/3.
This fatty metamorphosis in NAFLD is usually reversible once metabolic control of diabetes is achieved. Regular weight loss (0.5-1kg/week), good blood sugar control (Hba1c <7g/dl), and regular exercise form the basis of the treatment in NAFLD in diabetics. One of the drugs that have been shown to be effective in the treatment is metformin, which is still widely used today.
Diabetes and hepatitis C (HCV)
Diabetes is more common in patients with hepatitis C than in the normal population. While the prevalence of diabetes is 7.8% in the normal population and 7.3% in those with non-hepatitis C liver disease, this rate is 14.5% in patients with hepatitis C.
Advanced age, obesity, presence of advanced fibrosis in the liver, and a family history of diabetes are risk factors that increase diabetes in patients with hepatitis C. Alpha-interferon, which is used for the treatment of HCV, may also be associated with the development of diabetes.
Diabetes and cirrhosis
The causes of cirrhosis that can progress with diabetes are NAFLD, hemochromatosis (see Hemochromatosis), and hepatitis C infection. Patients with cirrhosis and diabetes may experience signs of insulin resistance and may require higher insulin doses for blood glucose regulation.
When anemia develops due to hypersplenism or hemorrhages in patients with cirrhosis, Hba1c levels may be falsely low. Because the glucose storage capacity of the liver is reduced, patients with cirrhosis are prone to hypoglycemia and malnutrition (Hypoglycemia; low blood sugar). Therefore, extreme dietary restrictions should be avoided in diabetic cirrhosis.
Among the drugs used in the treatment of diabetes, those in the thiazolidinedione group (Troglitazone) should not be used in diabetics with cirrhosis, since they have a toxic effect on the liver.
Diabetes and hemochromatosis
The incidence of idiopathic hemochromatosis has doubled in diabetes (4/1000 in the normal population, 9.6/1000 in the diabetic population). In diabetic patients with abnormality in function tests, joint pain, and family history, transferrin saturation should be checked and hemochromatosis should be sought.
Gallstone
The incidence of gallstone formation is increased in diabetic patients. The decrease in gallbladder contractions due to autonomic neuropathy and the change in bile content, making it prone to stone formation (lithogenous bile) are the factors that facilitate the formation of gallstones.
The fact that the patients are mostly obese and hyperlipidemic also increases this risk. The risk of developing pancreatitis due to gallstones is increased in type 2 diabetics compared to non-diabetics. Unlike non-diabetic patients, diabetic patients with asymptomatic (silent) gallstones should be advised to have cholecystectomy (removal of the gallbladder) under elective conditions.
Diabetes and pancreas
 |
Autopsy studies have shown that 7% of non-obese individuals and 19% of obese individuals may have pancreatic adiposity. Pancreatic lubrication usually does not cause a complaint and is detected incidentally in ultrasonography performed for another reason.
Pancreatic enzymes are at normal levels. Fat accumulation in pancreatic islet cells (islets with insulin-secreting beta cells in the pancreas, islets of Langerhans) reduces insulin secretion from these cells. This may explain the development of type-2 diabetes to some extent if the excessive insulin requirement that occurs in obese individuals with insulin resistance cannot be met. Pancreatic fat is also a strong indicator of the presence of nonalcoholic fatty liver disease.
Mild to moderate pancreatic exocrine insufficiency is seen in 15% of patients with type 2 diabetes (the inability of the pancreas to secrete digestive enzymes that it produces and empties into the intestine). This condition usually does not give any clinical symptoms.
When exocrine insufficiency is severe, greasy stools and diarrhea may occur. The situation is different in chronic pancreatitis. Since diabetes develops in advanced stages of the disease (type-3 diabetes) in patients with chronic pancreatitis, fatty diarrhea due to chronic pancreatitis is common in these patients.
0 Comments