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18.7: Disorders of the Gastrointestinal Tract - Biology

18.7: Disorders of the Gastrointestinal Tract - Biology


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Crohn’s Rash

If you had a skin rash like the one in Figure (PageIndex{1}), you probably wouldn’t assume that it was caused by a digestive system disease. However, that’s exactly why the individual in the picture has a rash. He has a gastrointestinal (GI) tract disorder called Crohn’s disease. This disease is one of a group of GI tract disorders that are known collectively as inflammatory bowel disease. Unlike other inflammatory bowel diseases, signs and symptoms of Crohn’s disease may not be confined to the GI tract.

Inflammatory Bowel Disease

Inflammatory bowel disease is a collection of inflammatory conditions primarily affecting the intestines. The two principal inflammatory bowel diseases are Crohn’s disease and ulcerative colitis. Unlike Crohn’s disease, which may affect any part of the GI tract and the joints as well as the skin, ulcerative colitis mainly affects just the colon and rectum. Both diseases occur when the body’s own immune system attacks the digestive system. Both diseases also typically first appear in the late teens or early twenties and occur equally in all sexes and genders.

Crohn’s Disease

Crohn’s disease is a type of inflammatory bowel disease that may affect any part of the GI tract from the mouth to the anus, among other body tissues. The most commonly affected region is the ileum, which is the final part of the small intestine. Signs and symptoms of Crohn’s disease typically include abdominal pain, diarrhea (with or without blood), fever, and weight loss. Malnutrition because of faulty absorption of nutrients may also occur. Potential complications of Crohn’s disease include obstructions and abscesses of the bowel. People with Crohn’s disease are also at a slightly greater risk than the general population of developing bowel cancer. Although there is a slight reduction in life expectancy in people with Crohn’s disease, if the disease is well managed, affected people can live full and productive lives.

Crohn’s disease is caused by a combination of genetic and environmental factors that lead to impairment of the generalized immune response (called innate immunity). The chronic inflammation of Crohn’s disease is thought to be the result of the immune system “trying” to compensate for the impairment. Dozens of genes are likely to be involved, only a few of which have been identified. Because of the genetic component, close relatives such as siblings of people with Crohn’s disease are many times more likely to develop the disease than people in the general population. Environmental factors that appear to increase the risk of the disease include smoking tobacco and eating a diet high in animal proteins. Crohn’s disease is typically diagnosed on the basis of a colonoscopy, which provides a direct visual examination of the inside of the colon and the ileum of the small intestine.

People with Crohn’s disease typically experience recurring periods of flare-ups followed by remission. There are no medications or surgical procedures that can cure Crohn’s disease, although medications such as anti-inflammatory or immune-suppressing drugs may alleviate symptoms during flare-ups and help maintain remission. Lifestyle changes, such as dietary modifications and smoking cessation, may also help control symptoms and reduce the likelihood of flare-ups. Surgery may be needed to resolve bowel obstructions, abscesses, or other complications of the disease.

Ulcerative Colitis

Ulcerative colitis is an inflammatory bowel disease that causes inflammation and ulcers (sores) in the colon and rectum. Unlike Crohn’s disease, other parts of the GI tract are rarely affected in ulcerative colitis. The primary symptoms of the disease are lower abdominal pain and bloody diarrhea. Weight loss, fever, and anemia may also be present. Symptoms typically occur intermittently with periods of no symptoms between flare-ups. People with ulcerative colitis have a considerably increased risk of colon cancer and should be screened for colon cancer more frequently than the general population. However, ulcerative colitis seems to reduce primarily the quality of life and not the lifespan.

The exact cause of ulcerative colitis is not known. Theories about its cause involve immune system dysfunction, genetics, changes in normal gut bacteria, and lifestyle factors such as a diet high in animal protein and the consumption of alcoholic beverages. Genetic involvement is suspected in part because ulcerative colitis tends to “run” in families. It is likely that multiple genes are involved. Diagnosis is typically made on the basis of colonoscopy and tissue biopsies.

Lifestyle changes, such as reducing the consumption of animal protein and alcohol, may improve symptoms of ulcerative colitis. A number of medications are also available to treat symptoms and help prolong remission. These include anti-inflammatory drugs and drugs that suppress the immune system. In cases of severe disease, removal of the colon and rectum may be required and can cure the disease.

Diverticulitis

Diverticulitis is a digestive disease in which tiny pouches in the wall of the large intestine become infected and inflamed. Symptoms typically include lower abdominal pain of sudden onset. There may also be fever, nausea, diarrhea or constipation, and blood in the stool. Having large intestine pouches called diverticula (Figure (PageIndex{2})) that are not inflamed is called diverticulosis. Diverticulosis is thought to be due to a combination of genetic and environmental factors and is more common in people who are obese. Infection and inflammation of the pouches (diverticulitis) occur in about 10 to 25 percent of people with diverticulosis and is more common at older ages. The infection is generally caused by bacteria.

Diverticulitis can usually be diagnosed with a CT scan. Mild diverticulitis may be treated with oral antibiotics and a short-term liquid diet. For severe cases, intravenous antibiotics, hospitalization, and complete bowel rest (no nourishment via the mouth) may be recommended. Complications such as abscess formation or perforation of the colon require surgery.

Peptic Ulcer

A peptic ulcer is a sore in the lining of the stomach or the duodenum (the first part of the small intestine). If the ulcer occurs in the stomach, it is called a gastric ulcer; if it occurs in the duodenum, it is called a duodenal ulcer. The most common symptoms of peptic ulcers are upper abdominal pain that often occurs at night and improves with eating. Other symptoms may include belching, vomiting, weight loss, and poor appetite. However, many people with peptic ulcers, particularly older people, have no symptoms. Peptic ulcers are relatively common, with about 10 percent of people developing a peptic ulcer at some point in their life.

The most common cause of peptic ulcers is infection with the bacterium Helicobacter pylori, which may be transmitted by food, contaminated water, or human saliva (for example, by kissing or sharing eating utensils). Surprisingly, the bacterial cause of peptic ulcers was not discovered until the 1980s. The scientists who made the discovery are Australians Robin Warren and Barry J. Marshall. Although the two scientists eventually won a Nobel Prize for their discovery, their hypothesis was poorly received at first. To demonstrate the validity of their discovery, Marshall used himself in an experiment. He drank a culture of bacteria from a peptic ulcer patient and developed symptoms of peptic ulcer in a matter of days. His symptoms resolved on their own within a couple of weeks, but he took antibiotics to kill any remaining bacteria at his wife’s urging (apparently because bad breath is also one of the symptoms of H. pylori infection). Marshall’s self-experiment was published in the Australian Medical Journal and is among the most cited articles ever published in the journal.

Another relatively common cause of peptic ulcers is the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen. Additional contributing factors may include tobacco smoking and stress, although these factors have not been demonstrated conclusively to cause peptic ulcers independent of H. pylori infection. Contrary to popular belief, diet does not appear to play a role in either causing or preventing peptic ulcers. Eating spicy foods and drinking coffee and alcohol were once thought to cause peptic ulcers. These lifestyle choices are no longer thought to have much if any effect on the development of peptic ulcers.

Peptic ulcers are typically diagnosed on the basis of symptoms or the presence of H. pylori in the GI tract. However, endoscopy (Figure (PageIndex{3})), which allows direct visualization of the stomach and duodenum with a camera, may be required for a definitive diagnosis. Peptic ulcers are usually treated with antibiotics to kill H. pylori, along with medications to temporarily decrease stomach acid and aid in healing. Unfortunately, H. pylori have developed resistance to commonly used antibiotics, so treatment is not always effective. If a peptic ulcer has penetrated so deep into the tissues that it causes perforation of the wall of the stomach or duodenum, then emergency surgery is needed to repair the damage.

Gastroenteritis

Gastroenteritis, also known as infectious diarrhea, is an acute and usually self-limiting infection of the GI tract by pathogens. Symptoms typically include some combination of diarrhea, vomiting, and abdominal pain. Fever, lack of energy, and dehydration may also occur. The illness generally lasts less than two weeks, even without treatment, but in young children, it is potentially deadly. Gastroenteritis is very common, especially in poorer nations. Worldwide, up to five billion cases occur each year, resulting in about 1.4 million deaths. In the United States, infectious diarrhea is the second most common type of infection after the common cold.

Commonly called “stomach flu,” gastroenteritis is unrelated to the influenza virus, although viruses are the most common cause of the disease (Figure (PageIndex{4})). In children, rotavirus is most often the cause, whereas norovirus is more likely to be the cause in adults. Besides viruses, other potential causes of gastroenteritis include fungi, protozoa (including Giardia lamblia, described below), and bacteria (most often Escherichia coli or Campylobacter jejuni). Transmission of pathogens may occur due to eating improperly prepared foods or foods left to stand at room temperature, drinking contaminated water, or having close contact with an infected individual.

Gastroenteritis is less common in adults than children, partly because adults have acquired immunity after repeated exposure to the most common infectious agents. Adults also tend to have better hygiene than children. If children have frequently repeated incidents of gastroenteritis, they may suffer from malnutrition, stunted growth, and developmental delays. Many cases of gastroenteritis in children can be avoided by giving them a rotavirus vaccine. Frequent and thorough hand washing can cut down on infections caused by other pathogens.

Treatment of gastroenteritis generally involves increasing fluid intake to replace fluids lost in vomitus or diarrhea. Oral rehydration solution, which is a combination of water, salts, and sugar, is often recommended. In severe cases, intravenous fluids may be needed. Antibiotics are not usually prescribed because they are ineffective against viruses that cause most cases of gastroenteritis.

Giardiasis

Giardiasis, popularly known as beaver fever, is a type of gastroenteritis caused by a GI tract parasite, the single-celled protozoan Giardia lamblia (Figure (PageIndex{5})). The parasite inhabits the digestive tract of a wide variety of domestic and wild animal species in addition to human beings, including cows, rodents, and sheep as well as beavers (hence its popular name). Giardiasis is one of the most common parasitic infections in people the world over, with hundreds of millions of people infected worldwide each year.

Transmission of G. lamblia is via a fecal-oral route. Those at greatest risk include travelers to countries where giardiasis is common, people who work in child-care settings, backpackers and campers who drink untreated water from lakes or rivers, and people who have close contact with infected people or animals in other settings. In the United States, giardiasis occurs more often during the summer than in other seasons, probably because people spend more time outdoors and in wild settings at that time of year.

Symptoms of giardiasis can vary widely. About a third of people with the infection have no symptoms, whereas others have severe diarrhea with poor absorption of nutrients. Problems with absorption occur because the parasites inhibit intestinal digestive enzyme production, cause detrimental changes in microvilli lining the small intestine, and kill off small intestinal epithelial cells. The illness can result in weakness, loss of appetite, stomach cramps, vomiting, and excessive gas. Without treatment, symptoms may continue for several weeks. Treatment with an antibiotic may be needed if symptoms persist longer or are particularly severe.

Review

  1. What is inflammatory bowel disease?
  2. Describe typical symptoms of inflammatory bowel disease.
  3. Compare and contrast Crohn’s disease and ulcerative colitis.
  4. What is diverticulosis? How is it related to diverticulitis?
  5. Identify the locations and causes of peptic ulcers.
  6. Define and describe gastroenteritis.
  7. Identify the cause of giardiasis. Why may it cause malabsorption?
  8. Which of the following does not normally affect the small intestine?

    A. Peptic ulcers

    B. Crohn's disease

    C. Giardiasis

    D. Ulcerative colitis

  9. Name three disorders of the GI tract that can be due to bacteria.

  10. True or False. A colonoscopy can be used to examine the small intestine.

  11. True or False. Peptic ulcers are mainly due to diet.

  12. Name one disorder of the GI tract that can be helped by anti-inflammatory medications and one that can be caused by chronic use of anti-inflammatory medications.

  13. People with ulcerative colitis should be frequently screened for _________ cancer.

  14. Describe one reason why it can be dangerous to drink untreated water.

  15. Do you think the “stomach flu” can be prevented by an influenza vaccine? Why or why not?


Stem Cells in Repair of Gastrointestinal Epithelia

Among the endodermal tissues of adult mammals, the gastrointestinal (GI) epithelium exhibits the highest turnover rate. As the ingested food moves along the GI tract, gastric acid, digestive enzymes, and gut resident microbes aid digestion as well as nutrient and mineral absorption. Due to the harsh luminal environment, replenishment of new epithelial cells is essential to maintain organ structure and function during routine turnover and injury repair. Tissue-specific adult stem cells in the GI tract serve as a continuous source for this immense regenerative activity. Tissue homeostasis is achieved by a delicate balance between gain and loss of cells. In homeostasis, temporal tissue damage is rapidly restored by well-balanced tissue regeneration, whereas prolonged imbalance may result in diverse pathologies of homeostasis and injury repair. Starting with a summary of the current knowledge of GI tract homeostasis, we continue with providing models of acute injury and chronic diseases. Finally, we will discuss how primary organoid cultures allow new insights into the mechanisms of homeostasis, injury repair, and disease, and how this novel 3D culture system has the potential to translate into the clinic.

Copyright © 2017 Int. Union Physiol. Sci./Am. Physiol. Soc.

Conflict of interest statement

No conflicts of interest, financial or otherwise, are declared by the author(s).


Notes

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Even though anatomically part of the GI tract, diseases of the mouth are often not considered alongside other gastrointestinal diseases. By far the most common oral conditions are plaque-induced diseases (e.g., gingivitis, periodontitis, dental caries). Some diseases which involve other parts of the GI tract can manifest in the mouth, alone or in combination, including:

  • Gastroesophageal reflux disease can cause acid erosion of the teeth and halitosis. can be associated with failure of tooth eruption, supernumerary teeth, and dentigerous cysts. can cause dark spots on the oral mucosa or on the lips or the skin around the mouth.
  • Several GI diseases, especially those associated with malabsorption, can cause recurrent mouth ulcers, atrophic glossitis, and angular cheilitis (e.g., Crohn's disease is sometimes termed orofacial granulomatosis when it involves the mouth alone). can cause glossitis, angular cheilitis. [1]

Oesophageal diseases include a spectrum of disorders affecting the oesophagus. The most common condition of the oesophagus in Western countries is gastroesophageal reflux disease, [2] which in chronic forms is thought to result in changes to the epithelium of the oesophagus, known as Barrett's oesophagus. [3] : 863–865

Acute disease might include infections such as oesophagitis, trauma caused by the ingestion of corrosive substances, or rupture of veins such as oesophageal varices, Boerhaave syndrome or Mallory-Weiss tears. Chronic diseases might include congenital diseases such as Zenker's diverticulum and esophageal webbing, and oesophageal motility disorders including the nutcracker oesophagus, achalasia, diffuse oesophageal spasm, and oesophageal stricture. [3] : 853, 863–868

Oesophageal disease may result in a sore throat, throwing up blood, difficulty swallowing or vomiting. Chronic or congenital diseases might be investigated using barium swallows, endoscopy and biopsy, whereas acute diseases such as reflux may be investigated and diagnosed based on symptoms and a medical history alone. [3] : 863–867

Gastric diseases refer to diseases affecting the stomach. Inflammation of the stomach by infection from any cause is called gastritis, and when including other parts of the gastrointestinal tract called gastroenteritis. When gastritis persists in a chronic state, it is associated with several diseases, including atrophic gastritis, pyloric stenosis, and gastric cancer. Another common condition is gastric ulceration, peptic ulcers. Ulceration erodes the gastric mucosa, which protects the tissue of the stomach from the stomach acids. Peptic ulcers are most commonly caused by a bacterial Helicobacter pylori infection. [3] Epstein–Barr virus infection is another factor to induce gastric cancer. [4] [5]

As well as peptic ulcers, vomiting blood may result from abnormal arteries or veins that have ruptured, including Dieulafoy's lesion and Gastric antral vascular ectasia. Congenital disorders of the stomach include pernicious anaemia, in which a targeted immune response against parietal cells results in an inability to absorb vitamin B12. Other common symptoms that stomach disease might cause include indigestion or dyspepsia, vomiting, and in chronic disease, digestive problems leading to forms of malnutrition. [3] : 850–853 In addition to routine tests, an endoscopy might be used to examine or take a biopsy from the stomach. [3] : 848

The small and large intestines may be affected by infectious, autoimmune, and physiological states. Inflammation of the intestines is called enterocolitis, which may lead to diarrhea.

Acute conditions affecting the bowels include infectious diarrhea and mesenteric ischaemia. Causes of constipation may include faecal impaction and bowel obstruction, which may in turn be caused by ileus, intussusception, volvulus. Inflammatory bowel disease is a condition of unknown aetiology, classified as either Crohn's disease or ulcerative colitis, that can affect the intestines and other parts of the gastrointestinal tract. Other causes of illness include intestinal pseudoobstruction, and necrotizing enterocolitis. [3] : 850–862, 895–903

Diseases of the intestine may cause vomiting, diarrhoea or constipation, and altered stool, such as with blood in stool. Colonoscopy may be used to examine the large intestine, and a person's stool may be sent for culture and microscopy. Infectious disease may be treated with targeted antibiotics, and inflammatory bowel disease with immunosuppression. Surgery may also be used to treat some causes of bowel obstruction. [3] : 850–862

The normal thickness of the small intestinal wall is 3–5 mm, [6] and 1–5 mm in the large intestine. [7] Focal, irregular and asymmetrical gastrointestinal wall thickening on CT scan suggests a malignancy. [7] Segmental or diffuse gastrointestinal wall thickening is most often due to ischemic, inflammatory or infectious disease. [7] Though less common, medications such as ACE inhibitors can cause angioedema and small bowel thickening. [8]

Small intestine Edit

The small intestine consists of the duodenum, jejunum and ileum. Inflammation of the small intestine is called enteritis, which if localised to just part is called duodenitis, jejunitis and ileitis, respectively. Peptic ulcers are also common in the duodenum. [3] : 879–884

Chronic diseases of malabsorption may affect the small intestine, including the autoimmune coeliac disease, infective Tropical sprue, and congenital or surgical short bowel syndrome. Other rarer diseases affecting the small intestine include Curling's ulcer, blind loop syndrome, Milroy disease and Whipple's disease. Tumours of the small intestine include gastrointestinal stromal tumours, lipomas, hamartomas and carcinoid syndromes. [3] : 879–887

Diseases of the small intestine may present with symptoms such as diarrhoea, malnutrition, fatigue and weight loss. Investigations pursued may include blood tests to monitor nutrition, such as iron levels, folate and calcium, endoscopy and biopsy of the duodenum, and barium swallow. Treatments may include renutrition, and antibiotics for infections. [3] : 879–887

Large intestine Edit

Diseases that affect the large intestine may affect it in whole or in part. Appendicitis is one such disease, caused by inflammation of the appendix. Generalised inflammation of the large intestine is referred to as colitis, which when caused by the bacteria Clostridium difficile is referred to as pseudomembranous colitis. Diverticulitis is a common cause of abdominal pain resulting from outpouchings that particularly affects the colon. Functional colonic diseases refer to disorders without a known cause, including irritable bowel syndrome and intestinal pseudoobstruction. Constipation may result from lifestyle factors, impaction of a rigid stool in the rectum, or in neonates, Hirschprung's disease. [3] : 913–915

Diseases affecting the large intestine may cause blood to be passed with stool, may cause constipation, or may result in abdominal pain or a fever. Tests that specifically examine the function of the large intestine include barium swallows, abdominal x-rays, and colonoscopy. [3] : 913–915

Rectum and anus Edit

Diseases affecting the rectum and anus are extremely common, especially in older adults. Hemorrhoids, vascular outpouchings of skin, are very common, as is pruritus ani, referring to anal itchiness. Other conditions, such as anal cancer may be associated with ulcerative colitis or with sexually transmitted infections such as HIV. Inflammation of the rectum is known as proctitis, one cause of which is radiation damage associated with radiotherapy to other sites such as the prostate. Faecal incontinence can result from mechanical and neurological problems, and when associated with a lack of voluntary voiding ability is described as encopresis. Pain on passing stool may result from anal abscesses, small inflamed nodules, anal fissures, and anal fistulas. [3] : 915–916

Rectal and anal disease may be asymptomatic, or may present with pain when passing stools, fresh blood in stool, a feeling of incomplete emptying, or pencil-thin stools. In addition to regular tests, medical tests used to investigate the anus and rectum include the digital rectal exam and proctoscopy.

Hepatic Edit

Hepatic diseases refers to those affecting the liver. Hepatitis refers to inflammation of liver tissue, and may be acute or chronic. Infectious viral hepatitis, such as hepatitis A, B and C, affect in excess of (X) million people worldwide. Liver disease may also be a result of lifestyle factors, such as fatty liver and NASH. Alcoholic liver disease may also develop as a result of chronic alcohol use, which may also cause alcoholic hepatitis. Cirrhosis may develop as a result of chronic hepatic fibrosis in a chronically inflamed liver, such as one affected by alcohol or viral hepatitis. [3] : 947–958

Liver abscesses are often acute conditions, with common causes being pyogenic and amoebic. Chronic liver disease, such as cirrhosis, may be a cause of liver failure, a state where the liver is unable to compensate for chronic damage, and unable to meet the metabolic demands of the body. In the acute setting, this may be a cause of hepatic encephalopathy and hepatorenal syndrome. Other causes of chronic liver disease are genetic or autoimmune disease, such as hemochromatosis, Wilson's disease, autoimmune hepatitis, and primary biliary cirrhosis. [3] : 959–963, 971

Acute liver disease rarely results in pain, but may result in jaundice. Infectious liver disease may cause a fever. Chronic liver disease may result in a buildup of fluid in the abdomen, yellowing of the skin or eyes, easy bruising, immunosuppression, and feminization. [9] Portal hypertension is often present, and this may lead to the development of prominent veins in many parts of the body, such as oesophageal varices, and haemorrhoids. [3] : 959–963, 971–973

In order to investigate liver disease, a medical history, including regarding a person's family history, travel to risk-prone areas, alcohol use and food consumption, may be taken. A medical examination may be conducted to investigate for symptoms of liver disease. Blood tests may be used, particularly liver function tests, and other blood tests may be used to investigate the presence of the Hepatitis viruses in the blood, and ultrasound used. If ascites is present, abdominal fluid may be tested for protein levels. [3] : 921, 926–927

Pancreatic Edit

Pancreatic diseases that affect digestion refers to disorders affecting the exocrine pancreas, which is a part of the pancreas involved in digestion.

One of the most common conditions of the exocrine pancreas is acute pancreatitis, which in the majority of cases relates to gallstones that have impacted in the pancreatic part of the biliary tree, or due to acute or chronic hazardous alcohol use or as a side-effect of ERCP. Other forms of pancreatitis include chronic and hereditary forms. Chronic pancreatitis may predispose to pancreatic cancer and is strongly linked to alcohol use. Other rarer diseases affecting the pancreas may include pancreatic pseudocysts, exocrine pancreatic insufficiency, and pancreatic fistulas. [3] : 888–891

Pancreatic disease may present with or without symptoms. When symptoms occur, such as in acute pancreatitis, a person may suffer from acute-onset, severe mid-abdominal pain, nausea and vomiting. In severe cases, pancreatitis may lead to rapid blood loss and systemic inflammatory response syndrome. When the pancreas is unable to secrete digestive enzymes, such as with a pancreatic cancer occluding the pancreatic duct, result in jaundice. Pancreatic disease might be investigated using abdominal x-rays, MRCP or ERCP, CT scans, and through blood tests such as measurement of the amylase and lipase enzymes. [3] : 888–894

Gallbladder and biliary tract Edit

Diseases of the hepatobiliary system affect the biliary tract (also known as the biliary tree), which secretes bile in order to aid digestion of fats. Diseases of the gallbladder and bile ducts are commonly diet-related, and may include the formation of gallstones that impact in the gallbladder (cholecystolithiasis) or in the common bile duct (choledocholithiasis). [3] : 977–978

Gallstones are a common cause of inflammation of the gallbladder, called cholecystitis. Inflammation of the biliary duct is called cholangitis, which may be associated with autoimmune disease, such as primary sclerosing cholangitis, or a result of bacterial infection, such as ascending cholangitis. [3] : 977–978, 963–968

Disease of the biliary tree may cause pain in the upper right abdomen, particularly when pressed. Disease might be investigated using ultrasound or ERCP, and might be treated with drugs such as antibiotics or UDCA, or by the surgical removal of the gallbladder. [3] : 977–979


Gastrointestinal Physiology, Development, & Epithelial Biology

Basic, clinical, and translational research on GI development, diseases, and disorders.

The Gastrointestinal (GI) Physiology, Development, and Epithelial Biology program supports basic and translational research on the development, structure, and function of the GI tract in health and disease. This program focuses on GI development, regeneration, and healing, including the role of gastrointestinal stem cells and stem cell differentiation basic biology of the GI epithelium, including studies on the structure and function of the epithelium, interactions between the epithelium and other components of the GI tract, and the integrity of the epithelium as a barrier the cellular and molecular mechanisms regulating transport and absorption of water, ions, sugars, amino acids/peptides, lipids, vitamins, and minerals across the epithelium requirements, bioavailability, and metabolism of nutrients and other dietary components at the organ, cellular, and subcellular levels in normal and diseased states gut barrier function and permeability and normal and abnormal function of the enteric nervous system, including the structure and function of GI hormones peptides and bile acid metabolism. Also of interest are studies that explore the role of taste receptors in the GI tract in nutrient absorption and other metabolic functions.


Kidneys

The paired kidneys are often considered the main organs of excretion. The primary function of the kidneys is the elimination of excess water and wastes from the bloodstream by the production of the liquid waste known as urine . The main structural and functional units of the kidneys are tiny structures called nephrons. Nephrons filter materials out of the blood, return to the blood what is needed, and excrete the rest as urine. As shown in Figure 16.2.6, the kidneys are organs of the urinary system, which also includes the ureters, bladder, and urethra — organs that transport, store, and eliminate urine, respectively.

Figure 16.2.6 The urinary system consists of two kidneys and the structures that transport and store urine.

By producing and excreting urine, the kidneys play vital roles in body-wide homeostasis . They maintain the correct volume of extracellular fluid, which is all the fluid in the body outside of cells, including the blood and lymph. The kidneys also maintain the correct balance of salts and pH in extracellular fluid. In addition, the kidneys function as endocrine glands, secreting hormones into the blood that control other body processes. You can read much more about the kidneys in section 16.4 Kidneys.


5. ICC and GI Disorders

By defining the biology of ICC within the normal GI tract, some important links have been reported between ICC and GI disorders. Decreased or injured ICC have been documented in several human GI motility disorders, such as ageing [54], diabetic gastroparesis [63,73], Hirschsprung’s disease (HSCR) [74,75], and slow transit constipation [62,76,77]. However, direct translation between animal models and human GI physiology is yet to be fully established. A major limitation has been monitoring ICC loss or dysfunctions in the live human GI tract during disease development and progression. While animal models may be poor predictors of how novel therapies will perform in humans, they nevertheless have been useful in developing cellular and molecular frameworks to use in understanding normal biology and disease pathogenesis in humans.

5.1. ICC and Ageing

Alterations in GI motility have been linked to ageing, with a number of GI motility complications (such as constipation) occurring more frequently in the elderly population (reviewed in [78,79,80]). In one of the first studies to investigate the role of ICC in ageing, Gomez-Pinilla et al. [54] sampled gastric and colon tissue from patients aged 25� and 36� years old, respectively. The number and collective volume of KIT + ICC networks declined by 13% per decade of life in the muscle layer of gastric and colon tissue. Such findings have also been demonstrated in ageing mice. In the stomach, jejunum and colon, Kit + ICC numbers and networks decreased over a 24-month time period, which was correlated with reduced Kit protein levels [81]. Interestingly, loss of ICC was first observed in the stomach, followed by the intestine and colon, indicating that gastric ICC functionality may be the first affected during ageing. Additionally, similar changes in ICC network volumes have been found in the terminal bowel of ageing mice [82]. Whilst thorough molecular information regarding ICC and ageing is yet to be elucidated, these data indicate that a change in ICC functionality may, in part, affect GI motility with age.

5.2. ICC and Diabetic Gastroparesis

Reduced KIT + ICC numbers have been reported in the gastric muscles of diabetic patients [56], which is often linked to GI motility disorders such as gastroparesis. In humans, diabetic gastroparesis presents as delayed gastric emptying in the absence of obstruction or any other identifiable, non-diabetic cause [83]. Investigation of type 1 or type 2 diabetic patients has shown approximately that 42% exhibit normal gastric emptying and 58% abnormal emptying (36% with delayed emptying and 22% with accelerated emptying) [84]. Similar outcomes were seen in type 2 diabetic patients with poor glycaemic control i.e.,

66% had abnormal (though not always symptomatic) gastric emptying [85]. Other studies of gastroparesis have shown ultrastructural changes in ICC and disrupted slow-wave activity within the gastric antrum and corpus, termed ‘ICC-opathy’ (reviewed in [86]). More recently, some studies have suggested a link between inflammation and ICC loss in diabetic gastroparesis patients. Low numbers of CD206 + macrophages were found to be correlated to loss of KIT + ICC within the gastric corpus of diabetic gastroparesis patients [87]. Moreover, transcriptomic and proteomic analyses on gastric muscle biopsies from diabetic gastroparesis patients have further supported this hypothesis that innate immune signalling and inflammation may play a role in disease pathogenesis [88,89].

Delayed gastric emptying has also been observed in mouse diabetic models. Interestingly, reduced numbers of gastric Kit + cells and disrupted GI pacemaker activity have been reported in type 2 diabetic (db/db) mice [90], as well as diabetic GFP + ICC (Kit +/copGFP Lep ob/ob ) mice [39] and non-obese diabetic gastroparesis (NOD) mice [51]. Furthermore, a loss of Ho-1 (a cytoprotective molecule against oxidative stress) up-regulation was associated with decreased gastric Kit protein expression and delayed gastric emptying in NOD mice, suggesting a role of oxidative stress in diabetes [91]. Interestingly, administration of interleukin-10 (which activates the expression of Ho-1 protein) into NOD mice led to increased gastric emptying and more organised gastric Kit + ICC networks [92]. In a different study, depleted ICC in NOD mice were also accompanied by reduced Scf production and smooth muscle atrophy [93]. Moreover, in organotypic gastric muscle cultures, such ICC loss was inhibited by insulin or Igf-1 via rescue of smooth muscle cells and Scf expression, suggesting a potential role of smooth muscle cells in diabetic-associated loss of ICC. On the other hand, in female obese type 2 diabetic leptin receptor-mutant (Lepr db/db ) mice, hyperglycaemia and hyperinsulinemia were observed with elevated oxidative stress, rapid gastric emptying and increased gastric Kit + ICC [94]. Thus, while diabetes may be associated with both ICC gain and loss, the mechanisms underpinning these phenomena in humans are yet to be fully explored.

5.3. ICC and Other GI Motility Disorders

ICC loss has also been observed along with disrupted slow-wave activity in mouse models of intestinal surgical resection [52] and small bowel obstruction [53]. Interestingly, after removing the insult, ICC networks and slow-wave activity began to recover.

Hirschsprung’s disease (HSCR) is a congenital colon disorder that causes chronic constipation. Altered KIT + ICC networks have been documented in the bowel [75] and colon [74] of HSCR patients. Additionally, reduced ANO1 immunoreactivity and protein levels were found in the colon of HSCR patients [95]. Intriguingly, in human colon samples from both normal and HSCR patients, Kit low CD34 + Igf1r + candidate ‘ICC progenitors’ were identified at a frequency of 0.7% of total cells [61] (similar to the Kit low CD34 + Igf1r + candidate ‘ICC progenitors’ identified in the mouse stomach [38]). Reduced proportions of mature and progenitors of ICC were reported, along with ultrastructural ICC injury, in the narrow part of the HSCR colon.

5.4. ICC and Gastrointestinal Stromal Tumours (GISTs)

Gastrointestinal Stromal Tumours (GISTs) are the most common mesenchymal tumour of the gut. Some 60�% of GISTs occur in the stomach and contain activating mutations in the KIT or PDGFRA genes [96]. GISTs have been treated with imatinib, a tyrosine kinase inhibitor, but many patients eventually develop imatinib-resistance.

One hypothesis for the development of GISTs is that they may arise from KIT + CD34 + ICC in the human GI tract [97,98]. However, this hypothesis is controversial as others have reported that KIT + ICC are distinct from CD34 + cells [99,100]. Nonetheless, in mouse models of GIST, knock-in mutations in the Kit gene (K641E and KIT-Asp818Tyr) resulted in hyperplastic ICC and the development of GISTs, suggesting ICC may be involved in disease pathogenesis [101,102]. Lőrincz et al. [38] isolated Kit low CD44 + CD34 + Insr + Igf1r + ‘ICC progenitors’ (representing 0.6% of the total cells) by FACS from mouse gastric tissue. Interestingly, these cells were able to expand with Scf and differentiate into mature functional ICC with Igf-1 in vitro. Transplantation of this cell population into nude mice showed that these ‘ICC progenitors’ induced the formation of malignant tumours containing Kit + Ano1 + cells [103]. Furthermore, in vitro assessment of these cells indicated they were resistant to imatinib as well as being resistant to neutralising antibodies against Kit and Scf—treatments that would normally inhibit proliferation of mature ICC. A 2016 human microarray study showed that genes in the hedgehog signalling pathway, molecular regulators of GI mesenchymal development, were altered within GIST tissue compared to FACS-purified gastric-derived ICC [55]. It was suggested that dysregulated hedgehog signalling—possibly within ICC—may be involved in GIST development. At present, these data suggest a potential role of ICC in GIST pathogenesis. In particular, the mouse data suggests that ‘ICC progenitors’ may be GIST precursors and potential targets for GIST therapy.


Management of COVID-19-related GI manifestations

Diagnostic aspects

Most GI manifestations in patients with COVID-19 are mild and self-limiting. 93 In such patients, no further investigations specific to the GI system are needed. Routine endoscopy is not useful in the diagnosis of mild disease and should be performed cautiously due to the risk of exposure of healthcare workers. Mild cases have a normal endoscopy, but in one study, endoscopic biopsy showed plasma cells and lymphocytes in the lamina propria of the stomach, duodenum and rectum despite having a macroscopically normal GI epithelium. 22 Endoscopy is useful in selected patients with GI bleeding for both diagnostic and therapeutic purposes. Lin etਊl. 43 found multiple round herpetic erosions and ulcers in the oesophagus. Martin etਊl. 45 found gastric or duodenal ulcers in 80% of endoscopies for upper GI bleeding and rectal ulcers in 60% of endoscopies when there was lower GI bleeding. Mauro etਊl. 46 described 11 patients who had active peptic ulcers, erosive gastritis and bleeding from gastro-oesophageal varices. A summary of the reported investigation findings and treatments used are provided in Table  3 . 15,16,21,22,38� Although stool RT-PCR, peritoneal biopsies and peritoneal fluid RNA tests have been performed, their usefulness in management is limited. Selected patients with abdominal manifestations such as acute abdomen and peritonitis should have an abdominal computed tomography scan and angiogram. The reported positive findings include small bowel volvulus, acute enterocolitis, splenic flexure contrast extravasation, acute appendicitis, haemoperitoneum and haemopneumoperitoneum. As there are no accepted protocols for investigation of GI manifestations in COVID-19, the decision should be made based on individual circumstances considering the therapeutic benefit of the intervention and the potential risk of exposure to healthcare workers.

Table 3.

Assessment and treatment of patients with COVID-19 and GI manifestations

First author, year (country)Article typeTotal patients, NImagingEndoscopyPathologyGeneral management and nutritionDrugs specific for GI manifestationsComplications and surgical managementOutcome of GI manifestations and follow-up data
Chen, 2020 38 (China)RA99NANANANANoNoNA
Chen, 2020 39 (China)RA42NANANANANANoNA
Guan, 2020 40 (China)RA1099NANANANANANoNA
Han, 2020 15 (China)RA206NANADirect invasion of virus through the intestinal mucosaNANANoRecovered/discharged: 100%
Huang, 2020 41 (China)RA41NANANANANANoNA
Jin, 2020 42 (China)RA651NANANANANANoARDS 6.76%
Shock 1.35%
Liver injury 17.57%
Mechanical ventilation 6.76%
ICU care 6.76%
Death 1.35%
Lin, 2020 43 (China)RA96NAIn patients with GI bleeding, source of bleeding localised to the oesophagus by endoscopy at a distance of 26਌m from incisorsMultiple round herpetic erosions and ulcers in the oesophagus with a diameter of 4𠄶 mmNANANoIn hospital 61.1%Discharged 38.9%
Luo, 2020 44 (China)RA1141NANANANANANARecovered 96.2%
Death 3.8%
Martin,2020 45 (USA)RA41UGIB, NGUGIB, esophagogastroduodenoscopy (32%) treated with epinephrine injection, endoclips or cautery in 40%UGIB, gastric/duodenal ulcers in 80% of endoscopiesBlood transfusion and monitoringUGIB, high-dose PPIsGI bleeding (upper 31, lower 10) requiring blood transfusionICU care 46%
LGIB, CT angiogram in 1 patient 㺬tive extravasation at splenic flexure but angiography was negativeLGIB, flexible sigmoidoscopy or colonoscopy (50%)LGIB, rectal ulcers in 60% of endoscopies LGIB, NA Mechanical ventilation 46%
Death 27%
Mauro,2020 46 (Italy)RA4871Radiological embolization in 1 patient with an early rebleedUGIE in 11 patients treated with adrenaline injection and clips in 5, cyanoacrylate gel in 1UGIB, active peptic ulcers (44%), erosive or haemorrhagic gastritis (22%), variceal bleeding from gastro-oesophageal varices (4.5%)Blood transfusion and monitoringHigh-dose PPIsUpper GI bleeding in 23 patientsDischarged 78%
Endoscopic re-treatment in 1 patient with an early rebleed Vasoactive agent for suspicious variceal bleeding in 1 patient Death 22%
Mo, 2020 47 (China)RA155NANANANANANANA
Pan, 2020 16 (China)RA204NANANANANANoRecovered 81.55%
Death 18.45%
ICU care 5.94%
Seeliger, 2020 21 (France)RA7CT abdomen, small bowel ischaemia, appendicitis, sigmoid ischaemia, haemoperitoneum, haemopneumoperitoneum and stab wound in liverSigmoidoscopy, ulcerative and ischaemic changesSmall bowel ischaemia, appendicitis, sigmoid ischaemia, haemoperitoneum, haemopneumoperitoneum and stab wound in liverNANAComplications, small bowel ischaemia, sigmoid ischaemia, haemoperitoneum, haemopneumoperitoneum, abdominal compartment syndromeRecovered/discharged 40%
Surgical management, yes, open small bowel resection, laparoscopic appendectomy, open drainage of haemoperitoneum/haemopneumoperitoneum, reduction of incarcerated small bowelICU care 60%
Shi, 2020 48 (China)RA81NANANANANANANA
Wang, 2020 49 (China)RA138NANANANANANANA
Xu, 2020 50 (China)RA62NANANANANANANA
Xu, 2020 51 (China)RA10NANANANANANARecovered/discharged 100%
Mechanical ventilation 0
ICU care 0
Young, 2020 52 (Singapore)RA18NANANANANANAMechanical ventilation 25%
ICU care 50%
Recovered/discharged 100%
Death 0
Zhang, 2020 53 (China)RA505NANANANANANANA
Zhang, 2020 54 (China)RA140NANANANANANANA
Zhou, 2020 55 (China)RA191NANANANANANANA
Gadiparthi, 2020 56 (USA)BC3Patient 1, not doneNot donePatient 1, possibly from an anastomotic ischaemic ulcer from previous Roux-end-Y gastric bypassConservative management with blood transfusion and monitoringAll 3 patients were given high-dose PPIsComplications, GI bleeding requiring blood transfusionRecovered/discharged 33.3%
Patient 2, CT angiogram did not localize the bleeding vessel Patient 2, gastroduodenal bleeding Patient 3 underwent a faecal management system for large volume watery diarrhoeaNo surgical managementDeath 66.7%
Patient 3, not done Patient 3, rectal ulcer or direct trauma from faecal management system
Xiao, 2020 22 (China)BC73NAMucous epithelium of oesophagus, stomach, duodenum and rectum showed no significant damageInfiltration of occasional lymphocytes in oesophageal squamous epithelium. In lamina propria of stomach, duodenum and rectum, numerous infiltrating plasma cells and lymphocytes seen with interstitial oedema. Positive staining of GI epithelium for ACE2 and viral RNANANANANA
Case reports
Aloysius, 2020 57 (USA)CR1CT abdomen, normal gall bladder, normal biliary tract and unremarkable pancreasNAACE2 receptor mediated damage to pancreatic islet cells causing acute pancreatitisNothing by mouth, fluid resuscitation (crystalloid) Analgesia, not specifiedNoRecovered/discharged
Parenteral nutrition
Coccolini, 2020 58 (Italy)CR1CT abdomen, intestinal occlusion due to a small bowel volvulus with no signs of gut ischaemiaNAVolvulus due to omental band attached to RIF (past history of open appendectomy 20 years ago). Bowel vital and viable no perforation, no bowel ischaemia, no colonic diverticulaNANAComplications, intestinal occlusionSurgical management, yes, adhesiolysis without intestinal resectionRecovered
Holshue, 2020 59 (USA)CR1NANANANormal salineOndansetronNoRecovered
Hosoda, 2020 60 (Japan)CR1CT abdomen, acute enterocolitis without ileusNANANANANoRecovered

ARDS: acute respiratory distress syndrome BC: brief communication CR: case report LGIB: lower gastrointestinal endoscopy NA: not available RA: research article UGIE: upper gastrointestinal endoscopy.

Protective measures during endoscopy

Procedures such as upper and lower GI endoscopy should follow the recommended guidelines. 94 As positive viral RNA is seen in the oesophagus, stomach, duodenum and rectum, endoscopic procedures warrant extra precautions to ensure the safety of staff and prevent cross-contamination and nosocomial outbreaks among patients. During the COVID-19 pandemic, specific infection control guidelines have been implemented in different countries for endoscopic procedures. 94 Endoscopies should be performed only after clinical discussion and should be considered when it is essential for reaching a therapeutic decision that cannot be made using other non-invasive tests.

General measures and universal precautions

Human-to-human transmission of SARS-CoV-2 occurs mainly through the respiratory tract via infected droplets/aerosols. Contact with contaminated surfaces is another possible mode of transmission. Thus wearing proper face masks, hand hygiene and social distancing are fundamental for infection prevention. Healthcare workers should wear appropriate personal protective equipment. Since the virus is found in stools for varying lengths of time, extra precautions may be needed to avoid faecal–oral transmission. Contact with infected saliva or stools should be avoided. Appropriate infection prevention and control measures should be in place for preventing nosocomial spread. There are case reports of the detection of virus in peritoneal fluid during laparotomy. Therefore adherence to special precautionary infection control measures for preventing aerosolization of the virus during laparoscopic procedures or when using electrocautery in open procedures should be considered. 58

Supportive measures

As most virus-induced GI manifestations are mild and self-limiting, supportive care and symptomatic treatment are usually sufficient. 95� Supportive treatment with oxygen, optimal hydration, analgesics and anti-emetics may be necessary. 99 Although studies are limited, endoscopy in selected patients has shown ulceration and bleeding. Avoidance of non-steroidal anti-inflammatory drugs (NSAIDs) and gastric acid prophylaxis should be considered in patients with GI manifestations. Those with paralytic ileus or excessive vomiting may require nasogastric tube decompression and nothing by mouth. Patients with diarrhoea need appropriate rehydration therapy and anti-diarrheal medications. Those with GI manifestations have increased rates of electrolyte disturbance 42 and thus regular monitoring and correction of electrolytes is needed and medications that may induce electrolyte imbalance should be administered with caution. Those with severe GI manifestations or acute abdomen should be managed by a specialised multidisciplinary team including a physician, critical care specialist, nutritionist, gastroenterologist and surgeon.

Medications

To date, no specific antiviral medications have been shown to reduce mortality in COVID-19 patients. The antiviral drugs used for treatment of COVID-19 include remdesivir and lopinavir–ritonavir. Remdesivir was shown to reduce hospital stays in patients with severe disease. A myriad of other treatment modalities aimed at symptom control and management of complications have been used. Immunomodulatory agents including glucocorticoids, convalescent plasma and anti-cytokine therapy have been used to reduce the negative effects of the overwhelming systemic inflammatory response. 99 However, except for dexamethasone, the other agents have not shown definite therapeutic benefits, although they may be beneficial in selected subgroups. 100 Moreover, evidence on the efficacy of these agents in treating GI manifestations is limited and further studies are required. There is an ongoing debate about the use of ACE inhibitors and renin𠄺ngiotensin𠄺ldosterone system blockers in the treatment of COVID-19. Although beneficial mechanisms such as blocking viral entry into the host cell have been proposed, the clinical significance of these agents is yet to be conclusively proven. 101

The loss of gut mucosal integrity and dysfunction of intestinal flora are important complications in severe viral illnesses, including COVID-19. The use of probiotics has been suggested to improve GI symptoms of SARS-CoV-2 infection. 101 Irrational use of broad-spectrum antibiotics should be avoided, as they cause the loss of commensal intestinal flora and alteration of gut mucosal integrity. COVID-19 treatment guidelines in China have included the use of probiotics and micro-ecological regulators for maintaining gut mucosal integrity and to minimise secondary bacterial infections. 102

Nutrition

SARS-CoV-2 patients may have a reduced oral intake due to the severity of their disease or as a side effect of the medicines that are used. Enteral nutrition is important for maintaining gut mucosal integrity, especially in patients with severe disease. In patients with severe disease, specialist nutritional assessment should be done and a high-calorie, immunomodulatory diet should be administered. In patients who are mechanically ventilated, nasogastric or nasojejunal tube insertion and enteral feeding is an option. In patients who cannot tolerate enteral feeding, parenteral nutrition should be administered. However, enteral feeding should be commenced early following improvement of the clinical condition.

Surgical measures

Rarely, patients with COVID-19 may present with an acute abdomen either due to a complication of the disease or due to a coexisting pathology. Conditions such as acute pancreatitis and abdominal compartment syndrome have been reported in association with COVID-19. 57,103 Thus such conditions should be suspected in a deteriorating SARS-CoV-2 patient with an acute abdomen. As thrombotic complications are well-described in SARS-CoV-2 patients, mesenteric thrombosis should be suspected early in a clinically deteriorating patient with acute abdomen and appropriate anticoagulation should be initiated promptly after confirming the diagnosis through imaging. 104 In patients with GI bleeding that does not settle with medical management, therapeutic endoscopy with clipping or cautery has been found to be successful.

Surgical treatment has been reported for conditions such as intestinal obstruction, bowel ischaemia, acute appendicitis and haemoperitoneum/haemopneumoperitoneum in association with SARS-CoV-2 (Table  3 ). Such cases are extremely rare and require a high degree of clinical suspicion and relevant imaging to reach the diagnosis. Standard surgical procedures have been performed with appropriate personal protective equipment and infection control measures to prevent transmission of infection. 105,106 Furthermore, in such critically ill patients, postoperative care in an ICU is necessary. 107


2020 Award Recipients

Recognizing the critical role of research in advancing the understanding and care of chronic gastrointestinal (GI) illnesses in adults and children, IFFGD was pleased to award its 2020 Research Recognition Awards to three young investigators. With the cancellation of DDW in Chicago due to COVID-19, we were unable to award them in person. First established in 2003, these awards are intended to recognize and support the research accomplishments of young investigators actively engaged in research in neurogastroenterology, and especially, in the basic mechanisms and clinical aspects of functional GI and motility disorders. To date, the foundation has presented awards to 48 investigators from around the world.

The award recipients were selected by a committee of leaders in the medical and scientific community:

Peer-Review Selection Committee

  • William Whitehead, PhD, Chair
  • Gary Mawe, MD
  • Emeran Mayer, MD
  • Samuel Nurko, MD
  • Douglas Drossman, MD
  • Jan Tack, MD, PhD
  • Maura Corsetti, PhD

We are pleased to recognize the 2020 IFFGD Research Recognition Award recipients for their achievements and thank them for their commitment to research that will improve the diagnosis, treatment, and care of adults and children with chronic GI disorders.

The 2020 IFFGD Research Award Recipients Are:

Kyle Staller, MD, Massachusetts General Hospital and Harvard Medical School in Boston, Massachusetts, USA – Recipient of the 2020 award for Clinical Science Investigator

Kyle Staller, MD, MPH is a gastroenterologist and the director of the Gastrointestinal Motility Laboratory at Mass General. He is also an assistant professor of medicine at Harvard Medical School and a member of Clinical and Translational Epidemiology Unit. Dr. Staller specializes in disorders of gastrointestinal motility and neurogastroenterology and is a faculty member of the MGH Center for Neurointestinal Health and the MGH Center for Pelvic Floor Disorders. His clinical practice is devoted to treating patients with GI motility disorders and disorders of brain-gut interaction.

Christopher V. Almario, MD Cedars-Sinai Medical Center in Los Angeles, California, USA – Recipient of the 2020 award for Clinical Science Investigator

Christopher V. Almario, MD, MSHPM, is an Assistant Professor-in-Residence of Medicine and Health Services Research Scientist in the Divisions of Digestive and Liver Diseases and Health Services Research at Cedars-Sinai Medical Center in Los Angeles, CA. He earned his MD at Jefferson Medical College and then completed his internal medicine and gastroenterology training at the Hospital of the University of Pennsylvania and UCLA, respectively. While at UCLA, he also earned his MS in Health Policy and Management through the UCLA Fielding School of Public Health.

Maria Raffaella Barbaro, PhD University of Bologna, Italy – Recipient of the 2020 award for Basic/Translational Science Investigator

Dr. Maria Raffaella Barbaro is a researcher and adjunct professor at the University of Bologna, Italy. She graduated Summa cum Laude in Biological Sciences and she obtained her PhD in Molecular and Functional Biology from the University of Bologna. She qualified in Clinical Pathology in 2017. Since 2012, she has been working as researcher in the Neurogastroenterology and Motility Translational Laboratory at the Department of Medical and Surgical Sciences of the University of Bologna, Italy. Her research interests include functional gastrointestinal diseases, particularly irritable bowel syndrome, mucosal barrier function and immunology, as well as enteric nervous biology.


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