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Digital Tools in the Management of IBS/ Functional GI Disorders

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Tue, 09/26/2023 - 12:23
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Digital Tools in the Management of IBS/Functional GI Disorders
Author(s)
Eric D. Shah, MD, MBA, FACG

Click to view more from Gastroenterology Data Trends 2023. 

References
  1. Hasan SS et al. Neurogastroenterol Motil. 2023;35(4):e14554. doi:10.1111/nmo.14554
  2. Peters SL et al. Neurogastroenterol Motil. 2023;35(4):e14533. doi:10.1111/nmo.14533
  3. Zhou C et al. Neurogastroenterol Motil. 2019;31(2):e13461. doi:10.1111/nmo.13461
  4. Staudacher HM et al. Nat Rev Gastroenterol Hepatol. 2023;1-15. doi:10.1038/s41575-023-00794-z
  5. Qin HY et al. World J Gastroenterol. 2014;20(39):14126-14131. doi:10.3748/wjg.v20.i39.14126
  6. Varjú P et al. PLoS One. 2017;12(8):e0182942. doi:10.1371/journal.pone.0182942
  7. Saleh ZM et al. Am J Gastroenterol. 2023. doi:10.14309/ajg.0000000000002220
  8. Yu C et al. Clin Transl Gastroenterol. 2022;13(9):e00515. doi:10.14309/ctg.0000000000000515
  9. Jagannath B et al. Inflamm Bowel Dis. 2020;26(10):1533-1542. doi:10.1093/ibd/izaa191
  10. Zhang H et al. J Nutr. 2023;153(4):924-939. doi:10.1016/j.tjnut.2023.01.026
  11. Karakan T et al. Gut Microbes. 2022;14(1):2138672. doi:10.1080/19490976.2022.2138672
  12. Kordi M et al. Inform Med Unlocked. 2022;29:100891. doi:10.1016/j.imu.2022.100891
  13. Gubatan J et al. World J Gastroenterol. 2021;27(17):1920-1935. doi:10.3748/wjg.v27.i17.1920
  14. Boucher EM et al. Expert Rev Med Devices. 2021;18(suppl 1):37-49. doi:10.1080/17434440.2021.2013200
  15. Babel A et al. Front Digit Health. 2021;3:669869. doi:10.3389/fdgth.2021.669869
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Gastroenterology and Hepatology
University of Michigan, Michigan Medicine
Ann Arbor, MI

Click to view more from Gastroenterology Data Trends 2023. 

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References
  1. Hasan SS et al. Neurogastroenterol Motil. 2023;35(4):e14554. doi:10.1111/nmo.14554
  2. Peters SL et al. Neurogastroenterol Motil. 2023;35(4):e14533. doi:10.1111/nmo.14533
  3. Zhou C et al. Neurogastroenterol Motil. 2019;31(2):e13461. doi:10.1111/nmo.13461
  4. Staudacher HM et al. Nat Rev Gastroenterol Hepatol. 2023;1-15. doi:10.1038/s41575-023-00794-z
  5. Qin HY et al. World J Gastroenterol. 2014;20(39):14126-14131. doi:10.3748/wjg.v20.i39.14126
  6. Varjú P et al. PLoS One. 2017;12(8):e0182942. doi:10.1371/journal.pone.0182942
  7. Saleh ZM et al. Am J Gastroenterol. 2023. doi:10.14309/ajg.0000000000002220
  8. Yu C et al. Clin Transl Gastroenterol. 2022;13(9):e00515. doi:10.14309/ctg.0000000000000515
  9. Jagannath B et al. Inflamm Bowel Dis. 2020;26(10):1533-1542. doi:10.1093/ibd/izaa191
  10. Zhang H et al. J Nutr. 2023;153(4):924-939. doi:10.1016/j.tjnut.2023.01.026
  11. Karakan T et al. Gut Microbes. 2022;14(1):2138672. doi:10.1080/19490976.2022.2138672
  12. Kordi M et al. Inform Med Unlocked. 2022;29:100891. doi:10.1016/j.imu.2022.100891
  13. Gubatan J et al. World J Gastroenterol. 2021;27(17):1920-1935. doi:10.3748/wjg.v27.i17.1920
  14. Boucher EM et al. Expert Rev Med Devices. 2021;18(suppl 1):37-49. doi:10.1080/17434440.2021.2013200
  15. Babel A et al. Front Digit Health. 2021;3:669869. doi:10.3389/fdgth.2021.669869
References
  1. Hasan SS et al. Neurogastroenterol Motil. 2023;35(4):e14554. doi:10.1111/nmo.14554
  2. Peters SL et al. Neurogastroenterol Motil. 2023;35(4):e14533. doi:10.1111/nmo.14533
  3. Zhou C et al. Neurogastroenterol Motil. 2019;31(2):e13461. doi:10.1111/nmo.13461
  4. Staudacher HM et al. Nat Rev Gastroenterol Hepatol. 2023;1-15. doi:10.1038/s41575-023-00794-z
  5. Qin HY et al. World J Gastroenterol. 2014;20(39):14126-14131. doi:10.3748/wjg.v20.i39.14126
  6. Varjú P et al. PLoS One. 2017;12(8):e0182942. doi:10.1371/journal.pone.0182942
  7. Saleh ZM et al. Am J Gastroenterol. 2023. doi:10.14309/ajg.0000000000002220
  8. Yu C et al. Clin Transl Gastroenterol. 2022;13(9):e00515. doi:10.14309/ctg.0000000000000515
  9. Jagannath B et al. Inflamm Bowel Dis. 2020;26(10):1533-1542. doi:10.1093/ibd/izaa191
  10. Zhang H et al. J Nutr. 2023;153(4):924-939. doi:10.1016/j.tjnut.2023.01.026
  11. Karakan T et al. Gut Microbes. 2022;14(1):2138672. doi:10.1080/19490976.2022.2138672
  12. Kordi M et al. Inform Med Unlocked. 2022;29:100891. doi:10.1016/j.imu.2022.100891
  13. Gubatan J et al. World J Gastroenterol. 2021;27(17):1920-1935. doi:10.3748/wjg.v27.i17.1920
  14. Boucher EM et al. Expert Rev Med Devices. 2021;18(suppl 1):37-49. doi:10.1080/17434440.2021.2013200
  15. Babel A et al. Front Digit Health. 2021;3:669869. doi:10.3389/fdgth.2021.669869
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IBS can be a highly debilitating condition that negatively affects a person’s quality of life. The recent emergence of digital tools designed to help patients and caregivers better manage IBS and functional GI disorders has facilitated the formation of a new health care model with an ever-evolving landscape. These tools range from mobile apps, virtual health platforms, and wearable devices, to the use of AI and digital therapeutics.

These tools serve several purposes—such as telehealth services, symptom tracking, food journals, cognitive behavioral therapy, gut-directed hypnotherapy, and patient education—and can help increase patients’ access to safe, effective treatments.1,2 Further, AI-driven tools can assist health care providers in facilitating more accurate diagnoses and creating
more personalized treatment plans.

Regular exercise, stress management, and low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) dietary strategies are often recommended as nonpharmacologic approaches to IBS management.3-6 With the assistance of digital tools, patients can not only receive care, but also gain disease-specific knowledge, self-manage their diet, track physical activity, monitor stress and IBS symptoms remotely, and improve their quality of life with this new and expanding type of health care model.

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Anxiety and panic attacks

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Given the patient's insidious cognitive decline, as well as increased agitation, irritability, anxiety, social isolation, inability to fully manage finances, loss of routine hygienic practices, and loss of interest in regular meals, this patient is diagnosed with probable Alzheimer's disease (AD) dementia and is referred to a specialist for further testing.

AD is one of the most common forms of dementia. More than 6 million people in the United States have clinical AD or mild cognitive impairment because of AD. By 2060, the incidence of AD is expected to grow to 15 million people. AD is classified into four stages: preclinical, mild, moderate, and severe. Patients with preclinical AD — a relatively new classification currently only used for research — do not yet show abnormal results on physical exam or mental status testing, but areas of the brain are undergoing pathologic changes. Mild AD signs and symptoms include memory loss, compromised judgment, trouble handling money and paying bills, mood and personality changes, and increased anxiety. People with moderate AD show increasing signs of memory loss and confusion, problems with recognizing family and friends, and difficulty with organizing thoughts and thinking logically, and they repeat themselves in conversation, among other symptoms. Severe AD is generally described as a complete loss of self, with the inability to recognize family and friends, inability to communicate effectively, and complete dependence on others for care. 

Diagnosing AD currently relies on a clinical approach. A complete physical examination, with a detailed neurologic examination and a mental status examination, is used to evaluate disease stage and rule out comorbid conditions. Initial mental status testing should evaluate attention and concentration, recent and remote memory, language, praxis, executive function, and visuospatial function. Imaging studies may be performed to rule out other treatable causes of cognitive decline. In addition, volumetric studies of the hippocampus and 2-[18F]fluoro-2-deoxy-D-glucose PET with or without amyloid imaging can be used for early detection and differentiating dementia etiologies. Lumbar puncture as a diagnostic measure for levels of tau (which is often elevated in AD) and amyloid (which is often reduced in AD) is currently reserved for research settings.

Although the cause of AD is unknown, experts believe that environmental and genetic risk factors trigger a pathophysiologic cascade that, over decades, leads to Alzheimer's pathology and dementia. Universally accepted pathologic hallmarks of AD are beta-amyloid plaques and neurofibrillary tangles (NFTs). NFTs result from changes in the tau protein, a key chemical in neuronal support structures, and are associated with malfunctions in communication between neurons as well as cell death. Beta-amyloid plaques are dense, mostly insoluble deposits that develop around neurons in the hippocampus and other regions in the cerebral cortex used for decision-making, disrupting function and leading to brain atrophy. Risk factors for AD include advancing age, family history, APOE e4 genotype, insulin resistance, hypertension, depression, and traumatic brain injury.

After an AD diagnosis, physicians should encourage the involvement of family and friends who agree to become more involved in the patient's care as the disease progresses. These individuals need to understand the patient's wishes around care, especially for the future, when the patient is no longer able to make decisions. The patient may also consider establishing medical advance directives and durable power of attorney for medical and financial decision-making. Caregivers supporting the patient are encouraged to help balance the physical needs of the patient while maintaining respect for them as a competent adult to the extent allowed by the progression of their disease. 

Currently, AD treatments are focused on symptomatic therapies that modulate neurotransmitters — either acetylcholine or glutamate. The standard medical treatment includes cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist. Two amyloid-directed antibodies (aducanumab, lecanemab) are currently available in the US for individuals with AD exhibiting mild cognitive impairment or mild dementia. A third agent currently in clinical trials (donanemab) has shown significantly slowed clinical progression after 1.5 years among clinical trial participants with early symptomatic AD and amyloid and tau pathology.

 

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.

Jasvinder Chawla, MD, has disclosed no relevant financial relationships.


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Given the patient's insidious cognitive decline, as well as increased agitation, irritability, anxiety, social isolation, inability to fully manage finances, loss of routine hygienic practices, and loss of interest in regular meals, this patient is diagnosed with probable Alzheimer's disease (AD) dementia and is referred to a specialist for further testing.

AD is one of the most common forms of dementia. More than 6 million people in the United States have clinical AD or mild cognitive impairment because of AD. By 2060, the incidence of AD is expected to grow to 15 million people. AD is classified into four stages: preclinical, mild, moderate, and severe. Patients with preclinical AD — a relatively new classification currently only used for research — do not yet show abnormal results on physical exam or mental status testing, but areas of the brain are undergoing pathologic changes. Mild AD signs and symptoms include memory loss, compromised judgment, trouble handling money and paying bills, mood and personality changes, and increased anxiety. People with moderate AD show increasing signs of memory loss and confusion, problems with recognizing family and friends, and difficulty with organizing thoughts and thinking logically, and they repeat themselves in conversation, among other symptoms. Severe AD is generally described as a complete loss of self, with the inability to recognize family and friends, inability to communicate effectively, and complete dependence on others for care. 

Diagnosing AD currently relies on a clinical approach. A complete physical examination, with a detailed neurologic examination and a mental status examination, is used to evaluate disease stage and rule out comorbid conditions. Initial mental status testing should evaluate attention and concentration, recent and remote memory, language, praxis, executive function, and visuospatial function. Imaging studies may be performed to rule out other treatable causes of cognitive decline. In addition, volumetric studies of the hippocampus and 2-[18F]fluoro-2-deoxy-D-glucose PET with or without amyloid imaging can be used for early detection and differentiating dementia etiologies. Lumbar puncture as a diagnostic measure for levels of tau (which is often elevated in AD) and amyloid (which is often reduced in AD) is currently reserved for research settings.

Although the cause of AD is unknown, experts believe that environmental and genetic risk factors trigger a pathophysiologic cascade that, over decades, leads to Alzheimer's pathology and dementia. Universally accepted pathologic hallmarks of AD are beta-amyloid plaques and neurofibrillary tangles (NFTs). NFTs result from changes in the tau protein, a key chemical in neuronal support structures, and are associated with malfunctions in communication between neurons as well as cell death. Beta-amyloid plaques are dense, mostly insoluble deposits that develop around neurons in the hippocampus and other regions in the cerebral cortex used for decision-making, disrupting function and leading to brain atrophy. Risk factors for AD include advancing age, family history, APOE e4 genotype, insulin resistance, hypertension, depression, and traumatic brain injury.

After an AD diagnosis, physicians should encourage the involvement of family and friends who agree to become more involved in the patient's care as the disease progresses. These individuals need to understand the patient's wishes around care, especially for the future, when the patient is no longer able to make decisions. The patient may also consider establishing medical advance directives and durable power of attorney for medical and financial decision-making. Caregivers supporting the patient are encouraged to help balance the physical needs of the patient while maintaining respect for them as a competent adult to the extent allowed by the progression of their disease. 

Currently, AD treatments are focused on symptomatic therapies that modulate neurotransmitters — either acetylcholine or glutamate. The standard medical treatment includes cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist. Two amyloid-directed antibodies (aducanumab, lecanemab) are currently available in the US for individuals with AD exhibiting mild cognitive impairment or mild dementia. A third agent currently in clinical trials (donanemab) has shown significantly slowed clinical progression after 1.5 years among clinical trial participants with early symptomatic AD and amyloid and tau pathology.

 

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.

Jasvinder Chawla, MD, has disclosed no relevant financial relationships.


Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Given the patient's insidious cognitive decline, as well as increased agitation, irritability, anxiety, social isolation, inability to fully manage finances, loss of routine hygienic practices, and loss of interest in regular meals, this patient is diagnosed with probable Alzheimer's disease (AD) dementia and is referred to a specialist for further testing.

AD is one of the most common forms of dementia. More than 6 million people in the United States have clinical AD or mild cognitive impairment because of AD. By 2060, the incidence of AD is expected to grow to 15 million people. AD is classified into four stages: preclinical, mild, moderate, and severe. Patients with preclinical AD — a relatively new classification currently only used for research — do not yet show abnormal results on physical exam or mental status testing, but areas of the brain are undergoing pathologic changes. Mild AD signs and symptoms include memory loss, compromised judgment, trouble handling money and paying bills, mood and personality changes, and increased anxiety. People with moderate AD show increasing signs of memory loss and confusion, problems with recognizing family and friends, and difficulty with organizing thoughts and thinking logically, and they repeat themselves in conversation, among other symptoms. Severe AD is generally described as a complete loss of self, with the inability to recognize family and friends, inability to communicate effectively, and complete dependence on others for care. 

Diagnosing AD currently relies on a clinical approach. A complete physical examination, with a detailed neurologic examination and a mental status examination, is used to evaluate disease stage and rule out comorbid conditions. Initial mental status testing should evaluate attention and concentration, recent and remote memory, language, praxis, executive function, and visuospatial function. Imaging studies may be performed to rule out other treatable causes of cognitive decline. In addition, volumetric studies of the hippocampus and 2-[18F]fluoro-2-deoxy-D-glucose PET with or without amyloid imaging can be used for early detection and differentiating dementia etiologies. Lumbar puncture as a diagnostic measure for levels of tau (which is often elevated in AD) and amyloid (which is often reduced in AD) is currently reserved for research settings.

Although the cause of AD is unknown, experts believe that environmental and genetic risk factors trigger a pathophysiologic cascade that, over decades, leads to Alzheimer's pathology and dementia. Universally accepted pathologic hallmarks of AD are beta-amyloid plaques and neurofibrillary tangles (NFTs). NFTs result from changes in the tau protein, a key chemical in neuronal support structures, and are associated with malfunctions in communication between neurons as well as cell death. Beta-amyloid plaques are dense, mostly insoluble deposits that develop around neurons in the hippocampus and other regions in the cerebral cortex used for decision-making, disrupting function and leading to brain atrophy. Risk factors for AD include advancing age, family history, APOE e4 genotype, insulin resistance, hypertension, depression, and traumatic brain injury.

After an AD diagnosis, physicians should encourage the involvement of family and friends who agree to become more involved in the patient's care as the disease progresses. These individuals need to understand the patient's wishes around care, especially for the future, when the patient is no longer able to make decisions. The patient may also consider establishing medical advance directives and durable power of attorney for medical and financial decision-making. Caregivers supporting the patient are encouraged to help balance the physical needs of the patient while maintaining respect for them as a competent adult to the extent allowed by the progression of their disease. 

Currently, AD treatments are focused on symptomatic therapies that modulate neurotransmitters — either acetylcholine or glutamate. The standard medical treatment includes cholinesterase inhibitors and a partial N-methyl-D-aspartate antagonist. Two amyloid-directed antibodies (aducanumab, lecanemab) are currently available in the US for individuals with AD exhibiting mild cognitive impairment or mild dementia. A third agent currently in clinical trials (donanemab) has shown significantly slowed clinical progression after 1.5 years among clinical trial participants with early symptomatic AD and amyloid and tau pathology.

 

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.

Jasvinder Chawla, MD, has disclosed no relevant financial relationships.


Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

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THOMAS DEERINCK, NCMIR / Science Source

 

 

 

 

 

A 73-year-old man who lives independently presents to his primary care physician (PCP) with irritability, anxiety, and panic attacks. Last year, he saw his PCP at the urging of his brother, who noticed that the patient was becoming more forgetful and agitated. At that time, the brother reported concerns that the patient, who normally enjoyed spending time with his extended family, was beginning to regularly forget to show up at family functions. When asked why he hadn't attended, the patient would become irate, saying it was his family who failed to invite him. The patient wouldn't have agreed to seeing the PCP except he was having issues with insomnia that he wanted to address. During last year's visit, the physician conducted a complete physical examination, as well as detailed neurologic and mental status examinations; all came back normal. 

At today's visit, in addition to patient-reported mood fluctuations, the brother tells the physician that the patient has become reclusive, skipping nearly all family functions as well as daily walks with friends. His daily hygiene has suffered, and he has stopped eating regularly. The brother also mentions to the doctor that the patient has received some late-payment notices for utilities that he normally meticulously paid on time. The PCP orders another round of cognitive, behavioral, and functional assessments, which reveal a decline in all areas from last year's results, as well as a complete neurologic examination that reveals mild hyposmia.

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MASLD/MASH and Weight Loss

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MASLD/MASH and Weight Loss
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Arpan Mohanty, MD, MSc

Click to view more from Gastroenterology Data Trends 2023. 

References
  1. Younossi ZM et al. Gastroenterology. 2021;160(3):912-918. doi:10.1053/j.astro.2020.11.051
  2. Cusi K et al. Endocr Pract. 2022;28(5):528-562. doi:10.1016/j.eprac.2022.03.010
  3. Rinella ME et al. Hepatology. 2023;77(5):1797-1835. doi:10.1097/HEP.0000000000000323
  4. World obesity atlas 2023. World Obesity Day. Published March 2023. Accessed July 23, 2023. https://www.worldobesityday.org/assets/downloads/World_Obesity_Atlas_2023_Report.pdf
  5. Le MH et al. Clin Mol Hepatol. 2022;28(4):841-850. doi:10.3350/cmh.2022.0239
  6. Vilar-Gomez E et al. Gastroenterology. 2015;149(2):367-78.e5. doi:10.1053/j.gastro.2015.04.005
  7. Koutoukidis DA et al. Metabolism. 2021;115:154455. doi:10.1016/j.metabol.2020.154455
  8. Ma J et al. Gastroenterology. 2018;155(1):107-117. doi:10.1053/j.gastro.2018.03.038
  9. Ahern AL et al. Lancet. 2017;389(10085):2214-2225. doi:10.1016/S0140-6736(17)30647-5
  10. Newsome PN et al; NN9931-4296 Investigators. N Engl J Med. 2021;384(12):1113-1124. doi:10.1056/NEJMoa2028395
  11. Armstrong MJ et al. Lancet. 2016;387(10019):679-690. doi:10.1016/S0140-6736(15)00803-X
  12. Gastaldelli A et al. Lancet Diabetes Endocrinol. 2022;10(6):393-406. doi:10.1016/S2213-8587(22)00070-5
  13. Kahl S et al. Diabetes Care. 2020;43(2):298-305. doi:10.2337/dc19-0641
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Click to view more from Gastroenterology Data Trends 2023. 

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References
  1. Younossi ZM et al. Gastroenterology. 2021;160(3):912-918. doi:10.1053/j.astro.2020.11.051
  2. Cusi K et al. Endocr Pract. 2022;28(5):528-562. doi:10.1016/j.eprac.2022.03.010
  3. Rinella ME et al. Hepatology. 2023;77(5):1797-1835. doi:10.1097/HEP.0000000000000323
  4. World obesity atlas 2023. World Obesity Day. Published March 2023. Accessed July 23, 2023. https://www.worldobesityday.org/assets/downloads/World_Obesity_Atlas_2023_Report.pdf
  5. Le MH et al. Clin Mol Hepatol. 2022;28(4):841-850. doi:10.3350/cmh.2022.0239
  6. Vilar-Gomez E et al. Gastroenterology. 2015;149(2):367-78.e5. doi:10.1053/j.gastro.2015.04.005
  7. Koutoukidis DA et al. Metabolism. 2021;115:154455. doi:10.1016/j.metabol.2020.154455
  8. Ma J et al. Gastroenterology. 2018;155(1):107-117. doi:10.1053/j.gastro.2018.03.038
  9. Ahern AL et al. Lancet. 2017;389(10085):2214-2225. doi:10.1016/S0140-6736(17)30647-5
  10. Newsome PN et al; NN9931-4296 Investigators. N Engl J Med. 2021;384(12):1113-1124. doi:10.1056/NEJMoa2028395
  11. Armstrong MJ et al. Lancet. 2016;387(10019):679-690. doi:10.1016/S0140-6736(15)00803-X
  12. Gastaldelli A et al. Lancet Diabetes Endocrinol. 2022;10(6):393-406. doi:10.1016/S2213-8587(22)00070-5
  13. Kahl S et al. Diabetes Care. 2020;43(2):298-305. doi:10.2337/dc19-0641
References
  1. Younossi ZM et al. Gastroenterology. 2021;160(3):912-918. doi:10.1053/j.astro.2020.11.051
  2. Cusi K et al. Endocr Pract. 2022;28(5):528-562. doi:10.1016/j.eprac.2022.03.010
  3. Rinella ME et al. Hepatology. 2023;77(5):1797-1835. doi:10.1097/HEP.0000000000000323
  4. World obesity atlas 2023. World Obesity Day. Published March 2023. Accessed July 23, 2023. https://www.worldobesityday.org/assets/downloads/World_Obesity_Atlas_2023_Report.pdf
  5. Le MH et al. Clin Mol Hepatol. 2022;28(4):841-850. doi:10.3350/cmh.2022.0239
  6. Vilar-Gomez E et al. Gastroenterology. 2015;149(2):367-78.e5. doi:10.1053/j.gastro.2015.04.005
  7. Koutoukidis DA et al. Metabolism. 2021;115:154455. doi:10.1016/j.metabol.2020.154455
  8. Ma J et al. Gastroenterology. 2018;155(1):107-117. doi:10.1053/j.gastro.2018.03.038
  9. Ahern AL et al. Lancet. 2017;389(10085):2214-2225. doi:10.1016/S0140-6736(17)30647-5
  10. Newsome PN et al; NN9931-4296 Investigators. N Engl J Med. 2021;384(12):1113-1124. doi:10.1056/NEJMoa2028395
  11. Armstrong MJ et al. Lancet. 2016;387(10019):679-690. doi:10.1016/S0140-6736(15)00803-X
  12. Gastaldelli A et al. Lancet Diabetes Endocrinol. 2022;10(6):393-406. doi:10.1016/S2213-8587(22)00070-5
  13. Kahl S et al. Diabetes Care. 2020;43(2):298-305. doi:10.2337/dc19-0641
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Metabolic dysfunction–associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), affects about 20% to 30% of the world population. About 1 in 4 of these patients have metabolic dysfunction–associated steatohepatitis (MASH; formerly known as nonalcoholic steatohepatitis)—which is associated with significant morbidity and mortality.

Although they affect the liver, these conditions are associated with extrahepatic diseases such as obesity, type 2 diabetes mellitus, and cardiovascular disease, which contribute to poor outcomes. Evidence has shown that weight loss is a key intervention for reduction of steatosis, MASH, and fibrosis in both lean and obese patients with MASLD. Modifications recommended for weight loss include potential pharmacological, surgical, or endoscopic approaches (in cases of severe obesity) that can prevent progression of MASLD as well as improve diabetes and reduce cardiovascular events.1-3

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The Evolving Role of Surgery for IBD

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References
  1. Gul F et al. Ann Med Surg (Lond). 2022;81:104476. doi:10.1016/j.amsu.2022.104476
  2. Kotze PG et al. Clin Colon Rectal Surg. 2021;34(3):172-180. doi:10.1055/s-0040-1718685
  3. Bemelman WA; S-ECCO collaborators. J Crohns Colitis. 2018;12(8):1005-1007. doi:10.1093/ecco-jcc/jjy056
  4. Ricci C et al. Dig Liver Dis. 2008;40(suppl 2):S285-S288. doi:10.1016/S1590-8658(08)60539-3
  5. Lin X et al. Therap Adv Gastroenterol. 2022;15:17562848221104951. doi:10.1177/17562848221104951
  6. Parigi TL et al. Dis Colon Rectum. 2022;65(suppl 1):S119-S128. doi:10.1097/DCR.0000000000002548
  7. Pilonis ND et al. Transl Gastroenterol Hepatol. 2022;7:7. doi:10.21037/tgh.2020.04.02
  8. Misawa M et al. Clin Endosc. 2021;54(4):455-463. doi:10.5946/ce.2021.165
  9. de Sousa HT et al. Curr Opin Gastroenterol. 2018;34(4):194-207. doi:10.1097/MOG.0000000000000440
  10. Whitehead A, Cataldo PA. Clin Colon Rectal Surg. 2017;30(3):162-171. doi:10.1055/s-0037-1598156
  11. Cannon LM. The use of enhanced recovery pathways in patients undergoing surgery for inflammatory bowel disease. In: Hyman N, Fleshner P, Strong S, eds Mastery of IBD Surgery. Chicago, IL: University of Chicago Press; 2019:29-38. doi:10.1007/978-3-030-16755-4_4
  12. Ljungqvist O et al. World J Surg. 2020;44(10):3197–3198. doi:10.1007/s00268-020-05734-5
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References
  1. Gul F et al. Ann Med Surg (Lond). 2022;81:104476. doi:10.1016/j.amsu.2022.104476
  2. Kotze PG et al. Clin Colon Rectal Surg. 2021;34(3):172-180. doi:10.1055/s-0040-1718685
  3. Bemelman WA; S-ECCO collaborators. J Crohns Colitis. 2018;12(8):1005-1007. doi:10.1093/ecco-jcc/jjy056
  4. Ricci C et al. Dig Liver Dis. 2008;40(suppl 2):S285-S288. doi:10.1016/S1590-8658(08)60539-3
  5. Lin X et al. Therap Adv Gastroenterol. 2022;15:17562848221104951. doi:10.1177/17562848221104951
  6. Parigi TL et al. Dis Colon Rectum. 2022;65(suppl 1):S119-S128. doi:10.1097/DCR.0000000000002548
  7. Pilonis ND et al. Transl Gastroenterol Hepatol. 2022;7:7. doi:10.21037/tgh.2020.04.02
  8. Misawa M et al. Clin Endosc. 2021;54(4):455-463. doi:10.5946/ce.2021.165
  9. de Sousa HT et al. Curr Opin Gastroenterol. 2018;34(4):194-207. doi:10.1097/MOG.0000000000000440
  10. Whitehead A, Cataldo PA. Clin Colon Rectal Surg. 2017;30(3):162-171. doi:10.1055/s-0037-1598156
  11. Cannon LM. The use of enhanced recovery pathways in patients undergoing surgery for inflammatory bowel disease. In: Hyman N, Fleshner P, Strong S, eds Mastery of IBD Surgery. Chicago, IL: University of Chicago Press; 2019:29-38. doi:10.1007/978-3-030-16755-4_4
  12. Ljungqvist O et al. World J Surg. 2020;44(10):3197–3198. doi:10.1007/s00268-020-05734-5
References
  1. Gul F et al. Ann Med Surg (Lond). 2022;81:104476. doi:10.1016/j.amsu.2022.104476
  2. Kotze PG et al. Clin Colon Rectal Surg. 2021;34(3):172-180. doi:10.1055/s-0040-1718685
  3. Bemelman WA; S-ECCO collaborators. J Crohns Colitis. 2018;12(8):1005-1007. doi:10.1093/ecco-jcc/jjy056
  4. Ricci C et al. Dig Liver Dis. 2008;40(suppl 2):S285-S288. doi:10.1016/S1590-8658(08)60539-3
  5. Lin X et al. Therap Adv Gastroenterol. 2022;15:17562848221104951. doi:10.1177/17562848221104951
  6. Parigi TL et al. Dis Colon Rectum. 2022;65(suppl 1):S119-S128. doi:10.1097/DCR.0000000000002548
  7. Pilonis ND et al. Transl Gastroenterol Hepatol. 2022;7:7. doi:10.21037/tgh.2020.04.02
  8. Misawa M et al. Clin Endosc. 2021;54(4):455-463. doi:10.5946/ce.2021.165
  9. de Sousa HT et al. Curr Opin Gastroenterol. 2018;34(4):194-207. doi:10.1097/MOG.0000000000000440
  10. Whitehead A, Cataldo PA. Clin Colon Rectal Surg. 2017;30(3):162-171. doi:10.1055/s-0037-1598156
  11. Cannon LM. The use of enhanced recovery pathways in patients undergoing surgery for inflammatory bowel disease. In: Hyman N, Fleshner P, Strong S, eds Mastery of IBD Surgery. Chicago, IL: University of Chicago Press; 2019:29-38. doi:10.1007/978-3-030-16755-4_4
  12. Ljungqvist O et al. World J Surg. 2020;44(10):3197–3198. doi:10.1007/s00268-020-05734-5
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IBD can involve chronic inflammation of the GI tract that can lead to severe complications. Although surgery is not the first-line treatment for IBD, it may need to be considered in certain situations, such as when medication and other measures are ineffective, or in cases of certain disease manifestations.

Surgical options have evolved significantly over the years, with advancements in techniques, technologies, and perioperative care that have helped improve outcomes, reduce complications, and enhance quality of life for patients—especially with minimally invasive surgery (MIS) approaches. MIS procedures for IBD include multiport laparoscopy and robotics.1,2 Now, colorectal surgeons have specialized to treat IBD—especially in MIS fashion when applicable.3

Successful IBD management requires a collaborative approach—and surgeons play a crucial role within this framework.4 A multidisciplinary approach ensures that individuals with IBD receive comprehensive care that integrates medical, surgical, and supportive interventions (ie, nutrition, mental health, and peer support)—maximizing treatment outcomes, minimizing complications, and improving the overall quality of life for patients with IBD who require surgery.

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Hyperpigmented lesion on palm

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Hyperpigmented lesion on palm

Hyperpigmented lesion on palm

This patient had a posttraumatic tache noir (also known as talon noir on the volar aspect of the feet); it is a subcorneal hematoma. The diagnosis is made clinically. Dermoscopic evaluation of tache/talon noir will reveal “pebbles on a ridge” or “satellite globules.” Confirmation of tache/talon noir can be made by paring the corneum with a #15 blade, which will reveal blood in the shavings and punctate lesions.1

This patient noted that the knob of his baseball bat rubbed the hypothenar eminence of his nondominant hand when he took a swing. The sheer force of the knob led to the subcorneal hematoma. Tache noir was high on the differential due to his physician’s clinical experience with similar cases. Tache noir occurs predominantly in people ages 12 to 24 years, without regard to gender.2 The condition is commonly found in athletes who participate in baseball, cricket, racquet sports, weightlifting, and rock climbing.2-4

Talon noir occurs most commonly in athletes who are frequently jumping, turning, and pivoting, as in football, basketball, tennis, and lacrosse.

Tache noir can be differentiated from other conditions by the presence of preserved architecture of the skin surface and punctate capillaries beneath the stratum corneum. The differential diagnosis includes verruca vulgaris, acral melanoma, and a traumatic tattoo.

Talon/tache noir are benign conditions that do not require treatment and do not affect sports performance. The lesion will usually self-resolve within a matter of weeks from onset or can even be gently scraped with a sterile needle or blade.

This patient was advised that the lesion would resolve on its own. His knee pain was determined to be a simple case of patellofemoral syndrome or “runner’s knee” and he opted to complete a home exercise program to obtain relief.

‌

This case was adapted from: Warden D. Hyperpigmented lesion on left palm. J Fam Pract. 2021;70:459-460. Photos courtesy of Daniel Warden, MD

References

1. Googe AB, Schulmeier JS, Jackson AR, et al. Talon noir: paring can eliminate the need for biopsy. Postgrad Med J. 2014;90:730-731. doi: 10.1136/postgradmedj-2014-132996

2. Burkhart C, Nguyen N. Talon noire. Dermatology Advisor. Accessed October 19, 2021. www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/talon-noire-black-heel-calcaneal-petechiae-runners-heel-basketball-heel-tennis-heel-hyperkeratosis-hemorrhagica-pseudochromhidrosis-plantaris-chromidrose-plantaire-eccrine-intracorne/

3. Talon noir. Primary Care Dermatology Society. Updated August 1, 2021. Accessed October 19, 2021. www.pcds.org.uk/clinical-guidance/talon-noir

4. Birrer RB, Griesemer BA, Cataletto MB, eds. Pediatric Sports Medicine for Primary Care. Lippincott Williams & Wilkins; 2002.

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Hyperpigmented lesion on palm

This patient had a posttraumatic tache noir (also known as talon noir on the volar aspect of the feet); it is a subcorneal hematoma. The diagnosis is made clinically. Dermoscopic evaluation of tache/talon noir will reveal “pebbles on a ridge” or “satellite globules.” Confirmation of tache/talon noir can be made by paring the corneum with a #15 blade, which will reveal blood in the shavings and punctate lesions.1

This patient noted that the knob of his baseball bat rubbed the hypothenar eminence of his nondominant hand when he took a swing. The sheer force of the knob led to the subcorneal hematoma. Tache noir was high on the differential due to his physician’s clinical experience with similar cases. Tache noir occurs predominantly in people ages 12 to 24 years, without regard to gender.2 The condition is commonly found in athletes who participate in baseball, cricket, racquet sports, weightlifting, and rock climbing.2-4

Talon noir occurs most commonly in athletes who are frequently jumping, turning, and pivoting, as in football, basketball, tennis, and lacrosse.

Tache noir can be differentiated from other conditions by the presence of preserved architecture of the skin surface and punctate capillaries beneath the stratum corneum. The differential diagnosis includes verruca vulgaris, acral melanoma, and a traumatic tattoo.

Talon/tache noir are benign conditions that do not require treatment and do not affect sports performance. The lesion will usually self-resolve within a matter of weeks from onset or can even be gently scraped with a sterile needle or blade.

This patient was advised that the lesion would resolve on its own. His knee pain was determined to be a simple case of patellofemoral syndrome or “runner’s knee” and he opted to complete a home exercise program to obtain relief.

‌

This case was adapted from: Warden D. Hyperpigmented lesion on left palm. J Fam Pract. 2021;70:459-460. Photos courtesy of Daniel Warden, MD

Hyperpigmented lesion on palm

This patient had a posttraumatic tache noir (also known as talon noir on the volar aspect of the feet); it is a subcorneal hematoma. The diagnosis is made clinically. Dermoscopic evaluation of tache/talon noir will reveal “pebbles on a ridge” or “satellite globules.” Confirmation of tache/talon noir can be made by paring the corneum with a #15 blade, which will reveal blood in the shavings and punctate lesions.1

This patient noted that the knob of his baseball bat rubbed the hypothenar eminence of his nondominant hand when he took a swing. The sheer force of the knob led to the subcorneal hematoma. Tache noir was high on the differential due to his physician’s clinical experience with similar cases. Tache noir occurs predominantly in people ages 12 to 24 years, without regard to gender.2 The condition is commonly found in athletes who participate in baseball, cricket, racquet sports, weightlifting, and rock climbing.2-4

Talon noir occurs most commonly in athletes who are frequently jumping, turning, and pivoting, as in football, basketball, tennis, and lacrosse.

Tache noir can be differentiated from other conditions by the presence of preserved architecture of the skin surface and punctate capillaries beneath the stratum corneum. The differential diagnosis includes verruca vulgaris, acral melanoma, and a traumatic tattoo.

Talon/tache noir are benign conditions that do not require treatment and do not affect sports performance. The lesion will usually self-resolve within a matter of weeks from onset or can even be gently scraped with a sterile needle or blade.

This patient was advised that the lesion would resolve on its own. His knee pain was determined to be a simple case of patellofemoral syndrome or “runner’s knee” and he opted to complete a home exercise program to obtain relief.

‌

This case was adapted from: Warden D. Hyperpigmented lesion on left palm. J Fam Pract. 2021;70:459-460. Photos courtesy of Daniel Warden, MD

References

1. Googe AB, Schulmeier JS, Jackson AR, et al. Talon noir: paring can eliminate the need for biopsy. Postgrad Med J. 2014;90:730-731. doi: 10.1136/postgradmedj-2014-132996

2. Burkhart C, Nguyen N. Talon noire. Dermatology Advisor. Accessed October 19, 2021. www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/talon-noire-black-heel-calcaneal-petechiae-runners-heel-basketball-heel-tennis-heel-hyperkeratosis-hemorrhagica-pseudochromhidrosis-plantaris-chromidrose-plantaire-eccrine-intracorne/

3. Talon noir. Primary Care Dermatology Society. Updated August 1, 2021. Accessed October 19, 2021. www.pcds.org.uk/clinical-guidance/talon-noir

4. Birrer RB, Griesemer BA, Cataletto MB, eds. Pediatric Sports Medicine for Primary Care. Lippincott Williams & Wilkins; 2002.

References

1. Googe AB, Schulmeier JS, Jackson AR, et al. Talon noir: paring can eliminate the need for biopsy. Postgrad Med J. 2014;90:730-731. doi: 10.1136/postgradmedj-2014-132996

2. Burkhart C, Nguyen N. Talon noire. Dermatology Advisor. Accessed October 19, 2021. www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/talon-noire-black-heel-calcaneal-petechiae-runners-heel-basketball-heel-tennis-heel-hyperkeratosis-hemorrhagica-pseudochromhidrosis-plantaris-chromidrose-plantaire-eccrine-intracorne/

3. Talon noir. Primary Care Dermatology Society. Updated August 1, 2021. Accessed October 19, 2021. www.pcds.org.uk/clinical-guidance/talon-noir

4. Birrer RB, Griesemer BA, Cataletto MB, eds. Pediatric Sports Medicine for Primary Care. Lippincott Williams & Wilkins; 2002.

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Gastroenterology and Climate Change: Assessing and Mitigating Impacts

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Gastroenterology and Climate Change: Assessing and Mitigating Impacts
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Swapna Gayam, MD, FACG

Click to view more from Gastroenterology Data Trends 2023. 

References
  1. Karliner J et al. Eur J Public Health. 2020;30(suppl 5):v311. doi:10.1093/eurpub/ckaa165.843
  2. Vaccari M et al. Waste Manag Res. 2018;36(1):39-47. doi:10.1177/0734242X17739968
  3. Peery AF et al. Gastroenterology. 2019;156(1):254-272.e11. doi:10.1053/j.gastro.2018.08.063
  4. Sorge A et al. Endoscopy. 2023;55(suppl 2):S72-S73. https://www.esge.com/assets/downloads/pdfs/guidelines/ESGE_Days_2023.pdf
  5. Maurice JB et al. Lancet Gastroenterol Hepatol. 2020;5(7):636-638. doi:10.1016/S2468-1253(20)30157-6
  6. Gayam S. Am J Gastroenterol. 2020;115(12):1931-1932. doi:10.14309/ajg.0000000000001005
  7. Siau K et al. Tech Innov Gastrointest Endosc. 2021;23(4):344-352. doi:10.1016/j.tige.2021.06.005
  8. Namburar S et al. Gut. 2022;71(7):1326-1331. doi:10.1136/gutjnl-2021-324729
  9. Haddock R et al. Am J Gastroenterol. 2022;117(3):394-400. doi:10.14309/ajg.0000000000001604
  10. Donnelly MC et al. J Hepatol. 2022;76(5):995-1000. doi:10.1016/j.jhep.2022.02.01
  11. Leddin D, Macrae F. J Clin Gastroenterol. 2020;54(5):393-397. doi:10.1097/MCG.0000000000001336
  12. Pohl H et al. Hepatology. 2022;76(6):1836-1844. doi:10.1002/hep.32810
  13. Rodríguez de Santiago E et al. Endoscopy. 2022;54(8):797-826. doi:10.1055/a-1859-3726
  14. Sebastian S et al. Gut. 2023;72(1):12-26. doi:10.1136/gutjnl-2022-328460
  15. Cunha Neves JA et al. Gut. 2023;72(2):306-313. doi:10.1136/gutjnl-2022-327005
  16. Kaplan S et al. Issue Brief (Commonw Fund). 2012;29:1-14. PMID:23214181
  17. López-Muñoz P et al. Gut. 2023;gutjnl-2023-329544. doi:10.1136/gutjnl-2023-329544
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West Virginia University
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Click to view more from Gastroenterology Data Trends 2023. 

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References
  1. Karliner J et al. Eur J Public Health. 2020;30(suppl 5):v311. doi:10.1093/eurpub/ckaa165.843
  2. Vaccari M et al. Waste Manag Res. 2018;36(1):39-47. doi:10.1177/0734242X17739968
  3. Peery AF et al. Gastroenterology. 2019;156(1):254-272.e11. doi:10.1053/j.gastro.2018.08.063
  4. Sorge A et al. Endoscopy. 2023;55(suppl 2):S72-S73. https://www.esge.com/assets/downloads/pdfs/guidelines/ESGE_Days_2023.pdf
  5. Maurice JB et al. Lancet Gastroenterol Hepatol. 2020;5(7):636-638. doi:10.1016/S2468-1253(20)30157-6
  6. Gayam S. Am J Gastroenterol. 2020;115(12):1931-1932. doi:10.14309/ajg.0000000000001005
  7. Siau K et al. Tech Innov Gastrointest Endosc. 2021;23(4):344-352. doi:10.1016/j.tige.2021.06.005
  8. Namburar S et al. Gut. 2022;71(7):1326-1331. doi:10.1136/gutjnl-2021-324729
  9. Haddock R et al. Am J Gastroenterol. 2022;117(3):394-400. doi:10.14309/ajg.0000000000001604
  10. Donnelly MC et al. J Hepatol. 2022;76(5):995-1000. doi:10.1016/j.jhep.2022.02.01
  11. Leddin D, Macrae F. J Clin Gastroenterol. 2020;54(5):393-397. doi:10.1097/MCG.0000000000001336
  12. Pohl H et al. Hepatology. 2022;76(6):1836-1844. doi:10.1002/hep.32810
  13. Rodríguez de Santiago E et al. Endoscopy. 2022;54(8):797-826. doi:10.1055/a-1859-3726
  14. Sebastian S et al. Gut. 2023;72(1):12-26. doi:10.1136/gutjnl-2022-328460
  15. Cunha Neves JA et al. Gut. 2023;72(2):306-313. doi:10.1136/gutjnl-2022-327005
  16. Kaplan S et al. Issue Brief (Commonw Fund). 2012;29:1-14. PMID:23214181
  17. López-Muñoz P et al. Gut. 2023;gutjnl-2023-329544. doi:10.1136/gutjnl-2023-329544
References
  1. Karliner J et al. Eur J Public Health. 2020;30(suppl 5):v311. doi:10.1093/eurpub/ckaa165.843
  2. Vaccari M et al. Waste Manag Res. 2018;36(1):39-47. doi:10.1177/0734242X17739968
  3. Peery AF et al. Gastroenterology. 2019;156(1):254-272.e11. doi:10.1053/j.gastro.2018.08.063
  4. Sorge A et al. Endoscopy. 2023;55(suppl 2):S72-S73. https://www.esge.com/assets/downloads/pdfs/guidelines/ESGE_Days_2023.pdf
  5. Maurice JB et al. Lancet Gastroenterol Hepatol. 2020;5(7):636-638. doi:10.1016/S2468-1253(20)30157-6
  6. Gayam S. Am J Gastroenterol. 2020;115(12):1931-1932. doi:10.14309/ajg.0000000000001005
  7. Siau K et al. Tech Innov Gastrointest Endosc. 2021;23(4):344-352. doi:10.1016/j.tige.2021.06.005
  8. Namburar S et al. Gut. 2022;71(7):1326-1331. doi:10.1136/gutjnl-2021-324729
  9. Haddock R et al. Am J Gastroenterol. 2022;117(3):394-400. doi:10.14309/ajg.0000000000001604
  10. Donnelly MC et al. J Hepatol. 2022;76(5):995-1000. doi:10.1016/j.jhep.2022.02.01
  11. Leddin D, Macrae F. J Clin Gastroenterol. 2020;54(5):393-397. doi:10.1097/MCG.0000000000001336
  12. Pohl H et al. Hepatology. 2022;76(6):1836-1844. doi:10.1002/hep.32810
  13. Rodríguez de Santiago E et al. Endoscopy. 2022;54(8):797-826. doi:10.1055/a-1859-3726
  14. Sebastian S et al. Gut. 2023;72(1):12-26. doi:10.1136/gutjnl-2022-328460
  15. Cunha Neves JA et al. Gut. 2023;72(2):306-313. doi:10.1136/gutjnl-2022-327005
  16. Kaplan S et al. Issue Brief (Commonw Fund). 2012;29:1-14. PMID:23214181
  17. López-Muñoz P et al. Gut. 2023;gutjnl-2023-329544. doi:10.1136/gutjnl-2023-329544
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The health care industry, particularly in the United States, is a large contributor to climate change, with the field of GI being one of the top contributors to overall and hazardous waste emissions.1,2 One of the most important components of the carbon footprint of GI is the sheer volume of procedures performed. More than 18 million endoscopic procedures are performed each year in the US alone, and a significant portion are of low-value.3,4 Every endoscopic procedure uses substantial resources, including single-use consumables, water (including sterile water bottles), electricity, paper, and personal protective equipment (PPE), among others.5-7 Within the field of endoscopy, disposable endoscopes are an important area of concern; a complete switch to disposables could increase waste by up to 40%.8 Along with the impact of GI on climate change, there is also a bidirectional effect—climate change affects GI and liver health, worsening symptoms for many.9-11

To combat the contribution of GI to climate change, a GI multisociety task force was formed comprising members from 4 major US societies, including the AGA.12 A strategic plan was proposed to decrease the carbon footprint of GI, similar to a plan proposed by European and British societies.13,14 Multiple recent studies have shown positive effects of interventions such as waste segregation in reducing overall endoscopic waste and increasing recycled waste.15 Such measures also have been shown to have financial benefits, with estimated cost savings of around $5.4 billion dollars in 5 years.16

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References
  1. Jin Z et al. BioMed Eng OnLine. 2022;21(1):12. doi:10.1186/s12938-022-00979-
  2. Buendgens L, Cifci D, Ghaffari Laleh N, et al. Sci Rep. 2022;12(1):4829. doi:10.1038/s41598-022-08773-1
  3. Uche-Anya EN, Berzin TM. Artificial intelligence applications in colonoscopy. GI & Hepatology News. January 24, 2023. https://www.mdedge.com/gihepnews/article/260769/mixed-topics/artificial-intelligence-applications-colonoscopy
  4. Rondonotti E et al. Endoscopy. 2023;55(1):14-22. doi:10.1055/a-1852-0330
  5. Antonelli G et al. Ann Gastroenterol. 2023;36(2):114-122. doi:10.20524/aog.2023.0781
  6. van der Zander QEW et al. Endoscopy. 2021;53(12):1219-1226. doi:10.1055/a-1343-159
  7. Areia PM et al. Lancet Digital Health. 2022;4(6):e436-e444. doi:10.1016/S2589-7500(22)00042-5
  8. Sumiyama K et al. Dig Endosc. 2021;33(2):218-230. doi:10.1111/den.13837
  9. Berzin TM et al. Gastrointest Endosc. 2020;92(4):951-959. doi:10.1016/j.gie.2020.06.035
  10. Mori Y et al. Dig Endosc. 2023;35(4):422-429. doi:10.1111/den.14531
  11. Uche-Anya E et al. Gut. 2022;71(9):1909-1915. doi:10.1136/gutjnl-2021-326271
  12. Moor M et al. Nature. 2023;616(7956):259-265. 10.1038/s41586-023-05881-4
  13. Kather JN et al. NPJ Digit Med. 2022;5(1):90. doi:10.1038/s41746-022-00634-5
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References
  1. Jin Z et al. BioMed Eng OnLine. 2022;21(1):12. doi:10.1186/s12938-022-00979-
  2. Buendgens L, Cifci D, Ghaffari Laleh N, et al. Sci Rep. 2022;12(1):4829. doi:10.1038/s41598-022-08773-1
  3. Uche-Anya EN, Berzin TM. Artificial intelligence applications in colonoscopy. GI & Hepatology News. January 24, 2023. https://www.mdedge.com/gihepnews/article/260769/mixed-topics/artificial-intelligence-applications-colonoscopy
  4. Rondonotti E et al. Endoscopy. 2023;55(1):14-22. doi:10.1055/a-1852-0330
  5. Antonelli G et al. Ann Gastroenterol. 2023;36(2):114-122. doi:10.20524/aog.2023.0781
  6. van der Zander QEW et al. Endoscopy. 2021;53(12):1219-1226. doi:10.1055/a-1343-159
  7. Areia PM et al. Lancet Digital Health. 2022;4(6):e436-e444. doi:10.1016/S2589-7500(22)00042-5
  8. Sumiyama K et al. Dig Endosc. 2021;33(2):218-230. doi:10.1111/den.13837
  9. Berzin TM et al. Gastrointest Endosc. 2020;92(4):951-959. doi:10.1016/j.gie.2020.06.035
  10. Mori Y et al. Dig Endosc. 2023;35(4):422-429. doi:10.1111/den.14531
  11. Uche-Anya E et al. Gut. 2022;71(9):1909-1915. doi:10.1136/gutjnl-2021-326271
  12. Moor M et al. Nature. 2023;616(7956):259-265. 10.1038/s41586-023-05881-4
  13. Kather JN et al. NPJ Digit Med. 2022;5(1):90. doi:10.1038/s41746-022-00634-5
References
  1. Jin Z et al. BioMed Eng OnLine. 2022;21(1):12. doi:10.1186/s12938-022-00979-
  2. Buendgens L, Cifci D, Ghaffari Laleh N, et al. Sci Rep. 2022;12(1):4829. doi:10.1038/s41598-022-08773-1
  3. Uche-Anya EN, Berzin TM. Artificial intelligence applications in colonoscopy. GI & Hepatology News. January 24, 2023. https://www.mdedge.com/gihepnews/article/260769/mixed-topics/artificial-intelligence-applications-colonoscopy
  4. Rondonotti E et al. Endoscopy. 2023;55(1):14-22. doi:10.1055/a-1852-0330
  5. Antonelli G et al. Ann Gastroenterol. 2023;36(2):114-122. doi:10.20524/aog.2023.0781
  6. van der Zander QEW et al. Endoscopy. 2021;53(12):1219-1226. doi:10.1055/a-1343-159
  7. Areia PM et al. Lancet Digital Health. 2022;4(6):e436-e444. doi:10.1016/S2589-7500(22)00042-5
  8. Sumiyama K et al. Dig Endosc. 2021;33(2):218-230. doi:10.1111/den.13837
  9. Berzin TM et al. Gastrointest Endosc. 2020;92(4):951-959. doi:10.1016/j.gie.2020.06.035
  10. Mori Y et al. Dig Endosc. 2023;35(4):422-429. doi:10.1111/den.14531
  11. Uche-Anya E et al. Gut. 2022;71(9):1909-1915. doi:10.1136/gutjnl-2021-326271
  12. Moor M et al. Nature. 2023;616(7956):259-265. 10.1038/s41586-023-05881-4
  13. Kather JN et al. NPJ Digit Med. 2022;5(1):90. doi:10.1038/s41746-022-00634-5
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The availability of AI technologies to improve the overall quality of GI endoscopy has grown significantly over the last decade.1 AI algorithms have shown promise in detecting malignant, infectious, and inflammatory diseases in both upper and lower GI endoscopy imaging.2 Most AI research in endoscopy is currently focused on computer-aided detection (CADe) and diagnosis (CADx), but other computer vision tools are also in development, ranging from algorithms to measure IBD activity to dysplasia detection in Barrett's esophagus.2,3 

Improved lesion detection and classification with AI can support clinical decision-making and lead to better patient outcomes, cost savings, clinician time management, and other efficiencies within the health care system.2-7 However, some substantial barriers must be overcome and current projections must be validated with clinical and real-world trials before we can fully rely on AI in these settings.8-11

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References
  1. Di Bella S et al. Toxins (Basel). 2016;8(5):134. doi:10.3390/toxins8050134
  2. Turner NA, Anderson DJ. Clin Colon Rectal Surg. 2020;33(2):98-108. doi:10.1055/s-0040-1701234
  3. Czepiel J et al. Eur J Clin Microbiol Infect Dis. 2019;38(7):1211-1221. doi:10.1007/s10096-019-03539-6
  4. Sekirov I et al. Gut microbiota in health and disease. Physiol Rev. 2012;90(3):859-904. doi:10.1152/physrev.00045.2009
  5. Posteraro B et al. Expert Opin Biol Ther. 2018;18(4):469-476. doi:10.1080/14712598.2018.1452908
  6. Khanna S. J Intern Med. 2021;290(2):294-309. doi:10.1111/joim.13290
  7. Seekatz AM et al . Therap Adv Gastroenterol. 2022;15:17562848221134396. doi:10.1177/17562848221134396
  8. Federal Drug Administration. FDA approves first fecal microbiota product: Rebyota approved for the prevention of recurrence of Clostridioides difficile infection in adults [press release]. Published November 30, 2022. Accessed July 14, 2023. https://www.fda.gov/news-events/press-announcements/fda-approves-first-fecal-microbiota-product
  9. Bafeta A et al. Ann Intern Med. 2017;167(1):34-39. doi:10.7326/M16-2810
  10. Guh AY et al; Emerging Infections Program Clostridioides difficile Infection Working Group. N Engl J Med. 2020;382(14):1320-1330. doi:10.1056/NEJMoa1910215
  11. Centers for Disease Control and Prevention. What is C. diff? Last reviewed September 7, 2022. Accessed July 14, 2023. https://www.cdc.gov/cdiff/what-is.html
  12. Centers for Disease Control and Prevention. Patients and families: be antibiotics aware. C. diff infection—Am I at risk? Accessed July 14, 2023. https://www.cdc.gov/cdiff/pdf/FS-Cdiff-PatientsFamilies-508.pdf
  13. Centers for Disease Control and Prevention. 2019 annual report for the emerging infections program for Clostridioides difficile infection. Last reviewed February 1, 2023. Accessed July 14, 2023. https://www.cdc.gov/hai/eip/Annual-CDI-Report-2019.html
  14. Kelly CR et al. Am J Gastroenterol. 2021;116(6):1124-1147. doi:10.14309/ajg.0000000000001278
  15. Tariq R et al. Therap Adv Gastroenterol. 2021;14:1756284821994046. doi:10.1177/1756284821994046
  16. McDonald LC et al. Clin Infect Dis. 2018;66(7):e1-e48. doi:10.1093/cid/cix1085
  17. Wilcox MH et al. N Engl J Med. 2017;376(4):305-317. doi:10.1056/NEJMoa1602615
  18. Guilleman MM et al. Gene Ther. 2023;30:455-462. doi:10.1038/s41434-021-00236-y
  19. Sims MD et al; ECOSPOR IV Investigators. JAMA Netw Open. 2023;6(2):e2255758. doi:10.1001/jamanetworkopen.2022.55758
  20. Microbiota Restoration Therapy for Recurrent Clostridium Difficile Infection (PUNCHCD2). ClinicalTrials.gov identifier: NCT02299570. Updated January 2021. Accessed August 2023. https://classic.clinicaltrials.gov/ct2/show/results/NCT02299570
  21. Khanna S et al. Clin Infect Dis. 2021;73(7):e1613-e1620. doi:10.1093/cid/ciaa1430
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References
  1. Di Bella S et al. Toxins (Basel). 2016;8(5):134. doi:10.3390/toxins8050134
  2. Turner NA, Anderson DJ. Clin Colon Rectal Surg. 2020;33(2):98-108. doi:10.1055/s-0040-1701234
  3. Czepiel J et al. Eur J Clin Microbiol Infect Dis. 2019;38(7):1211-1221. doi:10.1007/s10096-019-03539-6
  4. Sekirov I et al. Gut microbiota in health and disease. Physiol Rev. 2012;90(3):859-904. doi:10.1152/physrev.00045.2009
  5. Posteraro B et al. Expert Opin Biol Ther. 2018;18(4):469-476. doi:10.1080/14712598.2018.1452908
  6. Khanna S. J Intern Med. 2021;290(2):294-309. doi:10.1111/joim.13290
  7. Seekatz AM et al . Therap Adv Gastroenterol. 2022;15:17562848221134396. doi:10.1177/17562848221134396
  8. Federal Drug Administration. FDA approves first fecal microbiota product: Rebyota approved for the prevention of recurrence of Clostridioides difficile infection in adults [press release]. Published November 30, 2022. Accessed July 14, 2023. https://www.fda.gov/news-events/press-announcements/fda-approves-first-fecal-microbiota-product
  9. Bafeta A et al. Ann Intern Med. 2017;167(1):34-39. doi:10.7326/M16-2810
  10. Guh AY et al; Emerging Infections Program Clostridioides difficile Infection Working Group. N Engl J Med. 2020;382(14):1320-1330. doi:10.1056/NEJMoa1910215
  11. Centers for Disease Control and Prevention. What is C. diff? Last reviewed September 7, 2022. Accessed July 14, 2023. https://www.cdc.gov/cdiff/what-is.html
  12. Centers for Disease Control and Prevention. Patients and families: be antibiotics aware. C. diff infection—Am I at risk? Accessed July 14, 2023. https://www.cdc.gov/cdiff/pdf/FS-Cdiff-PatientsFamilies-508.pdf
  13. Centers for Disease Control and Prevention. 2019 annual report for the emerging infections program for Clostridioides difficile infection. Last reviewed February 1, 2023. Accessed July 14, 2023. https://www.cdc.gov/hai/eip/Annual-CDI-Report-2019.html
  14. Kelly CR et al. Am J Gastroenterol. 2021;116(6):1124-1147. doi:10.14309/ajg.0000000000001278
  15. Tariq R et al. Therap Adv Gastroenterol. 2021;14:1756284821994046. doi:10.1177/1756284821994046
  16. McDonald LC et al. Clin Infect Dis. 2018;66(7):e1-e48. doi:10.1093/cid/cix1085
  17. Wilcox MH et al. N Engl J Med. 2017;376(4):305-317. doi:10.1056/NEJMoa1602615
  18. Guilleman MM et al. Gene Ther. 2023;30:455-462. doi:10.1038/s41434-021-00236-y
  19. Sims MD et al; ECOSPOR IV Investigators. JAMA Netw Open. 2023;6(2):e2255758. doi:10.1001/jamanetworkopen.2022.55758
  20. Microbiota Restoration Therapy for Recurrent Clostridium Difficile Infection (PUNCHCD2). ClinicalTrials.gov identifier: NCT02299570. Updated January 2021. Accessed August 2023. https://classic.clinicaltrials.gov/ct2/show/results/NCT02299570
  21. Khanna S et al. Clin Infect Dis. 2021;73(7):e1613-e1620. doi:10.1093/cid/ciaa1430
References
  1. Di Bella S et al. Toxins (Basel). 2016;8(5):134. doi:10.3390/toxins8050134
  2. Turner NA, Anderson DJ. Clin Colon Rectal Surg. 2020;33(2):98-108. doi:10.1055/s-0040-1701234
  3. Czepiel J et al. Eur J Clin Microbiol Infect Dis. 2019;38(7):1211-1221. doi:10.1007/s10096-019-03539-6
  4. Sekirov I et al. Gut microbiota in health and disease. Physiol Rev. 2012;90(3):859-904. doi:10.1152/physrev.00045.2009
  5. Posteraro B et al. Expert Opin Biol Ther. 2018;18(4):469-476. doi:10.1080/14712598.2018.1452908
  6. Khanna S. J Intern Med. 2021;290(2):294-309. doi:10.1111/joim.13290
  7. Seekatz AM et al . Therap Adv Gastroenterol. 2022;15:17562848221134396. doi:10.1177/17562848221134396
  8. Federal Drug Administration. FDA approves first fecal microbiota product: Rebyota approved for the prevention of recurrence of Clostridioides difficile infection in adults [press release]. Published November 30, 2022. Accessed July 14, 2023. https://www.fda.gov/news-events/press-announcements/fda-approves-first-fecal-microbiota-product
  9. Bafeta A et al. Ann Intern Med. 2017;167(1):34-39. doi:10.7326/M16-2810
  10. Guh AY et al; Emerging Infections Program Clostridioides difficile Infection Working Group. N Engl J Med. 2020;382(14):1320-1330. doi:10.1056/NEJMoa1910215
  11. Centers for Disease Control and Prevention. What is C. diff? Last reviewed September 7, 2022. Accessed July 14, 2023. https://www.cdc.gov/cdiff/what-is.html
  12. Centers for Disease Control and Prevention. Patients and families: be antibiotics aware. C. diff infection—Am I at risk? Accessed July 14, 2023. https://www.cdc.gov/cdiff/pdf/FS-Cdiff-PatientsFamilies-508.pdf
  13. Centers for Disease Control and Prevention. 2019 annual report for the emerging infections program for Clostridioides difficile infection. Last reviewed February 1, 2023. Accessed July 14, 2023. https://www.cdc.gov/hai/eip/Annual-CDI-Report-2019.html
  14. Kelly CR et al. Am J Gastroenterol. 2021;116(6):1124-1147. doi:10.14309/ajg.0000000000001278
  15. Tariq R et al. Therap Adv Gastroenterol. 2021;14:1756284821994046. doi:10.1177/1756284821994046
  16. McDonald LC et al. Clin Infect Dis. 2018;66(7):e1-e48. doi:10.1093/cid/cix1085
  17. Wilcox MH et al. N Engl J Med. 2017;376(4):305-317. doi:10.1056/NEJMoa1602615
  18. Guilleman MM et al. Gene Ther. 2023;30:455-462. doi:10.1038/s41434-021-00236-y
  19. Sims MD et al; ECOSPOR IV Investigators. JAMA Netw Open. 2023;6(2):e2255758. doi:10.1001/jamanetworkopen.2022.55758
  20. Microbiota Restoration Therapy for Recurrent Clostridium Difficile Infection (PUNCHCD2). ClinicalTrials.gov identifier: NCT02299570. Updated January 2021. Accessed August 2023. https://classic.clinicaltrials.gov/ct2/show/results/NCT02299570
  21. Khanna S et al. Clin Infect Dis. 2021;73(7):e1613-e1620. doi:10.1093/cid/ciaa1430
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Clostridioides difficile (C difficile) is a gram-positive anaerobic bacillus that produces toxins (enterotoxin A [TcdA] and cytotoxin B [TcdB]) that can damage the lining of the gastrointestinal tract and cause potentially life-threatening disease of the large intestine.1C difficile infection (CDI) is not only a common nosocomial infection, but an increasing incidence is seen in the community with a high disease burden, as reinfection often occurs.2 C difficile is very contagious and spreads easily via contaminated surfaces that act as reservoirs (especially in healthcare settings); the spores of this bacterium are very hard to kill.3

CDI often occurs either while the patient is taking antibiotics or soon after finishing them, as the intestinal (gut) microbiome and metabolism are altered, which allows for C difficile to proliferate.4 People with a compromised immune system or other comorbid conditions, or who are older than 65 years of age, are especially prone to CDI.1

Antibiotics are the first-line treatment for primary and recurrent CDI (rCDI), although they do not always kill the spores,3 and the dysbiosis caused by antibiotics within the gut environment still needs to be addressed.4 A humanized monoclonal antibody (an immunoglobulin G against the cytotoxin B), in combination with antibiotics, has been shown to help prevent rCDI in a subset of patients.5

Therapies that help restore the gut microbiota to a eubiotic state, especially after antibiotic treatment for C difficile, have been shown to help manage and prevent future rCDI. Experimental fecal microbiota transplantatio (FMT) performed under enforcement discretion from the FDA is one such microbiota restoration therapy.3 Microbes harvested from healthy donor stool are transplanted into the intestine of a recipient (usually via colonoscopy) to help restore the gut microbiome and prevent CDI.7

Two therapeutics are approved by the FDA for prevention of rCDI. The first one was approved in 2022 and is a rectal administration product derived from human donor stool (fecal microbiota live-jslm [Rebyota]).8 The other is an oral capsule (fecal microbiota spores live-bprk [Vowst]) containing live spores from fecal microbiota.6 With these exciting advances, we can now begin to address additional unmet needs with future research into microbiota restoration therapies.9

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Gastroenterology Data Trends 2023

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GI&Hepatology News and the American Gastroenterological Association present the 2023 issue of Gastroenterology Data Trends, a special report on hot topics in gastroenterology told through original infographics and visual storytelling.

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GI&Hepatology News and the American Gastroenterological Association present the 2023 issue of Gastroenterology Data Trends, a special report on hot topics in gastroenterology told through original infographics and visual storytelling.

In this issue:

GI&Hepatology News and the American Gastroenterological Association present the 2023 issue of Gastroenterology Data Trends, a special report on hot topics in gastroenterology told through original infographics and visual storytelling.

In this issue:

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GI Oncology
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Germline Genetic Testing in CRC: Implications for Familial and Population-Based Testing

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Germline Genetic Testing in CRC: Implications for Familial and Population-Based Testing
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References
  1. Weiss JM et al. J Natl Compr Canc Netw. 2021;19(10):1122-1132. doi:10.1164/jnccn.2021.0048
  2. Samadder NJ et al. JAMA Oncol. 2021;7(2):230-237. doi:10.1001/jamaoncol.2020.6252
  3. Pearlman R et al; Ohio Colorectal Cancer Prevention Initiative Study Group. JAMA Oncol. 2017;3(4):464-471. doi:10.1001/jamaoncol.2016.5194
  4. Stoffel EM et al. Gastroenterology. 2018;154(4):897-905.e1. doi:10.1053/j.gastro.2017.11.004
  5. Stoffel EM, Murphy CC. Gastroenterology. 2020;158(2):341-353. doi:10.1053/j.gastro.2019.07.055
  6. Cavestro GM et al; Associazione Italiana Familiarità Ereditarietà Tumori; Collaborative Group of the Americas on Inherited Gastrointestinal Cancer; European Hereditary Tumour Group, and the International Society for Gastrointestinal Hereditary Tumours. Clin Gastroenterol Hepatol. 2023;21(3):581-603.e33. doi:10.1016/j.cgh.2022.12.006
  7. Gupta S et al. Cancer. 2020;126(13):3013-3020. doi:10.1002/cncr.32851
  8. Stanich PP et al. Gastroenterology. 2021;160(5):1850-1852. doi:10.1053/j.gastro.2020.12.009
  9. Rustgi S et al. Universal screening strategies for the identification of Lynch syndrome in colorectal cancer patients and at-risk relatives. Research forum lecture #263 presented at: Digestive Disease Week (DDW) 2023; May 6-9, 2023; Chicago, IL.
  10. Tier 1 genomic applications and their importance to public health. Centers for Disease Control and Prevention. Reviewed March 6, 2014. Accessed August 15, 2023. https://www.cdc.gov/genomics/implementation/toolkit/tier1.htm
  11. Win AK et al. Cancer Epidemiol Biomarkers Prev. 2017;26(3):404-412. doi:10.1158/1055-9965.EPI-16-0693
  12. Yurgelun MB et al. J Clin Oncol. 2017;35(10):1086-1095. doi:10.1200/JCO.2016.71.0012
  13. Pearlman R et al. JCO Precis Oncol. 2021;5:PO.20.00525. doi:10.1200/PO.20.00525
  14. Patel R, Hyer W. Frontline Gastroenterol. 2019;10(4):379-387. doi:10.1136/flgastro-2018-101053
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Associate Professor of Medicine
Division of Digestive and Liver Diseases
Director, Gastrointestinal Cancer Risk and Prevention Program
Director, Muzzi Mirza Pancreatic Cancer
Prevention and Genetics Program
Columbia University Irving Medical Center
New York Presbyterian Hospital
New York, NY

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Author(s)
Fay Kastrinos, MD, MPH
Author(s)
Fay Kastrinos, MD, MPH
Author and Disclosure Information

Associate Professor of Medicine
Division of Digestive and Liver Diseases
Director, Gastrointestinal Cancer Risk and Prevention Program
Director, Muzzi Mirza Pancreatic Cancer
Prevention and Genetics Program
Columbia University Irving Medical Center
New York Presbyterian Hospital
New York, NY

Author and Disclosure Information

Associate Professor of Medicine
Division of Digestive and Liver Diseases
Director, Gastrointestinal Cancer Risk and Prevention Program
Director, Muzzi Mirza Pancreatic Cancer
Prevention and Genetics Program
Columbia University Irving Medical Center
New York Presbyterian Hospital
New York, NY

Click here to view more from Gastroenterology Data Trends 2023. 

Click here to view more from Gastroenterology Data Trends 2023. 

References
  1. Weiss JM et al. J Natl Compr Canc Netw. 2021;19(10):1122-1132. doi:10.1164/jnccn.2021.0048
  2. Samadder NJ et al. JAMA Oncol. 2021;7(2):230-237. doi:10.1001/jamaoncol.2020.6252
  3. Pearlman R et al; Ohio Colorectal Cancer Prevention Initiative Study Group. JAMA Oncol. 2017;3(4):464-471. doi:10.1001/jamaoncol.2016.5194
  4. Stoffel EM et al. Gastroenterology. 2018;154(4):897-905.e1. doi:10.1053/j.gastro.2017.11.004
  5. Stoffel EM, Murphy CC. Gastroenterology. 2020;158(2):341-353. doi:10.1053/j.gastro.2019.07.055
  6. Cavestro GM et al; Associazione Italiana Familiarità Ereditarietà Tumori; Collaborative Group of the Americas on Inherited Gastrointestinal Cancer; European Hereditary Tumour Group, and the International Society for Gastrointestinal Hereditary Tumours. Clin Gastroenterol Hepatol. 2023;21(3):581-603.e33. doi:10.1016/j.cgh.2022.12.006
  7. Gupta S et al. Cancer. 2020;126(13):3013-3020. doi:10.1002/cncr.32851
  8. Stanich PP et al. Gastroenterology. 2021;160(5):1850-1852. doi:10.1053/j.gastro.2020.12.009
  9. Rustgi S et al. Universal screening strategies for the identification of Lynch syndrome in colorectal cancer patients and at-risk relatives. Research forum lecture #263 presented at: Digestive Disease Week (DDW) 2023; May 6-9, 2023; Chicago, IL.
  10. Tier 1 genomic applications and their importance to public health. Centers for Disease Control and Prevention. Reviewed March 6, 2014. Accessed August 15, 2023. https://www.cdc.gov/genomics/implementation/toolkit/tier1.htm
  11. Win AK et al. Cancer Epidemiol Biomarkers Prev. 2017;26(3):404-412. doi:10.1158/1055-9965.EPI-16-0693
  12. Yurgelun MB et al. J Clin Oncol. 2017;35(10):1086-1095. doi:10.1200/JCO.2016.71.0012
  13. Pearlman R et al. JCO Precis Oncol. 2021;5:PO.20.00525. doi:10.1200/PO.20.00525
  14. Patel R, Hyer W. Frontline Gastroenterol. 2019;10(4):379-387. doi:10.1136/flgastro-2018-101053
References
  1. Weiss JM et al. J Natl Compr Canc Netw. 2021;19(10):1122-1132. doi:10.1164/jnccn.2021.0048
  2. Samadder NJ et al. JAMA Oncol. 2021;7(2):230-237. doi:10.1001/jamaoncol.2020.6252
  3. Pearlman R et al; Ohio Colorectal Cancer Prevention Initiative Study Group. JAMA Oncol. 2017;3(4):464-471. doi:10.1001/jamaoncol.2016.5194
  4. Stoffel EM et al. Gastroenterology. 2018;154(4):897-905.e1. doi:10.1053/j.gastro.2017.11.004
  5. Stoffel EM, Murphy CC. Gastroenterology. 2020;158(2):341-353. doi:10.1053/j.gastro.2019.07.055
  6. Cavestro GM et al; Associazione Italiana Familiarità Ereditarietà Tumori; Collaborative Group of the Americas on Inherited Gastrointestinal Cancer; European Hereditary Tumour Group, and the International Society for Gastrointestinal Hereditary Tumours. Clin Gastroenterol Hepatol. 2023;21(3):581-603.e33. doi:10.1016/j.cgh.2022.12.006
  7. Gupta S et al. Cancer. 2020;126(13):3013-3020. doi:10.1002/cncr.32851
  8. Stanich PP et al. Gastroenterology. 2021;160(5):1850-1852. doi:10.1053/j.gastro.2020.12.009
  9. Rustgi S et al. Universal screening strategies for the identification of Lynch syndrome in colorectal cancer patients and at-risk relatives. Research forum lecture #263 presented at: Digestive Disease Week (DDW) 2023; May 6-9, 2023; Chicago, IL.
  10. Tier 1 genomic applications and their importance to public health. Centers for Disease Control and Prevention. Reviewed March 6, 2014. Accessed August 15, 2023. https://www.cdc.gov/genomics/implementation/toolkit/tier1.htm
  11. Win AK et al. Cancer Epidemiol Biomarkers Prev. 2017;26(3):404-412. doi:10.1158/1055-9965.EPI-16-0693
  12. Yurgelun MB et al. J Clin Oncol. 2017;35(10):1086-1095. doi:10.1200/JCO.2016.71.0012
  13. Pearlman R et al. JCO Precis Oncol. 2021;5:PO.20.00525. doi:10.1200/PO.20.00525
  14. Patel R, Hyer W. Frontline Gastroenterol. 2019;10(4):379-387. doi:10.1136/flgastro-2018-101053
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Germline Genetic Testing in CRC: Implications for Familial and Population-Based Testing
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Scientific advances in DNA sequencing technologies have allowed for the simultaneous testing of multiple genes associated with an inherited susceptibility of CRC. As a result, CRC screening and treatment protocols have been affected by results from germline multigene panel testing,1,2 including but not limited to Lynch syndrome (LS), the most common inherited CRC syndrome, which is associated with mismatch repair deficiency and tumor microsatellite instability.3

A demographic of concern for which systematic genetic risk assessment is recommended is the early-onset (EO) population—people diagnosed with CRC before age 50 years. More than 15% of EO-CRC cases are due to pathogenic variants in cancer susceptibility genes3,4 irrespective of family cancer history, most of which are LS–related and most frequently detected as age at CRC diagnosis decreases.5 Thus, multiple international guidelines recommend that all individuals diagnosed with EO-CRC undergo germline genetic testing6; these results have implications for at-risk relatives, particularly when a familial pathogenic variant is detected and specialized cancer screening or risk-reducing strategies can be pursued in family members, many of whom are cancer-free. The alarming increase in EO-CRC rates has led to a focus on the assessment of familial and inherited CRC risk to optimize screening recommendations among the general population.7,8

Furthermore, universal germline testing of all individuals with CRC is cost-effective and provides optimal surveillance for cancer survivors while also increasing the pool of at-risk, cancer-free relatives who benefi most from cancer screening and prevention protocols.9 In fact, indications for universal germline testing for relatives of individuals with CRC to personalize screening recommendations also supports future consideration for population-based germline genetic testing for LS genes, as the prevalence of the condition is 1 in 279 individuals, with more than 1 million individuals in the United States affected but unaware of their diagnosis.10,11

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