Jump to content

Gastroparesis

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Keith D (talk | contribs) at 20:50, 25 September 2018 (Fix cite errors). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Gastroparesis
Pronunciation
  • (/,ɡæstroʊ,pəˈriːsɪs/)[1]
SpecialtyGastroenterology

Gastroparesis (GP also called delayed gastric emptying) is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract.

Signs and symptoms

The most common symptoms of gastroparesis are the following:[2]

Other symptoms include the following:

Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.[3]

Complications

Primary complications of gastroparesis include:

  • Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)[4]
  • General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it. This is especially true for vitamin deficiencies such as scurvy because of inability to tolerate fresh fruits.[5]
  • Severe fatigue and weight loss due to calorie deficit
  • Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)[4]
  • Small intestine bacterial overgrowth is commonly found in patients with gastroparesis.[6]
  • Bacterial infection due to overgrowth in undigested food[4]

Causes

Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

More than 50% of all gastroparesis cases is idiopathic in nature, with unknown causes. It is however frequently caused by autonomic neuropathy. This may occur in a minority of people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves.[7] The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis.[8]

Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease.[9] It may occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.[10] Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection.[citation needed] Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.[11] A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest.[3] Neither theory has been proven definitively.

Gastroparesis can be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency,[citation needed] as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) to properly empty itself of a meal.

On the molecular level, it is thought that gastroparesis can be caused by the loss of neuronal nitric oxide expression since the cells in the GI tract secrete nitric oxide. This important signaling molecule has various responsibilities in the GI tract and in muscles throughout the body. When nitric oxide levels are low, the smooth muscle and other organs may not be able to function properly.[12] Other important components of the stomach are the interstitial cells of Cajal (ICC) which act as a pacemaker since they transduce signals from motor neurons to produce an electrical rhythm in the smooth muscle cells.[13] Lower nitric oxide levels also correlate with loss of ICC cells, which can ultimately lead to the loss of function in the smooth muscle in the stomach, as well as in other areas of the gastrointestinal tract.[12]

Diagnosis

Gastroparesis can be diagnosed with tests such as barium x-rays, manometry, and gastric emptying scans.[14] For the x-ray, the patient drinks a liquid after fasting containing barium which will show up in the x-ray and the physician is able to see if there is still food in the stomach as well. This can be an easy way to identify whether the patient has delayed emptying of the stomach.[15] The clinical definition for gastroparesis is based solely on the emptying time of the stomach (and not on other symptoms), and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.[citation needed]

In other cases or if the x-ray is inconclusive, the physician may have the patient eat a meal of beef containing barium so they can watch as it is being digested and see how slowly the digestive tract is moving. This can be helpful for diagnosing patients who are able to digest liquids but not solid foods.[15]

Treatment

In cases of postinfectious gastroparesis, patients have symptoms and go undiagnosed for an average of 3 weeks to 6 months before their illness is identified correctly and treatment begins. Current treatment is limited and includes nutritional modifications, medications to stimulate gastric emptying, drugs that reduce vomiting, and rarely surgical approaches.[16]

Treatment includes dietary changes (low fiber diets) and, in some cases, restrictions on fat and/or solids. Eating smaller meals, spaced two to three hours apart has proved helpful. Avoiding foods that cause the individual problems, such as pain in the abdomen, or constipation, such as rice or beef, will help avoid symptoms.[17]

Metoclopramide, a dopamine D2 receptor antagonist, increases contractility and resting tone within the GI tract to improve gastric emptying.[18] In addition, dopamine antagonist action in the central nervous system prevents nausea and vomiting.[19] Similarly, the dopamine receptor antagonist domperidone is used to treat gastroparesis. Erythromycin is known to improve emptying of the stomach but its effects are temporary due to tachyphylaxis and wane after a few weeks of consistent use.

Sildenafil citrate, which increases blood flow to the genital area in men, is being used by some practitioners to stimulate the gastrointestinal tract in cases of diabetic gastroparesis.[20]

The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment.[21] This is due to its antiemetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as does the popular anti-emetic ondansetron.[22]

Camicinal is a motilin agonist for the treatment of gastroparesis.

In specific cases where treatment of chronic nausea and vomiting proves resistant to drugs, implantable gastric stimulation may be utilized. A medical device is implanted that applies neurostimulation to the muscles of the lower stomach to reduce the symptoms. This is only done in refractory cases that have failed all medical management (usually at least two years of treatment).[17] Medically refractory gastroparesis may also be treated with a pyloromyotomy, which widens the gastric outlet by cutting the circular pylorus muscle. This can be done laparoscopically or endoscopically.

Vertical sleeve gastrectomy, a procedure in which a part or all of the affected portion of the stomach is removed, has been shown to have some success in the treatment of gastroparesis in obese patients, even curing it in some instances. Further studies have been recommended due to the limited sample size of previous studies.[23][24]

Prognosis

Most cases of postinfectious gastroparesis are self‐limiting, with recovery within 12 months of initial symptoms but some cases last well over 2 years. The condition affects people of all ages, but in children the duration tends to be shorter and the disease course milder. In adolescents and adults, the duration of clinical symptoms can be prolonged.[16]

Prevalence

Postinfectious gastroparesis, which constitutes the majority of idiopathic gastroparesis cases, affects up to 4% of the American population. Women in their 20s and 30s seem to be susceptible. One study of 146 American gastroparesis patients found the mean age of patients was 34 years with 82% affected being women, while another study found the patients were young or middle aged and up to 90% were women.[16]

There has only been one true epidemiological study of idiopathic gastroparesis which was completed by the Rochester Epidemiology Project. They looked at patients from 1996-2006 who were seeking medical attention instead of a random population sample and found that the prevalence of delayed gastric emptying was four fold higher in women. It is difficult for medical professionals and researchers to collect enough data and provide accurate numbers since studying gastroparesis requires specialized laboratories and equipment.[25]

Etymology

The etymology of the term is (gastro- from Ancient Greek γαστήρ gaster, "stomach" and πάρεσις -paresis, "partial paralysis").

References

  1. ^ "How to pronounce gastroparesis in English". dictionary.cambridge.org.
  2. ^ "Gastroparesis: Symptoms". MayoClinic.com. 2012-01-04. Retrieved 2012-10-09.
  3. ^ a b "Summary for Oley Foundation by R. W. McCallum, MD". Oley.org. Archived from the original on 2005-12-12. Retrieved 2012-10-09. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)[unreliable medical source?]
  4. ^ a b c "Gastroparesis Complications – Mayo Clinic".
  5. ^ Lisa Sanders MD "Diagnosis" NY Times Magazine 3.4.18 p.16-18.
  6. ^ Bharadwaj S, Meka K, Tandon P, Rathur A, Rivas JM, Vallabh H, Jevenn A, Guirguis J, Sunesara I, Nischnick A, Ukleja A (May 2016). "Management of gastroparesis-associated malnutrition". Journal of Digestive Diseases. 17 (5): 285–94. doi:10.1111/1751-2980.12344. PMID 27111029.
  7. ^ "Spotlight on gastroparesis," unauthored article, Balance (magazine of Diabetes UK, no. 246, May–June 2012, p. 43.
  8. ^ "Gastroparesis Causes – Mayo Clinic".
  9. ^ "Gastroparesis – Your Guide to Gastroparesis – Causes of Gastroparesis". Heartburn.about.com. Retrieved 2012-02-10.
  10. ^ "Gastroparesis: Causes". MayoClinic.com. 2012-01-04. Retrieved 2012-10-09.
  11. ^ "Epocrates article, registration required". Online.epocrates.com. Retrieved 2012-10-09.
  12. ^ a b Oh JH, Pasricha PJ (January 2013). "Recent advances in the pathophysiology and treatment of gastroparesis". Journal of Neurogastroenterology and Motility. 19 (1): 18–24. doi:10.5056/jnm.2013.19.1.18. PMC 3548121. PMID 23350043.
  13. ^ Al-Shboul OA (2013). "The importance of interstitial cells of cajal in the gastrointestinal tract". Saudi Journal of Gastroenterology. 19 (1): 3–15. doi:10.4103/1319-3767.105909. PMC 3603487. PMID 23319032.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ "Gastroparesis Tests and diagnosis – Mayo Clinic".
  15. ^ a b "Gastroparesis". American Diabetes Association. Retrieved 2018-09-08.
  16. ^ a b c Thorn AR (March 2010). "Not just another case of nausea and vomiting: a review of postinfectious gastroparesis". Journal of the American Academy of Nurse Practitioners. 22 (3): 125–33. doi:10.1111/j.1745-7599.2009.00485.x. PMID 20236395.
  17. ^ a b "Treatment Options for Gastroparesis". Medtronic.com. Medtronic. 29 September 2014. Retrieved 9 March 2016.
  18. ^ "Metochlopramide Hydrochloride". Monograph. The American Society of Health-System Pharmacists. Retrieved 23 March 2016.
  19. ^ Rang, H. P.; Dale, M. M.; Ritter, J. M.; Moore, P. K. (2003). Pharmacology (5th ed.). Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.[page needed]
  20. ^ Gottlieb S (August 2000). "Sildenafil may help diabetic patients". BMJ. 321 (7258): 401A. PMC 1127789. PMID 10938040.
  21. ^ Kundu S, Rogal S, Alam A, Levinthal DJ (June 2014). "Rapid improvement in post-infectious gastroparesis symptoms with mirtazapine". World Journal of Gastroenterology. 20 (21): 6671–4. doi:10.3748/wjg.v20.i21.6671. PMC 4047357. PMID 24914393.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  22. ^ Kim SW, Shin IS, Kim JM, Kang HC, Mun JU, Yang SJ, Yoon JS (2006). "Mirtazapine for severe gastroparesis unresponsive to conventional prokinetic treatment". Psychosomatics. 47 (5): 440–2. doi:10.1176/appi.psy.47.5.440. PMID 16959934.
  23. ^ Samuel, Bankole; Atiemo, Kofi; Cohen, Phillip; Czerniach, Donald; Kelly, John; Perugini, Richard (2016). "The Effect of Sleeve Gastrectomy on Gastroparesis: A Short Clinical Review". Bariatric Surgical Practice and Patient Care. 11 (2): 84–9. doi:10.1089/bari.2015.0052.
  24. ^ https://www.sages.org/meetings/annual-meeting/abstracts-archive/sleeve-gastrectomy-for-the-treatment-of-diabetic-gastroparesis/[full citation needed]
  25. ^ Bharucha, Adil E. (March 2015). "EPIDEMIOLOGY AND NATURAL HISTORY OF GASTROPARESIS". Gastroenterology clinics of North America. 44 (1): 9–19. doi:10.1016/j.gtc.2014.11.002. ISSN 0889-8553. PMC 4323583. PMID 25667019.

Further reading

Retrieved from "https://en.wikipedia.org/w/index.php?title=Gastroparesis&oldid=861206107"