Gastroentestinal Disorder - A Quick Review (1)

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Is there anything to it? Creatine is a natural substance, largely found in muscle, that's sold as a supplement. There's some evidence that it can help young athletes build muscle mass and improve athletic performance that requires short bursts of muscle activity, such as sprinting. For that reason, it is banned by some, but not by all, sports organizations. However, there is little evidence that it can build muscle bulk or strength in older adults. Small studies have suggested that it might be helpful for people with certain diseases more common in older folks, including heart failure and Parkinson's disease.

In my judgment, there is currently no convincing evidence of adverse effects from doses that the manufacturers recommend, which are typically 2 to 3 grams per day.

The gut-brain connection

However, there are very few studies of sufficient size and duration to be confident about this. Note also that the FDA does not regulate the manufacturing of supplements as it does prescription drugs. So even if the creatine itself is fine, the other substances used to create a tablet or capsule could contain impurities. I think there's little, if any, evidence that creatine supplements could help you build or maintain muscle strength at your age, and, because of the lack of regulation of supplements, there is some potential for harm.

I wish there were more solid information, but there isn't.

The Centre for Digestive Diseases – The centre of excellence for gastroenerology

For now, to be on the safe side, I'd advise against taking creatine. Disclaimer: As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician. Pay attention to your gut-brain connection — it may contribute to your anxiety and digestion problems The gut-brain connection is no joke; it can link anxiety to stomach problems and vice versa.

Most patients with rapid gastric emptying present with abdominal symptoms that mimic those of gastroparesis 10 , Suspicion of gastroparesis is further supported by identifying risk factors, for example, long-standing diabetes mellitus 9. Conversely, suspicion of gastric dumping is supported by a history of upper gastrointestinal surgery Furthermore, upper gastrointestinal symptoms had a poor clinical specificity relative to the actual rate of gastric emptying on scintigraphy, underlining the need for function testing to guide treatment.

Because accelerated, normal and delayed gastric emptying cannot be differentiated reliably based on type or severity of gastrointestinal symptoms, objective measurement of clearly delayed gastric emptying gastric emptying time increased above the upper level of normal using well-validated techniques such as gastric emptying scintigraphy Fig. Standardized scintigraphic study of gastric emptying of solids with consumption of a kcal radiolabelled meal scrambled eggs labelled with 99m Tc; Mayo Clinic protocol 30 and imaging over 4 h.

In the individual with normal gastric emptying GE left panel , large amounts of the meal are emptied from the stomach at 2 h, and GE is completed at 4 h. The merit of gastric emptying studies for clinical management has been questioned because of variations in the reports of association between gastric emptying rates and symptoms. Several studies published during the past 7 years have shown a positive association between symptoms of gastroparesis and gastric emptying times 14 , 15 , 16 , 17 , 18 , Measurement of gastric emptying can also predict responsiveness to different therapeutic options 20 , For example, the presence of slow gastric emptying in patients with functional dyspepsia was associated with poor response to antidepressant medications that target visceral hypersensitivity On the other hand, one systematic literature review that used multiple methods, various symptom instruments and diverse treatments showed that most drugs that improved idiopathic and diabetic gastroparesis failed to show a statistically significant relationship with the degree of symptom improvement and acceleration of gastric emptying across studies Some groups have observed that the association between clinical improvement and acceleration of gastric emptying depends on the aetiology of gastroparesis 20 , 23 , which could partly explain inconsistent findings across studies Moreover, the modes of action of drugs used for acceleration of gastric emptying are extremely heterogeneous and potentially induce dysfunctions that cause symptoms.

For example, motilin receptor agonists markedly accelerate gastric emptying but simultaneously impair gastric accommodation and can induce dyspeptic symptoms 1. Several additional factors other than a global delay in gastric emptying — such as antral distension, antral hypomotility, gastric dysrhythmias, visceral hypersensitivity or psychological disturbances — could explain, in part, the symptoms experienced by patients with gastroparesis In unclear cases, provocation tests that prove dumping syndrome are the basis of diagnosis, which is supported by evidence of accelerated gastric emptying, preferably of liquids.

Dumping syndrome is a common complication of oesophageal, gastric or bariatric surgery and includes early and late dumping symptoms Early dumping occurs within 1 h after eating, when rapid emptying of food into the small intestine triggers rapid fluid shifts into the intestinal lumen and release of gastrointestinal hormones, resulting in gastrointestinal and vasomotor symptoms.

Late dumping occurs 1—3 h after carbohydrate ingestion and is caused by an incretin-driven hyperinsulinaemia. According to clinical experience, in patients with typical symptoms after surgery, gastric emptying tests Figs 1 , 2 usually add little to the diagnosis. Liquid test meals might better detect acceleration of early gastric emptying; studies using solid meals generally have low sensitivity and specificity for detecting accelerated gastric emptying 12 , The test principle underlying the 13 C-octanoic acid breath test part a is as follows: 13 C-octaonoic acid is rapidly absorbed after gastric emptying and transported to the liver.

Hepatic metabolism leads to production and exhalation of 13 CO 2. Thus, alterations of the 13 C: 12 C ratio in breath samples collected at multiple time points postprandially reflect gastric emptying. Examples part b of values for accelerated, normal and delayed gastric emptying are shown. In these conditions, delayed gastric emptying can be clinically relevant even without typical symptoms of gastroparesis, as the test identifies gastric dysfunction that could have clinical or therapeutic implications.

Thus, impaired coordination between nutrient delivery to the duodenum and onset of insulin effect can impair glycaemic control in patients with insulin-dependent diabetes and gastroparesis 9. Delayed gastric emptying could cause gastro-oesophageal reflux and regurgitation in a subset of patients with GERD 26 and systemic sclerosis Lung transplant recipients can have markedly impaired gastric emptying secondary to vagal injury with a risk of aspiration and post-transplant sequelae Delayed gastric emptying contributes substantially to fluctuations in symptom control in patients with Parkinsonism on long-term levodopa therapy In patients with generalized gastrointestinal motility disorders, particularly in those under consideration for abdominal surgery because of the motility disorder for example, colonic inertia , knowledge of gastric involvement is required to individualize therapy.

Detailed investigation of gastric contractility generally requires invasive techniques such as intraluminal manometry including stomach and small bowel and should, therefore, be limited to patients with severe symptoms.

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A consensus report 24 has recommended a standardized protocol for the performance of gastric emptying scintigraphy in the USA and has provided normal values. However, even in the USA, despite society guidelines, many centres continue to perform suboptimal studies duration 1—2 h that undermine the quality and utility of the test 4. In most other countries, including the European ones, there are no widely accepted standard procedures. For interpretation of test results, it has to be taken into account that clinical utility depends on complete consumption of adequate test meals and adequate duration of imaging.

Test meals labelled with the stable, nonradioactive isotope 13 C can be used to measure gastric emptying. The edible blue—green algae, 13 C-labelled Spirulina platensis 31 or the medium-chain fatty acid, 13 C-octanoic acid 13 C-OA 32 , is typically used to label solids; 13 C-acetate is used for liquids Subsequently, it is metabolized, usually in the liver, and finally excreted by the lungs as 13 CO 2.

For 13 C-acetate, an interaction has been demonstrated between the rate of 13 C delivery to the duodenum and 13 C recovery in breath Moreover, it has been hypothesized that 13 C-GEBTs might be inaccurate in conditions associated with substantial malabsorption or liver or lung diseases. Intraindividual and interindividual variabilities of all 13 C-GEBTs are high, but they are similar to the variations observed with scintigraphy 4 , 31 , 38 and, therefore, reflect day-to-day physiological variability in gastric emptying.

Results of the 13 C-labelled S. The test kit is commercially available USA only , and the protocol is exactly defined and has been validated in a large group of healthy volunteers and patients When using these tests, it is important to strictly follow a standardized, validated approach. The WMC for example, SmartPill, Medtronic, USA is a single-use, orally ingested, non-digestible, data-recording capsule that measures pH, pressure and temperature throughout the gastrointestinal tract 4.

A marked increase in pH units is used to estimate gastric emptying time Fig. However, as the WMC is a large, non-digestible, solid object, it does not empty with the meal but rather is most often cleared from the stomach by powerful interdigestive migrating motor complex MMC phase III Fig. Accordingly, passage of the WMC into the duodenum correlates only modestly with gastric emptying of nutrients 41 , These aspects must be taken into consideration for evaluation of the test.

Functional GI Disorders - Lynn S. Connolly, MD, MSCR - UCLA Digestive Diseases

Wireless motility recordings in a healthy male participant part a and a female patient with severe constipation part b are shown. Please note that the timescales are different for the left and right panels.

High-resolution gastroduodenal manometry plots are shown for normal fasting part a and postprandial part b motility. During the fasting state part a , there is a constant transition between phases I to III of the interdigestive migrating motor complex MMC with motor quiescence during phase I, irregular contractions that are propagated over only smaller segments during phase II and regular, aborally propagated contractions that usually start in the stomach and traverse long segments of the small bowel during phase III.

Postprandially part b , MMC activity is interrupted and replaced by irregular contractions that serve to mix the luminal contents and to slowly propel them towards the more distal intestine.

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Catheter-based manometry with multiple pressure sensors located in the antrum, pylorus and duodenum is the only clinically available test that enables detailed assessment of coordinated gastric contraction patterns 3 Fig. Severe small bowel dysmotility is usually identified by chronic disabling gastrointestinal symptoms, which are associated with dilatation of some part of the small bowel, with inconclusive results of endoscopic and radiological investigations or surgical exploration. It is frequently associated with impaired nutritional intake. Experts therefore agree that only abnormal results, based on recorded transit times clearly outside normative ranges, should be considered diagnostic.

Detailed clinical evaluation of antroduodenojejunal contraction patterns by manometry is available in only highly specialized centres Fig. A WMC can also measure amplitude of antral, small bowel and colonic contractions during its passage through the gastrointestinal tract Fig. Individual antral contractions detected by the WMC correlated closely with those observed on manometry, and in theory, many of the indications for antroduodenojejunal manometry should also apply to the WMC 3.

However, the WMC records pressure at a single recording site and cannot appraise propagation of contractions. Thus, it is uncertain whether the WMC can be a substitute for catheter-based manometric investigation of small bowel motility in terms of propagation of pressure waves.

An entirely normal result in a manometric study suggests that motor dysfunction of the upper gastrointestinal tract is not a cause of patient symptoms 44 and that it can differentiate a true motility disorder from a somatoform disorder in children Severe motor pattern alterations in combination with documented episodes mimicking mechanical obstruction enable the diagnosis of CIPO. However, studies comparing manometric and histological findings are weak, and in the absence of a gold standard, the sensitivity and specificity of manometry abnormalities for differentiating causes of motility diseases have not been extensively evaluated.

For the identification of manometric patterns that predict obstruction, manometry has been compared with the results of laparotomy However, with modern and more-sensitive imaging techniques such as CT enterography or magnetic resonance enteroclysis, manometry is seldom required for this indication in clinical practice. CIPO is a rare disease in which severe intestinal dysmotility impairs transit of chyme such that patients present with signs of subileus and ileus on imaging without mechanical obstruction 48 , Small intestinal manometry permits diagnosis of severe intestinal motility disturbances compatible with CIPO 50 even during mostly asymptomatic intervals.

Moreover, manometry can be used to determine which organs need to be transplanted isolated versus multivisceral transplantation in patients failing all other treatment options 3. Additional indications for small bowel manometry include detection of retrograde propagated contractions, for instance, after Roux-en-Y gastric surgery 51 , and exclusion of generalized dysmotility in patients with colonic inertia before subtotal colectomy.

This step is relevant because patients with additional upper gastrointestinal motor abnormalities have a worse long-term outcome after surgery Whereas small bowel manometry can confirm a diagnosis of rumination syndrome 3 , high-resolution oesophageal manometry with impedance 1 , 53 is now preferred for this indication. Scintigraphic assessment of small bowel transit time is usually performed as part of a whole-gut transit study 4. Scintigraphy directly visualizes passage of the radioactive marker throughout the small bowel and provides physiological and quantitative data.

However, the technique is not standardized, has wide normal ranges and is rarely performed outside the USA. The WMC uses pH landmarks to identify passage through the pylorus and through the ileocaecal junction for calculation of small bowel transit time Fig.

The LHBT is a semi-quantitative test that measures orocaecal transit time using the increase in H 2 exhalation associated with caecal delivery and subsequent bacterial metabolism of the nonabsorbable saccharide lactulose 56 , 57 Fig. The test can be easily performed and is widely available, inexpensive and not associated with radiation exposure However, lactulose is not an inert marker; it can accelerate orocaecal transit time through osmotic fluxes into the small intestine 59 , and it also delays gastric emptying time Moreover, misleading results with falsely short transit times are to be expected in patients with small intestinal bacterial overgrowth, which is particularly problematic because small bowel motility disturbances can cause this condition 61 , The test requires H 2 measurements at regular intervals after ingestion of lactulose.

This increase in H 2 exhalation normally occurs 50— min after ingestion of the marker substance normal range for OCTT marked in grey. Moreover, the LHBT does not specifically measure small bowel transit time; rather, it reflects the summation of gastric and small bowel transit. Gastric emptying of the liquid test solution occurs rapidly and might be negligible in healthy individuals.

However, in patients with gastrointestinal motility disturbances, gastric emptying may markedly influence the measured orocaecal transit time. This problem could be overcome by combining the LHBT and the 13 C-acetate GEBT such that small bowel transit time can be calculated as the difference between orocaecal transit time and the gastric emptying time Catheter-based manometry with multiple pressure sensors permits detailed assessment of small bowel contraction patterns 3 Fig.

Manometry sensors are usually placed in only the proximal small bowel duodenum and proximal jejunum for practical reasons, and tracings from these segments are assumed to reflect motility of the total small intestine 3 , although this aspect has not been tested rigorously. Ambulatory investigations are performed over 24 h by some centres, while other centres perform stationary manometry with recordings over 3—4 h in the fasting state and for an additional 2 h after ingestion of a test meal 3.

Signs and symptoms involving the digestive system and abdomen

Manometry can reveal low-amplitude contractions or disorganized contractile patterns or normal amplitudes, frequencies and patterns of contractions 3 Fig. Certain measurements of colonic motility might provide useful information in a subset of patients with diarrhoea. Severe colonic dysmotility usually impairs propagation of luminal contents and is consequently associated with slow-transit constipation.

Moreover, colonic scintigraphy or radiopaque marker ROM transit has been shown to differ between subtypes of functional disorders of the lower gastrointestinal tract and healthy individuals 64 , Transit was generally accelerated in diarrhoea and delayed in constipation, confirming that motor dysfunction is of pathophysiological importance. Thus, colonic transit measurement could identify subgroups more likely to respond to treatment directed at dysmotility. Colonic transit could accelerate, and symptoms can improve or even resolve with treatment of the evacuation disorder 68 , Thus, delayed colonic transit does not necessarily reflect colonic inertia and does not imply a colonic motility disorder as the sole cause of constipation.

Moreover, anatomical alterations such as large rectoceles or mucosal prolapse can impair stool evacuation. Both dyssynergic defecation 70 and anatomical alterations require specific treatments and should be identified before elaborate investigation of colonic motility.

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Clinical markers do not predict slow-transit constipation reliably. In particular, stool frequency is a poor surrogate for transit even in those with reduced stool frequency 71 , Hard stool form 1 or 2 on the Bristol Stool Chart predicts delayed versus normal transit, but only a moderate correlation exists between stool form and whole-gut or colonic transit time in adults with constipation Transit tests are, therefore, required to identify slow colonic transit and can optimize the choice of treatment However, transit measurements alone are not diagnostic of evacuation disorders and require confirmation by specialized tests of evacuation.

Regional scintigraphic transit profiles and distribution of ROM can give initial information on the pathophysiology of constipation 4 , 75 , 76 , Retention of ROM in the entire colon is expected in slow-transit constipation Fig. If dyssynergic defecation is present, biofeedback training is indicated 70 , However, transit can be slow in disorders of rectal evacuation, such that specialized tests such as anorectal manometry, the balloon evacuation test or defaecography are required to confirm functional or structural causes of evacuatory dysfunction Moreover, even if transit tests suggest that a specific segment of the colon is responsible for delayed transit, in the absence of localized megacolon, experts advise against segmental colonic resection in treatment-refractory slow-transit constipation A radiopaque marker test of a patient who ingested 10 markers every morning for 6 days is shown.

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  5. Note that in this case, the markers are evenly distributed throughout the colon, which is regarded as typical of, but is not completely specific for, slow-transit constipation. In such patients, colonic transit tests are mandatory.