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PubMed2001

Pain hypersensitivity in patients with functional gastrointestinal disorders: a gastrointestinal-specific defect or a general systemic condition?

Visceral hypersensitivity was shown in patients with functional gastrointestinal disorders (FGID). The mechanisms underlying this sensory dysfunction remain undetermined. The initial hypothesis of a generalized reduction in pain tolerance was rejected by further studies that suggested a normal tolerance to somatic stimuli and led to the generally accepted assumption that pain intolerance is specific and exclusive for visceral stimuli in these patients. We wanted to revisit this theory by examining whether patients with FGID reported perception and tolerance to somatic pain differently from normal subjects and whether the response to somatic pain stimulus was correlated to gastrointestinal symptoms or psychological status or distress. Thirty-three patients with FGID (Rome II criteria)(F/M: 26/7; mean age 48+/-9.9) and 33 normal controls (F/M: 24/9; mean age 44.1+/-6.8) were asked to immerse their nondominant hand into 4 degrees C water for as long as possible (maximum 120 sec). Time before appearance of: (1) discomfort, (2) pain, and (3) withdrawing of the hand were noted. The intensity of pain was rated on a visual analog scale from 0 to 100. Self-report questionnaires were used to assess the severity of gastrointestinal symptoms (St-Luc GI index) and the psychological distress (SCL-90) in the patient group. Data are expressed in seconds as mean +/- SEM. Discomfort sensory thresholds were similar in controls and FGID patients (28+/-3 and 24+/-2, respectively; NS) whereas pain and withdrawing were significantly lower in FGID (41+/-3 and 76+/-6 sec) than in controls (62+/-6 and 102+/-4; P < 0.05). Pain intensity was similar in both groups (64+/-4 vs 67+/-3; NS). Female patients showed lower sensory thresholds than male patients and control females (pain thresholds: 39.8+/-3.4 vs 67.8+/-16.7 and vs 56.8+/-8.7; P < 0.05). Sensory thresholds were not different in subgroups of patients with FGID (irritable bowel syndrome and functional dyspepsia). No correlation was shown between sensory thresholds and gastrointestinal index or SCL 90-test. In conclusion, FGID patients showed a threshold to painful somatic stimulus that was lower than in normal subjects. These findings suggest that patients with FGID may have hyperalgesia and low pain tolerance that is not limited to the viscera, but that is part of a systemic general condition.

Case-Control Studies↗

PubMed2002

Immune-mediated neural dysfunction in a murine model of chronic Helicobacter pylori infection.

BACKGROUND & AIMS: Neuromuscular changes producing dysmotility and hyperalgesia may underlie symptom generation in functional gastrointestinal disorders. We investigated whether chronic Helicobacter pylori-induced gastritis causes neuromuscular dysfunction. METHODS: In vitro muscle contractility and acetylcholine release were evaluated in mice before and after H. pylori eradication. H. pylori colonization and gastritis were graded histologically. Substance P (SP)-, vasoactive intestinal polypeptide (VIP)-, and calcitonin gene-related peptide (CGRP) immunoreactivity (IR) and macrophages were studied by immunohistochemistry. RESULTS: In Balb/c mice, chronic H. pylori infection did not affect muscle function but augmented antral relaxation after nerve electric field stimulation. Infected mice had lower acetylcholine release by electric field stimulation and had higher density of SP-, CGRP-, and VIP-IR nerves in the stomach and of SP- and CGRP-IR in the spinal cord. Cholinergic nerve dysfunction worsened progressively and was associated with increasing macrophage and mononuclear but not polymorphonuclear infiltrate or bacterial colonization. SCID mice had unchanged acetylcholine release despite high H. pylori colonization and macrophage infiltration. Eradication of H. pylori normalized functional and morphologic abnormalities except for increased density of gastric SP- and CGRP-IR nerves. CONCLUSIONS: H. pylori infection induces functional and morphologic changes in the gastric neural circuitry that are progressive and lymphocyte dependent, and some persist after H. pylori eradication. The data have direct implications regarding the role of H. pylori infection in functional dyspepsia.

Acetylcholine↗

PubMed2005

[Intraabdominal and hepatic infections in pediatric cancer patients].

Common complications involved in treating pediatric patients with cancer are bacterial, viral and fungal infections of the gastrointestinal tract including esophagitis, gastritis, duodenitis, colitis and hepatobiliar infections. In many cases there are multiple factors that predispose these patients to gastrointestinal infections, such as granulocytopenia, T-cell dysfunction, and mucosal damage. In addition, newer therapies have changed the spectrum of infection that is seen in these patients. The profound T-cell suppression associated with therapies such as stem cell transplantation has led to the emergence of previously rare infections including cytomegalovirus and adenovirus. This article provides the recommendations of the Infectious Diseases Working Party of the German Society for Pediatric Infectious Diseases (DGPI) and the German Society for Pediatric Hematology/Oncology (GPOH) for diagnosis, prevention, and management of local as well as invasive infections of the gastrointestinal tract.

Anti-Infective Agents↗

PubMed2002

[Sinus node dysfunction with intermittent sinus arrest and AV-nodal escape rhythm as initial manifestation of pheochromocytoma].

A 25-year-old male student complained about episodic palpitations, dizziness, nausea and headache 5 years prior to presentation. No otorhinolaryngic, neurologic or gastrointestinal causes were identified. Several ECG recordings revealed sinus node dysfunction with intermittent sinus arrest and AV-nodal escape rhythm. The patient was given a permanent DDD-pacemaker. Six months later, the clinical symptoms were unchanged. During an attack, physical examination revealed paleness, diffuse sweating and an arterial blood pressure of 250/130 mmHg, which decreased to 120/80 mmHg within a few minutes. Abdominal ultrasound and abdominal computed tomographic scan demonstrated the presence of a large (6.4 x 5.5 cm) left-sided adrenal mass. Two 24-h-urinary collections demonstrated elevated noradrenaline (mean 315 micrograms/24 h, normal < 80 micrograms/24 h) and adrenaline (mean 268 micrograms/24 h, normal < 20 mg/24 h) levels. Blood samples, which were drawn during excessive blood pressure rise, revealed elevation of plasma catecholamines (6.793 pg/ml for adrenaline (normal 50-150 pg/ml) and 10.424 pg/ml for noradrenaline (normal 200-500 pg/ml), so that the diagnosis of pheochromocytoma was considered established. The tumor was successfully removed during laparascopic surgery. After surgery, the patient remained well and normotensive. Three months later, several long-term ECG recordings showed sinus arrhythmia with no evidence of sinus arrest or AV-nodal escape rhythm, so that the DDD pacemaker was turned off. This case underlines that sinus node dysfunction with intermittent sinus arrest and AV-nodal escape rhythm is a potential early manifestation of a pheochromocytoma. These changes seem to disappear after successful removal of the tumor.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

Patient controlled analgesia and GI dysfunction.

A prospective randomized study of 300 total joint replacement patients was done comparing the gastrointestinal (GI) side effects of morphine, meperidine, and nalbuphine given by patient controlled analgesia (PCA). All three groups of patients developed some form of GI dysfunction, but no significant difference was found among the three narcotics used. It was found that normal GI assessment in the initial postoperative period does not guarantee that GI function will remain normal. This finding indicates a need for extended nursing assessment of the GI status of the postoperative PCA patient.

Analgesia↗

PubMed1996

Risk of cancer in relatives of testicular cancer patients.

The incidence of cancer at sites other than the testis has been investigated in the families of 797 Norwegian and 178 Swedish patients diagnosed with testicular cancer during 1981-91. In the families of the Norwegian patients, the total number of cancers in the relatives was significantly lower than the expected number derived from national incidence rates [observed number of cancers 250, expected number of cancers 281.92, standardised incidence ratio (SIR) 0.89, 95% confidence interval (CI) 0.78-1.00]. This finding can be accounted for almost entirely by the finding of fewer than expected prostate and gastrointestinal cancers in the parents of cases. The other common cancers were found at slightly lower than or near the expected levels in the relatives. In the Swedish cohort, which accounts for less than 20% of cases, the observed number of cancers was very close to the expected number. Fourteen fathers of cases had prostate cancer compared with 27.57 prostate cancers expected, giving a SIR of 0.51 (P=0.006). Mothers had more lung cancers (ten cases observed, SIR=2.11, P=0.04) and cancers of the endometrium than expected (13 cases observed, SIR=1.73, P=0.09). These findings may be interpreted as support for theories proposing hormonal dysfunction as causing testicular cancer. Fifty-four gastrointestinal cancers were observed in the parents compared with 68.48 expected (SIR=0.78, P=0.082). Furthermore, testicular cancer was not found to be associated with the known dominantly inherited cancer syndromes [Familial breast (-ovarian) cancer, hereditary no-polyposis colon cancer]. However, one patient belonged to a Li-Fraumeni family, raising the possibility that testicular cancer may be an infrequent component of this rare cancer syndrome. This study supports the hypothesis that families of testicular cancer patients are not prone to cancer.

Cohort Studies↗

PubMed2005

Alvimopan: an oral, peripherally acting, mu-opioid receptor antagonist for the treatment of opioid-induced bowel dysfunction--a 21-day treatment-randomized clinical trial.

Alvimopan has been shown to reverse the inhibitory effect of opioids on gastrointestinal transit without affecting analgesia. We evaluated oral alvimopan, 0.5 or 1 mg, versus placebo, once daily for 21 days, in 168 patients with opioid-induced bowel dysfunction (OBD) who were receiving chronic opioid therapy (minimum, 1 month) for nonmalignant pain (n = 148) or opioid dependence (n = 20). The primary outcome was the proportion of patients having at least one bowel movement (BM) within 8 hours of study drug on each day during the 21-day treatment period. Averaged over the 21-day treatment period, 54%, 43%, and 29% of patients had a BM within 8 hours after alvimopan 1 mg, 0.5 mg, or placebo, respectively (P < .001). Secondary outcomes of median times to first BM were 3, 7, and 21 hours after initial doses of 1 mg, 0.5 mg, and placebo, respectively (P < .001; 1 mg vs placebo). Weekly BMs and overall patient satisfaction were increased after the 1-mg dose (P < .001 at weeks 1 and 2 vs placebo, and P = .046, respectively). Treatment-emergent adverse events were primarily bowel-related, occurred during the first week of treatment, and were of mild to moderate severity. Alvimopan was generally well tolerated and did not antagonize opioid analgesia. Patients treated with chronic opioid therapy often experience opioid-induced bowel dysfunction as a result of undesirable effects on peripheral opioid receptors located in the gastrointestinal tract. Alvimopan, a novel peripheral opioid mu-receptor antagonist, has demonstrated significant efficacy for the management of opioid-induced bowel dysfunction without compromise of centrally mediated opioid-induced analgesia.

Administration, Oral↗

PubMed2004

Impaired gallbladder motility and delayed orocecal transit contribute to pigment gallstone and biliary sludge formation in beta-thalassemia major adults.

AIM: Gallbladder and gastrointestinal motility defects exist in gallstones patients and to a lesser extent in pigment gallstone patients. To investigated the role of gallbladder and gastrointestinal motility disorders in pigment gallstone formation in beta-thalassemia major. METHODS: Twenty-three patients with beta-thalassemia major (16 females; age range 18-37 years) and 70 controls (47 females, age range 18-40 years) were studied for gallbladder and gastric emptying (functional ultrasonography), orocecal transit (OCTT, H(2)-breath test), autonomic dysfunction (sweat-spot, cardiorespiratory reflex tests), bowel habits, gastrointestinal symptoms and quality of life (all with questionnaires). Gallbladder content (ultrasonography) was examined before and during 8-12 mo follow-up. RESULTS: Gallstones and/or biliary sludge were found in 13 (56%) patients. beta-thalassemia major patients had increased fasting (38.0+/-4.8 mL vs 20.3+/-0.7 mL, P = 0.0001) and residual (7.9+/-1.3 mL vs 5.1+/-0.3 mL, P = 0.002) volume and slightly slower emptying (24.9+/-1.7 min vs 20.1+/-0.7 min, P = 0.04) of the gallbladder, together with longer OCTT (132.2+/-7.8 min vs 99.7+/-2.3 min, P = 0.00003) than controls. No differences in gastric emptying and bowel habits were found. Also, patients had higher dyspepsia (score: 6.7+/-1.2 vs 4.9+/-0.2, P = 0.027), greater appetite (P = 0.000004) and lower health perception (P = 0.00002) than controls. Autonomic dysfunction was diagnosed in 52% of patients (positive tests: 76.2% and 66.7% for parasympathetic and sympathetic involvement, respectively). Patients developing sludge during follow-up (38%, 2 with prior stones) had increased fasting and residual gallbladder volume. CONCLUSION: Adult beta-thalassemia major patients have gallbladder dysmotility associated with delayed small intestinal transit and autonomic dysfunction. These abnormalities apparently contribute together with haemolytic hyperbilirubinemia to the pathogenesis of pigment gallstones/sludge in beta-thalassemia major.

Adolescent↗

PubMed1990

Gallbladder and gastrointestinal motility after hemorrhagic shock.

The alterations in fasting gallbladder and gastrointestinal motility during hemorrhagic shock were investigated. Eight opossums implanted with a gallbladder cannula, gastrointestinal bipolar electrodes, and a carotid catheter were subjected to hemorrhagic shock of 30 mm Hg for 60 minutes by the removal of arterial blood. Shed blood was reinfused after the shock period. Fasting gallbladder volume and gastrointestinal electrical activity were studied before, immediately after, and 24 hours after hemorrhagic shock. Control measurements demonstrated a slow-wave frequency maximal in the duodenum (18.1 +/- 1.1 waves/min), with a plateau in the proximal third of the small bowel, decreasing thereafter. The migrating motor complex (MMC) had a duration of 118 +/- 28 minutes. The average volume of the gallbladder before shock was 5.4 +/- 1.5 ml. Gallbladder volume fluctuated with the MMC, being maximal during phase I and minimal in phase III. The volume of blood removed to reduce mean arterial pressure to 30 mm Hg was 45 +/- 5 ml/kg. Immediately after the shock and blood reinfusion, slow-wave frequency decreased by 40% in the antrum and 25% in the small bowel. The MMC was of shorter duration (91 +/- 22 minutes; p less than 0.05), and gallbladder volume increased to 7.0 +/- 1.7 ml (p less than 0.05). Fluctuations in gallbladder volume during the MMC were absent. Twenty-four hours after shock, slow-wave frequency, MMC, and gallbladder volume had returned to normal and were not different from control measurements. Ischemic damage to the gastrointestinal tract is postulated as the cause of gallbladder dysfunction and altered intestinal motility after hemorrhagic shock.

Animals↗

PubMed1982

Gastrointestinal manifestations of the muscular dystrophies.

Skeletal and cardiac muscle involvement is a recognized feature of the muscular dystrophies. Visceral smooth muscle involvement of the gastrointestinal tract is not as well appreciated. Gastrointestinal symptoms may herald the onset of a muscular disorder and may be the predominant feature of the disorder. In some instances, smooth muscle dysfunction may be the only clinical manifestation of the disease. The gastrointestinal manifestations of the various muscular dystrophies are reviewed. Clinical, radiographic, and histologic features are discussed. Further study of the histopathology and pathophysiology of visceral smooth muscle involvement in the muscular dystrophies will have a substantial impact on treatment that, to a large extent, remains empiric.

Adolescent↗

PubMed1975

The lower esophageal sphincter. Physiologic and clinical aspects.

Current concepts in physiology and pathophysiology of lower esophageal sphincteric mechanism are reviewed. With recent advances in manometric method for more accurate in-vivo human studies combined with in-vivo and in-vitro studies in animal models, there is much information regarding function of this sphincter. Three components of sphincter control have been identified: specialized circular smooth muscle at esophagogastric junction, autonomic nervous system, and probable physiology effects of gastrointestinal hormones, particularly gastrin. Clinical syndromes of sphincteric dysfunction have been identified relative to these three controlling elements. Foods and drugs that adversely effect sphincter pressure have been identified and indicate that anticholinergic agents, fatty foods, chocolate, alcohol, and cigarette smoking may have a harmful effect on a patient with heartburn. Drugs that increase the antireflux sphincter barrier have been studied. Clinical effectiveness of antacids and bethanechol in therapy of heartburn is supported by controlled treatment trials. Research continues on other medications producing increases in sphincter pressure.

Anemia, Pernicious↗

PubMed1994

Modulation of gastric perception and motility in man. Current concepts and correlation with symptoms.

Gastric function is controlled by central and peripheral modulation. Most often, afferent information from the stomach does not reach conscious level. At extremes of chemical and mechanical stimulation, however, afferent signals are perceived as pain. Whether or not a signal is perceived depends on gating of afferent signals at the levels of both spinal cord and brainstem. Inhibition of gastric tone and peristalsis during perceived discomfort largely results from stimulation via sympathetic neural pathways. These findings may be clinically relevant because upper gastrointestinal symptoms in many dyspeptic patients could be the result of primary afferent neuron dysfunction rather than motor dysfunction.

Afferent Pathways↗

PubMed2004

Functional dyspepsia: motor abnormalities, sensory dysfunction, and therapeutic options.

Functional dyspepsia is a common condition, but as yet, the underlying etiology is unclear. In this article, upper gastrointestinal motor and sensory physiology are reviewed and the current evidence for motor and/or sensory functional abnormalities causing dyspeptic symptoms is presented. The complex interrelationship between abnormal motor activity and sensation is explored, as well as the potential roles for autonomic dysfunction and psychological state in modulating gastrointestinal sensation and motor function. Finally, based on clinical trial evidence, a treatment pathway for functional dyspepsia is suggested.

Dyspepsia↗

PubMed1985

Gastrointestinal motility disturbances in patients with orthostatic hypotension.

Orthostatic hypotension syndromes may be associated with visceral denervation, resulting in disturbances of the gastrointestinal and urinary systems. This report analyzes the findings in 9 patients with neurogenic orthostatic hypotension and gastrointestinal symptoms. Antral and proximal small intestinal motor dysfunction was demonstrated in all patients: a significant reduction (p = 0.007) in the number of interdigestive motor complexes during 3 h of fasting (mean 0.4 vs. 1.3 controls); absence of gastric component in interdigestive motor complexes observed; incoordination of fasting and fed antral activity; and development of nonpropagating bursts of phase III-like activity in the intestine that were of at least 2-min duration, high amplitude and frequency, and associated with tonic elevations in baseline pressure. These motor abnormalities may provide a potential means for the diagnosis of impaired autonomic supply to the upper gut.

Adult↗

PubMed1984

Gastrointestinal transit in thyroid disease.

Diarrhea and malabsorption are common manifestations of hyperthyroidism, whereas constipation or obstipation frequently occur in hypothyroidism. Abnormalities of gastrointestinal motility have been proposed as the primary cause of these complaints, but documentation has been conflicting and largely limited to observations of the transit time of a barium meal. We studied gastrointestinal transit time in fasting patients with thyroid dysfunction using the pulmonary excretion of H2 after the ingestion of a nonabsorbable carbohydrate, lactulose, as an indicator of the rate of transit to the colon. Mean transit time of 10 hyperthyroid patients (29 +/- 4.0 min) was significantly less than that of 42 healthy controls (72 +/- 3.7 min, p less than 0.001), and of 6 hyperthyroid patients when they became hypothyroid after treatment (80 +/- 11.0 min, p less than 0.05). Transit time decreased significantly when hypothyroid patients were given thyroid replacement (p less than 0.01). These findings support the hypothesis that abnormal gut motility may be the primary cause of the diarrhea and malabsorption of hyperthyroidism, and the constipation and obstipation commonly seen in hypothyroidism.

Adult↗

PubMed1999

Long-term morbidity and quality of life in patients with localized prostate cancer undergoing definitive radiotherapy or radical prostatectomy.

PURPOSE: To assess morbidity, side effects, and quality of life (QoL) in patients treated for localized prostate cancer with curative aim. METHODS AND MATERIALS: This descriptive cross-sectional study comprises 154 patients who had undergone definitive radiotherapy (RAD) and 108 patients with radical prostatectomy (PRECT) at the Norwegian Radium Hospital during 1987-1995. At least 1 year after treatment the patients completed several questionnaires assessing quality of life (European Organization for Research and Treatment of Cancer QLQ-C30 instrument [EORTC QLQ-C30]), lower urinary tract symptoms (LUTS): International Prostate Symptom Score (IPSS), or sexuality (selected questions from the Psychosocial Adjustment to Illness Scale [PAIS]). Urinary incontinence and bowel distress were evaluated by ad hoc constructed questionnaires. A control group (OBS) consisted of 38 patients following the watch-and-wait policy. RESULTS: Twenty percent of the patients from the RAD Group had moderate (14%) or severe (6%) LUTS as compared to 12% in the PRECT group. However, 35% of men from the latter group reported moderate to severe urinary incontinence. "Overall" sexuality was moderately or severely impaired in 71% of the PRECT and 50% of the RAD patients. In the former group high age was correlated with erectile impotency (p < 0.001). In the RAD comorbidity was associated with erectile impotency (p < 0.001). Between 13-38% of the patients recorded moderate or severe bowel distress (blood per rectum: 13%; bowel cramps: 26%; flatulence: 38%), without significant differences comparing patients who had received conventional small 4-field box radiotherapy and patients who had undergone strictly conformal radiotherapy. Despite malignancy and/or treatment-related morbidity, QoL was comparable in both groups with respectively 9% and 6% RAD and PRECT patients, reporting moderately or severely impaired QoL. In the multivariate analysis physical function, emotional function and fatigue were significantly correlated with QoL, whereas sexuality, lower urinary symptoms, and urinary incontinence correlated with QoL only in the univariate analysis. CONCLUSION: In spite of considerable malignancy and/or treatment-related morbidity QoL was good or only slightly impaired in the majority of patients with localized prostate cancer who presented with stable disease > 1 year after definitive radiotherapy or radical prostatectomy with no difference as compared to the age-matched normal population. Clinicians should be aware of the fact that general QoL dimensions (physical function, emotional function, fatigue) are as a rule of greater significance for QoL than sexuality and lower urinary tract symptoms.

Aged↗

PubMed2005

Impact of COX-2 inhibitors in common clinical practice a gastroenterologist's perspective.

Non-selective NSAIDs enhance the risk of serious ulcer complications (bleeding, perforation, obstruction), hospitalization and death about 3-10-fold. The gastrointestinal side effects of NSAIDs have a considerable economical burden, since they are responsible for 5-10 billion dollars in hospitalization charges and lost work time. NSAIDs cause gastrointestinal damage by both topical and systemic effects. COX-1-mediated inhibition of prostaglandin synthesis is probably the most relevant mechanism, but NSAIDs can cause gastrointestinal injury also by COX-independent pathways. COX-2-selective inhibitors (Coxibs) such as celecoxib, rofecoxib or valdecoxib have been developed to achieve an equal relief of pain and inflammation as classical NSAIDs but without their risk of gastrointestinal side effects. Within the first three months, celecoxib became the fastest selling drug in history. The gastrointestinal safety of classical NSAIDs and Coxibs has been compared in a variety of endoscopic investigations, meta-analyses and outcome studies. In conclusion, these studies have clearly shown, that Coxibs are associated with significantly less dyspeptic symptoms, erosions, ulcers and ulcer complications. In contrast, Coxibs seem to delay gastric ulcer healing to the same extent as traditional NSAIDs. Besides their effects on the upper gastrointestinal tract, NSAIDs can cause small intestinal inflammation, ulcers of the small and large intestine, ileal dysfunction, intestinal strictures, colitis and NSAID enteropathy. In addition, NSAIDs increase the risk of lower gastrointestinal complications including bleeding, perforation and obstruction. Current data suggest, that Coxibs are associated with a significantly lower risk of serious lower GI events than traditional NSAIDs. It is now under debate, who should receive COX-2-selective inhibitors instead of classical NSAIDs, since Coxibs are much more expensive. Data from cost-effectiveness studies suggest, that Coxibs should currently be used only in patients with high risks of GI complications.

Animals↗

PubMed1991

Breath hydrogen test using water-diluted lactulose in patients with gastrointestinal amyloidosis.

To investigate small bowel motility in gastrointestinal amyloidosis, lactulose breath hydrogen tests were performed on 16 patients with histologically proven amyloidosis and 12 age- and sex-matched controls. Fasting breath hydrogen concentration (FBHC) was not significantly different between the two groups, but there was a tendency for FBHC in symptomatic amyloidosis patients (median 31.5, range 3-78 ppm) to be higher than in asymptomatic amyloidosis patients (4, 0-34 ppm, 0.05 less than P less than 0.1) and controls (6, 1-19 ppm, 0.05 less than P less than 0.1). Orocecal transit time (OCTT) was significantly delayed in the amyloidosis group (median 150, range 40-220 min) when compared to the controls (60, 20-110 min, P less than 0.01), but OCTT was not statistically different between symptomatic and asymptomatic amyloidosis patients. These data suggest an impaired motility of the stomach and small intestine in gastrointestinal amyloidosis and the possible role of small intestinal dysfunction such as bacterial overgrowth and malabsorption in the occurrence of symptoms in this disorder.

Adult↗