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PubMed2000

[Postural orthostatic tachycardia syndrome (POTS): etiology, diagnosis and therapy].

BACKGROUND: Since the renaissance of tilt table testing in clinical cardiology some 15 years ago, the syndromes of autonomic dysfunction with orthostatic intolerance underwent improved differentiation and classification. In the present review a variant of autonomic dysfunction with orthostatic intolerance--POTS (postural orthostatic tachycardia syndrome)--will be discussed. DIAGNOSIS AND TREATMENT: The affected patients present with orthostatic intolerance, postural tachycardia, exercise intolerance, fatigue, dizziness and in some cases with other dysautonomic symptoms such as gastrointestinal or sudomotor dysfunction. Together with the clinical history, tilt table testing is the cornerstone of diagnostic evaluation by which the syndrome can be distinguished from typical neurocardiogenic disorders. POTS is characterized by different subtypes; accordingly, therapy for relief of symptoms is variable and includes beta blockers for patients with the hyperadrenergic type and alphamimetics for those with partial dysautonomia. CONCLUSION: Although it is now possible to differ POTS from other forms of autonomic dysfunction, further research is warranted to clarify the pathophysiology of this syndrome and its subtypes and to improve therapeutic interventions.

Adrenergic Agents↗

PubMed1995

[Sympathetic skin response in Parkinson syndrome].

Several tests of cardiovascular and gastrointestinal function have been approved for the diagnosis of autonomic regulation dysfunction in Parkinson's disease. In the present study we compared the diagnostic value of the sympathetic skin response (SSR) with the established methods. Ninety percent of the 20 patients we examined (10 women, 10 men, 46 to 80 years) showed pathological results in the cardiovascular function test. Fifty-five percent had a prolonged colon transit, indicating a gastrointestinal dysfunction. We saw pathologically prolonged latencies of the SSR in 35% of the patients, 55% had borderline results. Three of the 20 patients had pathological results in all of the functions examined. Half of the patients had two pathological results, whereas 7 patients were pathological in only one of the three examinations. We were unable to establish any correlation between the SSR and other results, and we also found no relationship between prolonged SSR and the duration of the disease.

Aged↗

PubMed2001

Autopsy pathology of pediatric posttransplant lymphoproliferative disorder.

OBJECTIVES: Posttransplant lymphoproliferative disorder (PTLD) causes significant morbidity and mortality, is related to Epstein-Barr virus (EBV) infection, and is more common in children than in adults. We reviewed autopsies of children who died with PTLD to compare postmortem with antemortem PTLD histology, to assess the extent of PTLD, to document associated pathology, and to identify cause of death. METHODS: Postmortem examinations were performed on 7 patients after bone marrow (n = 3) or liver (n = 4) transplant. PTLD was classified histologically as hyperplasia or lymphoma. In situ hybridization for EBER1 messenger RNA was performed on tissue samples from all cases. EBV serologies were used to categorize infections as negative, primary, or reactive. RESULTS: PTLD was diagnosed in 5 children 12 to 35 (mean: 22) days before death, and 1.5 to 4 (mean: 3) months after transplant; PTLD was diagnosed in 2 cases at autopsy 2.5 and 4 months after transplant. Postmortem PTLD histology resembled antemortem histology; 5 PTLDs were lymphoma, 1 was hyperplasia, and 1 contained both lymphoma and hyperplasia. EBER1 messenger RNA was detected in 6 B-cell PTLDs, including lesions from patients who did not have EBV serology that indicated active infection. Complete autopsy of 4 patients who died with biopsy-proven PTLD revealed widely disseminated disease, and lymph node, brain, gastrointestinal tract, and kidney were involved in all 4 patients. Cases diagnosed at autopsy were 1 widely disseminated PTLD that had been suspected but not proven antemortem, and 1 PTLD confined to abdominal lymph nodes that was not suspected antemortem. Severe organ dysfunction (renal failure, gastrointestinal hemorrhage) was caused by massive PTLD infiltration in 2 patients. The conditions other than PTLD that contributed to morbidity and death were organ infection (5 cases), infarcts (4 cases), and diffuse alveolar damage (3 cases). CONCLUSIONS: PTLD may occur within weeks after transplant in children. The distribution of PTLD comprises a spectrum from localized and subclinical to widely disseminated and symptomatic. PTLD may cause demise quickly after the onset of signs and symptoms, through massive organ infiltration or associated conditions, such as diffuse alveolar damage. EBV serology may not accurately reflect the presence or extent of PTLD. Autopsy studies of transplant patients are necessary to identify the true incidence, natural history, and response to treatment of PTLD.

Autopsy↗

PubMed2004

Management of opioid-induced bowel dysfunction in cancer patients.

The gastrointestinal (GI) effects of morphine and other opioids may result in opioid-induced bowel dysfunction (OBD) and the need for treatment. Although OBD is very common in morphine-treated patients, it is usually under-diagnosed. Opioids deliver their GI effect through central and peripheral mechanisms. Laxatives are the pharmaceuticals prescribed most in this area. Prokinetics as well as cholinergic agonists have been used satisfactorily. One-third of patients with OBD have to be treated rectally. The use of opioid antagonists has been favored, but the bioavailability of oral forms is poor. Opioid antagonists with a quaternary structure have a high affinity for peripheral opioid receptors and therefore do not interfere with the analgesia, nor do they generate alkaloid withdrawal syndrome. Opioid rotation is another strategy for maintaining or improving analgesic quality directed toward decreasing the effects of previous opiates on the GI tract.

Analgesics, Opioid↗

PubMed1995

Stimulated duodenal/bile juice aspiration for diagnosis of enteric pathogens in HIV-infected patients.

Gastrointestinal and biliary abnormalities are common in the acquired immunodeficiency syndrome. Although obviously related to opportunistic infections in many cases, often no infectious agent can be identified. The specific diagnosis depends on invasive methods such as endoscopic retrograde cholangiography and liver histology. To evaluate an alternative and less invasive first-line approach, we conducted a prospective study of microscopic examination of aspirated duodenal/bile juice, to try to identify microbial causes of human immunodeficiency virus (HIV)-related gastrointestinal and biliary tract disease. Sixty-four HIV-infected patients underwent upper gastrointestinal endoscopy with biopsies from the esophagus, stomach, and duodenum, and aspiration of stimulated duodenal/bile juice. Biopsies, duodenal/bile juice, and stool samples were examined for enteric pathogens. Twenty-seven intestinal infections were found in 22 of the 64 patients (34%), 12 (44%) of which were diagnosed by duodenal/bile juice examination. Seven of the 27 infections (26%) were diagnosed exclusively in duodenal/bile juice, whereas 5 were found in biopsies or stool samples as well. Twenty infections (74%) were demonstrated in intestinal biopsies and/or stool samples, 15 without any positive result in duodenal/bile juice. The proportion of patients with elevated alkaline-phosphatase and gamma-glutamyl-transpeptidase activities was higher in patients with infectious agents detected in duodenal/bile juice (5 of 11, 45%), than in patients with infectious agents found exclusively in intestinal biopsies and/or stool samples (2 of 11, 18%). Analysis of duodenal/bile juice is a simple, rapid, and effective method for the detection of enteral pathogens in HIV-related gastrointestinal and biliary dysfunction. It increases the diagnostic yield above the results of intestinal biopsies and stool examinations alone.

Adult↗

PubMed2004

Colonic transit time, sphincter EMG, and rectoanal videomanometry in multiple system atrophy.

Both constipation and fecal incontinence are prominent lower gastrointestinal tract (LGIT) dysfunctions that occur frequently in multiple system atrophy (MSA). We investigated the mechanism of constipation and fecal incontinence in MSA. Colonic transit time (CTT), sphincter electromyography (EMG), and rectoanal videomanometry were performed in 15 patients with MSA (10 men, 5 women; mean age, 63.5 years; mean duration of disease, 3 years; decreased bowel frequency [< 3 times a week] in 9; difficulty in expulsion in 11; fecal incontinence in 3) and 10 age-matched healthy control subjects (7 men and 3 women; mean age, 62 years; decreased bowel frequency in 2; mild difficulty in expulsion in 2; fecal incontinence in none). Compared to the control subjects, MSA patients had significantly prolonged CTT in the rectosigmoid segment and total colon. Sphincter EMG showed neurogenic motor unit potentials in none of control subjects but in 93% of MSA patients. At the resting state, MSA patients showed a lower anal squeeze pressure (external sphincter weakness) and a smaller increase in abdominal pressure on coughing. During rectal filling, MSA patients showed smaller amplitude in phasic rectal contraction, which was accompanied by an increase in anal pressure that normally decreased, together with leaking in 3 patients. During defecation, most MSA patients could not defecate completely and had larger postdefecation residuals. MSA patients had weak abdominal strain, smaller rectal contraction on defecation, and larger anal contraction on defecation (paradoxical sphincter contraction on defecation), although these differences were not statistically significant. These findings in MSA patients were similar to those in Parkinson's disease patients in our previous study, except for the sphincter denervation and weakness in MSA. Constipation in MSA most probably results from slow colonic transit, decreased phasic rectal contraction, and weak abdominal strain, and fecal incontinence results from weak anal sphincter due to denervation. The responsible sites for these dysfunctions seem to be both central and peripheral nervous systems that regulate the LGIT.

Aged↗

PubMed2002

Aging and neural control of the GI tract. I. Age-related changes in the enteric nervous system.

As we enter the 21st century, the segment of the population that is the most rapidly expanding is that comprised of individuals 85 yr of age and older. Dysfunctions of the gastrointestinal (GI) system, including dysphagia, constipation, diarrhea, and irritable bowel syndrome are more common complaints of the elderly, yet our knowledge of the aging GI tract is incomplete. Compared with the rapid advances in the neurobiology of aging in the central nervous system, the understanding of age-related changes in the enteric nervous system (ENS) is poor. In this brief review, I recap experiments that reveal neurodegenerative changes and their functional correlates in the ENS of mice, rats, and guinea pigs. Clinical literature seems indicative of similar structural and functional age-related changes in the human ENS. Current studies that address the mechanisms underlying age-related changes in the ENS are introduced. The future directions for this field include physiological and pharmacological studies, especially at cellular and molecular levels. Research in the aging ENS is poised to make major advances, and this new knowledge will be useful for clinicians seeking to better understand and treat GI dysfunction in the elderly.

Aging↗

PubMed1986

Chronic intestinal pseudoobstruction in young children.

We studied 8 young children (4 boys and 4 girls) with chronic intestinal pseudoobstruction. Intestinal pseudoobstruction, recurrent urinary tract infections, and dysuria occurred between the ages of a few weeks to 5 yr old. All had marked dilatation of the entire gastrointestinal tract distal to the esophagus, and megacystis. Conventional pathologic examinations of the full-thickness specimens of the gastrointestinal tract were normal in 5 and abnormal in 2 patients. The abnormalities included increased fibrosis and lipofuscin pigment in the smooth muscle cells. Myenteric plexus examination, using the Smith's method in 2 patients, was normal. Biopsy specimens from urinary bladders examined in 3 patients revealed separation of individual smooth muscle cells by collagen fibers. Intestinal manometric studies performed in 3 patients showed only weak and infrequent contractions during fasting and after feeding. Severe and extensive dysfunction of the gastrointestinal and urinary tracts with relatively normal histologic appearance are typical for these children.

Abdomen↗

PubMed2003

Autonomic nervous system function in multiple sclerosis.

Autonomic dysfunction causes significant disability in patients with multiple sclerosis (MS). Abnormalities of bladder, bowel and sexual function have been well documented in previous studies but cardiovascular and sudomotor autonomic changes have been less frequently reported. The present study has documented autonomic symptoms and results of cardiovascular and sudomotor autonomic function tests in 63 MS patients and correlated these changes with the clinical features of MS.Autonomic symptoms were common in MS patients, the most common being disorders of micturition, impotence, sudomotor and gastrointestinal disturbances, which were associated with increased MS severity. There was no significant association between autonomic symptoms and abnormalities of autonomic investigations. Abnormalities of one or more autonomic function tests, not including those of bladder, gastrointestinal or sexual dysfunction, were present in more than one half of the MS patients. Autonomic dysfunction, defined as abnormalities in two or more tests, was found in 18% of patients and was associated with increased MS severity. Postural hypotension was very uncommon. Parasympathetic cardiovascular autonomic abnormalities occurred in 16% of patients and were associated with increased MS severity. Sympathetic cardiovascular abnormalities were present in 13% of patients and showed no significant association with MS severity. The sympathetic skin response(SSR) was abnormal in nearly one half of the patients and also showed no significant association with MS severity. There was a variable and heterogenous pattern of autonomic test abnormalities found in the MS patients, which were of minor clinical significance except for postural hypotension. Cardiovascular and sudomotor autonomic abnormalities in MS patients are likely to be due to plaques distributed throughout the brainstem and spinal cord affecting anatomically widespread autonomic regulatory areas and their connections.

Adult↗

PubMed2000

Persistence of abnormal gastrointestinal motility after operation for Hirschsprung's disease.

OBJECTIVE: Recent studies in patients with Hirschsprung's disease (HD) suggest that morphological abnormalities of the intramural intestinal plexuses are not restricted to the colon. In this report, symptoms and objective tests of gastrointestinal (GI) motor dysfunction were determined long after operative treatment to see whether evidence of a more widespread and relevant motility disturbance could be detected. METHODS: Twenty-one children were available for study an average of 6.6 yr after surgery for HD. All of these patients underwent evaluation of bowel frequency per week, total GI transit time (TGTT), and a scintigraphic gastric emptying test using solid food; anorectal manometry and segmental colonic transit times were performed in a subset of patients. Results were compared with findings in appropriately matched controls. RESULTS: Frequency of defecation per week in patients with HD after surgery was not different from that in control children, but TGTT was significantly longer (p < 0.01). Percentage retention of gastric isotope at 60 min exceeded the normal range in 12 of 21 (57.1%) patients, and colonic transit was abnormal in all six children studied. Symptoms persisted in two-thirds of patients postoperatively, and transit abnormalities were more common in the symptomatic subset (p = 0.026). CONCLUSIONS: Our data show that, in a subset of patients with HD, GI motor dysfunction persists long after surgical correction. The heterogeny of basic defects responsible for HD could provide the substrate for these motor abnormalities that, in turn, seem at least partially responsible for continuation of the symptomatic state.

Adolescent↗

PubMed1996

Pharmacology of the gastrointestinal tract.

Oral health care providers must have a basic understanding of gastrointestinal and hepatic dysfunction, principles of medical management, and the influence these factors may have on the dental management of these patients and on the selection and dosage regimen of drugs for the treatment of oral/odontogenic conditions.

Anti-Ulcer Agents↗

PubMed2003

[Visceral hypersensitivity: a concept within our reach].

Despite significant advances in the recognition of etiological factors and pathological mechanisms, the pathophysiology of functional gastrointestinal disorders (FGD) is still not fully understood. Visceral hypersensitivity has been recognized as a characteristic of patients with FGD, especially in patients with irritable bowel syndrome (IBS). Visceral afferent input is modulated by a variety of mechanisms, operating between the gastrointestinal tract and the brain. Dysfunction of these regulatory mechanisms could distort gastrointestinal perceptions. Recent findings suggest that in the majority of cases of IBS the primary abnormality may be at the periphery with alterations of the motor and secretory sensory activity. Although imaging techniques indicate that there are also differences in cortical activation. Furthermore, selective serotonin reuptake inhibitors may benefit FGD. Recent pharmacological studies suggest that 5-HT3 antagonist such as alosetron and cilansetron, and 5-HT4 agonist such as legaserod and prucalopride may also have a potential use in FGD.

Chest Pain↗

PubMed2006

CCK1 antagonists: are they ready for clinical use?

Cholecystokinin (CCK) is a peptide hormone which is found both in the gastrointestinal tract throughout the human small intestine and nerves in the myenteric plexus of the enteric nervous system and in the central nervous system. This dual location constitutes the anatomical basis for this in functions as a hormone and a neurotransmitter implicated in the regulation of both systems. CCK regulates not only motor functions in the gastrointestinal tract like lower oesophageal sphincter relaxation, gastric secretion and emptying, gall bladder contractility and bile secretion into the duodenum, intestinal and colonic motility, but also sensory functions and plays a role in the regulation of food intake. These effects are mediated through selective receptors CCK1 and CCK2. Over the last few years, research has focused on understanding the role of CCK, its receptors with antagonists at the biological, pharmacological, clinical and therapeutic level. As far as the CCK1 antagonists is concerned, important inroads have been made in the potential role of these antagonists in the treatment of GERD, IBS and pancreatitis. They have also shown encouraging results in sphincter of Oddi dysfunction and some gastrointestinal cancers. This review focuses on the recent ad vances of the biological role of CCK and their CCK1 antagonists: their current basic and clinical status in gastroenterology, with particular emphasis on the potential therapeutic role of the CCK1 antagonists and future research directions.

Cholecystokinin↗

PubMed1999

Gastrointestinal immunity in health and disease.

The gastrointestinal lymphoid tissue (GALT) is under constant antigenic challenge from bacteria and food and must be able to distinguish between benign and pathogenic organisms. Recent advances in understanding the organization and function of GALT reveal how it is able to direct appropriate immune responses according to the nature of the antigen and how inappropriate immune responses can lead to local and systemic immunopathology and/or infection. The interaction of the normal bowel flora and GALT is critical to normal local and systemic immune function and plays a major role in the pathogenesis of some immune-related diseases. This review draws upon information from veterinary, human, and laboratory animal studies to provide an update of mechanisms and consequences of function and dysfunction in the gastrointestinal immune system.

Animals↗

PubMed2004

Simultaneous absence of dopamine D1 and D2 receptor-mediated signaling is lethal in mice.

Dopamine (DA) controls a wide variety of physiological functions in the central nervous system as well as in the neuroendocrine and gastrointestinal systems. DA signaling is mediated by five cloned receptors named D1-D5. Knockout mouse models for the five receptors have been generated, and, albeit impaired for some important DA-mediated functions, they are viable and can reproduce. D1 and D2 receptors are the most abundant and widely expressed DA receptors. Cooperative/synergistic effects mediated by these receptors have been suggested, in particular, in the control of motor behaviors. To analyze the extent of such interrelationship, we have generated double D1/D2 receptor mutants. Interestingly, in contrast to single knockouts, we found that concurrent ablation of the D1 and D2 receptors is lethal during the second or third week after birth. This dramatic phenotype is likely to be related to altered feeding behavior and dysfunction of the gastrointestinal system, especially because major anatomical changes were not identified in the brain. Similarly, in the absence of functional D1, heterozygous D2 mutants (D1r(-/-);D2r(+/-)) showed severe growth retardation and did not survive their postweaning period. The analysis of motor behavior in D1r/D2r compound mutants showed that loss of D2-mediated functions reduces motor abilities, whereas the effect of D1r ablation on locomotion strongly depends on the experimental paradigms used. These studies highlight the interrelationship between D1 and D2 receptor-mediated control of motor activity, food intake, and gastrointestinal functions, which has been elusive in the single-gene ablation studies.

Animals↗

PubMed2000

Epidemiology of multiple organ dysfunction syndrome in critical surgical illness.

Multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality in surgical intensive care units (SICUs). Multiple organ dysfunction syndrome remains the most important factor associated with mortality in the SICU. Illness severity scores such as the Acute Physiology and Chronic Health Evaluation-III (APACHE III) and the magnitude of the systemic inflammatory response syndrome (SIRS) at the time of SICU admission are useful in stratifying patients at risk for MODS and subsequent mortality. Assessment of key organ systems shows that mortality correlates with the overall severity of organ dysfunction and the number of involved organ systems, as well as to individual organs that fail. Despite the prognostic utility of SIRS/MODS, definitions of dysfunction of individual organs have shortcomings. The problem with quantitating MODS lies in the inability to adequately define organ dysfunction, especially of the gastrointestinal tract, liver, and central nervous system. Biological indicators of organ dysfunction may prove to be better markers for MODS in the future.

Critical Illness↗

PubMed1996

Acute gastrointestinal complications after cardiac surgery.

Gastrointestinal problems, with an incidence of about 1%, may complicate the postoperative period after cardiovascular surgery, increasing morbidity, length of stay, and mortality. Several risk factors for the development of these complications, including preexisting conditions; advancing age; surgical procedure, especially valve, combined bypass/valve, emergency, reoperative, and aortic dissection repair; iatrogenic conditions; stress; ischemia; and postpump complications, have been identified in multiple research studies. Ischemia is the most significant of these risk factors after cardiovascular surgery. Mechanisms that have been implicated include longer cardiopulmonary bypass and aortic cross-clamp times and hypoperfusion states, especially if inotropic or intra-aortic balloon pump support is required. These risk factors have been linked to upper and lower gastrointestinal bleeding, paralytic ileus, intestinal ischemia, acute diverticulitis, acute cholecystitis, hepatic dysfunction, hyperamylasemia, and acute pancreatitis. Gastrointestinal bleeding accounts for almost half of all complications, followed by hepatic dysfunction, intestinal ischemia, and acute cholecystitis. Identification of these gastrointestinal complications may be difficult because manifestations may be masked by postoperative analgesia or not reported by patients because they are sedated or require prolonged mechanical ventilation. Furthermore, clinical manifestations may be nonspecific and not follow the "classic" clinical picture. Therefore, astute assessment skills are needed to recognize these problems in high-risk patients early in their clinical course. Such early recognition will prompt aggressive medical and/or surgical management and therefore improve patient outcomes for the cardiovascular surgical population.

Aged↗

PubMed1999

Roles of IL-1 and TNF in the decreased ileal muscle contractility induced by lipopolysaccharide.

Gastrointestinal stasis during sepsis may be associated with gastrointestinal smooth muscle dysfunction. Endotoxin [lipopolysaccharide (LPS)] impairs smooth muscle contraction, in part through inducible nitric oxide synthase (NOS II) and enhanced nitric oxide production. We studied the roles of tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) in this process by using TNF binding protein (TNFbp) and IL-1 receptor antagonist (IL-1ra). Rats were treated with TNFbp and IL-1ra, or their vehicles, 1 h before receiving LPS or saline. At 5 h after LPS, contractility was measured in strips of ileal longitudinal smooth muscle, and NOS II activity was measured in full-thickness segments of ileum. LPS decreased maximum stress (mean +/- SE) from 508 +/- 55 (control) to 355 +/- 33 g/cm2 (P < 0.05). Pretreatment with TNFbp plus IL-1ra prevented the LPS-induced decrease. Separate studies of TNFbp alone or IL-1ra alone indicated that, at the doses and timing used, TNFbp was more effective. LPS also increased NOS II activity by >10-fold (P < 0.01) over control. This increase was prevented by TNFbp plus IL-1ra (P = not significant vs. control). We conclude that the LPS-induced increase in NOS II activity and the decrease in ileal muscle contractility are mediated by TNF and IL-1.

Animals↗