UNIVERSITY OF NAPLES PhD Program “Human ... - FedOA

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INTRODUCTION Pediatric functional gastrointestinal disorders (FGIDs) include conditions in which a variable combination of often, age-dependent, chronic, or recurrent symptoms, such as vomiting, constipation, abdominal pain, are not explained by structural or biochemical abnormalities. As the child is programmed to develop, some functional disorders which occur during childhood accompany normal development, or may triggered by age appropriate but maladaptive behavioral response to internal or external stimuli. According to a biopsychosocial conceptualization of the pathogenesis and clinical expression of the FGIDs, early in life and genetics, in addition to environmental factors such as family influences on illness expression, abuse, major losses, or exposure to infections, may affect one’s psychosocial development in terms of one’s susceptibility to life stress or psychological state and coping skills, as well as susceptibility to gut dysfunction, abnormal motility, altered mucosal immunity, or visceral hypersensitivity. Furthermore, these “brain-gut” variables reciprocally influence their expression. Therefore, FGIDs are the clinical product of this interaction of psychosocial factors and altered gut physiology via the brain-gut axis (1). Genetic factors may predispose some individuals to develop FGIDs, whereas in others, environmental factors contribute to the phenomic expression of these conditions, as well as patient attitudes and behaviours (including health care seeking) relating to it. Some infants may inherit a genetic susceptibility to FGIDs characterized by a particular gastrointestinal reactivity to stress. This temperament-sensitive reactivity seems to be associated to other biological systems such as the cardiovascular, neuroendocrine and immunologic (2). Several pathways may be involved in this genetic predisposition, including lower levels of IL-10 (an anti-inflammatory cytokine) in some patients with IBS (3) that may effect gut mucosal neural sensitivity, serotonin reuptake transporter polymorphisms that can effect levels of 5-HT neurotransmitter, or the response to 5-HT blocking agents (4,5) g-protein polymorphisms that can affect both CNS and gut-related actions (6) and 2adrenoreceptor polymorphisms that affect motility (7). Serotonin reuptake transporter polymorphisms have effects on mood disturbances (8) and may be a genetic link to disorders of brain-gut function such as IBS. This represents an interesting area for future studies. The aggregation of FGIDs in families (9) is not only genetic. Also environmental factors during early life may play a role in the development of FGIDs. Plasticity of the neonatal brain allows early life events to program physiologic response to stress during infancy that may be perpetuated into adulthood (10). Furthermore, what children learn from parents may contribute to the risk of developing an FGID(11, 12) In fact, children of adult patients with IBS make more health care visits (and incur more health care costs) than children of non-IBS parents (13,14), so the family should be aware about the role that psychosocial factors play in the development and perpetuation of FGIDs. Nevertheless psychosocial factors do not define the FGIDs and are not required for diagnosis, research in this field yields three general observation: 1) psychological stress exacerbates GI symptoms; 2) psychosocial factors modify the experience of illness and illness behaviours such as health care seeking; 3) a functional gastrointestinal disorder may have psychosocial consequences on one’s general well-being, daily function status, one’s sense of control over the symptoms, in one word on one’s quality of life. Patients with FGDIs often exhibit sensory afferent dysfunction of the digestive tract that is manifested as altered sensitivity to luminal distention or other stimuli, and that selectively affects the visceral territory (15). Sensation and motility represent the two aspects of gut physiology most relevant to the FGIDs. In health, physiological stimuli from the gut induce motor reflexes, but these remain largely unperceived, with the exception of those related to ingestion and excretion. Depending on specific organs affected, visceral hypersensitivity may underline common symptoms in the FGIDs such as chest pain, abdominal discomfort, abdominal bloating, urgency defecation. Gut sensitivity is intimately related to gut motility. Sensory and motor functions of the 4
gastrointestinal tract are mediated through the enteric nervous system (ENS) and through the extrinsic nerves that connect the gastrointestinal tract to the central nervous system. The major functions of human digestive tract motility are to accomplish propulsion along the gut, to mix gut contents with digestive secretions and expose them to the absorptive surface, to facilitate temporary storage in certain regions of the gut, to prevent retrograde movement of contents from one region to another, and to dispose of residues. Motility is controlled by reflexes, both central and peripheral, as well as by descending modulation from the brain-gut axis. Communication between various regions of the gut is facilitated by the transmission of myogenic and neurogenic signals longitudinally along the gut (16). Gastrointestinal contractions may be classified on the basis of their duration; contractions may be of short duration (phasic contractions) or may be more sustained (tone). Tone is clearly recognized in organs with reservoir function, such as the proximal stomach (accommodation response to a meal) and the colon (response to feeding), as well as in sphincter regions. Compliance refers to the capability of a region of the gut to adapt to its content; it is expresses as the ratio of the change in volume to the change in pressure and is obtained from the pressure-volume curve. Compliance reflects the contribution of several factors, including the capacity (diameter) of the organ, the resistance of surrounding organs, the elastic properties of the gut wall, and its muscular activity. Wall tension, related to compliance, describes the force acting on the gut wall and results from the interaction between intraluminalcontent and the elasticity of the wall. Gut sensation is influenced by tonic or phasic contractions, and several observations suggest that this is mediated in part by an effect on wall tension; assessment of wall tension is therefore important in the interpretation of results of tests assessing perception of visceral stimuli. Transit refers to the time taken for intraluminal contents to traverse a specified region of the gastrointestinal tract. It reflects the combined effects of the various phenomena outlined earlier. Most measurements of transit are based on detecting intraluminal movements of an extrinsic marker labelling the luminal content. Transit depends on many factors, such as the physical (eg, solid, liquid, and gas) and chemical (eg, pH, osmolality, and nutrient composition) nature of both gut contents and the administered marker. Measurement of transit is influenced by the state of gut motility at the time of marker administration (eg, fasted vs fed motility) and any preparation of the gut (eg, cleansing of the colon). Some symptoms characteristic of the FGIDs, such as constipation and diarreha, are suggestive of dysmotility including alteration in contractile activity, tone, compliance and transit in various regions of the GI tract. In the context of the FGIDs, gastrointestinal dysmotility can develop through dysfunction of the control mechanisms at any level from the gut to the CNS. For example, inflammatory, immune, infiltrative, degenerative, or other processes may directly affect the muscle and/or other elements of the enteric nervous system,whereas psychosocial stressors can induce profound alterations in motility (17-26). Because patients with FGID tend to have a greater gastrointestinal motor response to stressful conditions than do healthy subjects, psychosocial stressors are particularly relevant to the symptomatic manifestations of the FGIDs (27-31). In the FGIDs, sustained and inappropriate gut hypersensitivity, as well as gut dysmotility, are well documented. These sensory-motor dysfunctions seem related to alterations in neural processing in the brain-gut axis and in visceral reflex pathways. Their underlying causes and their relevance to symptom generation are the subject of ongoing research. Despite recent progress in our understanding of pathophysiologic mechanisms underlying some forms of FGIDs, no biologic marker exists yet to allow a final diagnosis of FGID. Without any anatomic or biochemical labels, the FGID have required a classification based solely on symptoms. 5
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Page 3: -Boccia G, Manguso F, Miele E, Buon
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Page 11 and 12: Hernell O, Schmitz J (eds): Feeding
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Page 43 and 44: CHAPTER 2 EPIDEMIOLOGY AND PHATOPHY
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Page 47 and 48: INTRODUCTION Gastroesophageal reflu
Page 49 and 50: METHODS In Italy all children from
Page 51 and 52: RESULTS Fifty-nine out of 75 random
Page 53 and 54: DISCUSSION Regurgitation in infants
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eported to induce lower esophageal
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References 1) Nelson SP, Chen EH, S
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FIGURE LEGENDS Fig. 1: I-GERQ score
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Tab. 2 - Risk factors for GERD Risk
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I-GERQ Score Fig.2 16 14 12 10 8 6
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Dyspeptic symptoms in children: the
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INTRODUCTION Dyspeptic symptoms inc
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Dyspeptic symptoms and bowel habit
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RESULTS Eighty of 99 consecutively
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DISCUSSION Studies in children and
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ulcer identified at endoscopy and H
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8. Youle MS, Read NW. Effect of pai
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29. Riezzo G, Chiloiro M, Guerra V,
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Table 1. Rome II functional dyspeps
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Table 3. Frequency of reported dysp
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Figure 2 91
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CHAPTER 3 DIAGNOSIS AND TREATMENT O
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ABSTRACT Objectives: To evaluate in
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elated to acid in children with chr
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A drop in pH below 4.0 lasting at l
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DISCUSSION Chronic unexplained coug
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andom symptom-reflux association. T
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REFERENCES 1. Morice AH. Epidemiolo
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21. Goldani HA, Silveira TR, Rocha
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Table 1 . Model of the contingency
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Table 3. Distribution of the 3 symp
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CONCLUSIONS WHAT THESE STUDIES ADD
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the appearance of peristalsis using
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REFERENCES 1) Jones MP, Dilley JB,
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31) Tache Y, Martinez V, Million M,
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