Epidemiological studies suggest that RAP affects 8 to 25% of school-age children ages 9-12-years-old (e.g., Apley, 1975; Devanarayana, de Silva, & de Silva, 2008; Huguet & Miro, 2007; Konijnenberg, de Graeff-Meeder, van der Hoeven, Klimpen, Buitelaar, & Uiterwaal, 2006), and is more prevalent among girls (Apley,1975; Colletti, 1998). RAP accounts for 2 to 4% of pediatric office visits (Starfield, Katz & Gabriel, 1984), and many children with RAP go through potentially risky and possibly unnecessary hospitalizations, tests and procedures, thus placing heavy burden on the medical community (Walker, Garber, Van Slyke & Greene, 1995). Medical evaluations reveal organic disease in fewer than 5% of children evaluated in primary care settings (Stickler & Murphy, 1979). Nonetheless, nearly one-third to one-half of children with RAP continue to complain of abdominal pain and related symptoms after they reach adulthood (Walker, Garber et al., 1995). RAP is defined as “functional” because, in most cases, no organic cause can be found to e
JGPN 2008 .
Resultan de un grupo heterogéneo de causas o es la expresión variable del mismo transtorno.
El objetivo es restablecer el funcionamiento normal . No necesita ser definido como liberación de los sintomas El manejo empieza con el Dx positivo de Dolor abdo minal funcional, explicar la naturaleza de los sínt. Decir: El dolor es real, causado por una respuesta intensa del músculo intestinal alterado o por una hipersensibilidad a diferentes estímulos normales. Hay vulnerabilidad genética, es crónico. Los niños y padres deben saber que no existe enfermedad orgánica seria. Se les habla de criterios de síntomas y hallazgos clínicos que están ausentes en la presentación clínica que excluye una evaluación profunda. ........
RECOMMENDATIONS 1. The term “recurrent abdominal pain” as currently used clinically and in the literature should be retired. Functional abdominal pain is the most common cause of chronic abdominal pain. It is a specific diagnosis that needs to be distinguished from anatomic, infectious, inflammatory, or metabolic causes of abdominal pain. Functional abdominal pain may be categorized as one or a combination of: functional dyspepsia, irritable bowel syndrome, abdominal migraine, or functional abdominal pain syndrome (see Table 1). 2. Functional abdominal pain generally can be diagnosed correctly by the primary care clinician in children 4 to 18 years of age with chronic abdominal pain when there are no alarm symptoms or signs, the physical examination is normal, and the stool sample tests are negative for occult blood, without the requirement of additional diagnostic Evaluation.
RECOMMENDATIONS 1. The term “recurrent abdominal pain” as currently used clinically and in the literature should be retired. Functional abdominal pain is the most common cause of chronic abdominal pain. It is a specific diagnosis that needs to be distinguished from anatomic, infectious, inflammatory, or metabolic causes of abdominal pain. Functional abdominal pain may be categorized as one or a combination of: functional dyspepsia, irritable bowel syndrome, abdominal migraine, or functional abdominal pain syndrome (see Table 1). 2. Functional abdominal pain generally can be diagnosed correctly by the primary care clinician in children 4 to 18 years of age with chronic abdominal pain when there are no alarm symptoms or signs, the physical examination is normal, and the stool sample tests are negative for occult blood, without the requirement of additional diagnostic Evaluation.
Ursodeoxycholic acid (UDCA), previously used for cholesterol gallstone dissolution, is currently considered the first choice therapy for many forms of cholestatic syndromes. Many mechanisms and sites of action have been proposed for UDCA, but definitive data are still missing regarding the key points of its efficacy and optimal dosage in order to achieve a sustained clinical effect. Among the suggested mechanisms of action of UDCA, changes in bile acid pool composition, hepatocyte membrane protection, immunomodulatory effects and bicarbonate-rich hypercholeresis have been extensively studied. However, recent evidence indicate that UDCA is a potent intracellular signalling agent that counterbalances impaired biliary secretion, inhibits hepatocyte apoptosis and protects injured cholangiocytes against toxic effects of bile acids. It is clear that the relative contribution of these mechanisms to the anticholestatic action of UDCA depends on the type and stage of the liver injury. Available clinical evidence suggest that UDCA treatment has to be initiated as early as possible and that higher doses could be more efficacious in inducing and maintaining clinical remission of cholestatic diseases. The future availability of UDCA derivatives will possibly enhance the chances to effectively treat chronic cholestatic diseases.
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