Serologic markers include IgA antiendomysial antibody and IgA tissue transglutaminase antibody. Because IgA deficiency iscommon in celiac disease, total serum IgA also must be measured to document the accuracy of these tests. In the absence ofIgA deficiency, either test yields a sensitivity and specificity of95%. An endoscopic small bowel biopsy is essential to confirm the diagnosis and should be performed while the patient is stilltaking gluten. The biopsy specimen shows various degrees ofvillous atrophy (short or absent villi), mucosal inflammation,crypt hyperplasia, and increased numbers of intraepitheliallymphocytes. When there is any question about response totreatment, a repeat biopsy specimen may be obtained severalmonths later. Other laboratory studies should be performed torule out complications, including complete blood count, calcium, phosphate, vitamin D, iron, total protein and albumin,and liver function tests. Mild elevations of the transaminases are common and should normalize with dietary therapy.
Treatment consists of complete elimination of gluten from the diet. Consultation with a dietitian experienced in celiac disease is helpful, as is membership in a celiac disease support group. Lists of prepared foods that contain hidden gluten are particularly important for patients to use. Starchy foods that are safe include rice, soy, tapioca, buckwheat, potatoes, and (pure) oats. Many resources also are available via the Internet to help families cope with the large changes in diet that are required. Most patients respond clinically within a few weeks with weight gain, improved appetite, and improved sense of well-being. Histologic improvement lags behind clinical response, requiring several months to normalize.
SEE CHAPTER 34.
Intussusception is the “telescoping” of a segment of proximalbowel (the intussusceptum) into downstream bowel (the intussuscipiens). Most cases occur in infants 1 to 2 years old; in this age group, nearly all cases are idiopathic. Viral-induced lymphoidhyperplasia may produce a lead point in these children. In olderchildren, the proportion of cases caused by a pathologic leadpoint increases. In young children, ileocolonic intussusceptionis common; the ileum invaginates into the colon, beginning at ornear the ileocecal valve. When pathologic lead points are present,the intussusception may be ileoileal, jejunoileal, or jejunojejunal.
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An infant with intussusception has sudden onset of crampy abdominal pain; the infant’s knees draw up, and the infant cries out and exhibits pallor with a colicky pattern occurring every 15 to 20 minutes. Feedings are refused. As the intussusception progresses, and obstruction becomes prolonged, bilious vomiting becomes prominent, and the dilated, fatigued intestine generates less pressure and less pain. As the intussuscepted bowel is pulled further and further into the downstream intestine by motility, the mesentery is pulled with it and becomes stretched and compressed. The venous outflow from the intussusceptum is obstructed, leading to edema, weeping of fluid, and congestion with bleeding. Third space fluid losses and “currant jelly” stools result. Another unexpected feature of intussusception is lethargy. Between episodes of pain, the infant is glassy-eyed and groggy and appears to have been sedated. A sausage-shaped mass caused by the swollen, intussuscepted bowel may be palpable in the right upper quadrant or epigastrium.