Case 16: A Failed Preschool Art Project
1. In what percentile for height and weight is Justin?
Justin is below the 50th percentile for weight and height at 2 years & 2 months old and proceeds to the 10th percentile at 3 and 4 years old. 2. Describe how Justin’s villi differ from normal.
Justin’s villi have a smaller surface area and atrophy of fingertip ridges compared to normal villi. 3. What functions of the villi are impaired as a result of Justin’s condition?
Justin’s villi have a reduced ability to absorb nutrients.
4. What caused the diarrhea? What is the technical term for this type of diarrhea? Justin’s condition causes malabsorption of fat content, leading to a type of diarrhea termed steatorrhea. 5. How does Justin’s skin differ from normal?
Justin’s skin has a rash consisting of red, fluid-filled bumps. Justin also has faint fingerprints most likely due to epidermal ridge atrophy. 6. What condition does Justin have, and what causes it?
Justin has celiac disease, which can be caused by a genetic predisposition in combination with exposure to prolamins found in wheat, rye, oats, and barley. Exposure to gluten in the body activates an immune response to attack cells in the small intestine and produce auto-antibodies against tissue transglutaminase (tTG). Absorbed gluten by the small intestine gets metabolized by tTG and broken down to amide and deamidated gluten proteins. The deamidated gluten proteins get processed and presented by macrophages to T-helper cells, which induces an inflammatory response, cytokine production, and ultimately, destruction of intestinal epithelial cells by killer T-
cells. In addition, auto-antibodies are produced by B-cells. These auto-antibodies are anti-tTG and anti-gliadin. Anti-tTG mainly deposits and generates non-digestive complications, such as dermatitis herpetiformis in the skin and chronic kidney disease in the renal glomeruli.
7. What is the etiology of this condition, and how frequent is it?
Celiac disease originates from a genetic predisposition in combination with exposure to gluten found in wheat, rye, oats, and barley. 1 in 100 people have the condition, and many are undiagnosed.
8. What other disease is frequently associated with Justin’s condition?
Celiac disease is associated with other autoimmune disorders, such as type-1 diabetes, thyroiditis, rheumatoid arthritis, SLE, and Addison’s disease. 9. For which disease will Justin be at increased risk over the long term?
Justin will be at increased risk of intestinal lymphoma cancer, chronic kidney disease, anemia, and dermatitis herpetiformis over the long term if his celiac disorder is poorly controlled. 10. How can this condition be treated?
1. In what percentile for height and weight is Justin?
Justin is below the 50th percentile for weight and height at 2 years & 2 months old and proceeds to the 10th percentile at 3 and 4 years old. 2. Describe how Justin’s villi differ from normal.
Justin’s villi have a smaller surface area and atrophy of fingertip ridges compared to normal villi. 3. What functions of the villi are impaired as a result of Justin’s condition?
Justin’s villi have a reduced ability to absorb nutrients.
4. What caused the diarrhea? What is the technical term for this type of diarrhea? Justin’s condition causes malabsorption of fat content, leading to a type of diarrhea termed steatorrhea. 5. How does Justin’s skin differ from normal?
Justin’s skin has a rash consisting of red, fluid-filled bumps. Justin also has faint fingerprints most likely due to epidermal ridge atrophy. 6. What condition does Justin have, and what causes it?
Justin has celiac disease, which can be caused by a genetic predisposition in combination with exposure to prolamins found in wheat, rye, oats, and barley. Exposure to gluten in the body activates an immune response to attack cells in the small intestine and produce auto-antibodies against tissue transglutaminase (tTG). Absorbed gluten by the small intestine gets metabolized by tTG and broken down to amide and deamidated gluten proteins. The deamidated gluten proteins get processed and presented by macrophages to T-helper cells, which induces an inflammatory response, cytokine production, and ultimately, destruction of intestinal epithelial cells by killer T-
cells. In addition, auto-antibodies are produced by B-cells. These auto-antibodies are anti-tTG and anti-gliadin. Anti-tTG mainly deposits and generates non-digestive complications, such as dermatitis herpetiformis in the skin and chronic kidney disease in the renal glomeruli.
7. What is the etiology of this condition, and how frequent is it?
Celiac disease originates from a genetic predisposition in combination with exposure to gluten found in wheat, rye, oats, and barley. 1 in 100 people have the condition, and many are undiagnosed.
8. What other disease is frequently associated with Justin’s condition?
Celiac disease is associated with other autoimmune disorders, such as type-1 diabetes, thyroiditis, rheumatoid arthritis, SLE, and Addison’s disease. 9. For which disease will Justin be at increased risk over the long term?
Justin will be at increased risk of intestinal lymphoma cancer, chronic kidney disease, anemia, and dermatitis herpetiformis over the long term if his celiac disorder is poorly controlled. 10. How can this condition be treated?
