Treatment of a Male, Pediatric Crohn’s Disease Patient with the Speci c Carbohydrate Diet (SCD)

Faller, L., Scudiere, J., Davies, Y.

 

 

BRIEF SYNOPSIS

 

     Here we report the treatment of a pediatric Crohn’s disease patient with the Speci c Carbohydrate Diet (SCD) and without medications. e SCD excludes most dairy products and complex carbohydrates to reduce bacterial growth. is is thought to decrease local in ammation and allow the gastrointestinal tract to heal.2 Some studies suggest that this diet can help control and improve symptoms of Crohn’s disease.8,9

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INTRODUCTION

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     Crohn’s disease is an immune-mediated in ammatory condition that can a ect any part of the gastrointestinal tract.1 Although the cause is thought to be multifactorial and the precise mechanisms are not entirely clear, the fundamental defect is believed to be host immune system recognition of native intestinal bacteria as foreign. is triggers an immune response that leads to in ammation of the gastrointestinal mucosa and culminates in the development of erosions, ulcers, and (if prolonged) structuring.2

e mainstay of current Crohn’s disease therapy is pharmacologic management tailored to the speci c needs of the patient and consists predominantly of aminosalicylates (e.g., mesalamine), immunomodulators (e.g., 6-mercaptopurine, azathioprine), and biologics (e.g., anti-TNFa monoclonal antibody). However, an array of elimination diets and enteral nutrition regimens have been tested as alternatives to pharmalogic therapy, and their use has been associated with symptomatic improvement in some Crohn’s disease patients.3,4,5,6,7 e Speci c Carbohydrate Diet (SCD) is one diet that has been found to control and improve signs and symptoms of Crohn’s disease in a small number of patients.8,9 e SCD excludes most dairy products, re ned sugars, and all complex carbohydrates, in order to decrease the amount of carbohydrate available for bacteria to consume.2 e premise is that mucosal in ammation decreases enzymes necessary for breakdown of complex carbohydrates and that this favors metabolism by intestinal bacteria via fermentation and generation of harmful pro-in ammatory byproducts.2 Restriction of dietary carbohydrate is thought to reduce the pro-in ammatory bacterial byproducts and presumably block further in ammation and injury to the gastrointestinal tract. is diet was developed in the 1920s by Dr. Sidney Valentine Haas, a U.S. pediatrician who authored Management of Celiac Disease.12 e speci c details are outlined in Breaking the Vicious Cycle by the mother of one of his patients who studied biology, nutritional biochemistry and cellular biology.2,10 In this paper, we report the successful treatment

of a pediatric Crohn’s disease patient by utilizing the Speci c Carbohydrate Diet without any medications.

 

     A 6-year-old boy presented with a history of persistent diarrhea and mouth sores. e patient claims to have been following a gluten-free diet, but is still complaining about persistent diarrhea and mouth sores. His IBD speci c p-ANCA test showed a peri-nuclear distribution, a pattern associated with ulcerative colitis.11 A small-bowel follow- through imaging study revealed evidence of terminal ileitis. Subsequent upper endoscopy revealed ulcers in the duodenum as well as active in ammation in the duodenum, terminal ileum, descending colon, and rectum. e pathologic di erential diagnosis included Crohn’s disease and based on the clinical and laboratory information listed above, this patient was diagnosed with Crohn’s disease.

 

 

METHODS

The Specific Carbohydrate Diet restricts all food items that contain grain, re ned sugar, dairy, or any other complex carbohydrates. The diet mainly consists of:

• fruits, except plantains
• vegetables, except corn, yams and potatoes
• unprocessed meats
• dairy products that have been fermented for 24 hours or very aged cheeses such as hard cheddar cheese and parmesan.
 

The complete list of items excluded and included in the SCD can be found in the book, Breaking the Vicious Cycle by Elaine Gottschall or online at www.breakingtheviciouscycle. com. e patient strictly adopted the diet on the honors system and was routinely evaluated in clinic before and during the treatment for one year. However, the patient is still on the diet to date. e patient did not record the amount of carbohydrates consumed daily, but rather focused on the types of carbohydrates consumed, as described above. After nine months of treatment, VSL #3, a probiotic, was added to the daily regimen. ere was no speci c reason of adding it at this time point in therapy, other than the physician had been having success with this brand of probiotic with other gastrointestinal patients. After eighteen months of treatment, a SCD multivitamin and sh oil was added to the daily regimen. Again, there was no speci c reason of adding it at this time point in therapy, other than the parent was concerned about the patient growing and getting enough vitamins and nutrients being on the SCD. However, this is not a standard part of the SCD diet. An upper endoscopy was completed 14 months after initiation of treatment to compare to the biopsies collected before treatment. Routine hematoxylin-and-eosin-stained slides (Fig. 1) were evaluated.

 

RESULTS

 

Clinical Response

After one month of the diet, the patient had already gained weight and the persistent diarrhea ceased. Examinations in clinic were completed after four, seven, nine, twelve, eighteen and twenty two months of treatment. At each visit, the patient consistently reported feeling well with no diarrhea. e patient’s caregiver reported a stable body weight in between visits. is patient is currently maintained on the SCD with no medications and to date is doing well.

 

Upper Endoscopy

e rst set of biopsies showed patchy active in ammation in the duodenum, terminal ileum, descending colon, and rectum. e duodenum showed mildly active peptic-type duodenitis with villous blunting and gastric mucin cell metaplasia. While the villi showed blunting, there was no prominence of surface or crypt intraepithelial lymphocytes. Goblet cells were present and evenly distributed. e lamina propria showed a mild lymphoplasmacytic in ltrate. As shown in gure 1A, the terminal ileum showed features compatible with Crohn’s disease, including a patchy lymphoplasmacytic lamina propria in ltrate, erosions, and active in ammation. In one focus, the active in ammation extended f rom the luminal surface to the super cial submucosa, where a loose, non- caseating granuloma was present. Architectural distortion was minimal in this sample. While biopsies from the cecum, ascending colon, transverse colon, and sigmoid colon were essentially unremarkable, the descending colon and rectum showed a few areas of active in ammation. Additionally, poorly cohesive noncaseating microgranulomas were seen in both the descending colon and rectum. Correlation of the histologic ndings with clinical and endoscopic ndings produced a diagnosis of Crohn’s disease.

In the second set of biopsies taken approximately one year after the rst set, peptic-type changes were persistent in the duodenum, including minimal villous blunting and gastric mucin cell metaplasia. Absent, however, was the active in ammation identi ed in the rst duodenal sample. Likewise, the terminal ileum, colon, and rectum showed a marked decrease in in ammation in gure 1B. Active in ammation was not observed in the descending colon or rectum, and mucosal architecture was preserved. e only residual evidence of Crohn’s disease was a few lamina propria microgranulomas found adjacent to prominent lymphoid nodules.

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Figure 1

A. Histologic sections of the terminal ileum. Before treatment, the ileum showed active in ammation, a lymphoplasmacytic lamina propria in ltrate, non-caseating granulomas, and reactive epithelial changes (A). After treatment, the ileum showed essentially unremarkable mucosa (B) with a few lamina propria microgranulomas (not pictured). Hematoxylin-eosin, original magni cation 100x.

 

 

DISCUSSION

We describe the successful use of the Speci c Carbohydrate Diet in the treatment of Crohn’s disease. Not only did the patient’s symptoms improve but also the comparison of biopsy micrographs before and after the SCD revealed a return to normal mucosal architecture. is case is another example suggesting the SCD may be an e ective alternative therapy to pharmacologic therapy for treatment of Crohn’s disease.8,9 However, as the number of Crohn’s disease patients enrolled in the previous studies was quite small and studies that directly compare the e cacy of the SCD to standard pharmacologic therapy and investigate the long-term e ects of the diet are currently lacking, much more research is needed.8,9

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REFERENCES

1. 1  “What Is Crohn’s Disease?” CCFA: What Is Crohn’s Disease? Crohn’s & Colitis Foundation of America, 2014. Web. 21 Feb. 2014. <http:// www.ccfa.org/what-are-crohns-and-colitis/what-is-crohns-disease/>.

2. 2  Gottschall, Elaine Gloria. Breaking the Vicious Cycle: Intestinal Health through Diet. Kirkton, Ont.: Kirkton, 1994. Print.

3. 3  Berg, D., J. C. Clemente, and J. F. Colombel. “Can In ammatory Bowel Disease Be Permanently Treated with Short-term Interventions on the Microbiome?” Expert Review Gastroenterology Hepatology 10 (2015): 1-15. PubMed. Web. 22 Feb. 2015.

4. 4  Lee, D., L. Albenberg, C. Compher, R. Baldassano, D. Piccoli, J. D. Lewis, and G. D. Wu. “Diet in the Pathogenesis and Treatment of In ammatory Bowel Diseases.” Gastroenterology (2015): n. pag. PubMed. Web. 22 Feb. 2015.

5. 5  Charlebois, A., G. Rosenfeld, and B. Bressler. “ e Impact of Dietary Interventions on the Symptoms of In ammatory Bowel Disease: A Systematic Review.” Critical Reviews in Food Science and Nutrition 8 (2015): n. pag. Pubmed. Web. 22 Feb. 2015.

6. 6  Gibson, Peter R., Jane Varney, Sreepurna Malakar, and Jane G. Muir. “Food Components and Irritable Bowel Syndrome.” Gastroenterology (2015): n. pag. PubMed. Web. 22 Feb. 2015.

7 Simpson, H. L., B. J. Campbell, and J. M. Rhodes. “IBD: Microbiota Manipulation through Diet and Modi ed Bacteria.” Digestive Diseases 1 (2014): 18-25. PubMed. Web. 22 Feb. 2015.

8 Cohen, S. A., B. D. Goldacre, S. Oliva, J. Lewis, A. Stallworth, B. Koch, L. Eshee, and D. Mason. “Clinical and Mucosal Improvement with Speci c Carbohydrate Diet in Pediatric Crohn Disease.” Journal of Pediatric Gastroenterology and Nutrition 59.4 (2014): 516-21. PubMed. Web. 22 Feb. 2015.

9 Suskind, D. L., G. Wahbeh, N. Gregory, H. Vendettuoli, and D. Christie. “Nutritional erapy in Pediatric Crohn Disease: e Speci c Carbohydrate Diet.” Journal of Pediatric Gastroenterology and Nutrition 58.1 (2014): 87-91. PubMed. Web. 22 Feb. 2015.

10 Haas, Sidney Valentine; Haas, Merrill P. (2011). e Management of Celiac Disease. Literary Licensing. ISBN 1-258-19621-2.

11 Seidman EG. “Emerging prognostic markers in IBD.” Gastroenterology & Hepatology 3 (12 Supl 36) (2007): 5-6. PubMed. Web. 18 March 2015.

12 Haas, Sidney and Haas, Merrill. Management of Celiac Disease. Lippincott: Philadelphia, 1951. Print.

UC DAVIS HEALTH STUDENT REVIEW | CASE REPORT 3