Dysbiosis from Corticosteroid Use

Summary

The common assumption that prolonged courses of corticosteroid treatment can precipitate Candida yeast infections have never been so evident as in this case.

This content was created by the Metametrix Institute

History

This is a case of a 60-year-old woman with a long history of inflammatory bowel disease (Crohn's). She had undergone a ductal resection of the small intestine ileum – about a foot of intestine was removed. She still complains of recurrent episodes of bowel dysfunction and experiences occasional diarrhea with blood presenting in the stool.

In an effort to alleviate the pain and inflammation, she has repeatedly been subject to prolonged courses of corticosteroid therapy. All other attempts at treatment and dietary intervention have been unsuccessful.

It is common knowledge in medical literature that excessive use of oral or inhalant corticosteroids increases the risk of contracting oral and intestinal Candidia infections.

Age

60

Gender

Female

Description of Results

It appears that, in this case, Candida is a problem directly attributable to chronic corticosteroid therapy – as evident by EXTREMELY high levels of  the yeast/fungal marker D-Arabinitol.  At the same time, though, Candida may not have been the cause of this patients presenting complaint – Crohn's disease. There are several other elevated dysbiosis markers that may better represent Crohn's. Notice elevation in benzoate/hippurate markers; phenylpropionate; p-Hydroxyphenylacetate; and tricarballylate. All of these markers are microbiological products. Their simultaneous elevations may reflect distinct pathological colonies responsible for precipitating inflammatory bowel disorders, like Crohn's, colitis, or celiac disease.

Other typical findings with chronic inflammatory bowel diseases are seen in the Amino Acid Plasma analysis.  Almost all of this patients values are low-normal or deficient. Low glycine and threonine suggest long-term amino acid deficiency status. Considering the age of this woman (60 yrs) and her chronic status, it is no surprise shes been having trouble absorbing and digesting protein for such a long time. It seems her lean tissue is no longer able to sustain continued catabolism of branched chain amino acids – while some elevated histidine may illustrate further possibility of tissue sources of amino acids.

Multiple vitamin deficiencies are glaringly evident in the Organix profile. Examining the triad of formiminoglutamate, methylmalonate, and kynurenate, its no surprise that homocysteine is elevated  – as it relies heavily on these nutrients to detoxify.

Lipid peroxides are high for two very simple reasons. 1. As a whole, her serum lipids are high.  With such elevations in the blood, peroxidation is more likely to occur; 2. She is probably unable to efficiently oxidize fatty acids for energy because she is showing solid deficiency markers for carnitine and CoQ10 (see elevations in Krebs intermediates, succinate, malonate, fumarate and lactate). Both L-carnitine and CoQ10 are necessary intermediates in the efficient use of fat as a n energy source by the mitochondria. CoQ10, and the remainder of intermediates in the cytochrome pathway are important electron acceptors. Being unable to donate electrons, fatty acids and other substrates are more likely to undergo uncontrolled free radical reactions – producing oxidative damage to tissues. Elevated lipid peroxides and 8-hydroxy-2-deoxyguanosine corroborate this assumption – one representing fatty acid oxidative damage, and the other DNA damage.

Carnitine is manufactured in the body from the essential amino acid lysine. Lysine is low-normal in this patient, which may account for her apparent deficiency. CoQ10 in built borrowing from the same metabolic pathway as cholesterol. In this patient, hydroxymethylglutarate is very high – evidence that cholesterol is not being manufactured efficiently. CoQ10 also requires smooth operation of this pathway and, as a result, its production is inhibited as well.

Recommendations

Discussion with the physician who order this test led to three treatment recommendations.

1. Eradicate yeast overgrowth. Diflucan was chosen over Flagyl for various degrees of dysbiosis because Diflucan is not well absorbed in the gut, a good idea, because of the high toxicity indicators in the Organix test.  Flagyl is more avidly absorbed through the gut and carries with it far more toxic potential than other, less absorbed, treatments for yeast. High p-hydroxyphenylacetate has been associated with ileal resection with blind loop and anaerobic bacterial overgrowth in the small intestine.

2. This patient needs aggressive antioxidant therapy to minimize DNA damage and proliferative lipid destruction by peroxidation. CoQ10, Vitamin C, Beta-carotene, grape seed extract, and N-acetylcysteine come to mind as recommendations.

3. Take the custom amino acid formula, high in glycine, threonine, arginine, glutamine, aspartate, methionine, and tryptophan to shore up specific deficiencies

Other Comments

It is suspected that the high levels of Candida and other pathological microorganisms are providing an ample toxicological burden, combined with ileal resection – vitamins, along with amino acids, simply are not being assimilated. The necessary cofactors from proper fatty acid, protein, and glucose metabolism do not exist in appropriate quantities.

These results suggest a pathogenic microorganism etiology, and brings to mind recent conclusions drawn from research on ulcerative colitis. In this study, six patients with ulcerative colitis were inoculated with healthy human (cultured) microflora via retention enema for 10 minutes every day for five days. Within a week improvements in symptoms were seen: fewer inflammatory episodes, less pain, better stool consistency, etc. After 4 months, there was a complete reversal of symptoms in 100 percent of the patients – well after treatment had been discontinued. At follow-up 1 to 13 years after treatment, there was no evidence clinically or histologically that there had been a problem with these patients in the first place. (Brody TJ, et al. Treatment of ulcerative colitis using fecal bacteriotherapy. J Clin gastroenterol 2003; 37: 42-47.)