I’m going on four months with elevated liver enzymes. My aspartate aminotransferase and alanine aminotransferase fluctuate between normal to above normal. My alkaline phosphatase steadily remains triple to quadruple the normal level. I continue getting biweekly bloodwork to watch for any changes.
My liver biopsy in early July didn’t reveal any signs of rejection, recurrent primary sclerosing cholangitis, fatty liver disease, or other disorders. The sonographer who performed the ultrasound to guide the biopsy needle even praised how beautiful my liver was.
Having run out of options, the hepatology team is taking a wait-and-see approach. If my alkaline phosphatase remains high but stable, they’ll keep an eye on my bloodwork. However, if my numbers continue to rise, they’ll insert a stent in my slightly dilated biliary duct.
In the meantime, I’ve started my own investigation. Like a detective, I’m combing for clues that my doctors might’ve missed. It’s not that I don’t trust their expertise. I just have more of a vested interest.
I got a new lead a couple of weeks ago during my annual nephrology appointment. My nephrologist was pleased with my normal renal function but expressed concern about my alkaline phosphatase. After I told him my liver team was aware of it, he commented that the intestines also produce alkaline phosphatase.
I had recently discovered the enzyme is found in bones as well and had questioned my team about it. However, learning about intestinal alkaline phosphatase piqued my curiosity. My liver enzymes had increased as my flare subsided. Was there a correlation?
What is alkaline phosphatase?
The four types of alkaline phosphatase are distinguished between tissue-nonspecific and tissue-specific. Tissue-nonspecific alkaline phosphatase comes from the liver, bone, and kidneys. Tissue-specific alkaline phosphatase includes intestinal alkaline phosphatase, placental alkaline phosphatase, and germ cell alkaline phosphatase. The enzyme plays a part in a wide range of bodily functions, including bone formation and growth, brain cell production, and vitamin B6 metabolism. It can also signal inflammation in the body.
The blood test ordered by my doctors measures the combined total of liver, bone, and intestinal alkaline phosphatase. However, the lab can further break down the enzyme’s makeup by the percentage of the three types. A fractionated analysis might hold important clues.
What’s special about intestinal alkaline phosphatase?
Intestinal alkaline phosphatase maintains gut health by regulating fatty acid absorption, detoxifying harmful bacteria, and absorbing calcium. Of the total amount of alkaline phosphatase in the blood, about 14% is intestinal.
Eating a fatty meal can elevate intestinal alkaline phosphatase levels, especially in people with O and B blood types. Bowel perforation or ulcers in the stomach, duodenum, small intestine, or colon can also cause an increase.
I can confidently rule out food because I normally don’t fast for bloodwork, and I’m AB+. Also, when I fasted for my liver biopsy, my alkaline phosphatase level went up. On the other hand, my numbers increased drastically after my flare, indicating it could be linked to intestinal damage or inflammation caused by Crohn’s.
Can IBD influence alkaline phosphatase levels?
IBD-related liver diseases, like primary sclerosing cholangitis and fatty liver disease, can affect liver function. Also, some IBD medications — such as Remicade (infliximab), which I take to control Crohn’s — can injure the liver. In my case, my liver biopsy confirmed neither of these was responsible. Another source of increased liver enzymes is gallstones, which IBD patients are more prone to develop. I no longer have a gallbladder, so this wasn’t possible, either.
Interestingly, a small study submitted to the journal Inflammatory Bowel Diseases found that 93.3% of Crohn’s disease patients with abnormal liver enzymes had colonic lesions. Another study published in the Journal of Surgical Research reported that inflamed intestinal tissue samples obtained from IBD patients during colonoscopies expressed decreased intestinal alkaline phosphatase while non-inflamed tissue had normal amounts.
If intestinal alkaline phosphatase were leaking into the bloodstream, wouldn’t that mean less of it would be in the bowels? If so, I could be hot on the trail and close to nailing down the suspect.
Making my case
Was my liver ever the source of my elevated alkaline phosphatase? Could it have been caused by higher percentages of bone or intestinal alkaline phosphatase? After all, my level spiked only after I began exercising more intensely and frequently and I had suffered the worst flare I’ve had in years.
The colonoscopy I had on Monday could show lesions and inflammation. The bone density scan I’m having next Monday might indicate fractures or extreme bone growth. I’ll share the evidence with my transplant team on Tuesday. Maybe I can convince them to order the blood test that breaks down the makeup of my alkaline phosphatase. Then, we’ll know for certain whether the culprit is my liver, bones, or intestines.
Note: IBD News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health providers with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of IBD News Today, or its parent company, BioNews, and are intended to spark discussion about issues pertaining to IBD.
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