December 2, 2020 at 10:20 am #15957Jenny LivingstonKeymaster
For years and years, I thought everyone with CF was pancreatic insufficient. However, as I met more people in the CF community online, I learned that’s not the case. I have several friends who have never needed to take enzymes (which kind of still blows my mind).
As a child, my digestion was more problematic than my lungs. My enzyme dosage increased through the years until finding my “sweet spot” in my 20’s. As long as I was taking them consistently, things seemed to be under control.
After starting Trikafta, I experienced some pretty severe bloating, pain, and constipation. Over a few months, I slowly decreased my enzyme dosage which seemed to help. Now, a year later, my digestion is more comfortable and better than ever! For years and years, I’d taken 5 Creon with meals and now, I only take 2. I didn’t expect that after 33 years my pancreatic sufficiency would improve, but it’s definitely been a pleasant surprise.
What about you? Are you pancreatic sufficient or insufficient? Has your enzyme dosage changed throughout the years? If you’re on Trikafta, has that changed your enzyme needs?
December 3, 2020 at 2:43 pm #15967Christina KolassaParticipant
What do the docs attribute the decreased need for enzymes? I’m wondering if they’ve figured that out yet. Trikafta is bringing new and exciting news in the CF community on a daily basis. Go Vertex!
December 4, 2020 at 9:01 am #15969Paul met DebbieParticipant
I need the enzymes. Not many, but definitely.
One of my earliest memories (1967?) was the powdered version, which came in little folded pieces of paper. The powder was sprinkled over the food on the plate and did not improve the taste of what was served.
Later there were the granules that came in a metal can. Opening the can released a horrible smell. Putting the correct amount of granules (30 for a light meal and 60 for diner) in an egg cup was probably how I learned counting. Incidentally one would chew on a granule and that ruined the taste of anything in the mouth.
The next stage was the replacement of the egg cup by little capsules of edible wafer paper. The counting and filling was still my job, until the pharmacist delivered them ready to go much later. They were quite large and swallowing them whole was an acquired art.
And finally came the capsules like we know them nowadays, although they were larger in the beginning. I carry a pill container in my pocket as long as I can remember. I don’t mind and never forget to take them, but the fact that they are produced from piggs pancreases bothers me. I would much prefer synthetic enzymes and hope they will be made in the near future.
I don’t take trikafta, but I imagine when some pancreatic function is still available, the production and the flow of enzymes from the pancreas into the intestines is reduced because of the viscosity of the mucoid fluid. Too high internal enzyme levels in the pancreas is what leads to the typical damage of the organ with CF patients I always understood. After trikafta this viscosity might improve (more watery) and more enzymes will reach the intestines, just like the mucus in the airways becomes more fluid. Hence the need for less added enzyme capsules.
The positive effect of restoring pancreatic function was also reported with Kalydeco and Orkambi and it was advised to monitor pancreatic function after being stabilized on drugs like these to prevent pain and cramps from too high enzyme levels. There are also reports of patients needing less insuline after taking modulator drugs. Other patients however reported needing more added enzymes due to eating more. The balance seems to be very individual.
December 4, 2020 at 9:04 pm #15975Tim BlowfieldParticipant
Not surprising but great to hear that you need less pancreatic enzymes nor that it often takes time for the body to adjust to Trikafta. CF is such a chameleon of a disability with every cell in the body having the faulty gene affecting the Chloride pump in every call. Trikafta may be expected to work in every cell providing it gets into the cell. Does it pass the blood/brain barrier? I don’t know. But there again what is the effect of the faulty CFTR in neurological cells? Does anyone know? I doubt.
We live in exciting times.
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