Best treatment options for PD during an exacerbation of Inflammatory Bowel disease (IBS): By Dr. De Leon

As I have been dealing with severe Gi complications from both PD and history of ulcerative colitis, I thought I would cover this topic today on how to manage living with both illnesses. Not an easy task I assure you. As you may know, people with inflammatory bowel disease are at higher risk of having PD. But having PD can also compromise our immune systems making flare ups and exacerbation’s much more common.
Not only are colitis exacerbation’s a medical emergency due to possible severe dehydration that can occur but depending on the severity of disease and location down the Gi tract may require surgery. On top of the colitis Parkinson’s symptoms can also spin out of control lengthening recovery period and possibly prolonging hospitalization and rehab if we are not careful.

First, what is IBS- term used to describe disorders involving chronic inflammation of gi tract.
These compromise 2 diseases:

Ulcerative colitis (UC) – only involves colon and rectum
Crohn’s disease- involves the entire digestive tract

Complications of BOTH:
• Colon cancer need colonoscopy every 10years or more often
• Skin, eye and joint inflammation- PD can also cause joint pain in shoulder, hip and can cause eczema.
• Primary sclerosing cholangitis -scaring of the bile ducts leading to liver damage
• Increase blood clots- remember that PD increases risk of clots especially in those of us with migraines.

• Toxic megacolon- rapid expansion and swelling of colon extremely serious condition
• Perforated colon
• Severe dehydration

• Ulcers
• Malnutrition
• Bowel obstruction

• Nutritional support
• Calcium and vitamin D supplement especially important since we as PD patients already have Vitamin D deficiency
• Iron supplement- we may also already be anemic due to B12 deficiency
• Antidiarrheal –
• Desetin for irritation of your hiney
• Wear adult diapers for security till symptoms resolve
• Pain relievers- like Tylenol – avoid Nsaids like Motrin which make symptoms worse
• Antibiotics
• Anti-inflammatory drugs steroids and aminosalicylates (e.g. Asacol), balsalazide (Colazal) and olsalazine (Dipentum)
• Immunosuppressants methotrexate, azathioprine, cyclosporine-

 Important to note that some of these medicines cause b6 and b12 deficiency and can cause numbness and tingling which can already be present in PD. They can also increase the shakiness, can also cause nausea, vomiting, increase in BP, and cause dizziness. Therefore, it is extremely important to have a direct communication between your neurologists and Gi doctor. Especially, if these medicines will be taken for a long period of time. These can also cause osteoporosis so may have to take medication to prevent given that PD meds already increase risk of this. Plus can worsen headaches many of us already have migraines with PD.

• Tumor necrosis factors (TNF) e.g. Humira, Entyvio, Tyrabri, Stelara
• Dietician consult if losing too much weight
• Add multivitamin can be a melt
• May need to increase nausea meds since many PD drugs also cause nausea. Take ginger, mint, and peppermint teas to help with this. I have been on a diet of peppermint and mint tea for last 3 weeks along with Zofran to control severe nausea.

• Limit dairy products
• Low fat foods
• Eating fiber can exacerbate symptoms – steam vegetables instead of raw

 Things in cabbage family like cauliflower and broccoli usually make things worse
 Avoid nuts, fresh fruit especially those with skin like apple –if you do eat peel first, no popcorn, seeds or corn. Things like watermelon, pineapple, bananas,
• Avoid caffeine, alcohol and spicy foods- there goes my coffee, sweet tea, Mexican food and margaritas!!! My, my, what am I to do?

• Eat small meals -5-6 meals – this will help both PD and colitis
• Drink lots and lots and lots of water!!!
Can have jell-o, Popsicle, Gatorade, even Iv fluids if necessary to avoid dehydration

PD medications will have to be given either at higher doses to compensate for loss during exacerbation or be given in alternate route. For instance, if colitis is severe and intractable perhaps pump and /or DBs would be best. During the exacerbation you may also need to switch levodopa to oral disintegrating I.e. Parcopa, use 24 hour amantadine (Gicovri), Neupro patch and apomorphine either injection or melt strip once available. This will keep you from losing effect of medication because of gi malabsorption and diarrhea. We don’t want to decrease medication dose because not only will you have risk of falling but also of aspiration which would only complicate matters.
Best thing is be proactive in avoiding things that can trigger an exacerbation not always possible to control but we can alter our life style to reduce chance. This means decreasing stress through meditation, exercise, eating small meals regularly on time, drinking lots of fluids and sleeping well. Don’t forget routine check -ups!


all rights reserved by Maria De Leon

Parkinson’s Disease: an Autoimmune DIsease? By Dr. De Leon


For some time me and others like myself have been toying with the idea could it be possible that Parkinson’s is yet another autoimmune disease like diabetes or thyroid disease or even pernicious anemia? Or even an inflammatory disorders like ulcerative colitis? Perhaps some genetic subtypes can more easily fall into this category than others. For instance, it is interesting that the majority of Parkinson’s Disease (PD) patients have B12 deficiency as a co morbidity. Or that the type of Gaucher patients that are most likely to develop and have an increase risk of developing PD are type I patients – those without central nervous system involvement.

Patients who posses Gaucher and are carriers of a GBA gene mutation have increased risk of developing Parkinson’s disease and parkinsonism. Gaucher patients carry a deficiency of the enzyme glucocerobrosidase.  This enzyme is typically acts on the glycolipid glucocerobroside. So, when the enzyme is defective, glucosylceramide aggregates and accumulates in white cells (which are responsible for mounting immune attack but particularly like to congregate in the macrophages. The macrophages are like “Pac Man” hungry white blood cells gobbling up invading bacteria. They are formed in response to an infection or accumulating damage or dead cells. Thus, they are unable to break down fatty acids and they have abnormal accumulation into the white cells and macrophages which are the ones responsible for being able to mount an appropriate immune response against a foreign attack like bacteria or virus. But, if these cells who are to destroy the offending viruses etc. are unable to take them up because already full with unwanted stored up material then more white cells, T cells and macrophages have to be created jamming up the system and thus indiscriminately attacking normal cells throughout the body and brain. Some evidence of this is present in the preliminary data in a study I am involved at the University Of Texas Houston Center. My friend and colleague has informed me that my blood levels of T cells and other inflammatory and immune markers have been measured and found to be elevated and have improved as my disease has been treated. Data hopefully will be released soon.(this is all preliminary and confidential).

The other subtype of PD which points to an inflammatory and autoimmune component is the LRRK2 gene phenotype. Many of these patients with this type of phenotype have a history of inflammatory bowel disease most often ulcerative colitis. Ulcerative colitis (UC) is another autoimmune disease characterized by T-cells infiltrating the colon. Although Crohn’s disease another inflammatory bowel disease which is much more extensive beyond the colon as compared to UC has also been seen in this group of PD patients, once again making a case for a possibility of our immune system going haywire and attacking the nervous system. In medicine, it is dogma to say that once a patient has one autoimmune disease they are at higher risk for contracting another and we frequently see this in our practices. But, until recently, no one had really dared to contradict the underlying notion that “neurons” were somehow protected from attacks from the immune system. Although, we have clear evidence of instances of where there is an autoimmune reaction in the central and peripheral nervous system after vaccine injections causing “Acute disseminated encephalomyelitis” and also MS but these have only targeted the connections not destroyed or actually damaged actual Neurons! Therefore, if it is true that Parkinson’s neuronal loss is a result of attack of the immune system itself it would revolutionize not only our thinking but our way of preventing and going after treatments for Parkinson’s.

So, recently researchers tested this hypothesis to see if indeed living neurons would display antigens (like bacteria or viruses) which then trigger an immune mediated response to neutralize this force. Drs. Sutzer and Cebrian from Columbia University used in vitro mouse and human neurons from embryonic stem cells. Their studies revealed that under certain circumstances- including those known to occur in PD. These neurons produced a special protein which presented an antigen which was recognized by the T cells and triggered an attack on these neurons. They prove an autoimmune process can happen and neurons can be attacked but is not known if this is the initial or final response or if all Parkinson’s is started this way or only those subtypes I alluded to previously. One thing is for sure future is bright and field is ripe for new and novel treatment options!

For more information on the subject go to:






Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at you can also learn more about Parkinson’s disease at or at;,

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