Showing posts with label studies. Show all posts
Showing posts with label studies. Show all posts
Thursday, April 12, 2012
PBC and Gluten Sensitivity
Here is an Article talking about PBC and gluten Sensitivity. Mentions that there are more than 200 studies already linking gluten sensitivity and liver disease...
Tuesday, April 10, 2012
Gluten Sensitivity and Celiac
“Celiac disease and gluten sensitivity are subsets of gluten intolerance"
There is some debate whether a celiac is more likely to contract autoimmune disease than a gluten sensitive patient, but the jury is still out. I can only state that clinically I have seen many patients with autoimmune disease who were gluten sensitive.
http://www.celiaccentral.org/research-news/Celiac-Disease-Research/134/vobid--2264/
http://en.wikipedia.org/wiki/Gluten_sensitivity
There is some debate whether a celiac is more likely to contract autoimmune disease than a gluten sensitive patient, but the jury is still out. I can only state that clinically I have seen many patients with autoimmune disease who were gluten sensitive.
We also know that gluten, in sensitive individuals, extends its negative effects far beyond the gastrointestinal tract. Cellular & Molecular Life Sciences 2005 reported: “celiac disease has also been termed gluten sensitive enteropathy because the small intestine is the main target of injury; however, the clinical manifestations are extremely diverse, suggesting the disorder is in fact a multi-systemic disorder.”
Hepatology Journal 2007 found: “liver blood test abnormalities affect patients with classical celiac disease or may be the sole presentation of atypical celiac disease.” “A gluten free diet leads to normalization of the blood in 75% to 95% of patients with celiac disease, usually within a year of adherence to the diet.” “Even more, celiac disease was found to be associated with an 8-fold increased risk of death from liver cirrhosis.”
http://en.wikipedia.org/wiki/Gluten_sensitivity
Prevalent Role of Gluten Sensitivity and PBC
57% of patients with acute liver failure have anti-transglutaminase antibodies suggesting a role of gluten sensitivity in primary biliary cirrhosis, and primary biliary cirrhosis is considerably more common in gluten sensitive enteropathy than the normal population
I know it's just wikipedia, just saying it's becoming more common knowledge!
http://en.wikipedia.org/wiki/Primary_biliary_cirrhosis
I know it's just wikipedia, just saying it's becoming more common knowledge!
http://en.wikipedia.org/wiki/Primary_biliary_cirrhosis
PBC Familial Clusters Involve Mother-Daughter Pairs
Whether coeliac disease leads to severe liver disease and failure is the subject of ongoing debate. Patients with chronic liver disease have been found to have a higher prevalence of coeliac disease than the general population. A study of 327 patients with 'chronic liver disease' from Sweden found the prevalence of coeliac disease was increased at least 15-fold. Patients with severe liver disease were investigated in a study from Finland. In those considered for liver transplant for gross liver disease, coeliac disease was found in four and on a gluten-free diet a dramatic response ensued in the three compliant patients and in the fourth, a poorly compliant patient, a partial response followed. A related study of 185 Finnish patients who underwent liver transplantation found eight had adult coeliac disease; four to 10 times the expected prevalence. Seven of the eight adult coeliac disease patients were non-compliant long term. The liver biopsies showed a number of pathologies; autoimmune hepatitis (one), primary biliary cirrhosis (two), steatosis, primary biliary cirrhosis (one), primary sclerosing cholangitis (one), congenital liver fibrosis (one), chronic active hepatitis (one), secondary sclerosing cholangitis following cholecystectomy (one).
There are, moreover, numerous reports of a link to primary biliary cirrhosis with evidence of improvement on a gluten-free diet, leading to the recommendation that all patients with primary biliary cirrhosis be screened for coeliac disease.
There is evidence for links between coeliac disease, often silent, and a wide variety of liver diseases particularly a mild silent hepatitis and primary biliary cirrhosis.
http://www.medscape.com/viewarticle/500797_3
And if anyone doubts my worry for Zoe:
...data suggest that first-degree relatives of PBC patients have an increased risk of developing the disease. Most often, these familial clusters involve mother-daughter pairs, which is consistent with the female preponderance of the disease...
I am justified to worry!
http://www.hindawi.com/journals/ad/2011/189585/
There are, moreover, numerous reports of a link to primary biliary cirrhosis with evidence of improvement on a gluten-free diet, leading to the recommendation that all patients with primary biliary cirrhosis be screened for coeliac disease.
There is evidence for links between coeliac disease, often silent, and a wide variety of liver diseases particularly a mild silent hepatitis and primary biliary cirrhosis.
http://www.medscape.com/viewarticle/500797_3
And if anyone doubts my worry for Zoe:
...data suggest that first-degree relatives of PBC patients have an increased risk of developing the disease. Most often, these familial clusters involve mother-daughter pairs, which is consistent with the female preponderance of the disease...
I am justified to worry!
http://www.hindawi.com/journals/ad/2011/189585/
Is Gluten Intolerance The Cause of Autoimmune Disease
...There has been proof for many years that the intestine is not the only tissue targeted by the immune reaction to gluten...Now, more recent research reveals that perhaps a vast number of autoimmune diseases may also involve an immune response to dietary gluten...And potentially on and on it goes to include many of the 100s of autoimmune diseases afflicting millions of Americans. Can you now see why gluten has such far-reaching effects that damage other systems of the body?
Dr. Alessio Fasano performed a brilliant study on rats that were genetically predisposed to develop type 1 diabetes...This study was the first time that an autoimmune disease was prevented by blocking intestinal permeability...This study opens a new field of investigation into the relationship between the health of the intestine and the basis of many diseases. Imagine if the “unknown trigger” of autoimmune disease turns out to be gluten and its effect of creating a leaky gut!
A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases. They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age 2 to almost 35% by age 20. Imagine if screening of all children for gluten intolerance resulted in reductions of future autoimmune diseases!
...have their children evaluated for gluten intolerance, especially if there is any incidence of autoimmune disease in their family tree...
...we do see some very exciting reversals in autoimmune disease symptoms once a patient has removed gluten from their diet...
http://www.healthnowmedical.com/blog/2011/07/05/is-gluten-intolerance-the-cause-of-autoimmune-disease/
Dr. Alessio Fasano performed a brilliant study on rats that were genetically predisposed to develop type 1 diabetes...This study was the first time that an autoimmune disease was prevented by blocking intestinal permeability...This study opens a new field of investigation into the relationship between the health of the intestine and the basis of many diseases. Imagine if the “unknown trigger” of autoimmune disease turns out to be gluten and its effect of creating a leaky gut!
A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases. They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age 2 to almost 35% by age 20. Imagine if screening of all children for gluten intolerance resulted in reductions of future autoimmune diseases!
...have their children evaluated for gluten intolerance, especially if there is any incidence of autoimmune disease in their family tree...
...we do see some very exciting reversals in autoimmune disease symptoms once a patient has removed gluten from their diet...
http://www.healthnowmedical.com/blog/2011/07/05/is-gluten-intolerance-the-cause-of-autoimmune-disease/
Leaky Gut
What is the Leaky Gut Syndrome (LGS)?
Leaky gut syndrome is a term often used in complementary or alternative medicine circles and by the lay public that describes a collection of symptoms believed to be due to what medical researchers call increased intestinal permeability or altered intestinal or gut barrier function. This concept is increasingly recognized as one of the most important problems, if not the most important, in the prevention or development of various diseases such as celiac disease, Crohn's disease and various autoimmune disorders. An intact gut barrier is part of the innate immune system defense mechanism that is important for health and prevention of disease. The intestine is lined with a single layer of epithelial cells, called enterocytes in the small bowel and colonocytes in the large bowel or colon. These epithelial cells constitute the intestinal barrier or defensive wall from what enters our body when we eat.
Can gluten cause leaky gut with or without celiac disease?
Chronic gluten exposure has been shown to activate zonulin resulting in increased intestinal permeability (or leaky gut) even in the absence of celiac disease. ...
Study Sheds Light On Gluten Sensitivity - WSJ.com
Very interesting article. Like I keep saying- this information is still very new, but it's real!
http://online.wsj.com/article/SB10001424052748704893604576200393522456636.html
http://online.wsj.com/article/SB10001424052748704893604576200393522456636.html
Is gliadin really safe for non‐coeliac individuals?
"The data obtained in this pilot study support the hypothesis that gluten elicits its harmful effect, throughout an IL15 innate immune response, on all the individuals. This innate response is found in both patients with and without CD, although the triggering of an adaptive response is CD specific. We propose that somehow patients with CD need to be DQ2 and also have a lower threshold for triggering an adaptive TH1 response. This lower threshold could be mediated by the higher basal levels of immune mediators, like IFNγ mRNA, found in patients with CD, a defect in the CD permeability or even a higher IL15‐sensitive response under the same stimulus, which might be mediated by a higher density of IL15 receptor in patients with CD."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1954879/?tool=pmcentrez
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1954879/?tool=pmcentrez
Thursday, March 29, 2012
Not the best news but could be worse I guess
It could always be worse...I just gotta remember that.
So I found out yesterday that I am in Stage 2 of Primary Biliary Cirrhosis...Ugh. There are 4 stages, I was hoping for stage 1 (Or Zero- That would mean no damage at all yet, but I knew that'd be asking for too much...).
{Pre-UDCA [The Medicine I take]}
In a study involving 916 biopsy specimens from 222 patients followed in the pre-UDCA era, cirrhosis developed within four years in 31 and 50 percent who presented initially with stage I or II disease, respectively
The presence of cirrhosis (stage IV), is associated with a worse prognosis and identifies a group of patients at risk for development of complications related to cirrhosis including variceal bleeding and development of hepatocellular carcinoma. In a study of 256 patients seen in the pre-UDCA era, 31 percent developed esophageal varices during a median of 5.6 years of follow-up. One- and three-year survival rates were 83 and 59 percent, respectively, after the development of varices.
{With UDCA}
In another study, the presence of ductopenia {"refers to the associated reduction in the number of intrahepatic bile ducts, a process that ultimately leads to cholestasis"[bile not flowing and destroying liver]}on a baseline liver biopsy predicted histologic progression despite UDCA
In a trial of 180 patients at one medical center, UDCA led to a significant decrease in the plasma levels of aminotransferases, alkaline phosphatase, and bilirubin. Although there were also fewer deaths in the treatment arm, there was no improvement in fatigue, pruritus, liver histology, or referral for liver transplantation. In a follow-up report in which treatment had been continued for a total of three years, UDCA was associated with a significant reduction in the risk of death and need for transplantation
Similar findings were noted in a multicenter Canadian study of 222 patients. The active therapy group had lower plasma levels of the aminotransferases, alkaline phosphatase, bilirubin, IgM, and cholesterol. Fatigue, pruritus, and the rates of liver transplantation and death were unchanged. There was, however, a beneficial effect on liver histology as manifested by decreased progression of periportal hepatocellular ballooning and bile duct loss.
_________________________________________
{Random interesting tidbit I found. Sucks it's still coming back to bite me after 4 years quit!}
Cigarette smoking — An association between PBC and cigarette smoking has been suggested in epidemiologic studies. At least two studies also suggested that cigarette smoking is associated with more advanced fibrosis stage. In one of the studies, never-smokers were significantly less likely to have advanced fibrosis (METAVIR fibrosis score of 3 or 4) than patients who had smoked in the past or were current smokers (16 versus 33 percent). For each pack-year increase in smoking, there was a 5 percent increase in the likelihood of advanced fibrosis.
_______________________________________
So Anyway, what now? Now I get more tests! Yay! I have to get blood work drawn in 2 weeks, 3 months and 6 months. Then see the doctor again. Hopefully we'll see a downward trend of the numbers and can assume the meds (and diet changes) are helping. Depending on how it's going, at some point I'll get another liver biopsy to see what stage I'm in then.
My hope is that the meds slow down the progression and my diet changes help to start sealing my gut and EVENTUALLY (I'm talking several years here), I MIGHT see some reversal of this. And then after even more time, maybe I'll actually beat this disease. I mean I know it's supposedly 'incurable', but I have already met people that have cured their Auto Immune disease and read about lots more by doing what I'm doing. So my hopes are high.
I'm just going to stay on top of this and see where it goes.
________________________________________
Now I also know to stress even more to Zoe to not smoke (which of course I would already, but here's even another reason) and to eat right. I really don't want my little girl to get this ("familial clustering of autoimmunity has long been recognized" "Inheriting certain genes can make it more likely to get an autoimmune disease. But a combination of genes and other factors may trigger the disease to start"). And it's not just PBC I have to worry about- "Children {and anyone} with one autoimmune disease tend to run a higher risk of developing another"- Which is what has happened to me- I got lichen sclerosis first (AI disease) and now PBC...What next??
Heredity: A child inherits certain genes from her parents that make her susceptible to a particular disease.
Environmental factors: The disease doesn’t actually reveal itself until it’s “triggered” by something.
Hormonal factors: Given that many autoimmune diseases tend to affect adolescent girls and young women, the presence or amount of certain naturally occurring hormones in the body may also play a role in when these illnesses come to the fore.
So this is how it could have happened with me:
I am predisposed to get an AI; I eat Gluten all my life; I cause holes in the gut and gluten travels around my body; My immune system attacks the Gluten; Then I get my Sphincter of Oddi Dysfunction attacks; That 'triggered' my immune system some how to get confused and start attacking my body giving me LS and PBC
[" When the immune system attacks the gluten protein it can confuse other bodily proteins for gluten due to their similar molecular structure. The term used to describe this phenomenon is “cross-reactivity”. This cross reactivity is the cause of the immune system attacking “self”. It believes it’s attacking a toxin, in this case gluten. In some cases the trigger to attack self can be an infection"]
Of course, there's no way to know if I've had the PBC before the LS and just didn't know about it - the LS just makes itself KNOWN! Maybe it was the time I tried the Depo Shots that triggered it, or the hormonal changes from quitting smoking or being pregnant, or the stress of a kindey stone or gall stone, or that really high fever I had that one time- Just making a point, that there's really no way to determine the 'trigger', could be anything, which is why it's so important for me to try to prevent the leaky gut in the first place for Zoe!
Ugh. Just sucks to know I have probably passed the genes on to Zoe to develop AI disease(s).
Welcome to the world! You're beautiful! Smart! Funny! And, oh yea, here's a little something extra...
Great job mommy!
________________________________
Sources:
UpToDate.com Unfortuantely, my trial is almost over! :(
ChildrensHospital.org
WomensHealth.gov
ncbi.nlm.nih.gov
So I found out yesterday that I am in Stage 2 of Primary Biliary Cirrhosis...Ugh. There are 4 stages, I was hoping for stage 1 (Or Zero- That would mean no damage at all yet, but I knew that'd be asking for too much...).
- Stage one: Inflammation and/or abnormal connective tissue confined to the portal areas
- Stage two: Inflammation and/or fibrosis confined to portal and periportal areas
- Stage three: Bridging fibrosis
- Stage four: Cirrhosis
Histologic stage — PBC is classified histologically into four stages.
As noted above, the natural history of PBC involves histologic progression along these stages, although treatment with UDCA may slow disease progression. {Pre-UDCA [The Medicine I take]}
In a study involving 916 biopsy specimens from 222 patients followed in the pre-UDCA era, cirrhosis developed within four years in 31 and 50 percent who presented initially with stage I or II disease, respectively
The presence of cirrhosis (stage IV), is associated with a worse prognosis and identifies a group of patients at risk for development of complications related to cirrhosis including variceal bleeding and development of hepatocellular carcinoma. In a study of 256 patients seen in the pre-UDCA era, 31 percent developed esophageal varices during a median of 5.6 years of follow-up. One- and three-year survival rates were 83 and 59 percent, respectively, after the development of varices.
{With UDCA}
In another study, the presence of ductopenia {"refers to the associated reduction in the number of intrahepatic bile ducts, a process that ultimately leads to cholestasis"[bile not flowing and destroying liver]}on a baseline liver biopsy predicted histologic progression despite UDCA
In a trial of 180 patients at one medical center, UDCA led to a significant decrease in the plasma levels of aminotransferases, alkaline phosphatase, and bilirubin. Although there were also fewer deaths in the treatment arm, there was no improvement in fatigue, pruritus, liver histology, or referral for liver transplantation. In a follow-up report in which treatment had been continued for a total of three years, UDCA was associated with a significant reduction in the risk of death and need for transplantation
Similar findings were noted in a multicenter Canadian study of 222 patients. The active therapy group had lower plasma levels of the aminotransferases, alkaline phosphatase, bilirubin, IgM, and cholesterol. Fatigue, pruritus, and the rates of liver transplantation and death were unchanged. There was, however, a beneficial effect on liver histology as manifested by decreased progression of periportal hepatocellular ballooning and bile duct loss.
_________________________________________
{Random interesting tidbit I found. Sucks it's still coming back to bite me after 4 years quit!}
Cigarette smoking — An association between PBC and cigarette smoking has been suggested in epidemiologic studies. At least two studies also suggested that cigarette smoking is associated with more advanced fibrosis stage. In one of the studies, never-smokers were significantly less likely to have advanced fibrosis (METAVIR fibrosis score of 3 or 4) than patients who had smoked in the past or were current smokers (16 versus 33 percent). For each pack-year increase in smoking, there was a 5 percent increase in the likelihood of advanced fibrosis.
_______________________________________
So Anyway, what now? Now I get more tests! Yay! I have to get blood work drawn in 2 weeks, 3 months and 6 months. Then see the doctor again. Hopefully we'll see a downward trend of the numbers and can assume the meds (and diet changes) are helping. Depending on how it's going, at some point I'll get another liver biopsy to see what stage I'm in then.
My hope is that the meds slow down the progression and my diet changes help to start sealing my gut and EVENTUALLY (I'm talking several years here), I MIGHT see some reversal of this. And then after even more time, maybe I'll actually beat this disease. I mean I know it's supposedly 'incurable', but I have already met people that have cured their Auto Immune disease and read about lots more by doing what I'm doing. So my hopes are high.
I'm just going to stay on top of this and see where it goes.
________________________________________
Now I also know to stress even more to Zoe to not smoke (which of course I would already, but here's even another reason) and to eat right. I really don't want my little girl to get this ("familial clustering of autoimmunity has long been recognized" "Inheriting certain genes can make it more likely to get an autoimmune disease. But a combination of genes and other factors may trigger the disease to start"). And it's not just PBC I have to worry about- "Children {and anyone} with one autoimmune disease tend to run a higher risk of developing another"- Which is what has happened to me- I got lichen sclerosis first (AI disease) and now PBC...What next??
Heredity: A child inherits certain genes from her parents that make her susceptible to a particular disease.
So this is how it could have happened with me:
I am predisposed to get an AI; I eat Gluten all my life; I cause holes in the gut and gluten travels around my body; My immune system attacks the Gluten; Then I get my Sphincter of Oddi Dysfunction attacks; That 'triggered' my immune system some how to get confused and start attacking my body giving me LS and PBC
[" When the immune system attacks the gluten protein it can confuse other bodily proteins for gluten due to their similar molecular structure. The term used to describe this phenomenon is “cross-reactivity”. This cross reactivity is the cause of the immune system attacking “self”. It believes it’s attacking a toxin, in this case gluten. In some cases the trigger to attack self can be an infection"]
Of course, there's no way to know if I've had the PBC before the LS and just didn't know about it - the LS just makes itself KNOWN! Maybe it was the time I tried the Depo Shots that triggered it, or the hormonal changes from quitting smoking or being pregnant, or the stress of a kindey stone or gall stone, or that really high fever I had that one time- Just making a point, that there's really no way to determine the 'trigger', could be anything, which is why it's so important for me to try to prevent the leaky gut in the first place for Zoe!
Ugh. Just sucks to know I have probably passed the genes on to Zoe to develop AI disease(s).
Welcome to the world! You're beautiful! Smart! Funny! And, oh yea, here's a little something extra...
Great job mommy!
________________________________
Sources:
UpToDate.com Unfortuantely, my trial is almost over! :(
ChildrensHospital.org
WomensHealth.gov
ncbi.nlm.nih.gov
Friday, March 23, 2012
Some videos concerning gluten and our health
So there are tons of things to find that will talk about gluten and how it negatively impacts our health. I find more stuff all the time.
Here's a different mode. Instead of giving more articles to read (which I will soon anyway :). Here are some videos to watch/listen to. Good info...I'm sure I'll find more soon. They are all over the place.
Video 1
Video 2
Video 3
A TED MED Presentation
Here's a different mode. Instead of giving more articles to read (which I will soon anyway :). Here are some videos to watch/listen to. Good info...I'm sure I'll find more soon. They are all over the place.
Video 1
Video 2
Video 3
A TED MED Presentation
Monday, March 5, 2012
A start to the gluten auto immune connection
So here is a website with tons of links to studies with information about gluten and auto immune diseases:
http://www.glutenfreesociety.org/gluten-free-society-blog/gluten-and-the-autoimmune-disease-spectrum/
This is a video, it's free to watch- there's stuff on the page to buy info, but it's free to watch the video:
http://www.glutenology.net/glutenology-health-matrix-free-video/
That'll get ya started. Many more to come!
http://www.glutenfreesociety.org/gluten-free-society-blog/gluten-and-the-autoimmune-disease-spectrum/
This is a video, it's free to watch- there's stuff on the page to buy info, but it's free to watch the video:
http://www.glutenology.net/glutenology-health-matrix-free-video/
That'll get ya started. Many more to come!
Some statistics and information I gathered
I guess I just can't get too much information...Not so sure that's a good thing.
Here are some random tidbits about PBC:
The prevalence of PBC in families with one affected member is estimated to be 1000 times greater than that in the general population. The disease primarily affects women. {So think I'm worried about my daughter? Hell yea...}
The average age of patients undergoing liver transplantation for PBC is in the range of 53 to 55 years (mean age of diagnosis is 39).
{The part about "debilitating bone fractures" sounds fun?!}
In addition to considering the MELD score and Mayo model, we suggest that patients with PBC be referred for transplantation evaluation if one or more of the following is present:
•The plasma bilirubin concentration is greater than 5 mg/dL and is increasing
•The serum albumin concentration is below 2.8 g/dL (28 g/L) and is decreasing
•Signs of decompensation or portal hypertension develop, such as ascites, variceal bleeding, coagulopathy malnutrition, or encephalopathy
•The patient has intractable pruritus
•The patient has recurrent, debilitating, nontraumatic bone fractures
{Oh goody, liver transplant doesn't even fix it anyway!}
Recurrence of PBC in the transplanted liver — It is now generally accepted that PBC can recur following liver transplantation.
In a report of 421 patients from Pittsburgh, PA, recurrent PBC was observed in 8 percent of patients after five years, and 22 percent after 10 years [11]. Higher rates were described in a series of 400 patients from Birmingham, England, where recurrence was observed in 18 percent at five years and 30 percent at 10 years [9]. A later report from the same group involving 485 patients found a recurrence rate of 23 percent during a median follow-up of 79 months.
Primary biliary cirrhosis remains one of the top five indications for liver transplantation in the USA. Survival rates of patients and grafts after liver transplantation are reported to approach 92% and 85% at 1-year and 5-year intervals, respectively.137 Fatigue and pruritus usually resolve, with metabolic bone disease improving after transient worsening in the first 6–12 months after liver
transplantation.
{Thankfully I'm asymptomatic right now, so I guess I have 16 years?! Nice to know when my timer will ding...}
Generally, the median survival duration from the time of diagnosis is 7.5 years for patients who are symptomatic and 16 years for patients who are asymptomatic.
{I like how it says 'delays' ugh}
Reports suggest that UDCA delays the need for transplantation or delays death.
{FINALLY, something that actually sounds positive! Lets hope I'm responsive to the UDCA treatment!!!}
Patients who achieve biochemical response to UDCA after 1 year of treatment reportedly have a similar survival rate to the matched control population, and this observation might be used to identify the population of nonresponders who will require alternative or additional treatments
{Or not...}
Liver transplantation appears to be the only life-saving procedure.
15-20 mg/kg of UDCA (ursodiol) provided best out come.
{My sources, along with a trial UpToDate membership...}
http://emedicine.medscape.com/article/171117-overview
http://www.med.upenn.edu/gastro/documents/LancetPBC.pdf
So honestly, I'm being a little sarcastic with my comments. I mean, all the data does sound super bleak, BUT I've also been doing a lot of research on autoimmune diseases as a whole for a while now because I was trying to control my lichen sclerosis...SO, I've found that there is A LOT of evidence pointing toward grains (specifically the protein in grains known as gluten) causing 'leaky gut' which is then associated with causing all the auto immune diseases. I will post PLENTY of references on that as time goes on. But for now, I just wanted to say I'm not feeling nearly as negative as my comments sound. I actually have very good hopes for my grain free diet and increased vitamins to help me cure or at the very least, slow down progression. That along with my UDCA treatment will hopefully give me a normal life...
Looking forward to my appointment tomorrow! Need to find out where I stand and get started on the treatment! I have a kid that needs me to stick around a good long while! :)
Here are some random tidbits about PBC:
The prevalence of PBC in families with one affected member is estimated to be 1000 times greater than that in the general population. The disease primarily affects women. {So think I'm worried about my daughter? Hell yea...}
The average age of patients undergoing liver transplantation for PBC is in the range of 53 to 55 years (mean age of diagnosis is 39).
{The part about "debilitating bone fractures" sounds fun?!}
In addition to considering the MELD score and Mayo model, we suggest that patients with PBC be referred for transplantation evaluation if one or more of the following is present:
•The plasma bilirubin concentration is greater than 5 mg/dL and is increasing
•The serum albumin concentration is below 2.8 g/dL (28 g/L) and is decreasing
•Signs of decompensation or portal hypertension develop, such as ascites, variceal bleeding, coagulopathy malnutrition, or encephalopathy
•The patient has intractable pruritus
•The patient has recurrent, debilitating, nontraumatic bone fractures
{Oh goody, liver transplant doesn't even fix it anyway!}
Recurrence of PBC in the transplanted liver — It is now generally accepted that PBC can recur following liver transplantation.
In a report of 421 patients from Pittsburgh, PA, recurrent PBC was observed in 8 percent of patients after five years, and 22 percent after 10 years [11]. Higher rates were described in a series of 400 patients from Birmingham, England, where recurrence was observed in 18 percent at five years and 30 percent at 10 years [9]. A later report from the same group involving 485 patients found a recurrence rate of 23 percent during a median follow-up of 79 months.
Primary biliary cirrhosis remains one of the top five indications for liver transplantation in the USA. Survival rates of patients and grafts after liver transplantation are reported to approach 92% and 85% at 1-year and 5-year intervals, respectively.137 Fatigue and pruritus usually resolve, with metabolic bone disease improving after transient worsening in the first 6–12 months after liver
transplantation.
{Thankfully I'm asymptomatic right now, so I guess I have 16 years?! Nice to know when my timer will ding...}
Generally, the median survival duration from the time of diagnosis is 7.5 years for patients who are symptomatic and 16 years for patients who are asymptomatic.
{I like how it says 'delays' ugh}
Reports suggest that UDCA delays the need for transplantation or delays death.
{FINALLY, something that actually sounds positive! Lets hope I'm responsive to the UDCA treatment!!!}
Patients who achieve biochemical response to UDCA after 1 year of treatment reportedly have a similar survival rate to the matched control population, and this observation might be used to identify the population of nonresponders who will require alternative or additional treatments
{Or not...}
Liver transplantation appears to be the only life-saving procedure.
15-20 mg/kg of UDCA (ursodiol) provided best out come.
{My sources, along with a trial UpToDate membership...}
http://emedicine.medscape.com/article/171117-overview
http://www.med.upenn.edu/gastro/documents/LancetPBC.pdf
So honestly, I'm being a little sarcastic with my comments. I mean, all the data does sound super bleak, BUT I've also been doing a lot of research on autoimmune diseases as a whole for a while now because I was trying to control my lichen sclerosis...SO, I've found that there is A LOT of evidence pointing toward grains (specifically the protein in grains known as gluten) causing 'leaky gut' which is then associated with causing all the auto immune diseases. I will post PLENTY of references on that as time goes on. But for now, I just wanted to say I'm not feeling nearly as negative as my comments sound. I actually have very good hopes for my grain free diet and increased vitamins to help me cure or at the very least, slow down progression. That along with my UDCA treatment will hopefully give me a normal life...
Looking forward to my appointment tomorrow! Need to find out where I stand and get started on the treatment! I have a kid that needs me to stick around a good long while! :)
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