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It is important to know that even though there are about different symptoms, some people have none. The sooner you know, the sooner you can get the gluten out of your diet and the greater your chance of avoiding serious, sometimes fatal consequences. I have a friend who cannot be diagnosed with celiac for the simple reason that you need to eat gluten for a while before the biopsy, and eating gluten puts her in the hospital.
Thanks to all who have shared, being able to relate to alot of the symptoms, bad experiences is a great help. I owe my diagnosis to a lovely, helpful opthalmologist. He diagnosed me with iritis, and gently pressed me as to whether I had any other auto-immune disorders. After several years of feeling increasingly unwell, this was my impetus to get properly diagnosed and start eating appropriately. NO horror story — just a blessing. I willingly made the house GF 3 years ago. Will felt better.
In January , I managed to severely fracture my fibula, requiring emergency surgery and insertion of a metal plate and screws into my ankle. I never had intestinal issues. Hardly ever got sick, except the yearly flu. Suddenly I felt sick all the time.
At just 21 years old, I was worried. By the summer of , I had severe abdominal cramping all the time. It was sometimes so bad that my face would turn ghastly white, and I would vomit. I would curl up in bed and just lie there. I explained what was going on, and the doctor ordered an ultrasound to check out my gallbladder, as gallbladder issues run in the family. When my gallbladder was found to be normal, I was told nothing was wrong.
I knew a few people who had celiac, so I asked student health at my university if they could do the blood work to test for the antibodies. I started to have some strange symptoms. This is when I sought out a doctor in the area who, having celiac disease herself, claims to be very thorough, and asked me to come in to explain my symptoms.
I was experiencing extreme fatigue. I could barely get through a day of class without taking a nap. When I did take a nap, it was nearly impossible to get out of bed. I missed quite a few classes because of this. I was also having trouble concentrating in class and having the motivation to study.
I am now in my last year of undergrad, study health and human physiology and hoping to go to PA school in the near future you better believe I want to help people battle gluten! I would normally consider myself to be somewhat nerdy about my school work, as I am very passionate about physiology and the human body. Studying and paying attention in class have never been an issue for me. As a 21 year old college student, I do my fair share of social drinking, and have never been one to get a hangover.
Now, all of a sudden, every time I would have a night of drinking beer, I would be woken up suddenly at 6 in the morning with severe abdominal cramps and vomiting. I would lay in bed for two days straight. I did not matter if I had 2 beers or 6. As someone who does not normally get hungover at all, this is not normal for me.
My doctor said that it was. Needless to say, I stopped drinking beer right away. Next, I explained that I was having frequent bloody noses. At least twice a week, my nose would bleed. Before that summer, I had never even had one bloody nose in my 21 years of life. My doctor told me that this was probably just because it was dry…. I live in the midwest, and our summers are actually quite humid… my living conditions had not changed, and I had never experienced it before, dry whether or not.
Again, not normal for me. If anything I was gaining more weight. I am not new to working out, and I have seen my body respond positively to exercise in the past. Being only 21 years old, I should be able to lose the weight from surgery rather quickly. Finally, the digestive issues. The fun ones. Now, I was using the washroom upwards of 8 times per day. Definitely not normal for me. Not only that, but I would often have to run to the washroom… if you know what I mean. Without going into too much detail, it seems as though my food was not digesting properly.
My doctor was, however very thorough with her tests. She ordered full celiac antibody blood panel, blood work to test my liver enzymes, genetic testing for the celiac genes, blood work to test my iron levels, blood work to test my thyroid, and common allergen tests. However, the doctor never called me to share the results, nor did she request that I set up a follow up appointment. So, I called. I was told that my antibodies were within the normal ranges, so I definitely do not have celiac disease.
I do however, have one of the celiac genes. My thyroid levels were normal. I have an allergy to shellfish. Yes, I am thankful to not have celiac, but can you really just rule it out that quickly? And what about my iron levels? Turns out the doctor neglected to tell me that I am extremely anemic, according to the bloodwork, so I was prescribed an iron supplement. She told me that I was healthy other than that. December rolls around and I am fed up with these symptoms that are affecting my school work and ability to go to class, not to mention my ability to feel good and to be a healthy 21 year old, so I scheduled blood work one more time.
Again, the antibody test came back negative. The doctor told me that I could try and give up gluten, and see what happens. I gave up gluten for about two months, and it turned my world right side up again. I am still following a gluten free diet, and am feeling much, much better despite the once in a while glutening. No more unexplained vomitting. No more bloody noses. The bags under my eyes that I attributed to long hours of studying have gone away!
I cannot explain my frustration. The fact that I have one of the genes means that I may have celiac, and have been getting false negatives. Even if I do not have celiac, gluten makes me feel awful, so why would I want to cheat? However, gluten intolerance is not very studied, and the severity and long term repercussions are not known.
I would just like to be taken seriously! I am still fatigued, and blood work shows that my iron levels are still extremely low. I accidentally get glutened sometimes, and feel awful. Since going off of gluten, when I have a reaction, it is much worse than it used to be. I emailed my doctor on numerous occasions with questions, seeking advice.
I started using a new shampoo and broke out into a horrible, itchy rash on my neck and shoulders. Upon reading the label, I found that it contained gluten. Thanks for mentioning that before. Even prior to my other symptoms, I have always suffered from migraine headaches and dysmenhorrea, and take advil migraine and advil liquigels fairly regularly for relief.
I read somewhere that these items may contain gluten. When I asked my doctor she said that they sure do. Again, thank you for letting me know. I am sick of not being taken seriously. Whether I am gluten intolerant, have celiac disease, or whatever else, I know this: my body does not like gluten, and it makes me very sick. I still think I should be tested more for celiac, maybe by endoscopy, but am not looking forward to putting gluten into my body again, as my reaction to it seems to be getting more severe.
Do you think its worth it? Should I just be happy with the fact that I know gluten is my problem? Has anyone else not been taken seriously by a doctor who knows celiac? It sounds like even though you are now gluten free, an endoscopy might reveal past damage, and even villi in the healing stage so you would know more. If you can find a dr who will schedule a biopsy it would be good to do it now, rather than later.
I was much like you through my early adulthood and had no idea why I had symptoms like fatigue and bloating and so many cavities. Just in the past few years I have finally been able to keep my iron levels up and am feeling like my body is appreciating the efforts I make to keep it healthy. I am still debating the endoscopy.
I do believe it would be a good idea to have one, but I feel like if I subject myself to such a test, I should probably partake in the suggested one month of glutening myself. I am also happy to say that I have managed to get my iron levels under control! I saw another doctor, and he increased my dosage of the iron supplement.
For about three months I took that supplement, and when I was tested next, my iron levels were good- on the high side of healthy even! Well, you are doing that, do your own research online and in the latest books, call companies numbers to check medications, and stay away form it.
However, I do think that a diagnosis would help me be taken a bit more seriously by some of my doctors. I am still debating the one month of glutening and then the scope- but we will see! Please read the recent studies by Dr. Non-Celiac Gluten Sensitivity is a bona-fide diagnosis now and has been since It is diagnosed in those who have negative CD tests and no other known GI illness, but who respond well to the gluten free diet. He estimates that 18 million Americans have this condition, many more than have true CD.
Please trust your own instincts. He estimates that there are 18 million Americans who suffer from this, many more than have true CD. Patients have similar symptoms to CD, but test negative for Celiac. If you google his name you can learn more about this. I was checked for gallbladder problems too before I was diagnosed. And I understand what you said about the beer. I could drink plenty of wine or even vodka and never had a hangover.
For me, the biopsy gave me closure. And besides, why should you have to put yourself through that just so you can prove something to someone else? It makes no sense. Doctors need to realize that everyone is different and even one disease can show up differently in a lot people. My doctor told me today that these symptoms are anxiety and that there is no such thing as an allergy to gluten or wheat. And there are no specialists either. The problem is that I am getting severe reactions to airborne gluten now and this reaction is not taken lightly at my workplace due to the continuous bias surrounding this allergy.
Believe it or not, your symptoms may be due to anemia. Keep up with the iron tablets for twelve months and get regular blood tests every three months to make sure you do not take too much iron. Taking too much iron can make you sick too so do get tested every once in a while. So my mom was the person who came across this Celiac disease the other day and showed it to me.
I have been struggling with excessive weight gain, sever night terrors, bloating, ALOT of diarrhea for months now, sleeping issues, and several other symptoms that associate with Celiac disease and I am floored!!! Can I really have this disease?
Can someone explain more of this disease to me! I want to know more! Technically, if you think you may have Celiac, you should get tested. It is a very dangerous disease that can be deadly if not treated properly. If it helps, then continue living strictly gluten free. I was recently diagnosed, after what I would consider to be years of misdiagnosis.
It started in high school. I lost a bunch of weight, and I was exhausted. I was tested for Lymphoma, and the test came back indeterminate. Since then my fatigue got worse. Every day was just a variation of how exhausted I was. Eventually I started falling asleep at work.
I was afraid to drive more than 15 minutes. I would come home from work and sleep until I went back to work. I was given a referral to have a sleep study. Aka your brain has problems. Thanks guys. Their solution? A 12 hour, time released speed pill. I felt so incredibly awful, I quit after 5 months. I ended up dating someone who introduced me to the raw food diet.
I was happily functioning off of raw fruits, veggies, nuts and seeds. However I was still consuming raw oats and some pre-made raw items that contained gluten, so I was still somewhat tired. I would tell my doctors that my diet made me better and I was always given a lecture on how I needed to be eating more grains. This year I finally had it and saw a naturopath.
Our first visit was only an interview, and she knew I had Celiac. We tested for it, and its changed my life!!! On top of that, when I consume gluten I always end up with severe asthma attacks a few hours later which usually lands me in the hospital hooked up to oxygen and or a breathing treatment. Over time, my asthma kept getting worse and I started to get new symptoms as well headaches, all over body rashes, depressed mood swings. So they threw in more asthma meds, steroid cream for the rashes and a strong antidepressant for the mood swings.
Ended up being a total of 15 medications daily. Nothing helped. Finally one night, my mom and I made the connection: all the ER visits happened after I ate large amounts of gluten pasta, garlic bread, etc. Tried giving it up strictly for a month and never looked back since. No more headaches, bloating, all over skin rashes are gone, I actually know what normal bowel movements feels like and best of all, no more asthma attacks.
I really wish that the doctors would have suggested the gluten free diet earlier. All those ER visits as a kid could have been easily prevented. Unfortunately, most doctors are quick to throw pills at a patient rather than look at the root of the problem.
It took at least 30 years for me to be diagnosed at age My parents told me I was just lazy and need to go play. I was never slight. I was always ravenous. I had abdominal pain and fatigue my whole life. In middle school the reflux started.
By my senior year of high school I was living on tums. Depression and fatigue were my near constant companions. While pregnant at 21 with my first child I became unable to keep anything down. Being told I was just trying to keep thin and being told my lack of weight gain was my own fault.
Later I was told by general practitioners that I was lazy, fat, and crazy in regard to my constant pain. I was exhausted and hurting all of the time, my reflux was never controlled. At about age 26 I started taking serious tumbles and forgetting things. I was sent to a neurologist to look for MS. I was dismissed repeatedly.
At nearly 30 I was finally sent to a GI. I did have a biopsy done and I was treated for my reflux, it only got marginally better. My biopsy came back negative for celiac. At 32, my gal bladder finally came out after repeated trips to the ER for attacks. The falls continued and the winter I was You can have celiac and it wont show up. Do you have internet?
Then after at least a month, try to reintroduce. If you have problems then you have celiac. They call this gluten sensitive, but it is celiac. I had many of the neurological symptoms, many more than mentioned here. Pain, numbness, forgetfulness, confusion, seizures, fatigue…the list goes on. In hind sight is is clear to all of the doctors that this was the problem.
I get no follow up care. The rheumatologist just tells me to go to a GI, the GI says I need to be monitored by a rheumatologist…I still have bouts of lichen planus, fatigues, muscles get tired faster than a normal person, trace contact makes me flare up. We only have each other as guides once diagnosed.
We need more comprehensive literature from authoritative sources to hand our friends and family members. All of my kids have it. I see it looking at them and what they all have going on. My baby 11 yrs old has autism and is the only one on the diet. We need more medical awareness. Have you thought about trying the Autoimmune Protocol diet described by Sarah Ballentyne? She also has lichen planus.
Google it! I kept telling the Pediatrician I had this feeling that my daughter had stopped growing or was growing very slowly. He assured me that I was petite and she was just taking after me. He acted as though I was worried about her being a short adult when in fact, I was worried she was not healthy. I should also add she had been exhibiting GI problems trouble defecating without daily rounds of Miralax and a host of behavioral problems including trouble sleeping, anxiety, major outbursts and possible ADHD.
Again we were reassured that the potty problems were probably behavioral and that Miralax was a perfectly acceptable solution and could be used daily in a four year old. We were given parenting advice and told to enlist the help of an occupational therapist to help her work through her frustrations in an appropriate manner.
At her 6 year old check-up the Pediatrician FINALLY agreed with me that her growth curve was not an actual curve and that she had, in fact, not been growing for some time. He sent me to get her hands x-rayed to see her growth plates. In the time it took between appointments to hear back from him on the results, I took to the Internet and researched ADHD and Autistic diets. I came across lots of information on gluten free diets and decided to try it.
AFter one week on a gluten free diet my daughter could use the potty without any medication and it was not painful for the first time in years. She also seemed to be calmer and her checks seemed to have actual color in them. The growth plates showed she was a year behind schedule and that made the Pediatrician believe she was just immature. He tried to talk me out of it and told me about false positives. She tested positive and when his nurse called to give me the results she also went on and on about false positives and told me not to rely on this test.
Fast forward a few weeks and we are at the Pediatric GI getting my daughter scoped. The GI says it was so obvious to him she had Celiac from the state of her intestines, tells me to put her on a gluten free diet and that he will see her in a year. Basically felt like he confirmed my fears and then sent me off with a sick child and no support system or medical assistance.
That was almost two years ago. She is still petite and we still see some issues lack of sleep, ADHD like symptoms and anxiety are the biggest concerns but compared to where she was 2 years ago we will take it. But the biggest hurdle has been jumped. We have a starting place. And yes, I changed Pediatricians immediately after her diagnosis. God gave Mothers an instinct to protect their children. Wow, Mary Beth.
Our stories are so similar. We saw an N. The N. Usually I have a tough time with anything she has to ingest. The hope is to get her back in whack at least to the point where some of the suspected gluten-induced sensory issues I had these, too will calm down so that she can successfully work with an OT about making some new dietary introductions.
Eventually, hopefully in just a few short months or sooner?? Getting people my husband, my in-laws, school, etc. My impression is that they all think I am a little eccentric and that I make this stuff up. I hope your daughter is doing better. I can look back and pinpoint hundres of celiac symptoms right from birth. I started seeing my gp regularly from january — december because of constant sinus infections and then for an horrible rash on my breats.
Nothing was ever taken seriously and she only offered options other of antibiotics or topical creams. The root of the issue was never considered. Fortunately I saw a naturopath in December who immediately pinpointed the cause and knew my family history.
I had been suffering from vertigo and mild fatigue for a few years when things started to get a lot worse about a year ago. My vertigo became very debilitating and I started having numbness, tingling, muscle weakness and extreme fatigue. Having been the type that rarely visited the dr. I suddenly found myself at the Dr every week. And each time I was made to feel like I was crazy.
Saw an intern when my Dr. She wanted to give me a prescription for sleeping pills. This Dr. Got very angry, yelled at me, insisted I take the sleeping pill prescription, tapped her watch and told me I was out of time but I need to book another appt and address my anxiety. A few more months of seeing neurosurgeons my Dr. My Dr. My husband got me an appt with a Dr. In a neighbouring town that had an great reputation. He first discovered I had a severe B12 deficiency which led to the celiac testing.
My blood tests came back positive for Celiac but strangely enough, my biopsy was negative. I went completely gluten free after the biopsy and have been slowly getting better. Because of the negative biopsy they dx me as Non — Celiac gluten intolerance. The couple times I have been glutened I have had the exact same reaction: Severe Vertigo, numbness, tingling and muscle twitching.
Oh, and of course, loose stools. Between my new wonderful Dr. And a great naturopath who happens to have Celiac disease I feel very optimistic and continue to improve. Our yr-old daughter was 2 when we began looking for answers for her health issues. He encouraged milkshakes. Ignorant fool! I followed his instructions for another 3 months and finally removed gluten myself just before she turned 3.
The change was immediate and when my visiting MIL provided a gluten challenge, I knew we had found the problem. When she entered 9th grade public school we had to have a diagnosis to get gf meals so I had her records sent to our local clinic where there is an NP who was diagnosed celiac as a child.
She took one look at the biopsy results and said of course she has celiac disease. I removed gluten from my diet after the birth of my son almost 14 years ago and have never regretted it. I did have the lab tests from Entero Labs done before going gluten free, which showed a gluten sensitivity. In retrospect…I am sure my dad was a functioning celiac. MDs told him it must be a lactose intolerance or a parasite. He ultimately had open heart surgery and died a year later—still anemic, still bloated, still gassy.
I was the sickly kid, always had tummy aches, always tired. Typical Midwestern diet, meat, potatoes, flour gravy, dumplings, etc. In my 20s a diagnosis for low thyroid seemed to help for a bit, my doctor even gave me uppers at one point for fatigue. The rheumatologist kept pushing pills on me, saying I had arthritis, this after so many tests for every other autoimmune disease he could think of. In my thirties fatigue took over my life. I started having odd itchy rashes, and now came the tests for lupus and ms again!
I began doing online research after being told that things would get worse and start on these new pills. It took a good couple months to start putting the pieces together, my parents are deceased but my sister remembered some of my childhood issues like throwing up a lot, having allergy shows, and how I was hospitalized several times before I was 5 cause I always was sickly.
I called my PCP when I woke up with my rash and she got me into the dermatologist immediately for a biopsy. The derm said it was surely not related to gluten but did the skin biopsy. I got the call that it was DH and was told to quit eating bread! On a GF diet my aches and pains disappeared and my energy is back!
I have been gluttoned and when it happens I get stomach cramps nearly immediately and hives as well. If diagnosed via a skin biopsy, an upper GI with small bowel biopsy is not needed, because you already know you have celiac disease if you have DH. If anyone suffers from a VERY itchy skin rash, find a dermatologist who knows about celiac disease and get a skin biopsy.
If you are positive for DH, a form of CD, join a local support group or at least connect on line to get the help you need. Peter Green. Off to the doctor the next day and told I had Luekemia and would be bald within a week! My memory is fairly sketchy, thank god, but I saw specialist after specialist, was treated for alopecia and severe eczema including on the face , and on steroids for around 6 months at one stage. No one had a clue what was wrong with me. Finally saw a doctor who actually knew what coeliacs was, off I went for a biopsy and bang there it is.
Sent to a dietician who also was a bit clueless so mum and I somehow navigated through. But Mum assures me it was hell… 6 months later another biopsy and back on the diet. I said in another section that it took two years for my diagnosis. For a while before my new wonderful doctor who is actually probably worthy of sainthood, I had one of the most useless doctors known to man. I had weight and digestive discomfort issues all my life, and so I was tested for diabetes routinely with always negative results.
When I was twelve and my sister was fifteen, we had to go to the doctor for severe headache issues and a disturbing amount of exhaustion respectively. He told me to suck it up, and did some blood tests for my sister. My headaches got worse, and we had to get the blood test results for my sister so we booked a follow up. To explain the pain of my headaches, all I can say is that I have broken bones and had ovarian cysts burst and not cried.
These headaches made me bawl my eyes out until I passed out from the pain and sheer exhaustion from trying to deal with day to day life. I got told that I was lying for attention and that it would be best for me to get on with my life.
It took her two days to be able to tell us what happened, at which point my mother was naturally mad as all Hell. She made one last appointment to get me checked once more and to get our physical medical records from the office with blood test results. Thankfully, he was sick and had a sub.
I got sent for emergency MRIs, CTs, and everything you can possibly think of because the sub was really terrified that it was a tumor based on my descriptions came back clean. My sister got put on heavy doses of TSH to try and get her thyroid to produce thyroxine, and she was put on some levothyroxine to make up for what her body lacked.
Complete turnaround thanks to her specialist. For the next few years we searched for a doctor, and this was when I started to get really really sick all the time. In the ninth grade, I started having panic attacks all the time. I was a different kind of kid, and people recognized that. He gave a recommendation for the doctor I have now who has been nothing but wonderful. I told her what was happening.
First thing tested was thyroid, not only because of an extraordinary prominence in my genetics every female in my family , but because I was retaining weight despite having what felt like the never ending flu from Hell, was easily confused, tired, and irate. My number did turn out to be low, but not low enough for what I was going through. I was put on medication and sent for additional testing because she was concerned. We tested my vitamin levels and she was horrified.
I was retaining none of the vitamins I was taking in. I was put on prenatal vitamin supplements while we started other tests because she wanted to make sure at least a little got through. I wanted to lose weight really badly, so I started doing low carb diets. I started to feel better and just stopped following up with my GP until I got some of the worst pains in my abdomen I was 16 and lazy, sorry guys.
It turned out to be a bladder infection, and while I was healing I went off my low carb diet because they had always been my comfort food. I felt a little better, and then a lot worse really fast. I went back begging for something to be done. She thought they might be ovarian cysts, once again due to family history, so she booked me an ultrasound.
We determined later that those initial pains were cysts based on what happened when they burst. It came out clean. I was put on a low fat diet. I was told that I may have to have my gallbladder removed in the future and that avoiding fats could help me avoid this.
I wanted to keep my organs inside of me, so I followed her advice for a few months until I reached the furthest depth of my sickness, which was maybe being healthy enough to go to school one to four times a month and doing the rest via email with my teachers and at home when I could stay awake. She said that this was going to mean revolutionizing my life. I would not be allowed wheat, barley, rye, and that any of the oats that were sold in our relatively small Albertan community would not be a good idea for me because they inevitably would set me off.
I was told that gluten free products were a waste of my money and was immediately put on a modified paleo diet based on previously diagnosed lactose intolerance, lipid intolerance, and several anaphylactic allergies including some of the agents used to bleach grains. She knew I took advil for my headaches, so she told me immediately that that was a product which contained gluten and had me taking aspirin instead.
As a person raised primarily on pasta and ibuprofen, I was horrified, but she has seen me every six weeks like clockwork since I was diagnosed in November to make sure that everything is working for me. I am so thankful to have her, especially since the repercussions from my previous doctor are still manifesting.
It was determined in January that because of the advil I had been told to take, my body actually had developed a chemical dependency. She helped me get on the correct headache medications which dealt with the fact that I have cluster headaches and not typical migraines and therefore cannot be treated with over the counter medications. If you think getting diagnosed with celiacs changed your life, try that one.
Google cluster headaches and you will find news reports of people committing suicide because of the pain, and testimonials of women claiming it is worse than childbirth. Wow, your family went thru hell, thank you for sharing. I an having many new issues, most likely from so many years of damage tomy body waitingfor diagnosis. Have horrible dizziness which is being. Tomorrow i get results for additional allergys. Blessings to u! Oh God. Gluten Ataxia would be Hell.
Good luck with your allergy tests! It took me 21 years to be diagnosed. When we had the second celiac turn up in our family, we started testing everyone, and my father, myself, my brother, and my daughter all have this. My son, who tested negative, turned out to be gluten sensitive.
So we spread the word to our cousins, especially down one family line. The grandmother there has been chronically ill for years, with dozens of gastro problems, heart issues, exhaustion, and so on. One granddaughter had a tumor that you supposedly only see in people over 50 years of age.
Two other granddsons have had chronic stomach pains and nausea for years. When they went to consult their doctor, they were told not to test for celiac disease. The chronic stomach pain was obviously just school anxiety. They trust this man. And so my family there has continued to get sicker and sicker and have never been tested. In short, she was given wheat crackers 5-minutes after her endoscopy and right after her doctor ordered a gluten free diet.
My senior year of high school I was exhausted all the time and my arms hurt so badly I could barely write or hold a fork. I was diagnosed with carpal tunnel syndrome and a knee problem, given physical therapy, and sent on my way. I went off to college. Carrying my books to class was painful. I think you have fibromyalgia. And then I went gluten free for my breastfeeding daughter. Miracle of miracles, I my fibromyalgia disappeared!
I recently had a genetic test done. I have the genes for celiac, which I have passed on to two out of my three kids. I knew that the delay in my diagnosis was not the only case, but it is very encouraging to read about others who have experienced similar circumstances. In , I went to the ER with digestive distress and severe pain for the sixth time in approximately nine months. I had previously been sent home without a definitive diagnosis after a few days as the pain subdued and I was rehydrated.
Finally, a GI Doc told me he was going to admit me for a week and thoroughly conduct tests to determine the cause of my symptoms. I was very grateful and felt hopeful that I would finally learn what was wrong with me and how to treat it. On the fifth day of this admission, the doctor returned to me with the test results. Unfortunately, the news was very disappointing. I remained grateful to him, however, for restoring my hope that I could find a diagnosis, and I subsequently persevered in doing just that.
Please do not let yourselves lose hope; if you persevere as I did, even in the most difficult of circumstances, you will find the answers. Remember that you are your best advocate; do not doubt yourself and you will eventually find someone who can help you. When I began having symptoms hives, rashes, extreme facial swelling, upset stomach, fatigue, memory loss I was misdiagnosed several times. First, I was told it was just from stress. Then another doctor diagnosed me for scabies.
Then I was told I had lupus. All wrong. I eventually diagnosed myself through extensive research, various online sources, and dietary experiment. By this time I had lost over half my hair, 25 pounds I was already thin and most of my sanity. I now trust no one better than my own body and what it tries to tell me.
Won court case, children returned 1st child diagnosed gluten intolerant at 8 2nd child at 10mths by homeopath I was diagnosed finally by then weighed only 47kgs Broken up extended family Schitzo and forced sale of house. When I was in University, I kept complaining to my doctor that I was suffering from extreme exhaustion. She told me I was simply doing too much and to cut my class load. By 22, I was near collapse. It was so bad I could barely get from my bed to the shower.
I used to lie down on my bathroom floor to rest before and after taking my shower, in order to be able to walk back to bed. My doctor diagnosed me with the flu, sent me home, I got worse. She did some tests, suspected mono, suspected Lukemia. Six weeks and many tests later, no answers, and getting worse. So we did, and sure enough, my B12 and iron were life threateningly low. I was put on daily injections of B12, and given iron supplements and sent home.
When I asked him why, he said it was because I was a vegetarian at the time. I am living on crackers and toast doctors orders nausea gets worse and worse. I research what to do the pediatrician said to wait it out, that by months he would probably be fine. My research suggests cutting gluten and dairy. Within 24 hours of my elimination diet, my son smiles for the first time, and the colic is gone.
My PPD also ebbs away. I stay off gluten for the year I breastfeed. When I weaned him, I go back to my normal diet. Within the year, I keep going to my doctor with various ailments that keep getting worse, it gets so bad that she finally orders a myriad of tests: a dermatologist for my weird skin rash, a gastroenterologist for my GI issues, a blood test for my anemia, a therapist for my brain fog, a physiotherapist for my weird gait in the morning, en endocrinologist to check my thyroid… I was presenting with an enormous cluster of Celiac symptoms, and it never occurred for her to test.
Even the gastroenterologist just had me do a barium test and told me that I looked fine. The dermatologist prescribed a cream, suggested I change detergents. The therapist wanted to talk about my childhood. My blood work came back normal. Food was becoming poison for me. I decide to stop eating gluten as a test, and within a month all my symptoms were gone. I am now ten years gluten-free and keep a gluten-free household. I went through dozens of specialists, did every test, and was never tested for Celiac.
All I know is I eat gluten, my whole body falls apart. Every so often, we mess up and I get glutened, and my self-diagnosis gets confirmed. I wish doctors knew more about this disease, and were educated about nutrition. I grew up normal. At about 15 I started having severe stomach pains, every once in a while.
I never could finish my plate, my stomach would start hurting. In I started having severe acid reflux. Super gross. A ENT did multiple tests, and told me food allergies had nothing to do with reflux. They scheduled the upper GI and lower, a week later. I adjusted to the diet and started to feel better.
My skin is healthy, and I feel better at the age of 30 than I ever did in highschool or college. I was Diagnosed two years ago, and have been diligently trying to get my family tested I suspect my mom and brother both have it.
Took me a year and a half of talking about it, and she finally agreed to ask her doctor. I felt a little sense of accomplishment at that moment. That all changed when she told me what her doctor said. Wait… Seriously? I was so mad when she told me this! All my work down the drain because of one ignorant, arrogant SOB.
I want to pose as a patient and go visit this man and tell him that I think I may have it and want a blood test. Then, when he tries to feed me that line, I can tell him that I actually have it and hand him a packet of information and tell him he is probably misdiagnosing many patients due to his ignorance.
So, so frustrating. Mindy, You are SO right! The little training doctors receive on celiac disease in med school includes a video that shows a skin and bones person with a distended abdomen. They are told that they will most likely NEVER see a patient who has celiac disease during their entire career as a medical professional.
Until doctors are required to stay updated on the latest medical information, we will unfortunately have to put up with their ignorance and be our own advocates. My whole life I had stomach issues. The doctor just told my mom it will go away when she gets older. When I was in 5th grade I was having the runs after everything I ate so the doctor took me off wheat and milk products, then had my boob sent to some lab to have it tested of course nothing was found so I go back on them.
Then ringing in my ears starts and other ear issues. More test are done and nothing is found. When I was in my mid twenties all of it starts again. Go to urgent care they cannot find anything, but tells me to go my primary care on Monday to get a referral for a gastro doctor. So I do that the primary care doctor says o just have a milkshake to test for lactose intolerance… After I said I am getting sick no matter what I eat… I go home and tell my she calls a gastro doctor the next day I have an appointment get a colonscopy and upper GI just finds h.
About 3 weeks later get blood test done for everything comes out good. I was negative by a blood test and never had a biopsy done. I have self diagnosed my self with celiac disease. Since being gluten free no stomach issues, no rashes likes I was getting or ear issues.. I changed primary care doctors. My new one said she would admitted me to the hospital and got every test ran. I will never go to a PAC ever again…. Ever since I could remember, I always struggled to gain weight and I was very short compared to most of the people in my family.
My doctor chalked it up to the fact that I was very active in multiple sports. When I started menstruating, my periods were so heavy that it almost always meant missing a week of school every month. No matter what I did, I always woke up in the morning in a puddle of blood. Basically any clothing I wore during my period was ruined.
Then when I was 15, I started a period that lasted an entire year. I literally bled every single day. I went to school maybe 2 or 3 days a week and when I did, I would be asleep within 5 minutes. I was tired all the time and suicidal. I started cutting myself and occasionally doing drugs. I went to the doctor and she thought I was exaggerating. At first she just told me to give it time and that it would probably stop. The next step was for her to humiliate me in front of my mom by asking if I could be pregnant.
I was a virgin, but she made me take a test anyway. Eventually the bleeding got so bad I could barely move. I was so weak and pale. I ended up in the hospital having a blood transfusion. The doctors in the ER suspected I had a fibroid tumor, but an ultrasound showed nothing wrong. So I was prescribed birth control and sent on my way. In 6 months I went from lbs to And I was only 5 feet tall.
The birth control regulated my periods, and it took a couple years but I lost most of the weight I had put on. From breakfast until bed time. My doctor ordered an ultrasound to check for gallstones, but nothing showed up. But I kept making appointments and telling her my symptoms. Would you like to see a specialist? Of course! The very first time I went to the specialist, he suspected celiac and wanted to do the biopsy 2 days later. I was so happy that this doctor was taking it seriously.
He personally called me 2 days later with the results. I was happy that it was him and not just a nurse. It seemed like he actually cared. He had me set up a follow-up appointment and my mom and I came in and he explained it to us and gave us lists of different foods and stuff. Before I was diagnosed, I was really afraid. This dermatosis may appear in several clinical forms, which vary according to the morphology and distribution of lesions.
In less than 0. This is a case report of a patient aged two years and eight months, who presented keratotic violaceous papules, affecting the abdomen, buttocks and right thigh, distributed along the lines of Blaschko. Histopathological examination confirmed a diagnosis of linear lichen planus.
Vulval lichen planus-lichen sclerosus overlap. Vulval lichen planus-lichen sclerosus overlap is an emerging observation. Few clinical reports exist with no reviews of literature. We present a focused update of this phenomenon and discuss a clinical case. We report a year-old woman with a year history of ulcerative vulvo-vaginitis, initially diagnosed as benign mucous membrane cicatricial pemphigoid. This led to prolonged treatment with oral corticosteroids with minimal improvement in symptoms.
Subsequent complications of long-term use of systemic corticosteroid ensued. A clinico-pathological diagnosis of severe erosive lichen planus was made on clinical findings and on non-specific biopsy changes of ulceration and inflammation. Treatment with topical clobetasol propionate 0. Clinical examination revealed Wickham's striae on the labia majora supporting the diagnosis.
Six years after commencement of topical clobetasol, white plaques were noticed on the labia majora, perineum and peri-anal region consistent with lichen sclerosus, confirmed by repeat vulval skin biopsy and on vulvectomy. This case highlights the challenge of diagnosis of extensive vulvo-vaginal ulceration and the necessity to re-examine a previous diagnosis if there is poor response to treatment.
Lichen planus is a chronic papulosquamous dermatoses in which both skin and mucosae are involved. There are various morphological forms of lichen planus. Hypertrophic lichen planus is one of the rare clinical variants. Herein, we report a very unusual presentation of hypertrophic lichen planus.
A similar presentation has not been reported in literature yet, to the best of our knowledge. Hyperkeratotic Palmoplantar Lichen Planus in a child. Lichen planus LP is a common idiopathic inflammatory disorder that affects the flexor aspect of the wrists, the legs, and the oral and genital mucosa. Depending upon the site of involvement, LP can be divided into mucosal, nail , scalp, or palmoplantar types.
Palmoplantar LP can pose a diagnostic problem to the clinician as it resembles common dermatoses like psoriasis, verruca, corn, calluses, lichenoid drug eruption, and papular syphilide of secondary syphilis. In this case report, we describe a 4-year-old male child who presented with highly pruritic erythematous to violaceous hyperkeratotic papules and plaques on his palms and soles.
Typical LP papules were noted on the upper back. Histopathology of the papular lesion showed features of LP. Dermatoscopy of a papule from the back showed the characteristic Wickham striae. We report this rare involvement of palm and soles in a case of childhood LP. Dermoscopic findings in different clinical variants of lichen planus. Is dermoscopy useful? Lichen planus LP is a papulosquamous dermatosis that involves the skin, scalp, nails and mucous membranes.
Although its pathogenesis is still unknown, there is evidence that an imbalance of immunologic cellular reactivity plays an important role. Histopathologic examination reveals characteristic interface dermatitis. Dermoscopy is a non-invasive tool, useful in the assessment of inflammatory dermatoses, such as lichen planus. In this paper we describe the dermoscopic findings of different variants of LP ungual, cutaneous, planopilaris, pigmentosus.
Upregulation of angiogenesis in oral lichen planus. As angiogenesis is fundamental to the pathogenesis of many chronic inflammatory disorders, this study investigated the expression of various vascular markers in oral lichen planus and non-specific oral mucosal inflammatory tissues. Nine representative sites at the epithelial-connective tissue junction and through the fibrous connective tissue were selected, and automated analysis techniques were used to determine the extent of positivity expressed as the percentage of positive cells.
The aims of the study are to assess the histopathologic characteristics of vulvar biopsies consistent with lichen planus LP in women with a previous or concurrent histopathologic diagnosis of vulvar lichen sclerosus LS and to describe the clinical features of comorbid LP and LS. Patients were included if a diagnosis of LP was confirmed after review of the hematoxylin and eosin slides and the histopathology reporting LS noted a band of abnormal collagen.
Data were collected on anatomic site, clinical appearance, histopathology, microbiology, treatment, and follow-up. There were 31 cases with a mean age of Thirty specimens showed erosive LP, of which 22 were from inner labium minus and 8 from vestibule. There were no significant differences between biopsy site in epithelial thickness, erosion, lymphocytic infiltrate, or basal layer pattern.
One third of cases showed a regenerative pattern of LP. Of the 26 patients with clinical records available, erythema at the biopsy site was noted in all cases; in 23 the notes specified central erythema and peripheral pallor. Forty-six percent were prescribed topical corticosteroids before biopsy.
Comorbid vulvar LP and LS are not rare; clinicians suspecting one should evaluate for the other and consider separate biopsies of morphologically distinct areas. Clinicopathological correlation is an invaluable tool in assessing biopsies when both diagnoses are suspected, because the regenerative pattern of LP may otherwise be overlooked or misdiagnosed. Treatment modalities of palmoplantar lichen planus : a brief review. Palmoplantar lichen planus is a localized and uncommon variant of lichen planus which is mostly resistant to treatment.
Our purpose was to discuss all treatment modalities proposed and tested for palmoplantar lichen planus in the literature. A systematic review of the literature was conducted to evaluate evidence regarding all treatment modalities proposed and tested for palmoplantar lichen planus in the literature. Two major databases PubMed, Google scholar were searched.
The review included all case reports, letters and original articles reporting any treatment for palmoplantar lichen planus but not treatment used in the other type of lichen planus , generalized lichen planus or other type of palmoplantar dermatoses. We have gone over more than 50 articles.
There are many drugs that have been used in the treatment of lichen planus and generalized lichen planus but the palmoplantar type is a rare variety of lichen planus. That is why we could not find any clinical trial on the subject and just case reports have been described in this manuscript. In spite of plentiful investigations carried out on lichen planus , there is no treatment modality that has proved to be utterly satisfactory in treatment of palmoplantar lichen planus.
Lichen planus is a mucocutaneous disease, predominantly affecting the middle-aged individuals and may be associated with a plethora of signs and symptoms related to the skin, scalp, nails and mucous membranes. The definitive etiology of lichen planus is not yet known and no therapeutic modality has yet been universally accepted. Lichen planus in pediatric patients is a rare phenomenon and its presence in the oral mucosa is even rarer.
The aim of this article is to present a rare case of a symptomatic oral lichen planus OLP occurring in a year old child that was managed successfully with a novel sequential modality of topical retinoids followed by aloe vera gel application. Successful treatment of bullous lichen planus with acitretin monotherapy. Review of treatment options for bullous lichen planus and case report. She was already receiving treatment for arterial hypertension, hyperlipidemia, atrial fibrillation and uncontrolled diabetes mellitus.
Acitretin was administered for 5 months with complete remission of BLP lesions and no major side effects. This is probably the first reported case of BLP treated with acitretin monotherapy. In this case acitretin was an efficacious and well-tolerated therapeutic option for BLP. Case Report: Dermoscopic features of oral lichen planus - the evolution of mucoscopy. Dermoscopy, a non-invasive technique for cutaneous diagnosis is being increasingly studied in various disorders of the skin, nails and scalp.
However, it has been under-utilized for the diagnosis and characterization of mucosal disorders. The dermoscopic characterization of cutaneous lichen planus and its variants has been well documented with Wickham's striae constituting the hallmark of the condition. However, the dermoscopic features of oral lichen planus with hand-held or videodermoscopy remain to be elucidated.
We present the case of a young adult man who presented with asymptomatic white lacy lesions over a bluish-black background over the tongue, patchy hyperpigmentation of the buccal mucosae and gingivae, and longitudinal melanonychia involving some nails.
History of intake of any drugs preceding the lesions, smoking, chewing of betel nut and dental implants was negative. Family history was non-contributory. There were no cutaneous lesions suggestive of lichen planus.
Mucoscopy dermoscopy of the mucosa, oral in this case and onychoscopy were done followed by biopsy from the tongue that confirmed the diagnosis of lichen planus. Oral mucoscopy of the tongue revealed a tri-colored pattern with structureless veil-like grey-white areas modified Wickham's striae , well-demarcated red glossy erosions, and violaceous-to-brown clods. Additionally, vascular pattern of dotted and linear to curved vessels along the borders of leukoplakia-like areas and erosions were observed.
Onychoscopy confirmed lichen planus -associated melanonychia. Dermoscopy also proved useful in conveniently ruling out other disorders typified by mucosal and nail pigmentation such as Laugier Hunziker syndrome and drug-induced changes.
Although direct oral microscopy has been used in defining features of oral lichen planus , to the best of our knowledge this case is the first report on mucoscopy or dermoscopy of oral lichen planus. Narrowband UVB-induced lichen planus pemphigoide.
Lichen planus pemphigoides LPP is an autoimmune disease characterised by evolution of subepidermal blisters on normal and lichen planus affected skin. We describe a case of LPP in a year-old Chinese woman. The patient presented with psoriasiform plaques and was diagnosed with guttate psoriasis. Narrowband ultraviolet B NBUVB therapy was commenced, and she experienced a generalised eruption of violaceous papules, bullae over the lower limbs, and Wickham's striae over the buccal mucosa.
Histology from a plaque revealed interface dermatitis, while a specimen from a blister showed subepidermal bulla. Direct immunofluorescence showed linear deposition of IgG and C3 along the basement membrane. A diagnosis of LPP was made on clinicopathological grounds. In this case report, we describe the pathological mechanism of NBUVB in the development of LPP and key features distinguishing LPP from bullous lupus erythematosus, bullous lichen planus , bullous pemphigoid, and psoriasis. Background and objective: Given the postulated the role of inflammation and possible contribution of lymphangiogenesis in oral lichen planus , this study aimed to assess any associated presence of VEGFR Material and Methods: This cross-sectional study was performed on 52 formalin fixed and paraffin embedded blocks of oral lichen planus pathological diagnosis based on Modified WHO criteria , comprising 25 of erosive and 27 of reticular type, along with 60 samples of normal mucosa with minimal inflammation from clinical and histopathological aspects obtained at crown lengthening surgery.
Four micron sections were cut from paraffin blocks and stained with H and E for confirmation of diagnosis and by immunohistochemistry with primary antibodies against VEGFR Negative controls were provided by omission of primary antibody and placenta was considered as a positive control.
Conclusion: It appears that VEGFR-3 expression might be involved in the pathogenesis of the oral lichen planus through increasing lymphatic vessels and lymphangiogenesis. Creative Commons Attribution License. A pigmented variant of lichen planus LP was first reported from India in by Bhutani et al. LP has a number of variants, one of which is LPP. This disease has also later been reported from the Middle East, Latin America, Korea, and Japan, especially in people with darker skin.
It has an insidious onset. Initially, small, black or brown macules appear on sun-exposed areas. They later merge to form large hyperpigmented patches. The disease principally affects the sun-exposed areas of the body such as the face, trunk, and upper extremities. The oral mucosa may rarely be involved. However, the palms, soles, and nails are not affected. Histologically, the epidermis is atrophic along with vacuolar degeneration of basal cell layer. The dermis exhibits incontinence of pigment with scattered melanophages and a sparse follicular or perivascular infiltrate.
There is a considerable similarity in histopathological findings between LPP and erythema dyschromicum perstans. However, there are immunologic and clinical differences between the two. These observations have led to a controversy regarding the identity of the two entities.
While some dermatologists consider them to be the same, others have opined that the two should be considered as distinctly different diseases. A number of associations such as hepatitis C virus infection, frontal fibrosing alopecia, acrokeratosis of Bazex and nephrotic syndrome have been reported with LPP. A rare variant, LPP inversus, with similar clinical and histopathological findings was reported in As opposed to LPP, this variant occurs in covered intertriginous locations such as groins and axillae and mostly affects white-skinned persons.
Lichen planus pemphigoides treated with ustekinumab. A year-old woman presented with pink to violaceous, flat-topped, polygonal papules on the volar wrists, extensor elbows, and bilateral lower legs of 3 years' duration. She also had erythematous, violaceous, infiltrated plaques with microvesiculation on the bilateral thighs of several months' duration. She reported pruritus, burning, and discomfort. Her medical history included type 2 diabetes mellitus, hypertension, and asthma with no history of skin rashes.
Workup revealed lichen planus pemphigoides LPP , a rare papulosquamous and vesiculobullous dermatosis that shares features of both lichen planus LP and bullous pemphigoid BP. Despite multiple traditional therapies, her disease continued to progress, further developing mucosal disease. After several conventional systemic therapies failed, we treated our patient with ustekinumab with favorable results.
Acitretin for the management of generalized cutaneous lichen planus. Lichen planus is an inflammatory disease that affects the skin, the oral mucosa, or both. Generalized cutaneous lichen planus may pose a therapeutic challenge for clinicians if the condition persists or flares after topical or systemic corticosteroid therapy.
Acitretin, a systemic retinoid, can be considered a potential second-line treatment for patients with generalized cutaneous lichen planus. Herein, we describe a postmenopausal woman with generalized cutaneous lichen planus who was successfully treated with acitretin. A year-old woman presented with generalized cutaneous lichen planus involving her upper and lower extremities as well as her lower back.
To review the literature on the use of acitretin in cutaneous lichen planus , we used the PubMed search engine and searched for the terms "acitretin" and "cutaneous lichen planus. There was no recurrence of disease as acitretin was tapered and discontinued. Generalized cutaneous lichen planus may pose a therapeutic challenge for the symptomatic relief of skin lesions.
Topical and systemic corticosteroids are first-line treatments. In patients who fail corticosteroids, relapse after corticosteroid therapy, or have contraindications to corticosteroids, acitretin may be considered a potential second-line therapy.
Cutaneous lichen planus : A systematic review of treatments. Various treatment modalities are available for cutaneous lichen planus. Two systematic reviews and nine relevant randomized controlled trials were identified. Acitretin, griseofulvin, hydroxychloroquine and narrow band ultraviolet B are demonstrated to be effective in the treatment of cutaneous lichen planus.
Sulfasalazine is effective, but has an unfavorable safety profile. KH, a vitamin D analogue, is not beneficial in the management of cutaneous lichen planus. Evidence from large scale randomized trials demonstrating the safety and efficacy for many other treatment modalities used to treat cutaneous lichen planus is simply not available. Surgical management of vulvovaginal agglutination due to lichen planus.
Lichen planus is a rare dermatological disorder that is often associated with painful and disfiguring vulvovaginal effects. At the University of Michigan Center for Vulvar Diseases, we see many women with vulvovaginal lichen planus each year, with marked scarring and vulvovaginal agglutination that precludes vaginal intercourse and causes difficulty with urination.
Through our experience, we developed a protocol for the operative management and postoperative care for severe vulvovaginal agglutination. Our objective is to share this protocol with a wider audience so that providers who see patients with these devastating effects of lichen planus can benefit from our experience to better serve this patient population.
The figure represents a case of erosive lichen planus with early vaginal agglutination. The video reviews the pathophysiology and presentation of lichen planus. We then present a case of scarring and agglutination in a young woman, including our surgical management and postoperative care recommendations. LP is the main representative and namesake of the group of lichenoid diseases, which are characterized by small papules often accompanied by severe itching.
Histologically, keratinocytes with vacuolar degeneration, leaving behind apoptotic Kamino bodies and the characteristic band-shaped lymphocytic infiltrate at the dermatoepithelial junction, are common to lichenoid diseases. The molecular pathogenesis, still partially hypothetical, assumes trigger factors leading to the presentation of intrinsic or foreign antigens. Other autoimmune diseases are often associated with LP. Classical anti-inflammatory-immunosuppressive therapeutic concepts dominate with systemic retinoids ranking first in the highest evidence class for cutaneous LP with limitations in treatment of both mucosal and adnexal LP.
More recently, interesting and new complementary phototherapeutics have been identified. Oral lichen planus OLP is a chronic inflammatory disease of unknown etiology with significant impact on patients' quality of life. Malignant transformation into oral squamous cell carcinoma OSCC is considered as one of the most serious complications of the disease; nevertheless, controversy still persists.
Various factors seem to be involved in the progression of malignant transformation; however, the mechanism of this process is not fully understood yet. Molecular alterations detected in OLP samples might represent useful biomarkers for predicting and monitoring the malignant progression. In this review, we discuss various studies which highlight different molecules as ominous predictors of OLP malignant transformation. Photodynamic therapy in treatment of severe oral lichen planus.
The aim of the study was to elaborate the rationale for the application of photodynamic therapy in complex treatment of patient with severe oral lichen planus. Complex clinical and laboratory examination and treatment was performed in 54 patients divided on 3 groups.
Diagnosis of oral lichen planus was based on clinical, histological and immunohistochemical features. Group 1 received standard treatment, in the second group photodynamic therapy was conducted in addition to conventional treatment, patients in the third group received only photodynamic therapy. The study results proved photodynamic therapy to be useful tool in complex treatment of severe oral lichen planus.
A potential peptide pathway from viruses to oral lichen planus. Oral lichen planus is an idiopathic inflammatory disease of oral mucous membranes, characterized by an autoimmune epidermis attack by T cells. It remains unknown, however, how such aggressive T cells are activated in vivo to cause epidermal damage. This study analyzes the relationship at the peptide level between viruses and oral lichen planus disease. The described peptide sharing might be of help in deciphering the still unexplained immunopathogenic pathway that leads to oral lichen planus.
Interleukin-6 and neopterin levels in the serum and saliva of patients with Lichen planus and oral Lichen planus. Lichen planus together with its oral variant is a chronic, inflammatory disease of the skin and the mucosa of unclear aetiology and with an unpredictable course that still poses a major problem in terms of diagnosis and treatment. The objective of this study was to assess the concentrations of interleukin-6 IL-6 and neopterin in saliva and serum of patients with lichen planus including reticular and erosive form of oral lichen planus and to compare them with the concentrations observed in healthy controls.
The study material comprised serum and saliva samples from 56 patients diagnosed with lichen planus and 56 healthy volunteers. The concentrations of neopterin were significantly higher in the serum but not in saliva of lichen planus patients vs. The differences observed in IL-6 levels in patients with erosive-atrophic forms of oral lichen planus may indicate a substantial role played by the cytokine in the disease.
The diagnosis easy at early stages may become difficult in ancient lichen planus ]. Dynamic concept of oral lichen planus. The diagnosis easy at early stages may become difficult in ancient lichen planus. Lichen planus is a chronic inflammatory dermatosis of the skin, skin appendages and mucous membranes, which frequently affects the oral mucosa. Its aetiology still remains unknown, and currently accepted pathogenesis is that of an autoimmune cell-mediated disease.
To the contrary of skin lichen planus , oral lichen planus is a long-term chronic disease with dynamic evolution, in which progressive and profound changes of the clinical and histopathological aspects occur over time and under the influence of various exogenous factors.
By convention, in the history of the oral lichen planus four successive stages can be distinguished without well-defined boundaries between them. These stages can be defined as an initial phase; a long intermediate phase with alternating periods of activity and quiescence, which has a gradually increasing risk of malignant transformation; a late stage which activity is traditionally diminished; and a post- lichen cicatricial stage with an absent or negligible and undetectable activity, often undiagnosed because clinically unrecognized; in this stage, the lesion does not respond to usual treatments, but retains the same risk of malignant transformation.
The purpose of this study is to present the clinical and radiographic findings of esophageal lichen planus. A search of computerized medical records identified 15 patients with pathologic findings of esophageal lichen planus on endoscopic biopsy specimens. Three other patients had presumed esophageal lichen planus , although no biopsy specimens were obtained.
These eight patients constituted our study group. The barium esophagrams and medical records of these eight patients were reviewed to determine the clinical, radiographic, and endoscopic findings of esophageal lichen planus as well as the treatment and patient outcome. All eight patients were women median age, Five patients had a small-caliber esophagus with diffuse esophageal narrowing. Esophageal lichen planus typically occurs in older women with longstanding dysphagia and often develops in the absence of extraesophageal disease.
Barium esophagrams may reveal a small-caliber esophagus or, less commonly, segmental esophageal strictures. Greater awareness of the radiographic findings of esophageal lichen planus hopefully will lead to earlier diagnosis and better management of this condition. Lichen Planus Pigmentosus-like Reaction to Guasha. Lichen planus pigmentosus LPP is an uncommon variant of lichen planus LP that manifests as macular hyperpigmentation involving chiefly the face and upper limbs.
Although its etiology has not been fully elucidated, a relationship with hepatitis C infection, restrictive underwear, localized friction, and sun exposure have been proposed. Rarely, exposure to mustard oil, amla oil, henna, or hair dyes has been reported. We herein describe an LPP-like reaction to Guasha. Oral lichen planus is a chronic inflammatory immune-mediated disease.
The aim of this study is the immunohistochemical evaluation of VCAM1 and ICAM1 in oral lichen planus and to compare these two markers with normal mucosa for evaluation of angiogenesis. This descriptive-analytical study was performed on 70 paraffined blocks of oral lichen planus and 30 normal mucosa samples taken from around the lesions.
Oral bullous lichen planus : Case report and review of management. A year-old female patient with the chief complaint of burning sensation in the oral cavity associated with generalized pruritis, scalp and skin lesions diagnosed as Bullous lichen planus and treated with systemic prednisolone, levamisole, benzydamine oral rinse. Patient is in follow up since 1 year and free of lesions. Here we report the case and review current modalities in the management of oral lichen planus.
Salivary proteomics in lichen planus : A relationship with pathogenesis? Oral lichen planus is a chronic, T-cell-mediated, inflammatory disease that affects the oral cavity. The oral lichen planus pathogenesis is still unclear, however, the main evidence is that the mechanisms of activation of different T lymphocyte pathway induce apoptosis with an increase in Th1 and Th17 subtypes cells, triggered by the release of cytokines.
This study analysed saliva proteomics to identify protein markers that might be involved in the pathogenesis and development of the disease. Proteins differentially expressed by oral lichen planus and healthy controls were screened using mass spectrometry; the proteins found in oral lichen planus were subjected to bioinformatics analysis, including gene ontology and string networks analysis.
The multiplex analysis validation allowed the correlation between the proteins identified and the involved cytokines in Th17 response. One hundred and eight proteins were identified in oral lichen planus , of which 17 proteins showed a high interaction between them and indicated an association with the disease.
Expression of these proteins was correlated with the triggering of cytokines, more specifically the Th17 cells. Proteins, such as SA8, SA9, haptoglobin, can trigger cytokines and might be associated with a pathological function and antioxidant activities in oral lichen planus. Association of classic lichen planus with human herpesvirus-7 infection. Lichen planus is a mucocutaneous papulosquamous itchy disease with unknown etiology.
A number of factors such as immune mechanisms, viral agents, and drugs have been implicated in pathogenesis of lichen planus. In recent years, several studies have indicated the role of viral agents in this disease, including human herpesvirus-7 HHV Studies have given contradictory results, which is why we decided to study the possible association between lichen planus with HHV In this case-control study, which was conducted on 60 cutaneous classic lichen planus samples as well as 60 healthy control skin samples after matching the two groups in terms of gender and age, tissue samples of patients and controls were studied by real time polymerase chain reaction to detect for HHV The results of this study support the likely role of HHV-7 in pathogenesis of lichen planus.
As an exogenous antigen, this virus may be involved in cellular immune-mediated destruction of keratinocytes. Emotional assessment of patients with oral lichen planus. Oral lichen planus is a chronic immune-mediated disease with an estimated prevalence of 0. Patients with oral lichen planus are often emotionally unstable and anxious and may develop concomitant systemic disorders. The objective of this study was to evaluate emotional characteristics of patients with oral lichen planus.
Two groups were studied: the first group consisted of 48 patients with a diagnosis of oral lichen planus , and the second group consisted of controls without the disease matched for age and gender at a proportion of The emotional state of the patients was evaluated using the State-Trait Anxiety Inventory, SF generic quality of life questionnaire, and the Self Reporting Questionnaire The present investigation demonstrated the presence of anxiety and depression in patients with oral lichen planus and a negative impact of the disorder on the patient's quality of life as indicated by impairment of the physical aspect, vitality, mental health, and social aspect domains.
This could indicate that associated psychological treatment may be important in the follow-up of these patients. Vulvovaginal-gingival lichen planus VVG-LP consists of a triad of symptoms: vulval, vaginal and gingival lichen planus lesions. The aim of this study was to analyse the prevalence of lesions in various anatomical locations in patients with VVG-LP.
The study included consecutive patients with lichen planus. Sixteen The new entity may be termed "vulvovaginal-gingival-pilar lichen planus " and our study indicates that SES-ANA is a marker of this type of lichen planus with extensive, severe and refractory-to-therapy involvement of the mucous membranes, skin and scalp.
Oral lichen planus : focus on etiopathogenesis. Lichen planus is a chronic mucocutaneous inflammatory disease, which frequently affects the oral mucosa of white females over 40 years old. Its aetiology remains uncertain and the pathogenesis is still the object of much speculation. The present paper presents the most well known antigens, and describes the action of different cells and proteins associated with the development of that disease, as well as the possible agents involved with its malignant transformation.
Regarding carcinogenesis, since it is a complex process and presents multifactorial origin, it is believed that there may be a synergism between intrinsic, such as inflammation mediators, and extrinsic agents tobacco, alcohol, viral infections for the OLP malignant transformation to occur.
However, further studies are needed to better understand the origin, pathogenesis and process of malignant transformation of OLP. Oral lichen planus : a report and review of an autoimmune-mediated condition in gingiva. Oral lichen planus OLP is a chronic autoimmune, mucocutaneous disease that affects the oral mucosa as well as the skin, genital mucosa, scalp, and nails. It is one of the most common dermatological diseases presenting in the oral cavity.
An immune-mediated pathogenesis is recognized in lichen planus , although the exact etiology is unknown. The disease most commonly affects middle-aged females. It is infrequently found in children, with a prevalence of about 0. The erosive and atrophic forms of OLP are less common, yet they are more likely to cause symptoms. OLP is the target of much controversy, especially in relation to its potential for malignancy.
Thus, it is important for clinicians to maintain a high index of suspicion for all intraoral lichenoid lesions. Periodic follow-up of all patients with OLP is recommended. In view of the above, the authors highlight a case of gingival erosive lichen planus affecting a year-old adolescent without concomitant cutaneous lesions, with special emphasis on clinical and microscopic characteristics of the condition and management with retinoids and steroid therapy.
No evidence for Helicobacter pylori in oral lichen planus. Oral lichen planus is a T-cell-mediated mucosal disease of unknown etiology. Numerous predisposing factors have been put forward in the etiology of this disease. This includes stress, drugs, genetic susceptibility, certain viruses, and bacterial infections. Recently, there have been studies published on possible role of Helicobacter pylori infection in pathogenesis of mucocutaneous diseases including oral lichen planus OLP.
The aim of this study was to detect immunohistochemically the presence of Helicobacter pylori in oral lichen planus. Paraffin-embedded tissue blocks of 50 cases of OLP and 10 cases of normal buccal mucosal biopsies and 6 endoscopic biopsies of patients with peptic ulcer control group were sectioned and stained by hematoxylin and eosin. Serial sections of same were stained immunohistochemically using Anti-Helicobacter pylori antibody and observed under microscope for presence or absence of Helicobacter pylori.
Except for the control group, none of the cases of OLP and normal buccal mucosal biopsies showed positivity for Helicobacter pylori. As we did not detect the presence of Helicobacter pylori in any of the OLP cases, we question the role of these organisms in the pathogenesis of OLP planus if any. Hypertrophic lichen planus is a chronic variant of lichen planus with controversial malignant association.
To describe and analyze the relationship of squamous cell carcinoma SCC and hypertrophic lichen planus. A retrospective chart review of patients with hypertrophic lichen planus and SCC was performed at the authors' institution. Thereafter, scientific databases were searched for articles reporting cases of SCC arising in hypertrophic lichen planus. Patient demographics, immune status, lichen planus features, and SCC data points were extracted for each patient and evaluated.
Thirty-eight cases of SCC in hypertrophic lichen planus occurred in 16 women, average age: Squamous cell carcinoma was uniformly located on the lower extremity. In the past, hypertrophic lichen planus and SCC have been considered isolated diseases. Based on an increasing number of cases, the association between hypertrophic lichen planus and keratinocyte malignancies warrants surveillance.
Treatment of recalcitrant erosive oral lichen planus and desquamative gingivitis with oral apremilast. Erosive oral lichen planus and desquamative gingivitis are uncommon but severe debilitating variants of oral lichen planus. Treatment of these presentations is difficult and challenging.
A year-old woman was referred to the dermatology clinic with chronic painful lichen planus -related gingivitis and buccal erosions. She has failed multiple treatments including topical clobetasol and tacrolimus, intralesional corticosteroids and several systemic and immunosuppressive agents. Following completion of three months of treatment with oral apremilast at a dose of 30 mg twice daily, significant improvement was noted in her disease activity.
Oral apremilast may be a safe and effective treatment for erosive oral lichen planus. Increased salivary aldehyde dehydrogenase 1 in non-reticular oral lichen planus. Oral lichen planus is a potentially malignant disorder. One of the malignant transformation markers is cancer stem cells. One of the proposed marker for the detection of cancer stem cells's in head and neck cancer is aldehyde dehydrogenase.
Recently it is shown that aldehyde dehydrogenase 1 expression in tissue samples is associated with oral lichen planus malignant transformation. This study evaluates salivary aldehyde dehydrogenase 1 in oral lichen planus. Thirty patients and 30 age and sex-matched healthy volunteers were recruited. Oral lichen planus was diagnosed based on the modified World Health Organization criteria.
Subjects in the case group were divided into reticular and non-reticular forms. Unstimulated salivary samples were collected at AM. The differences between aldehyde dehydrogenase levels in the oral lichen planus group compared with the control group were not significant but aldehyde dehydrogenase in non-reticular oral lichen planus was significantly higher than that of the reticular form. This is a cross-sectional study, thus longitudinal studies in oral lichen planus may present similar or different results.
The mechanism of malignant transformation in oral lichen planus is not defined. Previous analyses revealed that the aldehyde dehydrogenase 1 expression is significantly correlated with increased risk of transformation. This finding is consistent with our results because in the erosive and ulcerative forms of oral lichen planus , which have an increased risk of transformation, salivary aldehyde dehydrogenase 1 was overexpressed.
A higher salivary aldehyde dehydrogenase level in non-reticular oral lichen planus can be a defensive mechanism against higher oxidative stress in these groups. Aldehyde dehydrogenase may be one of the malignant transformation markers in oral lichen planus. Further studies are needed for introducing aldehyde dehydrogenase as a prognostic.
Background Oral lichen planus is a potentially malignant disorder. Objective This study evaluates salivary aldehyde dehydrogenase 1 in oral lichen planus. Method Thirty patients and 30 age and sex-matched healthy volunteers were recruited. Results The differences between aldehyde dehydrogenase levels in the oral lichen planus group compared with the control group were not significant but aldehyde dehydrogenase in non-reticular oral lichen planus was significantly higher than that of the reticular form.
Limitations of the study This is a cross-sectional study, thus longitudinal studies in oral lichen planus may present similar or different results. Conclusions The mechanism of malignant transformation in oral lichen planus is not defined. Disease scoring systems for oral lichen planus ; a critical appraisal. The aim of the present study has been to critically review 22 disease scoring systems DSSs on oral lichen planus OLP that have been reported in the literature during the past decades.
Although the presently available DSSs may all have some merit, particularly for research purposes, the diversity of both the objective and subjective parameters used in these systems and the lack of acceptance of one of these systems for uniform use, there is a need for an international, authorized consensus meeting on this subject.
Because of the natural course of OLP characterized by remissions and exacerbations and also due to the varying distribution pattern and the varying clinical types, e. Instead, one may consider to only look for a quality of life scoring system adapted for use in OLP patients. Key words:Oral lichen planus , disease scoring system, classification.
Interventions for treating oral lichen planus. Oral lichen planus OLP is a common chronic autoimmune disease associated with cell-mediated immunological dysfunction. Symptomatic OLP is painful and complete healing is rare. To assess the effectiveness and safety of any form of therapy for symptomatic OLP. There were no restrictions regarding language or date of publication.
All randomised controlled clinical trials RCTs of therapy for symptomatic OLP which compared treatment with a placebo or between treatments or no intervention were considered in this review. The titles and abstracts of all reports identified were scanned independently by two review authors. All studies meeting the inclusion criteria were assessed for risk of bias and data were extracted. The statistical unit was the patient. Meta-analyses were done only with studies of similar comparisons reporting the same outcome measures.
Pain is the primary outcome of this review because it is the indication for treatment of OLP, and therefore this review indicates as effective, only those treatments which significantly reduce pain. Although topical steroids are considered first line treatment for symptomatic OLP, we identified no RCTs that compared steroids with placebo. There is no evidence from the three trials of pimecrolimus that this treatment is better than placebo in reducing pain from OLP.
There is weak evidence from two trials, at. Unilateral lichen planus pigmentosus mimicking acral lentiginous melanoma. The authors report a case of a Latin American woman who developed progressive pigmentation primarily involving two digits of her right hand. She was scheduled for amputation based on a presumptive histologic diagnosis of melanoma with regression.
Dermatology consultation with repeat biopsies disclosed a lichenoid tissue reaction with marked pigment incontinence and no evidence of melanoma. This report should prompt physicians to include lichen planus pigmentosus in the differential diagnosis of acral lentiginous melanoma.
Salivary oxidative status in patients with oral lichen planus. Reactive oxygen species ROS are involved in the pathogenesis of many inflammatory diseases, including oral lichen planus. Therefore, determining the salivary markers of oxidative stress is an excellent alternative approach to diagnosing oral cavity diseases.
The objective of our study was to provide preliminary validation and determination of the salivary markers of oxidative stress in both patients with reticular and erosive forms of oral lichen planus as well as in healthy individuals without any oral lesions. In total, 62 patients with oral lichen planus OLP were enrolled in the study, including 31 with the reticular form of lichen planus The control group comprised 30 individuals without any oral lesions Lichen planus is a chronic inflammatory, immune-mediated disease that could affect the oral mucosa and is a pre-cancerous condition.
The disease usually develops in middle age with female predominance and is rare in children. In this retrospective study, cases with definitive histopathologic diagnosis of lichen planus , over a year period from to from a dermatologic hospital archive were evaluated. The prevalence of both cutaneous and oral lichen planus , the male:female ratio and site of involvement were calculated using SPSS version Two females 0. One patient had erosive, and one had bullous, oral lichen planus.
Case report and review of esophageal lichen planus treated with fluticasone. Lichen planus is a fairly common chronic idiopathic disorder of the skin, nails and mucosal surfaces. Esophageal involvement of this disease on the other hand is rare and only about 50 cases have been reported in literature. Given its rarity, it can be difficult to diagnose and may be easily misdiagnosed as reflux esophagitis.
Currently, there are no clear recommendations on the optimal management of this disease and little is known about the best treatment approach. Systemic steroids are usually the first line treatment and offer a favorable response. In this report, we would like to present a novel approach in the management of esophageal lichen planus in a middle-aged woman treated successfully with swallowed fluticasone propionate mcg twice a day for 6 wk, as evidenced by objective clinical findings.
Based on our review of related literature and experience in this patient, we feel that a trial of swallowed fluticasone may be a prudent approach in the management of these patients since it has a more favorable side effect profile than systemic treatment. Lichen planus and other lichenoid dermatoses: Kids are not just little people. Lichenoid dermatoses, a group of inflammatory skin conditions with characteristic clinical and histopathologic findings, range from common to rare.
Classic lichen planus typically presents as pruritic, polygonal, violaceous flat-topped papules and plaques; many variants in morphology and location also exist. Other lichenoid dermatoses share similar clinical presentations and histopathologic findings. These include lichenoid drug eruption, lichen planus -like keratosis, lichen striatus, lichen nitidus, and keratosis lichenoides chronica. Epidemiologic characteristics vary among each lichenoid disorder.
While classic lichen planus is considered a disease of adults, other lichenoid dermatoses may be more common in younger populations. The literature contains an array of reports on the variations in presentation and successful management of lichen planus and lichenoid dermatoses among diverse populations.
Familiarity with the characteristics of each lichenoid dermatosis, rare or common within each patient population, is key to accomplishing timely recognition and effective management. Facial follicular cysts: a case of lichen planus follicularis tumidus? Clinically, it presents with prominent purplish lesions or white-pigmented yellowish cysts and comedones. Histopathologically, it is similar to lichen planopilaris, and it is additionally characterized by follicles and cysts surrounded by a lichenoid lymphocytic infiltrate.
The most common location is the retroauricular region, and it may be associated with other variants of LP. Herein, we describe the case of a year-old woman with a history of lower limb hypertrophic LP who subsequently presented with multiple pink, tumid, pruritic plaques with white-yellow cysts and comedones extensively affecting the bilateral face. Histopathologic examination revealed a lichenoid infiltrate surrounding the follicles and cysts.
We diagnosed LPFT and began treatment with topical corticosteroids, antihistamines, systemic corticosteroids and oral acitretin without improvement. To date, the literature contains only 16 cases of LPFT. To our knowledge, this is the most severe case and is the only one with cessation of disease activity in response to cyclosporine. Oral lichen planus OLP is a relatively common chronic immunologic mucocutaneous disorder.
Although there are many presenting treatments, some of them proved its failure. Recently, the use of photodynamic therapy PDT has been expanding due to its numerous advantages, as it is safe, convenient, and non-invasive and has toxic effect towards selective tissues. This article provides comprehensive review on OLP, its etiology, clinical features and recent non-pharmacological treatments.
We also describe the topical PDT and its mechanisms. Our purpose was to evaluate the efficacy of PDT in treatment of OLP through collecting the data of the related clinical studies. Inclusion criteria were English publications only were concerned. In the selected studies of photodynamic treatment, adult patients more than 20 years were conducted and the OLP lesions were clinically and histologically confirmed.
Exclusion criteria were classical and pharmacological treatments of OLP were excluded and also the using of PDT on skin lesions of lichen planus. We established five clinical studies in this review where all of them reported improvement and effectiveness of PDT in treatment of OLP lesions. The main outcome of comparing the related clinical studies is that the photodynamic is considered as a safe, effective and promising treatment modality for OLP.
Treatment of oral lichen planus using nm excimer laser. Oral lichen planus OLP is a chronic inflammatory disease, has prolonged courses, repeated attacks and resistance to treatment. The traditional narrow spectrum UVB treatment has an established efficacy on skin lichen planus , and high safety. However, most of ultraviolet phototherapy devices have a huge volume, thereby cannot be used in the treatment of OLP. Lymphocytic infiltration is evident in the lesions of lichen planus , and the direct irradiation of nm excimer laser can induce apoptosis of the T lymphocytes in skin lesions, thereby has a unique therapeutic effect on the diseases involving T lymphocytes.
This study aims to investigate the efficacy of nm excimer laser in the treatment of OLP. A total of six OLP patients were enrolled into this study, and further pathological diagnosis was conducted, then nm excimer laser was used in the treatment. The efficacy of nm excimer laser in the treatment of OLP was satisfactory.
The clinical symptoms of five patients were significantly improved. In two patients, the erosion surface based on congestion and the surrounding white spots completely disappeared, and clinical recovery was achieved. Only one patients had developed mild pain during the treatment, and this symptom alleviated by itself. The nm excimer laser therapy can serve as a safe and effective treatment for OLP. To investigate the influence of IL in the pathogenesis of periodontitis and oral lichen planus , and the correlation between periodontitis and oral lichen planus patients.
The patients' basic information, probing depth, clinical attachment loss, gingival index, sulcus bleeding index were measured and collected. The concentration of IL in patients with periodontitis and oral lichen planus was significantly higher than that of other groups P lichen planus may increase the concentration of IL both in serum and GCF. The expression of IL was positively correlated with periodontitis and oral lichen planus. Comparative study of cell alterations in oral lichen planus and epidermoid carcinoma of the mouth mucosa.
Currently, much is discussed regarding the pre-malignant nature of mouth mucosa lichen planus. The present study aims at analyzing the alterations found in the epithelial cells present in the oral cavity lichen planus , comparing them to those found in epidermoid carcinoma.
Histological cross-sections of oral lichen planus and epidermoid carcinoma, dyed by hematoxylineosin, were analyzed through light microscopy. As to the types of alterations, the chi-squared test also revealed statistically significant differences among the lesions assessed in relation to the following cell alterations: nuclear excess chromatism, atypical mitoses, cellular pleomorphism and abnormal cell differentiation p lichen planus , the results obtained in this study show that the alterations present in oral lichen planus differ considerably from those seen in epidermoid carcinoma, thus showing how distinct these two diseases are.
Betel quid-induced oral lichen planus : a case report. The social use of betel nut is relatively common in certain geographic areas, especially India and Southeast Asia. The term betel nut does not truly describe the product that is chewed; rather, the term quid is more accurate because it refers to a substance or mixture of substances, including the areca nut, that are chewed and remain in contact with the mucosa. Betel quid is a type of quid that contains betel leaf.
Chewer's mucosa and oral submucous fibrosis are clinical entities that have been associated with betel quid use. We report a case of oral lichen planus induced by betel quid use in a year-old Cambodian woman. Oral lichen planus : a literature review and update.
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Sign up now. Are nail ridges in fingernails a sign of a health problem? Answer From Lawrence E. Multimedia Vertical nail ridges.