guitarman01

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  1. So if something like silent liver injury could be part of our issue , it looks like they might have numerous drugs in the pipeline that could be of benefit to us in the near future. and better test as opposed to a liver biopsy. http://cen.acs.org/articles/94/i39/silent-liver-disease-epidemic.html A silent liver disease epidemic For most people, the acronym NASH won’t ring any bells. But NASH, or nonalcoholic steatohepatitis, is stealthily showing up in the livers of millions of Americans. Marked by the accumulation of an unhealthy amount of fat and scar tissue in the liver, NASH is quietly reaching epidemic proportions across the globe. By 2020, NASH is projected to overtake hepatitis C as the leading cause of liver transplants in the U.S. The disease is poised to win that dubious honor because an alarming rise in obesity and type-2 diabetes—key risk factors for NASH—is coinciding with far better treatments for hepatitis C. Despite NASH’s prevalence, its obscurity isn’t surprising: It doesn’t cause obvious symptoms in most people, there’s no simple test to detect it, and no drugs have been approved to treat it. Within the next five years, that could change. The patient population is already sizeable and, barring vast lifestyle changes, it will continue to grow. NASH drugs could bring in as much as $8 billion annually—a figure that is grabbing the attention of companies both big and small. Today, the field has a packed pipeline of drugs, mostly small molecules, that offer multiple approaches to tackling the three hallmarks of NASH: fat accumulation, inflammation, and fibrosis on the liver. Reversing the course of the disease will take a combination of drugs, liver specialists believe. That scenario has prompted a flurry of deal-making around NASH in the past two years as players such as Allergan, Bristol-Myers Squibb, and Gilead Sciences build portfolios of complementary products. But even with heavy interest from drug developers and a rapidly advancing pipeline, there’s reason for caution. The field has so far only seen data from mid-stage clinical trials—results that range from encouraging to confusing to disappointing. And until researchers come up with a simpler way to diagnose NASH and detect whether fibrosis is improving, designing clinical trials that give a clear “yes” or “no” about a drug’s efficacy will be tricky. Hidden damage “This is a silent process, much like high blood pressure or diabetes,” explains Manal Abdelmalek, a liver disease specialist at Duke University. But unlike high blood pressure or diabetes, which doctors can detect with cheap and easy tests during a routine check-up, NASH is difficult to diagnose. Most people with scarring on their liver don’t display symptoms, and right now there’s no straightforward biomarker that a routine blood panel would pick up. The only reliable measure of fibrosis is a liver biopsy. Moreover, the disease progresses slowly—over years or even decades—and researchers have yet to figure out when someone with a fatty liver is at risk for developing the inflammation and fibrosis that define NASH. That subtle, slow-moving process begins with the build-up of fat in the liver, a condition called nonalcoholic fatty liver disease, or NAFLD, because it is not driven by alcohol consumption. According to the U.S. Centers for Disease Control & Prevention, up to 20% of the American population has NAFLD, which occurs when fat makes up more than 5% of the liver. For many people, a fatty liver will never become a real problem. As Abdelmalek notes, “If you have isolated fat, you may live and die with your fatty liver and never know it.” But a portion of that population—a number pegged at roughly 16 million people—will go on to develop NASH’s telltale inflammation and scarring. Anywhere from 1 million to 3 million people with NASH will go on to develop cirrhosis, where scarring has stiffened the liver so much that it can no longer function properly. From there, the outcomes can be grim: liver failure, liver transplant, or liver cancer. Right now, a doctor can only recommend lifestyle changes—better diet, more exercise, less alcohol—to stop or reverse damage to the liver, which has an amazing ability to regenerate healthy cells. Unfortunately, studies have shown again and again that people are unable to stick to a healthier regime, and liver specialists would like to be able to offer treatments. The need for drugs is made more urgent by the fact that obese, diabetic people are often low on the liver transplant list. But the road to NASH therapeutics is riddled with potholes. “The epidemiology of the disease is not particularly well described,” says Mike Burgess, who is in charge of Bristol-Myers Squibb’s fibrosis pipeline. Researchers still don’t know the speed at which NAFLD progresses, why some people with a fatty liver develop inflammation and scarring, and if particular groups of people are more at risk for developing cirrhosis. And although researchers have theories about what will work, some stemming from other fibrotic diseases, their ideas still need to play out in the clinic. “The challenge with fatty liver disease is that the targets are still not well characterized, the disease is very heterogeneous, the pathways are complex, and the animal models don’t characterize the human phenotype well,” Duke’s Abdelmalek says. Leading the pack [+]Enlarge Intercept’s FXR agonist obeticholic acid is an analogue of chenodeoxycholic acid, a bile acid that is the natural ligand for the receptor. Still, pharmaceutical companies are moving full steam ahead with a range of treatments for NASH. The most-watched drug in the pipeline is Intercept Pharmaceuticals’s obeticholic acid, which made headlines in 2014 when results from a Phase II study were published in the Lancet. Funded and run by the National Institutes of Health, the so-called FLINT study was, at the time, the largest to use liver biopsies to compare fibrosis before and after a drug was given to people with NASH. The study also looked at a wide panel of markers in the blood to assess whether the drug was having an effect on the underlying drivers of the disease. Of the 110 people given obeticholic acid, 45% saw a marked improvement in their “NAFLD score”—a measure of fat, inflammation, and swelling of liver cells—without their liver scarring getting worse. In contrast, only 21% of the 109 people given a placebo improved. Those results allowed Intercept to start a Phase III study of obeticholic acid. Because of the NASH population’s heterogeneity, the trial will be huge: The goal is to enroll 2,500 people, the majority of whom have Stage 2 or Stage 3 liver fibrosis, meaning they have significant scarring but are not yet considered cirrhotic. The launch of the study, which defines the patient improvements the U.S. Food & Drug Administration wants to see before it approves a drug, has been critical to researchers in the field. In working with FDA to come up with an acceptable trial design, Intercept laid out a blueprint for other companies to follow as they push their own NASH drugs into the clinic. For diseases without approved drugs, “having clarity and plans for designing a Phase III program that can be done in a finite period of time at a typical cost is important,” notes Lloyd Klickstein, head of translational medicine for Novartis’s new indication discovery unit. “It doesn’t make sense to start a program if you can’t finish it.” Industry confidence in the path to regulatory approval has contributed to the recent spate of licensing and acquisitions of NASH-related assets. Rohit Loomba, director of the University of California, San Diego’s NAFLD Translational Research Unit, who has designed many of the clinical studies of NASH treatments, noticed an almost immediate explosion in interest in the field after the FLINT trial results were published. “Suddenly we went from five to 15 companies overnight, and now we are at 50 companies,” he says. Recent notable deals include Bristol-Myers Squibb’s option to purchase Promedior and Gilead’s acquisition of Nimbus Therapeutics’s family of allosteric inhibitors of acetyl-CoA carboxylase (ACC), an enzyme critical in fatty acid synthesis. And last month, Allergan made a splashy entrance into NASH by buying two companies in one day: Tobira Therapeutics and Akarna Therapeutics. The price of entry for the acquirers has been high. Allergan, for example, agreed to pay up to $1.7 billion—19 times Tobira’s market value—to capture cenicriviroc, which blocks two immunomodulatory receptors, CCR2 and CCR5, and is poised for Phase III studies. Gilead’s deal with Nimbus, which brought an ACC inhibitor that just began Phase II studies, was similarly rich. “We had four offers on the table for the ACC program,” says Nimbus Chief Executive Officer Don Nicholson. Gilead didn’t make the highest bid, he adds, but the company’s existing NASH pipeline and experience in navigating combination therapies made it the most attractive. Backbone search In addition to sealing NASH’s fate as a hot therapeutic area, the FLINT data helped make the farnesoid X nuclear receptor (FXR) the drug target du jour. In addition to Intercept’s obeticholic acid, FXR agonists from multiple companies—including Gilead, Novartis, and Enanta Pharmaceuticals—are already in early to mid-stage studies. NASH drugs generally fall into two buckets: molecules that address the fat or inflammation that drive the disease and molecules that address the injury they cause, namely scarring and cell death. FXR has become an attractive target because it has a hand in regulating multiple contributors to the complex disease: the synthesis and transport of bile acids, the breakdown of lipids in the liver and intestine, and the maintenance of glucose levels. Obeticholic acid is an analogue of one of FXR’s natural ligands, the bile acid chenodeoxycholic acid. Hewing close to the bile acids made by our bodies gives obeticholic acid its activity but also carries liabilities: bile acids don’t just bind to and turn on one receptor, and that promiscuity opens up the possibility of side effects. Indeed, two side effects have emerged in studies of obeticholic acid, which has already been approved to treat another kind of liver disease. Many people given obeticholic acid experienced pruritis, or itchiness, a side effect that most have been able to control with other drugs or by taking a break from obeticholic acid. More worrisome for a drug serving a patient population that tends to have other health issues was an increase in LDL, or “bad,” cholesterol. Although the cholesterol can be lowered by pairing obeticholic acid with statins, competitors see an opening to synthesize non bile-acid compounds that are safer and more effective. Moreover, a second trial of obeticholic acid, involving Japanese people with NASH, did not show the efficacy seen in the FLINT study. Competitors think a more potent compound could improve the antifibrotic effect of FXR agonists. “That molecule is far from ideal in many respects,” says John McHutchison, executive vice president of clinical research at Gilead, which has an FXR agonist in Phase II studies. The obvious areas to improve upon are the potency and selectivity of FXR agonists. FXR is a straightforward target for medicinal chemists: Companies have easily developed potent compounds targeting other nuclear receptors, all of which have natural ligands. For example, the latest compound to enter the clinic, Enanta’s EDP-305, is 20 times as potent as obeticholic acid. Enanta CEO Jay Luly says his company’s chemists have already come up with next-generation compounds that boast 10,000 times the binding affinity for FXR of the Intercept molecule. Akarna was launched just 18 months ago, but by the time Allergan acquired the firm last month it had discovered a new class of FXR agonists with high selectivity for FXR. The firm’s lead molecule, AKN-083, is expected to enter the clinic in early 2017. Intercept’s CEO, Mark Pruzanski, is well aware of the bull’s-eye planted on his company’s lead compound. He counters competitors’ claims about obeticholic acid’s potency and selectivity limitations by noting that a handful of non bile-acid FXR agonists have already failed in early clinical studies in other diseases. Intercept will not have the first set of data from its Phase III study until 2019. Beyond FXR Many companies are pursuing FXR agonists because they believe their antifibrotic effect, if sufficiently potent, could make them a cornerstone therapy in the treatment of NASH. But the drug pipeline is also full of drugs—many repurposed from other diseases—that work by different mechanisms. Liver specialists agree that they will need multiple treatment options to serve a diverse population. “Different patients are likely getting to NASH by different routes, such as different genetic predispositions or environmental exposures,” says Brent Tetri of St. Louis University’s Liver Center. “I don’t think we’ll get that one blockbuster drug that works for everybody.” With that in mind, the big players in NASH are assembling portfolios of drugs with hopes of becoming leaders in a potentially lucrative market. When McHutchison, a liver specialist, came to Gilead from Duke in 2010, he helped map out a NASH strategy intended to address multiple symptoms and drivers of the disease—namely, fibrosis, inflammation, and glucose and lipid metabolism. “I thought that targeting all components that cause the disease was going to be far more successful than just focusing on one of them,” McHutchison says. Six years later, Gilead has four different types of drugs in the clinic. In addition to its early-stage FXR agonist, the company has simtuzumab, a monoclonal antibody in Phase II studies that tries to stop fibrosis by inhibiting the protein LOXL2; GS-4997, a small molecule meant to reduce inflammation and fibrosis by blocking the protein kinase ASK1; and GS-0976, an allosteric inhibitor of ACC that prevents fatty acid synthesis. Bristol-Myers Squibb has taken a different strategy over the past two years by building a broader antifibrosis portfolio through internal research and deals that include options to acquire Galecto Biotech and Promedior. It also collaborates with the California Institute for Biomedical Research. The company’s thinking is that its fibrosis assets, though initially positioned for other diseases, could be relevant in NASH. “One of the things we’re still not clear on as a community is to what extent fibrosis is generic,” BMS’s Burgess says. In other words, researchers still don’t know if a drug that addresses scarring in lung tissue could also address scarring in the liver. “We have reasons to believe that should be true,” he says, noting that BMS is now thinking about how Promedior’s treatment for idiopathic pulmonary fibrosis could be used for NASH. Allergan last month became the newest entrant in the NASH sweepstakes, buying an entire pipeline in one fell swoop with its acquisitions of both Tobira and Akarna. “We are putting a big marker on this disease,” Allergan CEO Brent Saunders said in a conference call after the deals were announced. The next trials As the NASH pipeline becomes increasingly crowded, researchers are seeking better ways to measure the disease’s hallmark fibrosis. Currently, the degree of liver fibrosis can be confidently detected only with a biopsy, a procedure that patients in a clinical trial need to endure before and after treatment to assess a drug’s efficacy. “We’re talking about sticking a big needle through your side, into your liver, and taking a tissue sample of your liver before and after” treatment, Intercept’s Pruzanski notes. For patients, biopsies are unpleasant and risky; for companies conducting the trials, biopsies are expensive and time consuming. And a liver biopsy is an imperfect way to measure fibrosis. Liver scarring is not evenly distributed, meaning the level of fibrosis seen in a sample depends on where the needle is inserted. To account for that natural variability, clinical trials such as Intercept’s Phase III study of obeticholic acid need to be huge. Without simple ways to reliably detect liver fat and fibrosis, the use of any drugs that make it to market could be limited. “Even if we have effective therapies for NASH, the reality is many patients will still come to us with cirrhosis or advanced fibrosis because it was never discovered,” Tetri, the liver specialist, says. UCSD’s Loomba has, over the past 15 years, become the leader in assessing how imaging tools and other techniques can be used to diagnose and treat NASH. Among his many efforts, Loomba has studied the use of MRI to measure liver fat—a test he is now hoping to show can be replaced by cheaper ultrasound techniques—as well as ways to use imaging to study liver stiffness. And researchers still need to work out how NASH drugs will be used in the real world. If the industry develops a drug that actually reverses the disease, the question will be, “Do you stay on it for a year or two and then stop? Or do you stay on it forever?” Gilead’s McHutchison asks. “We’ve been discussing this recently internally and would have to look at both options and design trials that address both.” Opinions on the subject differ. Some involved are convinced that—barring a significant change in diet and exercise to prevent fat from continuing to accumulate in the liver—people will need to be treated chronically, much like with a diabetes drug. Intercept’s Pruzanski says the treatment approach will likely come down to how effective drugs are at sustainably reversing the course of the disease. But with the right tools to measure the markers of NASH, some liver experts believe, it might be possible to treat for a finite period and then monitor for changes. UCSD’s Loomba, for example, is confident that doctors will eventually be able to use blood tests and imaging tools to understand how a patient is responding to a treatment, possibly allowing those with early-stage disease to be treated acutely rather than chronically. In the end, everyone agrees that treating NASH is a work in progress—albeit rapid progress. “I’m learning new things every two months,” Loomba says. “I say to myself, ‘Oh, I was so foolish I used to think that way.’ ”
  2. I just read over your blog and I think most of us would be glad to offer any information that may be helpful towards your research. Unfortunately we haven't gotten much help from the medical community ourselves, so we have kind of been spinning our wheels. The most I feel we can do at the moment is to eliminate causes of illness that we don't have post accutane through testing and go from there. Some of the other theories are more difficult to prove through standard blood testing or imaging. It seems like some victims must be more predisposed to ongoing health problems post accutane then others and I'm sure genetics plays a part in this.
  3. I was reading about this funnel web spider(one of this most deadliest) that bit this boy in australia. The only way he survived was taking a record 10 vials of anti-venom. The spiders venom attacks the nervous system. It causes foaming at the mouth, muscle spasms and death. Muscle spasms, twitches, nerve pain, sensitivity. I think something is definitely attacking our nervous system in some of these cases. Muscle spasms on the side effect list for accutane? I dont think some of this is a direct cause of accutane. but something accutane changed, for these side effects to sometimes pop up years down the line. You guys read into SOD 1/2 Mutations? This shit is starting to remind me of MS, Lupus, lyme disease, fibromyalgia, Sjogrens. same type of symptoms. I def understand needing relief and moving on with your life, but for me personally im not ready to go the narcotics route yet if I feel we can still dig a little deeper into the cause.
  4. http://www.medschat.com/Discuss/accutane-long-term-side-effects-191307_p14.htm You guys seen this website? Kind of like this one. But only 94 pages... The cases seem much more extreme then what I've seen on here for the most part. Alot of informed stuff though. Alot of depressing stuff actually.
  5. Anyone had the blood test? I do already eat alot of dairy and grains high in iodine according to this Iodine Blood Test Email to a Friend Print Page Add to Wishlist Add to Compare Add to Cart An Iodine Blood Test monitors exposure to iodine; evaluate for iodine deficiency disorders (IDDs), excessive iodine intake, or iodine in the workplace. Test #070034 Additional Info Preparation No Fasting Required. Test Type Blood Test Results 2-3 days Details The Iodine Blood Test is useful in the diagnosis of iodine deficiency or excess, iodine-induced hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid), and autoimmune thyroid diseases such as Graves' disease and Hashimoto's thyroiditis, as well as monitoring exposure to iodine. Iodine is a mineral listed by the World Health Organization (WHO) as one of the most important micronutrients. Adequate amounts are essential for proper thyroid function and critical during pregnancy for healthy development of the fetus. The body’s primary source of iodine is food; seafood, dairy products and whole grains tend to be good sources of the mineral in the U.S. Iodized salt is also a common source. Recommended daily intake varies by agency, but the WHO, International Council for the Control of Iodine Deficiency Disorders, and UNICEF recommend the following amounts: Up to 7 years old: 90 micrograms (mcg) 7-12 years old: 120 mcg 12 years and older: 150 mcg Pregnant/breastfeeding women: 200 mcg Throughout the world, iodine deficiency is the most common cause of brain damage. Deficiency in pregnant women can result in miscarriage or stillbirth, low birth weight, and congenital abnormalities such as cretinism, a severe condition characterized by stunted growth and mental retardation. In children, iodine deficiency can impair physical and mental growth and development, and in both children and adults, goiter (enlarged thyroid) ran result. High iodine intake may or may not result in symptoms because people vary widely in their tolerance of excess amounts. Most people who haven’t been iodine deficient can handle large amounts without problems, but some individuals may experience conditions such as hyperthyroidism or hypothyroidism. An Iodine Test is also known as Iodine Serum. No fasting is required prior to the test, and results will be available within two to three days. A prior doctor’s visit is not required to order this test. Patients also do not need insurance. See also Walk-In Lab’s Iodine Urine Test.
  6. wow ok that is a pretty high dose. did a doctor prescribe this? and for what reason? here is fda reports on accutane causing eosinophilic esophagitis. Looks legit but im not a 100 percent sure. but when you look at the timeline and compared to other drugs thats a pretty big number. About this FactMed analysis covering adverse side effect reports of ACCUTANE patients who developed EOSINOPHILIC OESOPHAGITIS. FactMed provides MD-approved analysis to help both patients, researchers, and physicians accurately assess the risk profile for more than 20,000 different pharmaceutical products. The below report offers compiled information from Food & Drug Administration and FactMed user submissions. Between January 2004 and October 2012, 20 individuals taking ACCUTANE reported EOSINOPHILIC OESOPHAGITIS to the FDA. A total of 26681 ACCUTANE drug adverse event reaction reports were made with the FDA during this time period. Often the FDA only receives reports of the most critical and severe cases; these numbers may therefore underrepresent the complication rate of the medication. Summary Statistics Reports of ACCUTANE causing EOSINOPHILIC OESOPHAGITIS: 20 Reports of any side effect of ACCUTANE : 26681 Percentage of ACCUTANE patients where EOSINOPHILIC OESOPHAGITIS is a reported side effect: 0.0750% FDA reports of any drug causing EOSINOPHILIC OESOPHAGITIS : 121 Average percentage for all medicated patients where EOSINOPHILIC OESOPHAGITIS is reported as a complication: 0.0008% http://factmed.com/study-ACCUTANE-causing-EOSINOPHILIC OESOPHAGITIS.php
  7. I was actually given 5mg low dose prednisone by a rheumatologist to treat joint and muscle pain. They use a low dose like this to treat rheumatoid arthritis. What kind of dose were you taking? I myself wouldnt take anything higher then 5mg without having a idea of what was going on. I'm getting a endoscopy on Monday and they will biopsy my tissue to see if I still have a elevated esophil count in my esophagus. If so, they will give me a oral flonase to swallow, the dose is around 800mcg prob along with a ppi of at least 40mg and maybe something to coat the esophagus. I have never tried the swallowed flonase before. If this was drug induced by Accutane I wonder if anyone else might have something similar going on. This could be a source of chronic inflammation. This could trigger chronic reflux that people might not be aware of. This could after awhile(especially when you sleep)start effecting your sinuses and eustachian tubes that could trigger the facial flushing ,ear fullness, Pressure feeling in head. Because your ears have closed up from the aspirations of the reflux. So you have a constant feeling of head fullness. This could irritate the eyes as well. Anyone feel the worst when they first wake up in the morning? would you describe your depression almost as a pain or headache? Here is a study i was talking about in regards to referred pain. if there was some kind of abnormal inflammation going on along the spine due to accutane, this could after time trigger nerve pain anywhere in the body which could maybe induce lack of blood flow which leads to muscle spasms, contractions,weakness because the muscles are constantly contracted. Anyways big could for some of this stuff but its possible. If my head just felt clear id be good, and this could be a reason why. again i stress could. Scientists tap into spinal response from gastric reflux Manash Pratim Gohain| TNN | Oct 1, 2013, 07.48 AM IST NEW DELHI: University of Adelaide researchers have made advances in the understanding of one of the world's most common medical conditions, gastric reflux, and how patients experience pain from it. Gastric reflux affects as many as one in five people in Western countries and is on the increase in Asia. Diet and lifestyle, as well as genetic and hormonal issues, are commonly considered to be major causes of gastric reflux. In laboratory studies, researchers have identified the nerve pathways in the spinal cord that transmit pain signals associated with gastric reflux to the brain. "This is the first time anyone has shown the pain pathways in the spinal cord that receive direct input from acid-sensitive nerve endings in the oesophagus," says Dr Andrea Harrington, an Australian Research Council (ARC) DECRA research fellow in the University's Nerve-Gut Laboratory. "This is important because we know that the oesophageal nerves undergo changes in gastric reflux patients that make them overly sensitive to acid. There is also evidence to suggest that the whole circuitry becomes abnormally sensitive in these patients, resulting in ongoing pain responses in the absence of actual acid reflux. Our research will enable us to identify such mechanisms," she says. Dr Harrington says it's important to better understand how we detect and perceive pain from gastric reflux. "Being able to know exactly how pain pathways connect to the brain will give us new insights, which in the years ahead could lead to improved treatment," she says. Dr Harrington says most current treatments focus on reducing the amount of acid in the stomach. "However, we think it's a much more complex issue than that. There might come a time when treatments are able to both address the amount of acid in the stomach while correcting the sensitivity of nerve endings. This would go a long way to providing more balanced relief to suffers of gastric reflux." The next step in this research is to find out how the pain pathways are changed in reflux sufferers. The results of Dr Harrington's work have been published in the journal Neurogastroenterology and Motility.
  8. So there is a possibility of this. It can happen as late as 5 years after initiation of drug. It can be progressive. It could maybe effect systems such as the skin and gut that aren't going to show up on blood test. its similar to an allergic reaction. Could be highly individualised depending on the person. Most effective treatment seems to consist of steroids. And this is more so for the people that seem to suffer multi-progressive symptoms over years and years that dont improve. Not just the dry skin post tane. Drug-induced eosinophilia The Pharmaceutical Journal8 JAN 2000By Ian Maidment , Caroline Williams This review looks at drugs that produce eosinophilia and explains how this condition may be managed Eosinophils are a type of white blood cell formed in the bone marrow from stem cells. They are granulocytes derived from the same progenitor cells as monocytes, macrophages, neutrophils and basophils. The usual blood eosinophil count is 350 per mm3 with diurnal variation; the peak occurs at night and the trough in the morning. The circulating half-life of most eosinophils is six to 12 hours with most eosinophils residing in tissues (eg, the upper respiratory and gastrointestinal tract).1 There are a number of hypotheses regarding the function of eosinophils. It has been suggested they modulate the intensity of immunoglobulin E (IgE) and IgG-mediated reactions, for example, in schistosomiasis.2 They are toxic to helminths in vitro and it is also possible that eosinophils protect against certain tissue invasive metazoan parasites such as Pneumocystis carinii.1,3Finally, they may act via hormones such as adrenaline, oestrogens or glucocorticoids.3 Eosinophilia is defined as a peripheral blood eosinophil count greater than 350 per mm3.1 (Hypereosinophilia is defined as a peripheral blood count greater than 1,500 per mm3.) It is a common allergic manifestation of many drugs and usually disappears when the drug is stopped. Unless very severe, the severity of eosinophilia is solely related to the allergic responses that accompany it. The parts of the body that tend to be affected are the heart, lungs, skin, joints, gut and central nervous system. Prolonged periods of eosinophilia may result in tissue damage although the exact mechanism by which this occurs is still unclear.1 There are a number of causes of eosinophilia, allergic and atopic diseases being among the most common.1 Infections, particularly parasitic infestation, may produce an eosinophilia, as may fungal infections. Generally, however, bacterial or viral infections are associated with eosinopenia.4 Neoplastic disease, for example Hodgkin’s disease, may occasionally cause an elevated eosinophil count.3 Connective tissue disorders and skin disorders, such as pemphigus, are often associated with eosinophilia.1 The eosinophilic pneumonias are a group of diseases of both known and unknown aetiology, characterised by eosinophilic pulmonary infiltration and peripheral blood eosinophilia. Simple pulmonary eosinophilia is known as L?ffler’s syndrome and may be associated with a low grade fever, minimal respiratory symptoms and prompt recovery.1 Relating eosinophilia to a particular drug can be difficult. Hypersensitivity reactions to substances such as nickel, ragweed, pollen, poison ivy extracts, helminthic infestations, brucellosis, amoebiasis and coccidioidomycosis have all been associated with eosinophilia.5 To confirm a drug reaction, these chemical and infectious causes must be excluded. Diagnosis is further complicated because the drug may worsen a pre-existing eosinophilia, particularly in an atopic patient.6 Given that allergic reactions may result in eosinophilia, it would appear to be a potential problem with many drugs, as dictated by the idiosyncratic response of the individual patient. Management If the eosinophilia is mild, transient and asymptomatic, there is no need to take action. If, however, the eosinophilia is more severe and producing symptoms, the most important management step is to discontinue any agent that may have caused the reaction. Eosinophilia usually occurs within eight weeks of any medicine being started, so agents started in this period should be discontinued initially. Symptoms have been reported to develop up to five years after initiation of a medicine.9Patients usually recover after the offending drug is withdrawn. It is also important to treat any renal, hepatic, pulmonary, CNS or any other complications of the eosinophilia. Corticosteroids are often used, but there are no placebo controlled trials assessing their effectiveness and their role is not clear. Some sources suggest they have little benefit and no effect on outcomes,56,70 while others suggest that they produce a more rapid response.50,55 It has been suggested that corticosteroids should be reserved for more serious reactions.55Corticosteroids are sometimes not prescribed because of concern about an infection causing the eosinophilia.57 There is also some debate about the dose required. There are reports of doses between 10?100mg prednisone being used.41 Generally, high doses tend to be used; for example, daily doses of 60?90mg of prednisone or prednisolone have been used to treat NSAID-induced eosinophilic pneumonia.55,75 There are reports of 30?40mg daily of prednisone being used to treat the mainly pulmonary symptoms of minocycline- or tetracycline-induced eosinophilia.23,76 In one case, there were persistent dermal complications which required more prolonged treatment with prednisone.23 Additionally, there is no clear consensus on the duration of corticosteroid therapy. Most patients receive two to six weeks’ treatment, although much longer courses have also been recommended and used. It has been reported that stopping steroid therapy, particularly in patients with chronic eosinophilia, may result in relapse.77 These patients sometimes require long-term corticosteroids.9
  9. Esophageal ulcers: A possible adverse effect of isotretinoin Article in The Turkish journal of gastroenterology: the official journal of Turkish Society of Gastroenterology 24(5):562-3 · December 2013 with 58 Reads DOI: 10.4318/tjg.2013.0560 · Source: PubMed Couple things im looking at here is what they describe as something similar to vasculitis, which is inflammation of the blood vessels. The other is possible migration of white blood cells to the esophagus that they are saying might be similar in the cases of IBD. Abstract To the Editor, Drug-induced esophageal injury is a common cause of esophageal diseases. Many drugs have beenreported to cause esophagitis and esophageal ulcers; among these are antibiotics such as doxycycline and tetracycline, nonsteroid anti-inflammatory drugs, aspirin, and potassium chloride (1). Isotretioin is a synthetic analogue of vitamin A and is widely used in the management of acne vulgaris. However, several adverse effects of this drug have been reported, including mucositis and chelitis (2). Among these, a possible association of inflammatory bowel disease with isotretioin deserves further attention (3). Although the exact mechanism is not clear, the possible role of isotretinoin in the inhibition of epithelial cell growth, induction of apoptosis, lymphocyte migration, and immunomodulation have been proposed. We report a patient with multiple esophageal ulcers in which the only possible cause was the oral ingestion of isotretioin. A 29-year-old woman who had no previous gastrointestinal complaints (including no reflux symptoms) and no serious medical or surgical history presented to our gastroenterology department with severe odynophagia. She had started to use isotretioin for acne vulgaris one month before and had not used any other medication recently. Her odynophagia began suddenly two days before presentation and was similar in intensity while swallowing solids and liquids. Her physical examination, routine laboratory tests, chest x-ray and upper abdominal ultrasonography were all within normal limits. An emergency endoscopy was performed and showed discrete esophageal ulcers (3-8 mm in size) starting 30 cm from the incisors and disappearing gradually towards the 38 th cm (Figure 1). At the gastroesophageal junction (40 cm), no signs of reflux esophagitis were seen. Histopathology of biopsy samples from the ulcers revealed evidence of ulcerative esophagitis, i.e. small obliterated vessels in the ulcerated area, reminiscent of vasculitis (Figure 2). No fungus was identified with PAS stain. Isotretinoin was stopped; paracetamol and sucralfate liquid (6 times daily once before and after each meal) were started. Investigations for other vasculitic or rheumatologic conditions (serum CRP, ANA, C-ANCA, P-ANCA and ACE) were all within normal values. In a few days, the patient's pain waned and finally disappeared after one week following the cessation of isotretinoin. Isotretioin was the probable etiologic agent of esophageal ulcers in this patient. Pill-induced esophagitis may occur due to several mechanisms (direct injury by caustic coatings, dissolution after prolonged contact and direct injury to the esophagus by the drug, etc.); the ulcer-causing mechanism of isotretinoin may be similar to that involved in the pathogenesis of inflammatory bowel disease.
  10. I think part of the problem is dermatologist need to use extreme discretion when prescribing accutane. It's for extreme disfiguring or scarring acne only as a last resort. Not for mild, moderate or persistent acne that alot of us probably would have just grown out of. Alot of dermatologist or the medical field in general aren't aware or deny the chronic side effects that happen after treatment.
  11. Lactoferrin test and supplement for dry eyes and dry nasal passage An Objective Look at Dry-Eye Syndrome A new test for the amount of the protein lactoferrin on the ocular surface might hold the potential for diagnosis and treatment. For decades, clinicians have had to rely on their subjective evaluation of signs and symptoms in order to accurately diagnose and treat dry eye and ocular surface disease. Recent years have witnessed a flurry of developments in the realm of objective dry-eye diagnosis, however, with several devices becoming available around the same time. The newest addition to these objective measurement tools is the Tear Microassay System from Advanced Tear Diagnostics. Here’s a look at how the system works. Lactoferrin Explained The Tear Microassay System measures the amount of the protein lactoferrin on a patient’s ocular surface, using it as a marker for dry eye. “Lactoferrin is a multifunctional protein that’s part of the transferrin family,” explains Terrence O’Brien, MD, professor of ophthalmology at the University of Miami’s Bascom Palmer Eye Institute. Dr. O’Brien has experience working with lactoferrin as a marker for dry eye, and is interested in seeing what this new test may bring to the clinic. “It’s more of a global marker, and it’s present not only in tears but also in saliva, mother’s milk and nasal secretions. It’s also one of the components of the immune response, has demonstrated significant antimicrobial activity and is part of the eye’s natural defenses. This antimicrobial aspect of it is one of the reasons why I’m interested in it. It’s been identified as one of the tear proteins that may be part of the innate defense of the mucosal surface, and it has bactericidal and even fungicidal properties. In addition to binding iron, which bacteria use as an element necessary for their growth, it also binds to the lipopolysaccharide of bacterial cell walls. The oxidized iron that’s part of lactoferrin oxidizes bacteria, forming peroxide. This action affects the membrane permeability and results in the breakdown of the bacteria. “My interest in this stems from this antimicrobial mechanism being part of the innate immune system, and I think the test may have broader applications,” adds Dr. O’Brien. “For example, it may be that lactoferrin levels can tell us which patients might be at risk for developing an infection from wearing contact lenses.” The Test The lactoferrin test consists of introducing a micropipette into the patient’s canthus and harvesting a very small sample of tears, 0.5 µl. The sample is put in a diluent and the mixture is shaken, a step that amplifies the amount of lactoferrin. The mix is then placed in a small well on a strip, and, according to Advanced Tear Diagnostics’ Jeffrey Busby, the diluent chases the tear up the strip and, when the sample is placed in the microassay system, the system determines how much lactoferrin is in the sample. A result of 1.4 is considered normal, and anything below that means the patient has dry eye. According to company studies, the test’s sensitivity is 83 percent, and it’s specificity is 98 percent. There is already a diagnostic code assigned to the test, as well. The system can also process different samples of tears to test for immunoglobulin E, to look for the presence of ocular allergy. Now that clinicians can use lactoferrin levels to determine if a patient has dry eye, Dr. O’Brien says the next step is to study the results and see how they correlate with signs, symptoms and disease severity levels. “We need to figure out the correlation between the quantitative nature of this test result and the severity of the disease,” he says. Some progress has been made along these lines: In a small, non-published study that Dr. O’Brien conducted with Duke University’s Alan Carlson, MD, several years ago, they found lactoferrin levels may be associated with postop LASIK results. In the study, the researchers tested the lactoferrin of 32 patients before their LASIK procedures and then prior to their post-LASIK follow-up exams. Preoperatively, six patients had low lactoferrin, 21 had normal levels, and five had elevated lactoferrin. “We found that those patients who had lower levels of lactoferrin preoperatively were more prone to regression of effect and a lesser outcome of laser vision correction,” says Dr. O’Brien. Elevated lactoferrin suggested an increased risk for postop hyperopia. All of the low-lactoferrin patients had a postop refraction of -0.25 to -1.5 D; only 19 percent of the normal patients were outside the -0.25- to +0.25-D range; and 80 percent of the high-lactoferrin patients had hyperopic refractions of +0.5 D or greater. “It’s possible that an LVC surgeon, or a surgeon planning on implanting an advanced technology IOL, who uses the lactoferrin test to screen patients could uncover individuals who have mild to moderate disease that could impact the outcome,” says Dr. O’Brien. “So, this might be a broad screening tool for OSD as well as a perioperative screening tool that could be used in advance of surgery to uncover patients who may be at risk for a lesser outcome. The surgeon could then treat them preoperatively in an effort to improve the ocular surface.” As for the steps after a clinician finds that a patient has low lactoferrin, there is some evidence that lactoferrin supplementation can help. In a non-published study outlined in a letter to the editor in Ophthalmology, physicians from Tokyo administered oral lactoferrin to 10 patients with Sjögren’s syndrome and used 14 eyes of seven other Sjögren’s patients as controls.1 The researchers reported that mean corneal sensitivity, tear breakup time, tear-film lipid layer thickness, vital staining, squamous metaplasia grades, symptoms and goblet cell densities all improved significantly after a month of lactoferrin supplementation. The parameters then worsened a month after supplementation ceased. The control group showed no significant changes. Dr. O’Brien cautions clinicians to evaluate oral supplements carefully, though. “If lactoferrin is low, there are supplements available,” he says. “But these aren’t tightly regulated by the FDA, so evidence is lacking in terms of trials to tell us which form of lactoferrin would be ideal, which dosage is best and if it’s harmful to take too much. We have this problem with other supplements that people may take without knowing their true safety.” Making Sense of It All Dr. O’Brien says clinicians now have to determine where lactoferrin testing fits into their dry-eye diagnostic paradigm. “We’re finding out that dry-eye disease involves a complex biological system of multiple molecules, with each playing a different role in terms of normal homeostasis of tear function,” he says. “I think the lactoferrin will be complementary to other tests such as those for tear-film osmolarity and MMP-9 to help us screen for dry eye. “Lactoferrin might also have other implications in terms of how the protein really functions in the natural prevention of infection from organisms that blow onto the tear film, in contact lens wearers and in surgery patients,” Dr. O’Brien continues. “However, more work needs to be done to bring a clinical meaning to the quantitative result of the test. To that end, studies are currently being coordinated and are getting under way, and I hope we’ll have some data soon in different clinical settings.”
  12. I don't think it's really a matter of oil production. There are plenty of people as they get older that don't have oily skin but still have healthy skin(ie can tan normally) Also for example I used to dry the hell out of my skin with soap and acne creams before accutane and it never caused facial flushing like I get post accutane. I think the bad skin is more due to thinness and inflammation. The skin thinness can go with the body's general inability for some of us to put on body fat post tane. There also might be some mild dehydration going on as well
  13. not sure if this has been posted as well. Seems like it could be a important study on the hormonal effects of accutane. 13-cis-retinoic acid competitively inhibits 3 alpha-hydroxysteroid oxidation by retinol dehydrogenase RoDH-4: a mechanism for its anti-androgenic effects in sebaceous glands? Karlsson T1, Vahlquist A, Kedishvili N, Törmä H. Author information Abstract Retinol dehydrogenase-4 (RoDH-4) converts retinol and 13-cis-retinol to corresponding aldehydes in human liver and skin in the presence of NAD(+). RoDH-4 also converts 3 alpha-androstanediol and androsterone into dihydrotestosterone and androstanedione, which may stimulate sebum secretion. This oxidative 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) activity of RoDH-4 is competitively inhibited by retinol and 13-cis-retinol. Here, we further examine the substrate specificity of RoDH-4 and the inhibition of its 3 alpha-HSD activity by retinoids. Recombinant RoDH-4 oxidized 3,4-didehydroretinol-a major form of vitamin A in the skin-to its corresponding aldehyde. 13-cis-retinoic acid (isotretinoin), 3,4-didehydroretinoic acid, and 3,4-didehydroretinol, but not all-trans-retinoic acid or the synthetic retinoids acitretin and adapalene, were potent competitive inhibitors of the oxidative 3 alpha-HSD activity of RoDH-4, i.e., reduced the formation of dihydrotestosterone and androstandione in vitro. Extrapolated to the in vivo situation, this effect might explain the unique sebosuppressive effect of isotretinoin when treating acne.
  14. T-flavanone might be one at first glance. looks like it might be in some expensive shampoos and serums. trans-3,4'-Dimethyl-3-hydroxyflavanone, a hair growth enhancing active component, decreases active transforming growth factor beta2 (TGF-beta2) through control of urokinase-type plasminogen activator (uPA) on the surface of keratinocytes. trans-3,4'-Dimethyl-3-hydroxyflavanone (t-flavanone) is a synthetic compound with hair growth enhancing activity that is effective against male pattern alopecia. t-Flavanone was designed as a derivative of astilbin, the active hair growth enhancing component of Hypericum perforatum extracts. This study was designed to elucidate the mechanism of hair growth enhancement by t-flavanone. We investigated the effects of t-flavanone on transforming growth factor beta (TGF-beta), a known catagen-inducing factor induced in hair papilla cells by male hormone. When t-flavanone was added to cocultures of human hair papilla cells and human keratinocytes, there was no change in the total level of TGF-beta2. However, levels of active TGF-beta2 were reduced, suggesting the involvement of t-flavanone in the activation pathway of TGF-beta2. In order to investigate the effects of t-flavanone on TGF-beta2 activation by human keratinocytes, we evaluated the level of active TGF-beta2 converted from the inactive form in t-flavanone-treated human keratinocytes. The amount of active TGF-beta2 was reduced compared with controls suggesting that t-flavanone suppresses the TGF-beta2 activation cascade in human keratinocytes. We then examined the activity of urokinase-type plasminogen activator (uPA), the rate-limiting enzyme in the TGF-beta2 activation cascade, in t-flavanone-treated human keratinocytes. We found that t-flavanone reduces uPA activity on the keratinocyte surface. t-Flavanone is a hair growth enhancing component that has a novel mechanism of action which suppresses TGF-beta2 activation, and thereby is expected to have therapeutic effects on other types of alopecia in addition to male pattern alopecia.
  15. Sometimes I feel the dermatologist is as much to blame as the drug itself. If not more. Was looking at this hormone. It's involved in retinoid metabolism 3α-HSD Biological process • cellular response to jasmonic acid stimulus • steroid metabolic process • daunorubicin metabolic process • doxorubicin metabolic process • androgen metabolic process • retinoid metabolic process • bile acid and bile salt transport • bile acid biosynthetic process • oxidation-reduction process Various antidepressants, including the SSRIsfluoxetine, fluvoxamine, sertraline, and paroxetine, the SNRI venlafaxine, and mirtazapine, have been found to activate certain 3α-HSD enzymes, resulting in a selective facilitation of 5α-dihydroprogesterone conversion into allopregnanolone. This action has been implicated in their effectiveness in affective disorders, and has resulted in them being described as selective brain steroidogenic stimulants (SBSSs). Have you tried Zantac or pepcid? They are h2 blockers. They shouldn't cause much dryness. Your shit don't look too bad actually. I mean you don't look sickly or anything. Seem to have good color in your skin. I'd try to focus on the positives and try to not let it consume you too much. Know it's hard though,especially when people got daily reminders of their sides
  16. Some info on retinoid induced hair loss. Not sure if this has been posted yet. Someone mentioned on a forum this is reversible. Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla. Foitzik K1, Spexard T, Nakamura M, Halsner U, Paus R. Author information Abstract Diffuse hair loss ranks among the most frequent and psychologically most distressing adverse effects of systemic therapy with retinoids, which severely limits their therapeutic use even where clinically desired. Since the underlying mechanisms of retinoid-induced effluvium are as yet unknown, we have investigated the influence of the prototypic retinoid all-trans retinoic acid (ATRA, tretinoin) on the growth of human scalp hair follicles (HF) in culture. HF in the anagen VI stage of the hair cycle were cultured in the presence of 10(-8) or 10(-10) M ATRA. Compared with controls, hair shaft elongation declined significantly already after 2 d in the ATRA-treated group, and approximately 80% of the ATRA-treated HF had prematurely entered catagen-like stage at day 6, compared with 30% in the control group. This corresponded to an upregulation of apoptotic and a downregulation of Ki67-positive cells in ATRA-treated HF. Since transforming growth factor (TGF)-beta has been implicated as a key inducer of catagen, we next studied whether ATRA treatment had any effect on follicular expression. TGF-beta2 immunoreactivity was detected in the outer root sheath of anagen VI scalp HF. In catagen follicles, TGF-beta2 was also expressed in the regressing epithelial strand. After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Therefore, topical TGF-beta2/TGF-beta receptor II antagonists deserve to be explored for the prevention and management of retinoid-induced hair loss.
  17. Accutane's Dangerous Side Effects Accutane is a source of relief for many acne sufferers. However, despite this acne breakthrough, Accutane carries with it numerous side effects, including: Hearing and vision damage Liver and kidney damage Pancreatitis Cardiovascular injuries Severe birth defects Early closure of growth plates Lupus Suicidal thoughts and behavior Have you guys looked into Lupus? http://www.lupus.org/ How is lupus diagnosed? In lupus, something goes wrong with your immune system, the part of the body that fights off viruses, bacteria, and germs (“foreign invaders” like the flu). Normally, our immune system produces proteins called antibodies that protect the body from foreign invaders. When you have lupus, your immune system cannot tell the difference between these foreign invaders and your body’s healthy tissues, so autoantibodies (auto means self and anti means against: against self) are made that damage and destroy healthy tissue. These autoantibodies cause inflammation, pain, and damage in various parts of the body. A doctor who is considering the possibility of lupus will look for signs of inflammation which include, pain, heat, redness, swelling, and loss of function at a particular place in the body. Inflammation can occur on the inside of your body (your kidneys or heart, for example), on the outside (your skin), or both. A physician will carefully review the following while evaluating a lupus diagnosis: your current symptoms your laboratory test results your medical history the medical history of your close family members (grandparents, parents, brothers and sisters, aunts, uncles, cousins) All of this information may be necessary for a doctor to make a diagnosis of lupus. A variety of laboratory tests are used to detect physical changes or conditions in your body that can occur with lupus. Each test result adds more information to the picture your doctor is forming of your illness. However, for a number of reasons listed below, laboratory tests alone cannot give a definite “yes” or “no” answer: No single laboratory test can determine whether a person has lupus. Test results that suggest lupus can be due to other illnesses or can even be seen in healthy people. A test result may be positive one time and negative another time. Different laboratories may produce different test results. If multiple criteria are present simultaneously, a physician—a family practitioner, internist or pediatrician—may reach a lupus diagnosis. If, however, as is often the case, symptoms develop gradually over time, the diagnosis may not be as obvious, and consultation with a rheumatologist may be needed.
  18. Pale skin can be a sign of chronic gastritis or inflammation of the lining of the stomach. This can be chronic and go undetected for years with no symptoms. There is a possibility there could have been a mucosal change in the lining of the stomach or thinning due to accutane. There could be other reasons as well. Like lack of good blood flow for various reasons. I too have noticed unusual pale skin from Time to time
  19. This sounds like it could be silent reflux. It can be extremely hard to discern. But you might have some type of irritation going on with those symptoms.
  20. im going to be looking into this. il get back to you guys when i get more information such as cost. looks like insurance might even cover it. These eye floaters are annoying as hell some days. BTW I didnt get eye floaters until I started experimenting with vitamin A for the second time. So a word of caution. Also now that I think about it, Accutane had zero effect on my eyes while I was on the drug for 4 to 6 months. It wasnt until quite a few years after accutane I noticed my eyes becoming sensitive to light(forced to wear sunglasses when i never had to before) and decreased night vision. And I dont just mean Utah for this treatment. Im sure it will become available at more laser eye surgery specialist. New Laser Procedure Available To Treat Eye Floaters Issue 3.16 A new laser procedure to treat eye floaters is now available in southern Utah. The procedure is being performed by the Dixie Ophthalmic Specialists at Zion Eye Institute. Jason Ahee, MD is the Executive Medical Director for Zion Eye Institute. “Eye floaters are a very common problem. They usually appear as obstructions in a persons’ vision. They typically move around but can also be stationary. While not always a serious concern, they can range from distracting and annoying to visually disabling. Our new laser procedure will be a great help for patients struggling with eye floaters,” said Dr. Ahee. Floaters are found in the vitreous body, the clear gel that occupies most of the inside of the eye. They are caused by normal aging changes in the vitreous gel and there is no way to prevent them. Prior to this new laser procedure, the only way to remove floaters was to undergo invasive eye surgery to remove the vitreous gel and the floaters along with it. Most patient were told to just “live with it” because of the risks associated with surgery. Laser floater removal, however, can be done with minimal risk. The procedure is quick and painless. It is performed in the office with virtually no recovery time, and it is covered by medical insurances, including Medicare. The vitreous gel is 99% water and 1% solid elements. Of the solid portion, there are collagen filaments and hyaluronic acid molecules. The ability of the solid elements to retain water molecules decreases with age, causing liquefaction of the vitreous gel. The solid elements coalesce and form condensations. These condensations may ‘float’ within the liquid vitreous giving the patient a sensation of floaters in their vision. The same process that causes floaters may cause flashes of light. When the vitreous pulls on the retina – which lines the inside of the eyeball like wallpaper – the photoreceptor cells in the retina are mechanically stimulated. The retinal cells are incapable of perceiving pain, pressure, or temperature. The only stimulus that the retina responds to is ‘light’. So when the retinal photoreceptors experience mechanical stimulation because of the vitreous pull, they send a signal to the brain in the form of disorganized light, which is perceived by the brain as a ‘flash’. With the accumulation of enough liquid vitreous, the vitreous framework collapses and the vitreous completely separates from the retina. This process is called posterior vitreous detachment which can cause large floaters but is otherwise benign. If the vitreous pulls the retina enough to cause a retinal tear or hole, this can lead to a retinal detachment which may cause vision loss if not repaired quickly. Any time a patient experiences new onset of flashes and/or floaters, it is recommended that they see their eye doctor for a thorough examination. Posterior vitreous detachment occurs in less than 10% people under 50 years of age but in more than 60% people who are over 70 years of age. It is more common for people who are nearsighted, who have had an eye injury, have undergone eye surgery, or have had inflammation inside the eye.
  21. I feel like it be like how they caught capone for tax invasion. Something minor. Like we know what it did. But we dont know what it did. thats the problem. So it have to be something more minor or targeted that was tangible that could be easily proven. like the eye floater thing i was mentioning. like eye floaters caused by reduced lactoferrin in tear tissue caused by accutane. im still going to look into this btw. unfortunately some people dont have a choice. Truejustice looks like he could be a step away from barrett's esophagus which increases the risk for esophageal cancer.This is definitely something to get under control. but yea accutane is a prime example of risk/reward. just nobody told us we wouldnt see it coming.
  22. Someone was saying they felt completely normal on prednisone, well thats the most powerful anti inflammatory you can get. Looking at something more contained that might work similar thats not systemic could be something like a regime from this study. and i dont mean just for the esophagus but might have a impact on the body as a whole. its a off the wall approach, but has anti-inflammatory impact on multiple fronts. Eight patients from a single, adult gastroenterology unit with EoE were identified. Diagnosis was made by histological findings in addition to clinical symptoms. All the patients received 12-week treatment with combined oral pantoprazole 40 mg, montelukast 10 mg and swallowed fluticasone 880 micrograms daily. No maintenance medication was routinely used after the treatment. All patients had eosinophilic infiltration more than 15 per high power field histologically. Five patients (62.5%) had resolved or improved symptoms after the treatment. Two patients (25%) had recurrent but less severe symptoms 2 and 12 months after the treatment, respectively. I just want to mention that pantoprazole also has anti inflammatory properties. One doctor, as this person mentions has treated many patients successfully with symptoms of IBS with 40mg of pantoprazole daily. I know most of us dont have this type of ibs, but it might be capable still of calming the stomach. On the flipside of this if accutane was capable of inducing hypochlorhydria, as similar in sjogren's, A ppi is the opposite of what a person would want to do. But if we had reduced stomach acid I think people would be coming up with multiple vitamin deficiencies. but ive had opposing theories on this. My IBS Cured I use to have what was diagnosed as IBS. I would go to the bathroom with loose stool or diarrhea at least 3 to 4 times a day. No matter what I changed in my diet it was there all the time. I hated leaving my house and I never ate when away from the house. I eventually got tired of living this way so I decided to talk to a new doctor and he changed my life. He said that he had given out Protonix to 100's of patients that had IBS and it seemed to work wonders. I was willing to try anything so I said count me in. Within a week I was getting better and after a month I was using the bathroom no more than 1 time a day (normal stool). I know that it is the Protonix because I was forced to change because my insurance wanted me to switch to Prilosac because it was cheaper, when I switched I was back to the loose stool and 3-4 times a day. I went right back on Protonix. It has been 5 yrs now and I am on a bathroom schedule of 1 a day :-) I posted this hoping that it might help someone else as I know IBS can really suck the life out of you..... Read more: http://www.healthboards.com/boards/irritable-bowel-syndrome-ibs/579459-my-ibs-cured.html#ixzz4Yi6jGbj5
  23. no I dont really believe accutane could cause a physical change like a hiatus hernia. I meant more like a drug induced change somewhere in the gi tract similar to an allergic reaction that could cause chronic inflammation.Thats what could cause excess eosinophils being produced.I was more so speaking for my case and about that other guy i found with eosinophilic esophagitis post tane. If Accutane was capable of causing this, which i dont know for sure, Maybe something similar could be going on with other people. Idk if this could resolve on its own, need short-term treatment, or become chronic and need lifelong treatment. As far as changes in the brain that could maybe be detected it prob have to be a sensitive test like a PET scan with before and after shots. I mentioned to a neurologist once about getting a PET scan and he made it sound like my insurance wouldnt cover it or i didnt have cause. Back to the reflux real quick and /or stomach inflammation for some people. if the inflammation was severe enough this might be capable of causing some nerve pressure or pain along some main nerves( like the spine) That could trigger anything from muscle weakness/spasms to joint pain,to chronic headaches. Even if people dont feel like they got this going on. You might. I've seen alot of people mention histamine type reactions to supplements or weird mucus production. this could just be your body triggering secretions to fight inflammation somewhere in the body.
  24. That is a pretty serious form of reflux if you actually had ulcers in your esophagus. These gi issues including chronic reflux are actually some of the symptoms they are lumping together in some of the lawsuits. It's basically ibs going in the other direction. Now that accutane has been off the market for awhile I think the statue of limitations will be running out soon, alot of us are years past this anyways. I wonder if there would be any exceptions if we really found something. Basically like a drug induced skin change from the inside induced by accutane that could be causing some of these symptoms.
  25. Just found this when looking up if esophillic esophagitis could be related to accutane. Looks like this dude got diagnosed with the same thing after a very large dose of tane. This esophillic condition is capable of happening anywhere in the GI tract. WadeNovember 18, 2010 at 1:38 pmReply I am currently 23 years old and reside in Canada and was taking accutane ~10years ago at 240mg/day for 6 months. I had the usual side effects while taking the drug, but started having troubles swallowing soon after. The problem persistened and worsened to the point of not being able to swallow most solid foods. 2 years of hospital and specialist visits was finally diagnosed with eosinophilic esophagitis by a scoping and clipping of the esophagus. (Had done barrium swallow, xrays, digital imaging, diets, etc… previous to the scoping) They also scoped the stomach and first part of the intestine and found eight Benign Tumors that they removed. All of these symptoms are related to accutane symptoms. I currently have to take some sort of steroid inhaler that I swallow for 30 days at a time and daily ran-pantoprazole to help with inflammation and esophagitis. Is there any lawsuits in Canada or is this done through the states??? Any info please let me know thanks. - See more at: http://www.aboutlawsuits.com/settlement-accutane-lawsuit-prior-to-trial-10157/#sthash.XmTAmGUu.dpuf