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Showing results for tags 'idiopathic'.
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Celiac.com 12/23/2022 - Compared with the general population, children with celiac disease are nearly three times as likely to develop juvenile idiopathic arthritis, while adults with celiac disease are nearly twice as likely to be diagnosed with rheumatoid arthritis. Celiac disease is tied to numerous immune-mediated conditions, but, so far, researchers haven't nailed down any solid epidemiological connection between celiac disease and juvenile idiopathic arthritis or rheumatoid arthritis. A new study changes that. Here's how. Population-based Cohort Study Using a population-based cohort, a team of researchers recently set out to determine the risk of juvenile idiopathic arthritis and rheumatoid arthritis in people with celiac disease. The research team included John B. Doyle, MD; Benjamin Lebwohl, MD, MS; Johan Askling, PhD; Anders Forss, MD; Peter H.R. Green MD; Bjorn Roelstraete, PhD; Jonas Söderling, PhD; Jans F. Ludvigsson, and Jonas MD, PhD. They are variously affiliated with the Celiac Disease Center, Department of Medicine, Columbia University Irving Medical Center, New York, New York, USA; the Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; the Department of Pediatrics, Orebro University Hospital, Orebro, Sweden. Celiac Disease Data Used to Spot Patients Using a national histopathology database in Sweden, the team identified patients diagnosed with biopsy-proven celiac disease between 2004 and 2017. They then matched each patient by age, sex, calendar year, and geographic region against people from the general population. They then used Cox proportional hazards models to calculate the incidence and estimated the relative risk of juvenile idiopathic arthritis in celiacs aged eighteen and under, and of rheumatoid arthritis in people with celiac disease aged eighteen and over. The team found just over 24,000 celiacs, whom they then matched to more than 117,000 people from the general population. Juvenile Idiopathic Arthritis Rates Triple for Celiac Youth & Rheumatoid Arthritis Rates Double for Adults Among people under 18 years old, the incidence rate of juvenile idiopathic arthritis was 5.9 per 10,000 person-years in patients with celiac disease and 2.2 per 10,000 person-years in the general population over a seven year follow-up. Among individuals 18 or over, the incidence of rheumatoid arthritis was 8.4 per 10,000 person-years in celiac disease and 5.1 per 10,000 person-years in matched comparators over a follow-up of 8.8 years. KIA is nearly three times more common among children with celiac disease than in the general population, while rheumatoid arthritis occurs nearly twice as often among adults with celiac disease. Based on their findings, the team advises clinicians caring for celiac patients with joint symptoms to be vigilant for signs of juvenile idiopathic arthritis or rheumatoid arthritis in those patients. Read more in the American Journal of Gastroenterology
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Celiac.com 05/30/2022 - A recent Italian study published in Pediatric Rheumatology indicates that juvenile idiopathic arthritis patients have higher rates of celiac disease, which suggests that celiac screening would be beneficial for IA sufferers, especially those with a family history of autoimmunity. Since many autoimmune disorders share similar immune triggers, mechanics and contributing factors, including genetics and environment, understanding the connections, along with the factors associated with an increased susceptibility, could help researchers and clinicians to design better case-finding strategies for certain at-risk populations. For their retrospective study, the team gathered information, including age at diagnosis, family history, other autoimmune disorders, juvenile idiopathic arthritis subtype, and medications, from a Southern Italian group of patients with juvenile idiopathic arthritis who were admitted to the Pediatric Rheumatology Unit between January 2001 and June 2019 who underwent celiac disease screening. Using the data, they were able to assess clinical features and disease course, along with associated risk factors when juvenile idiopathic arthritis and celiac disease happen together. The team evaluated juvenile idiopathic arthritis patients every 3 to 6 months and adjusted treatment in response to adverse events and disease effects. The team's analysis is limited in part by small sample size of patients with both juvenile idiopathic arthritis and celiac disease, and because patients with juvenile idiopathic arthritis and celiac disease had longer follow-up periods than patients with juvenile idiopathic arthritis alone. However, since most celiac disease diagnosis occurred within 12 months of juvenile idiopathic arthritis onset, the team believes this does not influence bias. The team concluded that: They also added that the "results highlight the importance of celiac disease screening in pediatric juvenile idiopathic arthritis patients." These results are also significant for juvenile idiopathic arthritis patients who also have celiac disease, as juvenile idiopathic arthritis looks to be more aggressive in those patients, who often need step-up therapy. They note that these patients might benefit from an early introduction of a biologic drug, but more study is needed to know for sure. They plan future studies to test whether first-line genetic testing followed by celiac disease-specific serological screening will produce better results than first-line serological screening. Stay tuned for more on this and related stories. Read more in Rheumatology Network
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Celiac.com 05/18/2022 - Idiopathic pulmonary hemosiderosis causes diffuse alveolar hemorrhage, but the mechanics of the cause remains unknown. Alveolar hemorrhage is a "life-threatening disorder characterized clinically by the presence of hemoptysis, falling hematocrit, diffuse pulmonary infiltrates and hypoxemic respiratory failure. Diffuse alveolar hemorrhage should be considered a medical emergency due to the morbidity and mortality associated with failure to treat the disorder promptly." The occurrence of idiopathic pulmonary hemosiderosis and celiac disease together has been noted in both children and adults, and is also known as Lane-Hamilton syndrome. A team of researchers recently set out to compare demographics, clinical and radiologic findings, treatment, and outcomes between adult patients with idiopathic pulmonary hemosiderosis and Lane-Hamilton syndrome. The research team included Biplab K. Saha, Praveen Datar, Alexis Aiman, Alyssa Bonnier, Santu Saha, and Nils T. Milman. They are variously affiliated with the Department of Clinical Biochemistry, University College Zealand in Næstved, Denmark; the department of Internal Medicine, New York Institute of Technology College of Osteopathic Medicine at Arkansas State University in Jonesboro, USA; the Pulmonary and Critical Care Medicine, Ozarks Medical Center · West Plains, USA; the center for Critical Care, Goldfarb School of Nursing at Barnes Jewish College · Saint Louis, USA; and the Internal Medicine, Saha Clinic in Narail, Bangladesh. For their systematic review of the literature, the team used proper search parameters to identify relevant articles in multiple databases. Their final review included a total of 60 studies reporting 65 patients. Forty-nine of these patients had idiopathic pulmonary hemosiderosis, while 16 had Lane-Hamilton syndrome. Thirteen of twenty-two patients screened, nearly sixty percent, were positive for anti-celiac antibodies. Patients with Lane-Hamilton syndrome showed earlier symptom onset and diagnosis of idiopathic pulmonary hemosiderosis, though both groups showed an average delay in diagnosis of about one year. Lane-Hamilton syndrome patients were most likely to show the classic symptom triad, although only one in five patients in the Lane-Hamilton syndrome group showed any significant gastrointestinal symptoms at the time of idiopathic pulmonary hemosiderosis diagnosis. A gluten-free diet alone was effective in the majority of patients. Fewer patients in the Lane-Hamilton syndrome cohort received systemic corticosteroid than the idiopathic pulmonary hemosiderosis cohort. The recurrence and mortality in patients with Lane-Hamilton syndrome appear to be less than in the idiopathic pulmonary hemosiderosis cohort. The results show that one in four adult patients with idiopathic pulmonary hemosiderosis has celiac disease. Patients with Lane-Hamilton syndrome may show milder effects than patients without celiac disease. Based on these results, the researchers are recommending that all idiopathic pulmonary hemosiderosis patients receive serologic screening for celiac disease. Read more at Cureus.com 14(3): e23482
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Celiac.com 12/13/2021 - Celiac disease is potentially connected to juvenile idiopathic arthritis (JIA). A team of researchers recently set out to determine the serological incidence of celiac disease in patients with JIA. For their study, the team enrolled seventy-eight patients children under 16 years of age with JIA, who had not responded well to routine treatment, and who visited the pediatric centers of Tehran University of Medical Sciences between 2017 and 2019. The team also assessed the various manifestations of celiac disease, and measured celiac disease-related serological screening tests. Average subject age was about 8 years old, plus or minus about 4 years. years. Three patients with oligoarticular JIA had Anti-TTG-Ab levels above normal. None had celiac symptoms. Data showed no significant statistical differences in terms of growth disorders, sex distribution, and different subtypes of JIA between the sero-positive and sero-negative groups. The team confirmed one case of celiac disease by pathology, and recommended a gluten-free diet for the patient. Their main takeaway from the data is that celiac disease is still possible, even in JIA patients with no celiac symptoms. Read more in the Archives of Iranian Medicine. 2021 Oct 1;24(10):783-785. The research team included N Payman Sadeghi, Kobra Salari, Vahid Ziaee, Nima Rezaei, and Kambiz Eftekhari. They are variously affiliated with the Children's Medical Center, Pediatrics Center of Excellence, Tehran University of Medical Sciences, Tehran, Iran; the Pediatric Rheumatology Iranian Society; the Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran; the Pediatric Gastroenterology and Hepatology Research Center, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran and the Department of Pediatrics, Bahrami Children's Hospital, Tehran University of Medical Sciences, Tehran, Iran.
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Celiac.com 07/31/2021 - Although my theory on the ultimate, underlying cause if idiopathic epilepsy (viruses) is only a theory (backed by mounds of data), the response of epileptic dogs (and people) to the elimination diet I propose is far from theoretical. It has halted seizures in even the most refractory of cases time and time again. It has stopped seizures overnight in dogs that were about to be euthanatized by board-certified veterinarians for “non-responsive” epilepsy. It has eliminated seizures in people with a lifetime of seizures, ranging from children to adults in their 40’s and 50’s, including those with head trauma-induced epilepsy. The response of theses individuals, in addition to the fact that there are more than 24 known viral causes of seizures, has led to my “theory” of chronic latent viruses being the ultimate reasons why one individual has epilepsy and the one next to them does not. This is no more far-fetched than what we know about cancer...viral information embedded in our very genome that is “unleashed” once the circumstances are correct. (Once we have done enough wrong to ourselves and our pets, actually.) I guess we could use the term “epileptogens” rather than carcinogens when discussing the things that cause epilepsy to begin between 6 months and 6 years of age, 2-14 years, and then again, after age 65 in people). Why the delay? Doesn’t that pattern in people smack of the same things that cause leukemia? My ultimate “cause” of epilepsy theory is driven by viral agents but the dietary management of these patients is a 6.5 year fact, supported by similar, published, and well-publicized work in human medical research into the ketogenic and now the “modified Atkins” diets. They are coming close to the real answer, which is my diet, but they are woefully deficient in what they are eliminating. The step from ketosis (for which NO healthy individual should ever volunteer) to a non-ketotic diet found in the “modified Atkin’s” is a step in the right direction. Are you familiar with these dietary developments in human medicine, studied extensively at John’s Hopkins and The Mayo Clinic? I’m sure you must be. What is it that they are eliminating that is making a difference in 30-50% of individuals to which they apply it? Why not 60, 70 or 90%. Why not 100% like we are experiencing. Yes 100% of patients with idiopathic epilepsy that I have been involved with have had a notable response, the majority of which stopped seizing completely. 100%. That is a stiff claim, isn’t it? It’s true, though. And it is the wellspring of the passion I have for this topic and why I spend my time writing on forums instead of playing golf. Why not speak at ACVIM meetings? Why not write in peer-reviewed journals? First, I am a solitary practitioner. Other than my internship at Angell Memorial, I have no clout. And believe me when I say that I tried to reach people in high places. Academia is an ivory tower that is difficult to approach, especially in human medicine. Thank God (literally) there are alternatives to simply trying to change the mind of the two professions before any help can be rendered to the masses. Thank God (again, literally) that the afflicted can now be their own best advocates and find answers on their own. Thank God for the Internet. The time has come for medicine to change. Our blind approach of masking symptoms with drugs has come to an end. Seizures serve a purpose just like every other symptom that occurs in our body and until we see that, we will never be better at curing disease that we are now, and our success is dismal at this point. Our limited understanding of nutrition is appalling. How any educated person can say that diet has nothing to do with epilepsy (or any other medical condition for that matter) is beyond me but that has been the response of almost every board certified vet or practitioner that has been presented with this idea by an interested client...just before their seizures were stopped by changes to the diet. The “startling” fact is that nutrition has everything to do with our body running on the nutrients it acquires from food. We don’t get proteins, fats, vitamins, and minerals from air, do we? Cellular metabolism and enzyme systems don’t run on oxygen alone, do they? So how could a board-certified doctor, human or veterinary, say that “nutrition has nothing to do with seizures”??? Do you sense my frustration? I have spent the past 7 years trying to get this word out to colleagues and doctors alike. My head is bloody from hitting it so hard against that wall. But the progress I have made in the private sector has been astounding. Now my time has come to share it with the professionals. If I waited to hear from my or the human medical profession, I would have died waiting. Google “DogtorJ” and you’ll see where I’ve been (other than car forums). I spoke at two AHVMA conferences. I recently spoke at an international conference of MDs. And I will be speaking at the upcoming NAVC conference in Orlando in January. Dr. Jean Dodds and I are in total agreement on this approach and correspond very regularly. I have doctors at both Johns Hopkins and Mayo interested in this work, and the director of integrative medicine at Mayo is trying to get an NIH grant to study it. Maybe this approach has been backwards when viewed from inside the ivory tower, but this is becoming the mode these days. Most of us are aware of the public’s rising level of dissatisfaction with medical care. If medicine was a government a revolution would be in the offing. The doctor jokes are exceeding the lawyer jokes now. My clients regularly volunteer to me how much they “hate” the medical profession. I didn’t think I would see that day. Why are they so vehement about their disdain for “us”? Simply put, they are waking up. They see the absurdity of taking fever-reducers for a fever ‘caused by a virus or bacteria because they intuitively know that the fever serves a vital purpose in our healing. Similarly, they don’t see the logic in treating cancer with more carcinogens. They don’t understand why you would treat a condition like MS or lupus that results in individuals with weakened immune systems with immunosuppressive drugs. The scary thing is that these treatments eem to make sense to those who prescribe those “remedies”, just as they did to me for 21 years. Now that’s a scary and humbling thought. It’s time for us all to wake up. And, it’s time for us to put aside our pompous attitudes, imagining that we know so much when we really understand so little. Hey, “idiopathic” is our favorite word. How can we be so smug when we know that this is true? Even worse, how can we let a word like that shut off our brains when there is a finite number of causes for any disease we care to discuss. We hold up that word like a banner while casting aside ideas that actually work. I do understand how the system works. Again, thank God there are alternatives to that system. Otherwise, conventional (internal) medicine would lead us all into our graves. Granted, they often squeeze another 15 years out of a human life using drugs, controlling heart disease and the like. But they have done nothing to halt the incidence of heart disease, immune-mediated diseases, and cancer. It has simply been a race to determine this year’s number one killer. It is time to actually prevent and even CURE these conditions. Our disbelief that this can be done only illustrates how far we have strayed from the proper path of the healing arts.
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Brain. 2003 Mar;126(Pt 3):685-91. Celiac.com 08/11/2005 – Researchers in the United Kingdom screened 224 patients with various forms of ataxia (59 with familial, 132 sporadic idiopathic, and 33 with clinically probable cerebellar variant of multiple system atrophy MSA-C) for the presence of antigliadin antibodies and found that 24% of the ataxia patients were sensitive to gluten, and 72% of them had the HLA DQ2 genetic marker. Their results were compared with those of 1,200 healthy controls. Among the familial ataxia group 8 or 59 (14%), 54 of 132 (41%) of the sporadic idiopathic group, 5 of 33 (15%) in the MSA-C group, and 149 of the 1,200 (1.24%) controls, screened positive for antigliadin antibodies. The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant. Gastrointestinal symptoms were present in only 13% of the ataxia patients. MRI testing found atrophy of the cerebellum in 79% and white matter hyperintensities in 19% of the ataxia patients, and 45% of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. The researchers conclude that gluten ataxia is the single most common cause of sporadic idiopathic ataxia, and antigliadin antibody testing is should be done immediately on everyone with symptoms of sporadic ataxia.
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Celiac.com 04/07/2009 - Idiopathic portal hypertension is a malady ofunknown cause, typically manifesting portal hypertension, splenomegalyand anemia secondary to hypersplenism. Recently, a team ofIranian researchers encountered the case of a a 54-year-old maleadmitted for evaluation of malaise, weight loss, abdominal swelling andedema of the lower limbs. The reporting team was made up ofdoctors Farhad Zamani, Afsaneh Amiri, Ramin Shakeri, Ali Zare, andMehdi Mohamadnejad, of the Department of Pathology, and theGastrointestinal and Liver Disease Research Center of FirouzgarHospital at the University of Medical Sciences in Tehran, and theDigestive Disease Research Center of Shariati Hospital at TehranUniversity of Medical Sciences. The patient's clinicalevaluation showed pancytopenia, large ascites, splenomegaly andesophageal anomalies associated with portal hypertension. Bloodtests and small intestinal biopsy showed the presence of celiacdisease. Patient's symptoms improved with a gluten-free diet, butimprovement was further impaired by ulcerative jejunoileitis, andintestinal T-cell lymphoma. From these results, the researchersconclude that celiac disease, by means of a heightened immune responsein the splenoportal axis, can lead to the development of idiopathicportal hypertension in susceptible affected patients. J Med Case Reports. 2009; 3: 68.
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