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Update on celiac disease – etiology, differential diagnosis, drug targets, and management advances
Scanlon SA, Murray JA
Clinical and Experimental Gastroenterology , 2011, DOI: http://dx.doi.org/10.2147/CEG.S8315
Abstract: ate on celiac disease – etiology, differential diagnosis, drug targets, and management advances Review (7531) Total Article Views Authors: Scanlon SA, Murray JA Published Date December 2011 Volume 2011:4 Pages 297 - 311 DOI: http://dx.doi.org/10.2147/CEG.S8315 Samantha A Scanlon1, Joseph A Murray1,2 1Department of Internal Medicine, 2Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA Abstract: Celiac disease (CD) is an immune-mediated enteropathy triggered by exposure to wheat gluten and similar proteins found in rye and barley that affects genetically susceptible persons. This immune-mediated enteropathy is characterized by villous atrophy, intraepithelial lymphocytosis, and crypt hyperplasia. Once thought a disease that largely presented with malnourished children, the wide spectrum of disease activity is now better recognized and this has resulted in a shift in the presenting symptoms of most patients with CD. New advances in testing, both serologic and endoscopic, have dramatically increased the detection and diagnosis of CD. While the gluten-free diet is still the only treatment for CD, recent investigations have explored alternative approaches, including the use of altered nonimmunogenic wheat variants, enzymatic degradation of gluten, tissue transglutaminase inhibitors, induction of tolerance, and peptides to restore integrity to intestinal tight junctions.
Update on celiac disease – etiology, differential diagnosis, drug targets, and management advances  [cached]
Scanlon SA,Murray JA
Clinical and Experimental Gastroenterology , 2011,
Abstract: Samantha A Scanlon1, Joseph A Murray1,21Department of Internal Medicine, 2Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USAAbstract: Celiac disease (CD) is an immune-mediated enteropathy triggered by exposure to wheat gluten and similar proteins found in rye and barley that affects genetically susceptible persons. This immune-mediated enteropathy is characterized by villous atrophy, intraepithelial lymphocytosis, and crypt hyperplasia. Once thought a disease that largely presented with malnourished children, the wide spectrum of disease activity is now better recognized and this has resulted in a shift in the presenting symptoms of most patients with CD. New advances in testing, both serologic and endoscopic, have dramatically increased the detection and diagnosis of CD. While the gluten-free diet is still the only treatment for CD, recent investigations have explored alternative approaches, including the use of altered nonimmunogenic wheat variants, enzymatic degradation of gluten, tissue transglutaminase inhibitors, induction of tolerance, and peptides to restore integrity to intestinal tight junctions.Keywords: immune-mediated enteropathy, gliadin, gluten, epidemiology, CD diagnosis, therapy
Recent advances in inflammatory bowel disease
K Pettengell
Continuing Medical Education , 2009,
Abstract: We have come some way in understanding the aetiology of inflammatory bowel disease, which has allowed advances in its management.
Genetics of Alzheimer's disease: recent advances
Dimitrios Avramopoulos
Genome Medicine , 2009, DOI: 10.1186/gm34
Abstract: Alzheimer's disease (AD), first described by Alois Alzheimer in 1907 [1], is a neurodegenerative disorder progressing from memory loss to profound dementia and death within an average of eight years. Although clinical diagnosis is reliable in more than 90% of cases, the definite diagnosis is assigned post mortem based on brain atrophy and the characteristic neuropathologic findings, which involve intracellular neurofibrillary tangles containing hyperphosphorylated tau protein and extracellular amyloid plaques containing deposits of beta amyloid (Aβ). AD is recognized today as the most common cause of dementia in the elderly.In the 1930s a number of reports described familial cases of AD with multiple affected individuals in each generation, consistent with an autosomal dominant mode of inheritance [2-4]. Like Alzheimer's first patient, the age of onset of the familial cases was most often below 65 years, which led physicians to identify AD as pre-senile dementia, distinguishing it from senile dementia. By 1980, however, it had become evident that the two types of dementia are essentially identical, named by Terry and Davies [5] as dementia of the Alzheimer type.Not surprisingly, the genes involved in the familial, auto-somal dominant AD (FAD) were quickly discovered during the golden years of gene mapping in the 1990s. Despite initial confusion and controversy due to the genetic heterogeneity of AD [6,7], extending even to the small subset of FAD, a combination of functional evidence, linkage analyses and sequence comparisons led to the identification of the three genes accounting for most FAD cases: APP [8], PSEN1 [9] and PSEN2 [10].The majority (95%) of AD cases, however, are of later onset and do not follow Mendelian inheritance, despite showing significant heritability [11,12]. Like most other psychiatric disorders, the genetics of the late-onset disease appear to be complex. AD is the first complex disorder for which a gene was identified through an association
Novel Therapeutic/Integrative Approaches for Celiac Disease and Dermatitis Herpetiformis  [PDF]
Alessio Fasano
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/959061
Abstract: Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. Gluten is a protein component in wheat and other cereals like rye and barley. At present, the only available treatment is a strict gluten-free diet. Recent advances have increased our understanding of the molecular basis for this disorder. Last decade has seen new scientific developments in this disease and led to the formulation of new concepts of pathophysiology that offer possible targets for new treatments or interventions integrative to the gluten-free diet.
Overactive Bladder Disease : Overview of the recent advances in Symptoms, Diagnosis and Treatment  [cached]
Anandi Krishnan,Prof. Dr. R. S. Gaud
Pharmaceutical Reviews , 2008,
Abstract: The ability to hold urine and maintain continence is dependent on normal function of the lower urinary tract, the kidneys, and the nervous system, plus the physical and psychological ability to recognize and appropriately respond to the urge to urinate.The bladder's ability to fill and store urine requires a functional sphincter (muscle controlling output) and a stable bladder wall muscle (detrusor). The bladder of an infant contracts automatically when a certain volume of urine is reached. As the individual learns to control urination, bladder muscle contraction is prevented by constant inhibition from the cerebral cortex (part of the brain). This allows urination to be delayed until the individual is ready. Undesired bladder muscle contraction may occur as the result of a break in the neurological pathway from the brain to the bladder. It can also occur if the bladder is irritated and the normal neurological impulses to inhibit urination are insufficient to keep the bladder relaxed as it fills. This is called Overactive bladder syndrome or urinary incontinence. This article reviews the recent advances, diagnosis and treatment of this disease state.
Hepatobiliary Disorders in Celiac Disease: An Update  [PDF]
Kaushal K. Prasad,Uma Debi,Saroj K. Sinha,Chander K. Nain,Kartar Singh
International Journal of Hepatology , 2011, DOI: 10.4061/2011/438184
Abstract: This communication reviews recent literature and summarizes hepatobiliary abnormalities that may complicate the clinical course of celiac disease. A wide spectrum of hepatobiliary diseases has been described, including asymptomatic elevations of liver enzyme levels, nonspecific hepatitis, nonalcoholic fatty liver disease, and autoimmune and cholestatic liver disease. Moreover, in the majority of patients, liver enzyme levels will normalize on a gluten-free diet. In addition, celiac disease may be associated with rare hepatic complications, such as hepatic T-cell lymphoma. Because many celiac patients do not have overt gastrointestinal symptoms, a high index of suspicion is required. Simple methods of detecting celiac disease such as serum antibody tests help in the early identification of the disease, thus preventing serious complications of the disorder. The IgG DGP antibody test and IgA tTG antibody test used in combination are an excellent screening test for suspected cases of celiac disease.
Celiac Disease  [PDF]
Nikolaos Fotos,Hero Brokalaki
To Vima tou Asklipiou , 2008,
Abstract: Celiac disease is a small intestine disease caused by the immunological response to gluten, a component of wheat, rye and barley. The worldwide prevalence of celiac disease ranges between 0.2% and 2.2 %. The clinical features of celiac disease includes diarrhea, steatorrhea, flatulence, abdominal pain and weight loss. The asymptomatic type of celiac disease is characterized by soft or normally shaped stool, weakness, lassitude and moderate weight loss. In children, celiac disease usually arises between the first and the third year of age, with diarrhea, flatulence and low weight. The malabsorption in small intestine causes many extaintestinal manifestations, such us anemia, bone abnormalities, hemorrhage and neuropathy. Celiac disease is diagnosed by histological examination of tissue samples taken by duodenum due gastroscopy and by the detection of certain antibodies in blood (anti-GL-IgG, anti-GL-IgA, ΕΜΑ-IgA και anti-tTg-IgA). The only therapeutic approach to celiac disease is a gluten-free diet and, if it is necessary, the administration of iron, folic acid, calcium and vitamins (K, B12). The prognosis of celiac disease is excellent, if there is an early diagnosis and the patient keeps for life a gluten free diet.
Recent Advances on the Neuroprotective Potential of Antioxidants in Experimental Models of Parkinson’s Disease  [PDF]
Sushruta Koppula,Hemant Kumar,Sandeep Vasant More,Byung Wook Kim,In Su Kim,Dong-Kug Choi
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms130810608
Abstract: Parkinson’s disease (PD), a neurodegenerative movement disorder of the central nervous system (CNS) is characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta region of the midbrain. Although the etiology of PD is not completely understood and is believed to be multifactorial, oxidative stress and mitochondrial dysfunction are widely considered major consequences, which provide important clues to the disease mechanisms. Studies have explored the role of free radicals and oxidative stress that contributes to the cascade of events leading to dopamine cell degeneration in PD. In general, in-built protective mechanisms consisting of enzymatic and non-enzymatic antioxidants in the CNS play decisive roles in preventing neuronal cell loss due to free radicals. But the ability to produce these antioxidants decreases with aging. Therefore, antioxidant therapy alone or in combination with current treatment methods may represent an attractive strategy for treating or preventing the neurodegeneration seen in PD. Here we summarize the recent discoveries of potential antioxidant compounds for modulating free radical mediated oxidative stress leading to neurotoxicity in PD.
Celiac disease
Wolfgang Holtmeier, Wolfgang F Caspary
Orphanet Journal of Rare Diseases , 2006, DOI: 10.1186/1750-1172-1-3
Abstract: Celiac disease (CD) in children and celiac sprue in adults are probably the same disorder with the same pathogenesis. The synonyms are: Coeliac disease (British spelling) – Celiac sprue – Nontropical sprue-Gluten-sensitive enteropathy – Idiopathic steatorrheaCeliac disease is a chronic intestinal disease mostly associated with malabsorption caused by intolerance to gluten. It is characterized by immune-mediated enteropathy (villous flattening), resulting in maldigestion and malabsorption. Clinical and histological improvement can be obtained after withdrawal of dietary gluten.Celiac disease is characterized by malabsorption and villous atrophy. However, diseases other than CD can cause marked villous flattening and increased intraepithelial lymphocytes (IEL) [1]. Differential diagnosis is of special importance for subjects in whom CD is suspected and who have negative serology. The following diseases, which can have similar features, must be ruled out [1-4]:? Tropical sprue? Collagenous colitis? Whipple's disease? Giardiasis? Viral enteritis? AIDS? Crohn's disease of the small intestine? Small intestinal lymphoma? Carbohydrate intolerance, cow's milk intolerance? Autoimmune enteropathy? Graft-vs-host disease? Radiation damagePrevalence of clinically overt celiac disease varies from 1/270 in Finland to 1/5,000 in North America. However, since celiac disease can be asymptomatic, most subjects are not diagnosed or they can present with atypical symptoms. In epidemiological studies aimed to assess CD prevalence, large cohorts in North America and Europe were screened for highly-sensitive endomysium or tissue transglutaminase antibodies. Besides, they underwent subsequent small intestinal biopsies when antibody testing was positive. The CD prevalence was found to be much higher than expected. Approximately 1/100 to 1/500 were found positive for antibodies and had villous atrophy of the small intestine [5-10]. Thus, up to 1% of a western population tests positive for celi
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