Symptoms of anemia include the following:

Shortness of breath

Passing out.

If a person appears pale and if they suffer from any of the above symptoms, they should see their family doctor for a complete evaluation. The leading cause of anemia is iron deficiency. Iron deficiency is generally caused by blood loss. In a woman between the ages of 14 and 50, the leading cause of anemia is menstral abnormalities. as a person ages, the anemia from blood loss is usually due to a problem in the gastrointestinal tract. this problem can take the form of ulcers, inflammation, diverticula, and tumors which include malignant (cancer) or benign (polyps). There are many other forms of anemia besides iron deficiency. A person should not take iron tablets, especially those 50 and older. Iron taken when it is not needed can lead to significant liver damage. The only time a person should take iron is on the advice of their physician. If a person believes that they are suffering from anemia, they should see their doctor for a complete evaluation.

Dr. Gordon J. Rafool is a specialist in family practice and geriatrics at Gessler Clinic, Winter Haven.

Pancreatic Cancer Late Signs – Colon Cancer Symptoms and Signs in Women

Cancer that affects the gastrointestinal tract can hit anywhere in the digestive tract, starting with the esophagus and then going to the gallbladder, liver, pancreas, stomach, small intestine, large intestine, and lastly, the rectum.

Colon Cancer Symptoms and Signs in Women

While we primarily think of asbestos as a carcinogen that attacks the lungs with cancers such as mesothelioma, it can actually cause gastrointestinal cancer as well. this is because asbestos can be ingested as well as inhaled. this happens when a person gets asbestos fibers in his or her mouth through exposure to things such as asbestos dust. The fibers can become caught in the saliva, which are then swallowed and passed into the digestive tract.

The problem with asbestos fibers, whether ingested or inhaled, is that our bodies cannot break them down. When they lodge into our systems, they are stuck there. Our bodies are forced to create nodules of extra tissue around the fibers, which can cause scarring that can turn into cancerous tumors. Additionally, these fibers are microscopic in scope, which means that you may not know that you are ingesting them.

Lung Cancer Secrets Revealed Click here

Sadly, the widespread use of asbestos during the 20th century meant that many people were exposed to the material before it was mostly banned in the late 1980s. while asbestos is not very susceptible to biodegradation, age and friction can both lead to the wearing down of the object containing the carcinogen, which leads to the release of fibers. For example, asbestos is often a part of brake pads. however, as we use our brakes, the friction from stopping the car leads to the breakdown of asbestos. When the pads are changed, it can release clouds of asbestos into the air.

Asbestos from the air can be ingested, resulting in gastrointestinal cancers. this is a broad spectrum of cancer that gains about 250,000 new cases per year in the United States alone. some common types of gastrointestinal cancers include: Colorectal – the third most common cancer overall in both men and women Pancreatic Stomach – also known as gastric Anal Extrahepatic bile duct Esophageal Gallbladder Liver Small intestine

When doctors operate to remove gastrointestinal cancerous tumors, it can remove parts of your body that are necessary to keep you alive. You may have to live on special intravenous liquid nutrition or have special reconstruction surgery to keep you functioning as normally as possible.

lung cancer treatment breakthroughs Click here

SupremeMasterTV.com • March 20 2010 marks the 25th anniversary of Meatout Day, one of the world’s largest annual grassroots information campaigns on the plant-based diet. in honor of this special occasion, we feature excerpts with experts and people from all backgrounds regarding the wholesome, green and compassionate vegan diet…

Pancreatic Cancer Late Signs

More : Pancreatic Cancer Late Signs

New York, NY (Vocus/PRWEB) March 18, 2011

the Crohn’s & Colitis Foundation of America today announced that Congressmen Ander Crenshaw (R-FL) and Jesse L. Jackson, Jr. (D-IL) have launched the Congressional Crohn’s and Colitis Caucus. This new caucus will work to promote awareness of Crohn’s disease and ulcerative colitis, collectively known as inflammatory bowel disease (IBD), the need for expanded research at the National Institutes of Health and Centers for Disease Control and Prevention, and the importance of accessible insurance and disability for patients with IBD, chronic and often debilitating digestive diseases affecting over 1.4 million Americans. Congressmen Crenshaw and Jackson are inviting all Congressional colleagues to become members of this new caucus.

“As a parent of a child with Crohn’s and colitis, I have witnessed first-hand the often debilitating effects of this disease,” says Congressman Crenshaw. “Alongside Congressman Jackson, I am continuing to help raise much-needed awareness about issues related to Crohn’s and colitis—across party lines.”

With continuous inflammation in the gastrointestinal tract, Crohn’s disease and ulcerative colitis patients suffer significant abdominal pain, intestinal pain, and weight loss, among many other symptoms. with no known cure or cause, Crohn’s disease and ulcerative colitis have a devastating impact on both patients and families. Complications include arthritis, osteoporosis, anemia, liver disease, kidney disease, and colon cancer.

For information on how you can make your voice heard and advocate for IBD patients, visit ccfa.org/advocacy.

About Crohn's Disease & Ulcerative Colitis Crohn's disease and ulcerative colitis are painful, medically incurable illnesses that attack the digestive system. Crohn's disease may attack anywhere from the mouth to the anus, while ulcerative colitis inflames only the large intestine (colon). Symptoms may include abdominal pain, persistent diarrhea, rectal bleeding, fever and weight loss. many patients require hospitalization and surgery. These illnesses can cause severe complications, including colon cancer in patients with long-term disease. Some 1.4 million American adults and children suffer from Crohn's disease or ulcerative colitis, with as many as 150,000 under the age of 18. Most people develop the diseases between the ages of 15 and 35.

About the Crohn's & Colitis Foundation the Crohn's & Colitis Foundation of America's mission is to cure Crohn's disease and ulcerative colitis, and to improve the quality of life of children and adults affected by these diseases. the Foundation ranks third among leading health non-profits in the percentage of expense devoted to research toward a cure, with more than 81 cents of every dollar the Foundation spends goes to mission-critical programs. the Foundation consistently meets the standards of organizations that monitor charities, including the Better Business Bureau's Wise Giving Alliance (give.org) and the American Institute of Philanthropy (charitywatch.org). for more information, contact the Foundation at 800-932-2423 or visit ccfa.org. Join CCFA on Facebook at apps.facebook.com/supportccfa/and follow CCFA on Twitter at twitter.com/ccfa.

Read the full story at prweb.com/releases/2011/3/prweb8217473.htm

Public release date: 27-Jan-2011 [ | E-mail | Share ] Contact: Abi Cantorpress@plos.org44-122-344-2823Public Library of Science

An investigation has found that celiac disease and Crohn’s disease, both inflammatory diseases of the gastrointestinal tract, share at least four genetic risk loci. together, researchers from the University of Groningen, the Netherlands; the Broad Institute, USA; the Universit? de Montr?al and Montreal Heart Institute in Canada performed a combined meta-analysis of genome-wide data for celiac disease and Crohn’s disease. This meta-analysis, published in the open-access journal PLoS Genetics on January 27, has identified two new shared risk loci and two shared risk loci that had previously been independently identified for each disease.

The pathogenesis of both celiac disease and Crohn’s disease is only partly understood, although it is known that they are affected by both genetic and environmental risk factors. at least one in every hundred individuals in the Western world develop celiac disease; Crohn’s disease is much less common but can be accompanied by more severe symptoms as it can affect the whole gastrointestinal tract. Celiac patients develop an inflammation of the small bowel in reaction to gluten, whereas there is no specific known autoantigen for Crohn’s disease. however, the primary cause of Crohn’s disease is thought to be a dysregulated immune response to gut bacteria. In order to gain a better understanding of the pathogenesis and to aid in developing therapies against these disorders, knowledge of the genetic background of the diseases is vital.

As it has previously been shown that celiac patients are at a higher risk of developing Crohn’s disease than non-sufferers, it had been thought that the two illnesses would share genetic risk loci. This study combined the results from the genetic investigations into both diseases to show that part of the genetic background of Crohn’s disease and celiac disease is shared, which confirms a common pathogenesis for these disorders. Although additional studies will be necessary to understand the mechanisms by which these variants influence both Crohn’s disease and celiac, the current study provides a proof of principle that risk factors shared across related diseases can be identified by directly combining genetic data from clinically distinct diseases.

FINANCIAL DISCLOSURE: the study was supported by the Celiac Disease Consortium, an Innovative Cluster approved by the Netherlands Genomics Initiative and partially funded by the Dutch Government (BSIK03009); by the Netherlands Organization for Scientific Research (NWO, VICI grant 918.66.620 to CW [one of the authors], AGIKO grant 92.003.533 to EAMF [author], KF grant 907.00.281 to RKW [author]); by the Wellcome Trust (grant WT084743MA to DAvH [author]); by the National Institutes of Allergy and Infectious Diseases (grant AI065687, AI067152 to JDR [author]); by the National Institute of Diabetes and Digestive and Kidney Diseases (grant DK064869, DK062432 to JDR); and by the Crohn’s and Colitis Foundation of America (grant SRA512 to JDR). EAMF is a MD-medical research trainee with financial support from the Netherlands Organisation for Health Research and Development. GT [author] was awarded a Ter Meulen Fund travel grant by the Royal Netherlands Academy of Arts and Sciences (KNAW). PCD [author] is a MRC Clinical Training Fellow (G0700545). the British 1958 Birth Cohort collection was funded by the UK Medical Research Council (grant G0000934) and the Wellcome Trust (grant 068545/Z/02). Funding for the project Wellcome Trust Case-Control Consortium 2 data was provided by the Wellcome Trust under award 085475. the funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

COMPETING INTERESTS: the authors have declared that no competing interests exist.

CITATION: Festen EAM, Goyette P, Green T, Boucher G, Beauchamp C, et al. (2011) a Meta-Analysis of Genome-Wide Association Scans Identifies IL18RAP, PTPN2, TAGAP, and PUS10 as Shared Risk Loci for Crohn’s Disease and Celiac Disease. PLoS Genet 7(1): e1001283. doi:10.1371/journal.pgen.1001283

PLEASE ADD THIS LINK TO THE FREELY AVAILABLE ARTICLE IN ONLINE VERSIONS OF YOUR REPORT (the link will go live when the embargo ends): plosgenetics.org/article/info:doi/10.1371/journal.pgen.1001283

PRESS-ONLY PREVIEW OF THE ARTICLE: plos.org/press/plge-07-01-rioux.pdf

CONTACT: Abi Cantor, PLoS Genetics

This press release refers to an upcoming article in PLoS Genetics. the release is provided by journal staff, or by the article authors and/or their institutions. any opinions expressed in this release or article are the personal views of the journal staff and/or article contributors, and do not necessarily represent the views or policies of PLoS. PLoS expressly disclaims any and all warranties and liability in connection with the information found in the releases and articles and your use of such information.

About PLoS Genetics

PLoS Genetics (plosgenetics.org) reflects the full breadth and interdisciplinary nature of genetics and genomics research by publishing outstanding original contributions in all areas of biology. all works published in PLoS Genetics are open access. everything is immediately and freely available online throughout the world subject only to the condition that the original authorship and source are properly attributed. Copyright is retained by the authors. the Public Library of Science uses the Creative Commons Attribution License.

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The Public Library of Science (PLoS) is a non-profit organization of scientists and physicians committed to making the world’s scientific and medical literature a freely available public resource. For more information, visit plos.org.

[ | E-mail | Share ]  

I'm not sure what I've ate, but I usually NEVER get indigestion.

Here are some symptoms:
1) when breath in , I get a stuffy chest pain. I can't really pinpoint a certain spot.
2) I had about one diarrhea.

So is this indigestion?
I took meds, but it's not clearing up my chest pain.

Very possible. Sounds like something you ate has had a negative effect on your entire Gastrointestinal tract. top to bottom.

It could also be the result of a viral/bacterial infection — but that is less likely.

Just give it time, and monitor the symptoms and things will get back to normal. take some pepto-bismal, or anything similar to settle the stomach. if you still have loose stool, take a bit of immodium.

HAV is responsible for acute hepatitis only. often, this is an anicteric illness, with clinical symptoms indistinguishable from other forms of viral gastroenteritis, particularly in young children.

The illness is much more likely to be symptomatic in older adolescents or adults, in patients with underlying liver disorders, and in those who are immunocompromised. it is characteristically an acute febrile illness with an abrupt onset of anorexia, nausea, malaise, vomiting, and jaundice.

Duration of Illness:   The typical duration of illness is 7–14 days

Other organ systems can be affected during acute HAV infection. Regional lymph nodes and the spleen may be enlarged. the bone marrow may be moderately hypoplastic, and aplastic anemia has been reported. Small intestinal tissue may show changes in villous structure, and ulceration of the gastrointestinal tract can occur, especially in fatal cases. Acute pancreatitis and myocarditis have been reported, though rarely, and nephritis, arthritis, vasculitis, and cryoglobulinemia can result from circulating immune complexes.

Complications:   Although most patients achieve full recovery, two distinct complications can occur:

1.Acute liver failure (ALF) from HAV infection, a rare but not infrequent complication of HAV. Those at risk for this complication are adults, but also patients with underlying liver disorders or those who are immunocompromised. the height of HAV viremia may be linked to the severity of hepatitis. whereas in the United States, HAV represents <0.5% of pediatric-aged ALF, it is responsible for up to 3% mortality in the adult population with ALF. in endemic areas of the world, HAV constitutes up to 40% of all cases of pediatric ALF.2.HAV can progress to a prolonged cholestatic syndrome that waxes and wanes over multiple months. Pruritus and fat malabsorption are problematic and require symptomatic support with antipruritic medications and fat-soluble vitamins. This syndrome occurs in the absence of any liver synthetic dysfunction and resolves with no sequelae

There is no specific treatment for hepatitis A. Supportive treatment consists of intravenous hydration as needed and antipruritic agents and fat-soluble vitamins for the prolonged cholestatic form of disease. Serial monitoring for signs of acute liver failure and early referral to a transplantation center can be lifesaving.

VN:F [1.9.3_1094]VN:F [1.9.3_1094]Clinical Features of Hepatitis A in children, 10.0 out of 10 based on 1 rating