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Cerebral Palsy (CP) – KidsHealth

Posted: December 16, 2017 at 7:42 pm

Cerebral palsy (CP) is a disorder that affects muscle tone, movement, and motor skills (the ability to move in a coordinated and purposeful way).

CP usually is caused by brain damage that happens before or during a baby’s birth, or during the first 3 to 5 years of a child’s life. This brain damage also can lead to other health issues, including vision, hearing, and speech problems; and learning disabilities.

There is no cure for CP, but treatment, therapy, special equipment, and, in some cases, surgery can help kids who are living with the condition.

Cerebral palsy is one of the most common congenital (existing at orbefore birth) disorders of childhood. About 500,000 children in the United States have the condition.

The three types of CP are:

Since cerebral palsy affects muscle control and coordination, even simple movements like standing still are difficult. Other functions that also involve motor skills and muscles such as breathing, bladder and bowel control, eating, and talking also may be affected when a child has CP.

Cerebral palsy does not get worse over time.

The exact causes of CP aren’t always known. But many cases are the result of problems during pregnancy when a fetus’ brain is either damaged or doesn’t develop normally. This can be due to infections, maternal health problems, a genetic disorder, or something else that interferes with normal brain development. Rarely, problems during labor and delivery can cause CP.

Premature babies particularly those who weigh less than 3.3 pounds (1,510 grams) have a higher chance of having CP than babies that are carried to term. So do other low-birthweight babies and multiple births, such as twins and triplets.

Brain damage in infancy or early childhood also can lead to CP. For example, a baby or toddler might suffer damage because of lead poisoning, bacterial meningitis, poor blood flow to the brain, being shaken as an infant (shaken baby syndrome), or being in a car accident.

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Cerebral palsy | Genetic and Rare Diseases Information Center …

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Cerebral palsy refers to a group of neurological disorders that can affect the brain and/or spinal cord. Signs and symptoms generally appear during infancy or early childhood and vary based on the type of cerebral palsy (spastic cerebral palsy, dyskinetic cerebral palsy, ataxic cerebral palsy, and mixed cerebral palsy), the severity of the condition and which area(s) of the brain are affected. Common features include a lack of muscle coordination when performing voluntary movements (ataxia); stiff or tight muscles and exaggerated reflexes (spasticity); walking with one foot or leg dragging; walking on the toes, a crouched gait, or a “scissored” gait; and muscle tone that is either too stiff or too floppy. Cerebral palsy is caused by abnormal brain development or damage to the developing brain. Most of these problems occur as the baby grows in the womb; however, they can happen at any time during the first 2 years of life. There is no cure for cerebral palsy, but treatment is available to alleviate some symptoms. This may include physical, occupational, and speech therapy; certain medications; surgery; and/or devices (i.e. braces, wheelchairs) to aid in mobility.[1][2][3]

Last updated: 11/18/2015

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Cerebral Palsy (CP) Information & More | Cleveland Clinic

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What is cerebral palsy?

Cerebral palsy is an umbrella term for describing a group of chronic disorders that impair a person’s ability to control body movement and posture. These disorders result from injury to the motor areas of the brain. Cerebral palsy affects two to six infants out of every 1,000 births, and is the most common disability among children in the U.S. The problem causing cerebral palsy may occur while the infant is still in the womb or after birth, and the problem is not always detectable during a child’s first year of life. Children with mild cerebral palsy may only have a minor limp or an uncoordinated walk, while patients with severe cases will require care and supervision throughout their lives. Many of the infants born with cerebral palsy also experience some degree of mental retardation and/or have seizures.

Spastic cerebral palsy is the most common form and is the type seen in 75 to 80 percent of cases. Patients with this form are unable to relax their muscles, which respond by tightening further if the patient or someone else tries to stretch them. This spasticity affects the function of individual muscles, especially flexor muscles.

When spasticity occurs in the arms, the flexors tighten, pulling the elbows toward the body, and hands and wrists toward the chin. The hands themselves form tight fists. This constant tightened state may in turn weaken the extensor muscles, stretching them to the point where some of their functionality is lost. When spasticity occurs in the legs, the flexor muscles in the calves are affected. When this happens, the heels become raised, pushing the toes downward and often causing a child to walk on their toes.

Spasticity in the legs also affects the adductor muscles (the inner thigh muscles). Adductor muscles pull a body part toward its midline, such as those that pull the arms to a person’s side or close a person’s legs. In patients with cerebral palsy, the inward pull of the adductor muscles is so strong that the legs cross over each other or scissor. This motion also rotates the legs inward at the hips, pulling them away from the hip sockets, which can lead to abnormal socket development and hip dislocation.

Other conditions associated with spastic cerebral palsy may include an exaggerated response to startle stimulation, a degree of mental impairment, and weak respiration. Some children with spastic cerebral palsy develop a curvature of the spine. This results from remaining in a constant upright position, which prevents the trunk muscles needed for supporting the spine from developing properly.

Whereas spastic cerebral palsy doesn’t permit the muscles to relax, with athetosis, the muscles are subjected to excessive and uncontrollable movement. These movements also increase with a child’s excitement and in response to surrounding environmental stimulation. Likewise, the more relaxed a child is, the less often these abnormal movements occur. When a child is sleeping, the movements stop altogether.

The movements of a stimulated child form what is called an extensor thrust. When this happens, the arms rapidly extend outward and back, the palms turn toward the floor, the fingers spread and overextend, the knees come together, and the feet turn inward with the toes up. The child’s neck flexes, pulling the head back and to the side, and the mouth opens with the tongue sticking out. These movements can present extreme difficulty for a child when eating and drinking. The child may also have shallow and irregular respiration, which affects oxygen flow to the brain and increases the chance for respiratory infections. Patients with athetotic cerebral palsy also have difficulty with balance and walking.

The characteristics of each of these syndromes are not mutually exclusive, and a child may have spastic cerebral palsy in his or her legs as well as a degree of athetosis elsewhere.

While some of the causes of cerebral palsy are still unknown, there are many known factors that can cause or contribute to brain damage before or after birth. Preventive methods, such as proper prenatal care, can eliminate some causes, while others are as yet unpreventable.

Some of the known causes or contributors to cerebral palsy include:

Patients with cerebral palsy can have a variety of symptoms. These symptoms usually do not worsen over time and include:

Cerebral palsy may affect one arm or leg, an arm and leg on the same side, only the legs, all four limbs, or any combination of arms and legs. Whatever the affected areas may be, the muscle types involved are often the same. Muscles that enable people to bend their arms and legs are called flexor muscles. Extensor muscles are the opposite of flexors and enable a person to straighten these limbs back out. It is the inability to control these and other muscles that defines the most common cerebral palsy syndromes.

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Cerebral Palsy – Kids Health

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Have you ever heard a family member talk about your first step or the first word you spoke? For kids with cerebral palsy, called CP for short, taking a first step or saying a first word may not be as easy. That’s because CP is a condition that can affect the things that kids do every day.

Some kids with CP use wheelchairs and others walk with the help of crutches or braces. In some cases, a kid’s speech may be affected or the person might not be able to speak at all.

Cerebral palsy (say: seh-REE-brel PAWL-zee) is a condition that affects thousands of babies and children each year. It is not contagious, which means you can’t catch it from anyone who has it. The word cerebral means having to do with the brain. The word palsy means a weakness or problem in the way a person moves or positions his or her body.

A kid with CP has trouble controlling the muscles of the body. Normally, the brain tells the rest of the body exactly what to do and when to do it. But because CP affects the brain, depending on what part of the brain is affected, a kid might not be able to walk, talk, eat, or play the way most kids do.

There are three types of cerebral palsy: spastic (say: SPASS-tik), athetoid (say: ATH-uh-toid), and ataxic (say: ay-TAK-sik). The most common type of CP is spastic. A kid with spastic CP can’t relax his or her muscles or the muscles may be stiff.

Athetoid CP affects a kid’s ability to control the muscles of the body. This means that the arms or legs that are affected by athetoid CP may flutter and move suddenly. A kid with ataxic CP has problems with balance and coordination.

A kid with CP can have a mild case or a more severe case it really depends on how much of the brain is affected and which parts of the body that section of the brain controls. If both arms and both legs are affected, a kid might need to use a wheelchair. If only the legs are affected, a kid might walk in an unsteady way or have to wear braces or use crutches. If the part of the brain that controls speech is affected, a kid with CP might have trouble talking clearly. Another kid with CP might not be able to speak at all.

For some babies, injuries to the brain during pregnancy or soon after birth may cause CP. Children most at risk of developing CP are small, premature babies (babies who are born many weeks before they were supposed to be born) and babies who need to be on a ventilator (a machine to help with breathing) for several weeks or longer.

But for most kids with CP, the problem in the brain happens before birth. Often, doctors don’t know why.

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Ulcerative colitis – Wikipedia

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Ulcerative colitisEndoscopic image of a colon affected by ulcerative colitis. The internal surface of the colon is blotchy and broken in places.SpecialtyGastroenterologySymptomsAbdominal pain, diarrhea mixed with blood, weight loss, fever, anemia[1]ComplicationsMegacolon, inflammation of the eye, joints, or liver, colon cancer[1][2]Usual onset1530 years or > 60 years[1]DurationLong term[1]CausesUnknown[1]Diagnostic methodColonoscopy with tissue biopsies[1]TreatmentDietary changes, medication, surgery[1]MedicationSulfasalazine, steroids, immunosuppressants such as azathioprine, biological therapy[1]Frequency112 million with Crohn’s (2015)[3]Deaths47,400 with Crohn’s (2015)[4]

Ulcerative colitis (UC) is a long-term condition that results in inflammation and ulcers of the colon and rectum.[1][5] The primary symptom of active disease is abdominal pain and diarrhea mixed with blood.[1]Weight loss, fever, and anemia may also occur.[1] Often symptoms come on slowly and can range from mild to severe.[1] Symptoms typically occur intermittently with periods of no symptoms between flares.[1] Complications may include megacolon, inflammation of the eye, joints, or liver, and colon cancer.[1][2]

The cause of UC is unknown.[1] Theories involve immune system dysfunction, genetics, changes in the normal gut bacteria, and environmental factors.[1][6] Rates tend to be higher in the developed world with some proposing this to be the result of less exposure to intestinal infections, or a Western diet and lifestyle.[5][7] The removal of the appendix at an early age may be protective.[7] Diagnosis is typically by colonoscopy with tissue biopsies.[1] It is a kind of inflammatory bowel disease (IBD) along with Crohn’s disease and microscopic colitis.[1]

Dietary changes may improve symptoms.[1] Several medications are used to treat symptoms and bring about and maintain remission, including aminosalicylates such as sulfasalazine, steroids, immunosuppressants such as azathioprine, and biological therapy.[1]Removal of the colon by surgery may be necessary if the disease is severe, does not respond to treatment, or if complications such as colon cancer develop.[1]Removal of the colon and rectum can cure the disease.[1][7]

Together with Crohn’s disease about 112 million people were affected as of 2015.[3] Each year it newly occurs in 1 to 20 per 100,000 people, and 5 to 500 per 100,000 individuals are affected.[5][7] The disease is more common in North America and Europe than other regions.[7] Often it begins in people aged 15 to 30 years, or among those over 60.[1] Males and females appear to be affected in equal proportions.[5] It has also become more common since the 1950s.[5][7] Together, ulcerative colitis and Crohn’s disease affect approximately a million people in the United States.[8] With appropriate treatment the risk of death appears the same as that of the general population.[2] The first description of ulcerative colitis occurred around the 1850s.[7]

The clinical presentation[11] of ulcerative colitis depends on the extent of the disease process. Patients usually present with diarrhea mixed with blood and mucus, of gradual onset that persists for an extended period (weeks). They may also have weight loss and blood on rectal examination. The inflammation caused by the disease along with the chronic bleeding from the GI tract leads to increased rates of anemia. The disease may be accompanied by different degrees of abdominal pain, from mild discomfort to painful bowel movements or painful abdominal cramping with bowel movements.

Ulcerative colitis is associated with a general inflammatory process that can affect many parts of the body. Sometimes these associated extra-intestinal symptoms are the initial signs of the disease, such as painful arthritic knees in teenagers, which also may be seen in adults. A diagnosis of ulcerative colitis may not occur until the onset of intestinal manifestations, however.

Ulcerative colitis is normally continuous from the rectum up the colon. The disease is classified by the extent of involvement, depending on how far the disease extends:

In addition to the extent of involvement, people may also be characterized by the severity of their disease.[12]

As ulcerative colitis is believed to have a systemic (i.e., autoimmune) origin, patients may present with comorbidities leading to symptoms and complications outside the colon. The frequency of such extraintestinal manifestations has been reported as anywhere between 6 and 47 percent,[13] and include the following:

No direct causes for ulcerative colitis are known, but many possible factors such as genetics and stress play a role.

A genetic component to the etiology of ulcerative colitis can be hypothesized based on the following:[14]

Twelve regions of the genome may be linked to ulcerative colitis, including, in the order of their discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3,[16] but none of these loci has been consistently shown to be at fault, suggesting that the disorder is influenced by multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease.[17]

Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. There may even be human leukocyte antigen associations at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates.[16]

Multiple autoimmune disorders have been recorded with the neurovisceral and cutaneous genetic porphyrias including ulcerative colitis, Crohn’s disease, celiac disease, dermatitis herpetiformis, diabetes, systemic and discoid lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren’s disease and scleritis. Physicians should be on high alert for porphyrias in families with autoimmune disorders and care must be taken with the use of potential porphyrinogenic drugs, including sulfasalazine.

Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis. They include the following:

Ulcerative colitis is an autoimmune disease characterized by T-cells infiltrating the colon.[28] In contrast to Crohn’s disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis usually involves the rectum and is confined to the colon, with occasional involvement of the ileum. This so-called “backwash ileitis” can occur in 1020% of patients with pancolitis and is believed to be of little clinical significance.[29] Ulcerative colitis can also be associated with comorbidities that produce symptoms in many areas of the body outside the digestive system. Surgical removal of the large intestine often cures the disease.[12]

Levels of sulfate-reducing bacteria tend to be higher in persons with ulcerative colitis, which could indicate higher levels of hydrogen sulfide in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine.[32]

An increased amount of colonic sulfate-reducing bacteria has been observed in some patients with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulfide. Human colonic mucosa is maintained by the colonic epithelial barrier and immune cells in the lamina propria (see intestinal mucosal barrier). N-butyrate, a short-chain fatty acid, gets oxidized through the beta oxidation pathway into carbon dioxide and ketone bodies. It has been shown that N-butyrate helps supply nutrients to this epithelial barrier. Studies have proposed that hydrogen sulfide plays a role in impairing this beta-oxidation pathway by interrupting the short chain acetyl-CoA dehydrogenase, an enzyme within the pathway. Furthermore, it has been suggested that the protective benefit of smoking in ulcerative colitis is due to the hydrogen cyanide from cigarette smoke reacting with hydrogen sulfide to produce the non-toxic isothiocyanate, thereby inhibiting sulfides from interrupting the pathway.[34] An unrelated study suggested that the sulfur contained in red meats and alcohol may lead to an increased risk of relapse for patients in remission.[32]

Ulcerative colitis patients typically present with rectal bleeding, diarrhea, tenesmus (urgent desire to evacuate the bowels but with the passage of little stool), and lower abdominal pain. The severity of disease at clinical presentation is important in determining the appropriate therapy. Patients with mildly active disease will have fewer than 4 bowel movements daily and no signs of toxicity. Individuals with moderate-severity UC have more frequent bowel movements with bleeding. Approximately 70% of patients with ulcerative colitis will have moderately active disease at presentation. Patients with severely active disease will have signs of toxicity with fever, tachycardia, and anemia. Patients with fulminant or toxic colitis or toxic megacolon often have more than 10 bowel movements in a day, continuous bleeding, abdominal distention and tenderness, and radiologic evidence of edema and, in some cases, bowel dilation. These people most often require immediate colectomy because 10% have perforated colon at the time of surgery.

The initial diagnostic workup for ulcerative colitis includes the following:[12][35]

Although ulcerative colitis is a disease of unknown causation, inquiry should be made as to unusual factors believed to trigger the disease.[12]

The simple clinical colitis activity index was created in 1998 and is used to assess the severity of symptoms.[36][37]

The best test for diagnosis of ulcerative colitis remains endoscopy. Full colonoscopy to the cecum and entry into the terminal ileum is attempted only if the diagnosis of UC is unclear. Otherwise, a flexible sigmoidoscopy is sufficient to support the diagnosis. The physician may elect to limit the extent of the exam if severe colitis is encountered to minimize the risk of perforation of the colon. Endoscopic findings in ulcerative colitis include the following:

Ulcerative colitis is usually continuous from the rectum, with the rectum almost universally being involved. Perianal disease is rare. The degree of involvement endoscopically ranges from proctitis or inflammation of the rectum, to left sided colitis, to pancolitis, which is inflammation involving the ascending colon.

Biopsies of the mucosa are taken to definitively diagnose UC and differentiate it from Crohn’s disease, which is managed differently clinically. Microbiological samples are typically taken at the time of endoscopy. The pathology in ulcerative colitis typically involves distortion of crypt architecture, inflammation of crypts (cryptitis), frank crypt abscesses, and hemorrhage or inflammatory cells in the lamina propria. In cases where the clinical picture is unclear, the histomorphologic analysis often plays a pivotal role in determining the diagnosis and thus the management. By contrast, a biopsy analysis may be indeterminate, and thus the clinical progression of the disease must inform its treatment.

The following conditions may present in a similar manner as ulcerative colitis, and should be excluded:

The most common disease that mimics the symptoms of ulcerative colitis is Crohn’s disease, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases since their courses and treatments may differ. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis.

Standard treatment for ulcerative colitis depends on the extent of involvement and disease severity. The goal is to induce remission initially with medications, followed by the administration of maintenance medications to prevent a relapse. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing remission, which involves relief of symptoms and mucosal healing of the colon’s lining, and then longer term treatment to maintain remission and prevent complications. Acute severe ulcerative colitis requires hospitalisation, exclusion of infections, and corticosteroids.[41]

For acute stages of the disease, a low fiber diet may be recommended.[42][43]

Ulcerative colitis can be treated with a number of medications, including 5-ASA drugs such as sulfasalazine and mesalazine. Corticosteroids such as prednisone can also be used due to their immunosuppressive and short-term healing properties, but because their risks outweigh their benefits, they are not used long-term in treatment. Immunosuppressive medications such as azathioprine and biological agents such as infliximab and adalimumab are given only if people cannot achieve remission with 5-ASA and corticosteroids. Such treatments are used less commonly due to their possible risk factors, including but not limited to increased risk of cancers in teenagers and adults,[44]tuberculosis, and new or worsening heart failure (these side effects are rare). A formulation of budesonide was approved by the FDA for treatment of active ulcerative colitis in January 2013.[45] The evidence on methotrexate does not show a benefit in producing remission in people with ulcerative colitis.[46] Off-label use of drugs such as ciclosporin and tacrolimus has shown some benefits.[47][48]Fexofenadine, an antihistamine drug used in treatment of allergies, has shown promise in a combination therapy in some studies.[49][50] Opportunely, low gastrointestinal absorption (or high absorbed drug gastrointestinal secretion) of fexofenadine results in higher concentration at the site of inflammation. Thus, the drug may locally decrease histamine secretion by involved gastrointestinal mast cells and alleviate the inflammation.

Sulfasalazine has been a major agent in the therapy of mild to moderate ulcerative colitis for over 50 years. In 1977, Mastan S. Kalsi et al. determined that 5-aminosalicylic acid (5-ASA and mesalazine) was the therapeutically active component in sulfasalazine.[51] Since then, many 5-ASA compounds have been developed with the aim of maintaining efficacy but reducing the common side effects associated with the sulfapyridine moiety in sulfasalazine.[52]

Biologic treatments such as the TNF inhibitors infliximab, adalimumab, and golimumab are commonly used to treat people with UC who are no longer responding to corticosteroids. Tofacitinib, vedolizumab, and etrolizumab can also produce good clinical remission and response rates in UC.[6] Usually, these medications are only used if other options have been exhausted (i.e., the person has received and not responded favorably to high-dose corticosteroids and immunomodulators such as azathioprine and mesalazine).

Unlike aminosalicylates, biologics can cause serious side effects such as an increased risk of developing extra-intestinal cancers,[44]heart failure; and weakening of the immune system, resulting in a decreased ability of the immune system to clear infections and reactivation of latent infections such as tuberculosis. For this reason, patients on these treatments are closely monitored and are often given tests for hepatitis and tuberculosis at least once a year.

Unlike Crohn’s disease, ulcerative colitis has a lesser prevalence in smokers than non-smokers.[53][54] Studies using a transdermal nicotine patch have shown clinical and histological improvement.[55]

In one double-blind, placebo-controlled study conducted in the United Kingdom, 48.6% of patients who used the nicotine patch, in conjunction with their standard treatment, showed complete resolution of symptoms. Another randomized, double-blind, placebo-controlled, single-center clinical trial conducted in the United States showed that 39% of patients who used the patch showed significant improvement, versus 9% of those given a placebo.[56] Use of a transdermal nicotine patch without the addition of other standard treatments such as mesalazine has relapse occurrence rates similar to standard treatment without the use of nicotine.

The gradual loss of blood from the gastrointestinal tract, as well as chronic inflammation, often leads to anemia, and professional guidelines suggest routinely monitoring for anemia with blood tests repeated every three months in active disease and annually in quiescent disease.[57] Adequate disease control usually improves anemia of chronic disease, but iron deficiency anemia should be treated with iron supplements. The form in which treatment is administered depends both on the severity of the anemia and on the guidelines that are followed. Some advise that parenteral iron be used first because patients respond to it more quickly, it is associated with fewer gastrointestinal side effects, and it is not associated with compliance issues.[58] Others require oral iron to be used first, as patients eventually respond and many will tolerate the side effects.[57][59] All guidelines advise that parenteral iron should be administered in cases of severe anemia (a hemoglobin level less than 100 g/L).

Inflammation of the colon is a characteristic symptom of ulcerative colitis, and a new series of drugs in development looks to disrupt the inflammation process by selectively targeting an ion channel. A crucial step involved in the inflammation signaling cascade involves an intermediate conductance calcium activated potassium channel (IK channel) known as KCa3.1;[60][non-primary source needed] a protein coded for in the human gene KCNN4.[61] Ongoing research seeks to prevent T-cell activation and inflammation by inhibiting the KCa3.1 channel, selectively.[62][non-primary source needed] Since there is an upregulation of IK channel activity during T cell activation,[60][non-primary source needed] inhibition of the KCa3.1 is able to disrupt the production of Th1 cytokines IL-2 and TNF-. Production of these cytokines decreases because inhibition of KCa3.1 reduces the efflux of K+, which in turn diminishes the influx of Ca2+. By lowering elevated intracellular Ca2+ in patients with ulcerative colitis, these novel drug candidates can inhibit the signaling cascade involved in the inflammation process[62][non-primary source needed] and help relieve many of the symptoms associated with ulcerative colitis.

Preclinical study results in 2012 indicated that these selective inhibitors decreased colon inflammation in mice and rats cloned with the human KCa3.1 protein as effectively as the standard inflammatory bowel disease treatment of sulfasalazine. However, these novel selective IK channel blockers are significantly more potent and theoretically would be able to be taken at a much more manageable dosage.[62][non-primary source needed]

Benzothiazinone, NS6180, is a novel class KCa3.1 channel inhibitor in development. Through a number of in vitro experiments, NS6180 was qualified for KCa3.1 channel inhibition. In vivo experiment of DNBS (2,4 – dinitrobenzene sulfonic acid) induced rat colitis, a frequently used animal model for inflammatory bowel disease, showed comparable efficacy and greater potency than sulfasalazine.[62][non-primary source needed]

Unlike in Crohn’s disease, the gastrointestinal aspects of ulcerative colitis can generally be cured by surgical removal of the large intestine, though extraintestinal symptoms may persist. This procedure is necessary in the event of: exsanguinating hemorrhage, frank perforation, or documented or strongly suspected carcinoma. Surgery is also indicated for patients with severe colitis or toxic megacolon. Patients with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life.

Ulcerative colitis affects many parts of the body outside the intestinal tract. In rare cases, the extra-intestinal manifestations of the disease may require removal of the colon.[12]

Another surgical option for ulcerative colitis that is affecting most of the large bowel is called the ileo-anal pouch procedure. This is a two- to three-step procedure in which the large bowel is removed, except for the rectal stump and anus, and a temporary ileostomy is made. The next part of the surgery can be done in one or two steps and is usually done at six- to twelve-month intervals from each prior surgery.

In the next step of the surgery, an internal pouch is made of the patient’s own small bowel, and this pouch is then hooked back up internally to the rectal stump so that the patient can once again have a reasonably functioning bowel system, all internal. The temporary ileostomy can be reversed at this time so that the patient is internalized for bowel functions, or, in another step to the procedure, the pouch, and rectal stump anastamosis can be left inside the patient to heal for some time while the patient still uses the ileostomy for bowel function. Then, on a subsequent surgery, the ileostomy is reversed and the patient has internalized bowel function again.

A type of leukocyte apheresis, known as granulocyte and monocyte adsorptive apheresis, still requires large-scale trials to determine whether or not it is effective.[66] Results from small trials have been tentatively positive.[67]

About 21% of inflammatory bowel disease patients use alternative treatments.[72] A variety of dietary treatments show promise, but they require further research before they can be recommended.[73]

Patients with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with “flares” of disease. Patients with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. Patients with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of the disease.

The risk of colorectal cancer is significantly increased in patients with ulcerative colitis after ten years if involvement is beyond the splenic flexure. Those patients with only proctitis or rectosigmoiditis usually have no increased risk.[12] It is recommended that patients have screening colonoscopies with random biopsies to look for dysplasia after eight years of disease activity, at one to two year intervals.[87]

Ulcerative colitis has a significant association with primary sclerosing cholangitis (PSC), a progressive inflammatory disorder of small and large bile ducts. As many as 5% of patients with ulcerative colitis may progress to develop primary sclerosing cholangitis.[88]

Research has not revealed any difference in overall risk of dying in patients with ulcerative colitis from that of the background population. The cause-of-death distribution may be different from that of the background population.[89] It is thought that the disease primarily affects quality of life, and not lifespan.

Changes that can be seen in chronic ulcerative colitis include granularity, loss of the vascular pattern of the mucosa, loss of haustra, effacement of the ileocecal valve, mucosal bridging, strictures and pseudopolyps.[90]

The geographic distribution of UC and Crohn’s disease is similar worldwide,[91] with the highest number of new cases a year of UC found in Canada, New Zealand, Scotland and the United Kingdom.[92] It begins most commonly between the ages of 15 and 25. A second peak of onset is the 6th decade of life.[93] In general, higher rates are seen in northern locations compared to southern locations in Europe[94] and the United States.[95]

As with Crohn’s disease, the rates of UC are greater among Ashkenazi Jews and decreases progressively in other persons of Jewish descent, non-Jewish Caucasians, Africans, Hispanics, and Asians.[29] Appendectomy prior to age 20 for appendicitis[96] and current tobacco use[97] are protective against development of UC (although former tobacco use is associated with a higher risk of developing the disease.[97])

As of 2004, the number of new cases of UC in the United States is between 2.2 and 14.3 per 100,000 per year.[98] The number of people affected in the United States is between 37 and 246 per 100,000.[98]

In Canada, between 1998 and 2000, the number of new cases per year was 12.9 per 100,000 population or 4,500 new cases. The number of people affected was estimated to be 211 per 100,000 or 104,000.[99]

In the United Kingdom 10 per 100,000 people newly develop the condition a year while the number of people affected is 243 per 100,000. Approximately 146,000 people in the United Kingdom have been diagnosed with UC.[100]

Helminthic therapy using the whipworm Trichuris suis has been shown in a randomized control trial from Iowa to show benefit in patients with ulcerative colitis.[101] The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of patients in the developed world may lead to inflammation. Both helminthic therapy and fecal bacteriotherapy induce a characteristic Th2 white cell response in the diseased areas, which was unexpected given that ulcerative colitis was thought to involve Th2 overproduction.[102]

Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human ICAM-1 messenger RNA through Watson-Crick base pair interactions in order to subdue expression of ICAM-1.[103] ICAM-1 propagates an inflammatory response promoting the extravasation and activation of leukocytes (white blood cells) into inflamed tissue.[103] Increased expression of ICAM-1 has been observed within the inflamed intestinal mucosa of ulcerative colitis sufferers, where ICAM-1 over production correlated with disease activity.[104] This suggests that ICAM-1 is a potential therapeutic target in the treatment of ulcerative colitis.[105]

Gram positive bacteria present in the lumen could be associated with extending the time of relapse for ulcerative colitis.[106]

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Ulcerative colitis – Wikipedia

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Ulcerative Colitis – Symptoms, Causes and Treatments of …

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Ulcerative colitis and Crohn’s disease are the most common types of inflammatory bowel disease. Ulcerative colitis affects only the colon and rectum. Crohn’s can affect any part of the digestive tract. To learn more about Crohn’s disease, see the topic Crohn’s Disease.

Ulcerative colitis is a disease that causes inflammation and sores (ulcers) in the lining of the large intestine (colon ). It usually affects the lower section (sigmoid colon) and the rectum. But it can affect the entire colon. In general, the more of the colon that’s affected, the worse the symptoms will be.

The disease can affect people of any age. But most people who have it are diagnosed before the age of 30.

Experts aren’t sure what causes it. They think it might be caused by the immune system overreacting to normal bacteria in the digestive tract. Or other kinds of bacteria and viruses may cause it.

You are more likely to get ulcerative colitis if other people in your family have it.

The main symptoms are:

Some people also may have a fever, may not feel hungry, and may lose weight. In severe cases, people may have diarrhea 10 to 20 times a day.

The disease can also cause other problems, such as joint pain, eye problems, or liver disease.

In most people, the symptoms come and go. Some people go for months or years without symptoms (remission). Then they will have a flare-up. About 5 to 10 out of 100 people with ulcerative colitis have symptoms all the time.1

Doctors ask about the symptoms, do a physical exam, and do a number of tests. Testing can help the doctor rule out other problems that can cause similar symptoms, such as Crohn’s disease, irritable bowel syndrome, and diverticulitis.

Tests that may be done include:

Ulcerative colitis affects everyone differently. Your doctor will help you find treatments that reduce your symptoms and help you avoid new flare-ups.

If your symptoms are mild, you may only need to use over-the-counter medicines for diarrhea (such as Imodium). Talk to your doctor before you take these medicines.

Many people need prescription medicines, such as aminosalicylates, steroid medicines, or other medicines that reduce the body’s immune response. These medicines can stop or reduce symptoms and prevent flare-ups.

Some people find that certain foods make their symptoms worse. If this happens to you, it makes sense to not eat those foods. But be sure to eat a healthy, varied diet to keep your weight up and to stay strong.

If you have severe symptoms and medicines don’t help, you may need surgery to remove your colon. Removing the colon cures ulcerative colitis. It also prevents colon cancer.

People who have ulcerative colitis for 8 years or longer also have a greater chance of getting colon cancer. The longer you have had ulcerative colitis, the greater your risk.2 Talk to your doctor about your need for cancer screening. These tests help find cancer early, when it is easier to treat.3

Ulcerative colitis can be hard to live with. During a flare-up, it may seem like you are always running to the bathroom. This can be embarrassing. And it can take a toll on how you feel about yourself. Not knowing when the disease will strike next can be stressful.

If you are having a hard time, seek support from family, friends, or a counselor. Or look for a support group. It can be a big help to talk to others who are coping with this disease.

WebMD Medical Reference from Healthwise

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Ulcerative Colitis – Symptoms, Causes and Treatments of …

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Ulcerative Colitis: Practice Essentials, Background, Anatomy

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Ulcerative Colitis: Practice Essentials, Background, Anatomy

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Ulcerative Colitis: Causes, Symptoms, and Treatments

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What is ulcerativecolitis?

Ulcerative colitis is an inflammatory bowel disease (IBD). IBD comprises a group of diseases that affect the gastrointestinal tract. Ulcerative colitis occurs when the lining of your large intestine (also called the colon), rectum, or both becomes inflamed. This inflammation produces tiny sores called ulcers on the lining of your colon. It usually begins in the rectum and spreads upward. It can involve your entire colon.

The inflammation causes your bowel to move its contents rapidly and empty frequently. As cells on the surface of the lining of your bowel die, ulcers form. The ulcers may cause bleeding and discharge of mucus and pus.

While this disease affects people of all ages, most people are diagnosed between the ages of 15 and 35. After age 50, another small increase in diagnosis for this disease is seen, usually in men.

Whatcauses ulcerative colitis?

Although the trigger for ulcerative colitis remains unclear, researchers understand that the immune system undergoes an abnormal response to the colon. Your genes, environment, and immune system all play a role.

Whois at risk for ulcerative colitis?

Most people with ulcerative colitis dont have a family history of the condition. However, youre more likely to develop it if a parent or sibling also has the condition.

Ulcerative colitis can develop in a person of any race, but its more common in Caucasians. According to the Mayo Clinic, if youre an Ashkenazi Jew, you have a greater chance of developing the condition than most other groups.

Some studies show a possible link between the use of the drug isotretinoin (Accutane, Amnesteem, Claravis, or Sotret) and ulcerative colitis. Isotretinoin treats cystic acne.

Whatare the symptoms of ulcerative colitis?

The seriousness of symptoms varies among affected people. According to Cedars-Sinai, about 50 percent of people diagnosed with ulcerative colitis have mild symptoms. However, symptoms can be severe. Common symptoms of ulcerative colitis include:

Ulcerative colitis may cause additional conditions such as:

Complicationsof ulcerative colitis

Ulcerative colitis increases your risk of colon cancer. The longer you have the disease, the higher your risk of this cancer. Because of this increased risk, your doctor will perform a colonoscopy and check for cancer when you receive your diagnosis. Regular screening helps lower your risk of colon cancer. Repeat screenings every one to three years are recommended thereafter. Follow-up screenings can detect precancerous cells early.

Other complications of ulcerative colitis include:

Howis ulcerative colitis diagnosed?

Different tests can help your doctor diagnose ulcerative colitis. This disorder mimics other bowel diseases such as Crohns disease. Your doctor will run multiple tests to rule out other conditions.

Tests to diagnose ulcerative colitis often include:

Blood tests are often useful in the diagnosis of ulcerative colitis. A complete blood count looks for signs of anemia (low blood count). Other tests indicate inflammation such as a high level of C-reactive protein and a high sedimentation rate. Your doctor may also order specialized antibody tests.

Whatare the treatments for ulcerative colitis?

Ulcerative colitis is a chronic condition. Treatment usually involves drug therapy or surgery. The goal of treatment is to reduce the inflammation that causes your symptoms.

Your doctor may prescribe a medication to reduce inflammation and swelling. These types of medications include sulfasalazine (Azulfidine), mesalamine (Asacol and Lialda), balsalazide (Colazal), and olsalazine (Dipentum). Reducing inflammation will help alleviate many of your symptoms.

More severe cases may need corticosteroids, antibiotics, medications that suppress immune function, or antibody medications, called biologics, that help block inflammation in a different way.

If your symptoms are severe, youll need to be hospitalized to correct the effects of dehydration and loss of electrolytes that diarrhea causes and to treat any complications

Surgery is necessary when there is massive bleeding, chronic and debilitating symptoms, perforation of your colon, or a severe blockage. A CT scan or colonoscopy can detect these serious problems.

Surgery involves removing your entire colon with the creation of a new pathway for waste. This pathway can be out through a small opening in your abdominal wall or redirected back through the end of your rectum.

To redirect waste through your abdominal wall, your surgeon will make a small opening in your abdominal wall. The tip of your lower small intestine, or the ileum, is then brought to the skins surface. Waste will drain through the opening into a bag.

If waste is able to be redirected through your rectum, your surgeon removes the diseased part of your colon and rectum, but retains the outer muscles of your rectum. The surgeon then attaches your small intestine to the rectum to form a small pouch. After this surgery, youre able to pass stool through your rectum. Bowel movements will be more frequent and watery than normal.

Howcan I prevent ulcerative colitis?

There is no solid evidence that indicates what you eat affects ulcerative colitis. You may find that certain foods aggravate your symptoms when you have a flare-up. Practices that may help include:

Also, ask your doctor if you should take a multivitamin.

Whatis the long-term outlook?

The only cure for ulcerative colitis is removal of the entire colon and rectum. Your doctor will usually begin with medical therapy unless you have a severe complication initially that requires surgery. Some may do well with medical therapy, but many will eventually require surgery.

If you have this condition, your doctor will need to monitor it, and youll need to carefully follow your treatment plan throughout your life.

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Ulcerative Colitis: Causes, Symptoms, and Treatments

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Ulcerative Colitis –

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What Is It?

Ulcerative colitis is an inflammatory disease. It usually begins in the rectum, then worsens to involve some or all of the large intestine. Ulcerative colitis is a lifelong condition.

Ulcerative colitis may begin with a breakdown in the lining of the intestine. The inside of the intestine, with its digested food, contains trillions of bacteria. Normally, the lining of the intestines keeps these bacteria from causing an infection of the wall of the intestine.

As long as the bacteria are contained, they remain invisible to your immune cells. They do not provoke a reaction. But when the intestine’s lining fails, bacteria that usually are harmless can activate your immune system.

Ulcerative colitis is an autoimmune disease. This means that the immune system, which is supposed to attack foreign things that get inside our bodies, instead attacks a part of the body.

In ulcerative colitis, the bowel bacteria provoke the immune system to attack the wall of the intestine itself, injuring the bowel.

There also is evidence that unusually large or small numbers of certain types of bacteria that normally live in everyone’s gut can make the gut vulnerable to ulcerative colitis.

Once the bowel inflammation has started, it can continue. It continues even if the immune system stops being exposed to the bowel bacteria.

Ulcerative colitis affects the inner lining of the rectum and colon. This causes the lining to:

Sometimes, other parts of the body are affected by the inflammation. These include the eyes, skin, liver, back and joints.

The disease is not contagious. Contact with another person cannot spread the disease.

Ulcerative colitis usually begins to cause symptoms between the ages of 15 and 40.

Ulcerative colitis substantially increases the risk of colon cancer.

The symptoms of ulcerative colitis vary. Some people with the disease have a burst of symptoms every few months. Others have symptoms all the time. Some, fortunately, have symptoms only rarely.

Typical symptoms include:

Cramping abdominal pain, especially in the lower abdomen

Bloody diarrhea, often containing pus or mucus

Little warning before you need to have a bowel movement

The need to wake from sleep to have bowel movements

Ulcerative colitis also may cause:

To confirm a diagnosis of ulcerative colitis, most patients have either flexible sigmoidoscopy or colonoscopy. Both procedures use a small camera and light to view the insides of your large intestine.

A biopsy may be done during either procedure. In a biopsy, small samples of tissue are clipped from the lining of the intestine. They may be examined for signs of inflammation.

Many temporary conditions, such as infections, cause the same symptoms as ulcerative colitis. Therefore, your doctor will want to test your stool for other conditions such as bacterial infections or parasite infections.

Blood tests may also be done to check for a low blood count or low iron levels. These can occur in ulcerative colitis.

Blood tests may be done to detect inflammation, and to check on your liver. Inflammation of the liver ducts occurs in some people with ulcerative colitis.

Ulcerative colitis is a lifelong condition, unless the large intestine is surgically removed. Most people with ulcerative colitis do not have their colon removed. That is because their symptoms can be controlled with medication. Or, they only have symptoms once in a while.

In ulcerative colitis, the inflammation is not always active. There can be long breaks between symptoms.

Each time ulcerative colitis acts up, symptoms can last for weeks or months. Often these flare-ups are separated by months or years of good health with no symptoms.

Some people notice that certain foods aggravate their symptoms. By managing their diet, these people can increase the time between flare-ups.

There is no way to prevent ulcerative colitis.

However, some people are able to decrease the frequency of symptoms. They do this by avoiding foods that seem to provoke flare-ups. For some people with ulcerative colitis, this includes spicy foods and milk products.

If you have ulcerative colitis, you can decrease the toll it takes on your body. To do this, eat a well-balanced, nutritious dietespecially when you are not having symptoms such as poor appetite and nausea that make it hard to eat. By doing so, you can decrease complications from malnutrition, such as weight loss or a low blood count.

Ulcerative colitis increases your risk of colon cancer. People with extensive inflammation in the whole colon have the highest risk. It is important to have your colon checked frequently for early signs of cancer. Ask your doctor how often you should have a colonoscopy.

Poor nutrition or the effect of colitis medicines can lead to osteoporosis. This disease weakens bones and can cause bones to break. Osteoporosis can be prevented with medicines, adequate exercise, calcium and vitamin D. If you have ulcerative colitis, discuss osteoporosis with your doctor.

Medications Medications are very effective for improving the symptoms of ulcerative colitis. Most of the medications used work by preventing inflammation in the intestine.

A group of anti-inflammatory medicines called aminosalicylates are usually tried first. These medicines are chemically related to aspirin. They suppress inflammation in the gut and in joints. They are given:

By mouth, as pills

Directly into the rectum, as a suppository. A suppository is a waxy capsule.

As an enema (liquid that is squeezed from a bag or bottle into the rectum)

Aminosalicylates clear up symptoms in most people. But you may need to receive treatment for three to six weeks before you are free of symptoms.

Other, more powerful anti-inflammatory medicines are prescribed when the disease is very active or it cannot be controlled with an aminosalicylate. Often, the first choice of an anti-inflammatory drug is a corticosteroid, such as prednisone. Newer biologic agents are being prescribed more frequently today.

However, doctors are always concerned about side effects from the anti-inflammatory medicines, especially the increased risk of infection. So the goal is to reduce the dose and then stop the anti-inflammatory drug once the disease is under control.

You may also be given medicines to decrease painful spasms of the colon.

When symptoms are severe or when diarrhea causes dehydration, you may need to be hospitalized. You will get fluids and sometimes nutrition intravenously while the colon recovers.

Surgery Surgery is used in people who have:

Severe symptoms that are not controlled by medicines

Unacceptable side effects from medicines

A very high risk of colon cancer because of extensive inflammation in the whole colon

After some surgeries, bowel movements will have to leave the body through an opening in the abdominal wall. This opening is called a stoma. The stoma replaces the function of the rectum. It may be connected to a drainage bag. The stoma may be used temporarily or permanently.

Newer surgical techniques allow many patients to keep the muscular layer of the rectum while still removing the rectal lining. This type of surgery has a cosmetic advantage. And, it allows bowel movements to pass through the rectum. Bowel movements are near normal, except that they are more frequent and contain more liquid.

New or changing symptoms often mean that additional treatment is needed. People who have ulcerative colitis should be in frequent contact with their physicians.

Common symptoms that require a doctor’s immediate attention are:

Fever, which could indicate infection or a ruptured intestine

Heavy bleeding from the rectum

A serious, but uncommon, complication is called toxic megacolon. This results when the colon inflammation is so severe that it stops the colon’s motion. Megacolon causes the abdomen to swell. This can cause vomiting or severe abdominal pain and bloating. Megacolon requires emergency treatment, often surgery.

Ulcerative colitis can affect people very differently. Many people have only mild symptoms. They do not require continuous treatment with medicines.

Others might require multiple medicines or surgery. Unless it is treated with surgery, this disease is a lifelong condition.

Ulcerative colitis requires people to pay special attention to their health needs. They must also seek frequent medical care. But most people can have normal jobs and productive lives.

It can be helpful for a person newly diagnosed with ulcerative colitis to join a support group of other people with the disease.

Crohn’s and Colitis Foundation of America 386 Park Ave. South 17th Floor New York, NY 10016 Phone: (212) 685-3440 Toll-Free: (800) 932-2423 Fax: (212) 779-4098

National Institute of Diabetes and Digestive and Kidney Disorders 31 Center Dr.Bethesda, MD 20892Phone: (301) 496-3583Fax: (301) 496-7422

Disclaimer: This content should not be considered complete and should not be used in place of a call or visit to a health professional. Use of this content is subject to specific Terms of Use & Medical Disclaimers.

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Ulcerative Colitis –

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Ulcerative Colitis | Beth Israel Deaconess Medical Center

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Ulcerative colitis is a disease characterized by chronic inflammation of the colon (large intestine) accompanied in severe cases by ulcers in the lining of the colon. It is most often diagnosed in people between the ages of 15 and 30, although it can develop at any age, in both children and adults.

The majority of patients have inflammation in their rectum, which spreads along the colon to varying extents. The inflammation may be limited to the:

When more than just the left colon is affected, it is termed “extensive colitis.” “Pancolitis” is the term used when the entire colon is inflamed.

Ulcerative colitis is a chronic condition in which individuals experience both periods of active disease (flares/relapses) and periods of mild or inactive disease (remission). Typical symptoms include:

Typical treatments involve anti-inflammatory medications (5-aminosalicylates) or immunomodulators (medications that modulate or suppress the immune system). Occasionally, medical treatment fails and surgical removal of the diseased colon becomes necessary.

Ulcerative colitis is predominantly a disease of the the developed world, and is uncommon in the developing world, possibly due to a higher prevalence of intestinal infections in the developing world. The exact reasons why some individuals develop ulcerative colitis are unknown, although a number of inherited and environmental factors increase the risk of developing the disease.

It is currently believed that ulcerative colitis is caused by an inappropriate response by an individuals immune system to bacteria normally present in the colon. The evidence for the role of bacteria comes from the observation that animals that are susceptible to developing colitis due to genetic mutations do not develop inflammation if kept in a bacteria-free environment.

Although the colon normally contains over 1 billion bacteria, no single organism has been identified as the cause of ulcerative colitis. Similarly, the association between genetic mutations and ulcerative colitis is relatively weak, and thus no single genetic test for ulcerative colitis currently exists [1]. A variety of inherited deficiencies in the control of immune responses to bacteria in the colon may allow normally benign bacteria to invade the colon. Interestingly, ulcerative colitis is less common in smokers, and patients who stop smoking are at increased risk of a flare of the disease. Some speculate that nicotine or its metabolites may have protective properties in strengthening colonic defences. As the precise triggers for the disease are unclear, current treatment focuses on suppressing the immune response that has been activated.

The typical symptoms of someone with ulcerative colitis are frequent loose watery, and often bloody bowel movements [2]. Patients with severe disease can report moving their bowels15-20 times a day. Moderate to severe colitis also can cause diarrhea at,night, a strong urge to pass stool that is difficult to ignore (urgency) and, occasionally, inability to hold in bowel movements (incontinence). Prolonged diarrhea may lead to weight loss in severe cases and anemia if there is blood loss or severe enough inflammation. Yet, paradoxically, patients who have disease localized to the rectum can also be constipated. The extent of colon affected by the disease and the location, as well as disease severity influences which symptoms dominate.

Crampy abdominal pain is also common, often relieved by passing stool. The pain is usually on the lower left side, but may be across the entire abdomen. A feeling of distension and bloating may also be present. About 30-50% of patients experience symptoms outside the intestinal tract, including joint pains, skin rashes, and eye irritation. Fever may occur during severe flares of the disease. Anemia can occur due to blood loss. As with many chronic diseases, malnutrition, psychological stress, and work disability may become problematic as a consequence of persistent active disease. Fertility may be affected by active UC, as well as by medications or surgery for the disease.

Fatigue is not specific to UC but can be often occur with other issues. Fever, particularly low-grade (below 101F) can be caused by UC, but it is important to make sure there is no ongoing infection. Temperatures greater than 101F are usually due to other causes such as infection, and would require you to notify your health care provider.

Unfortunately the symptoms described above are not exclusive to ulcerative colitis. In young adults with new-onset diarrhea, infections of the colon are the most important causes to consider. After these infections have been excluded, ulcerative colitis is an important consideration.In addition to these bowel related symptoms, UC can cause symptoms which are outside the bowel (or extra-intestinal manifestations). Joint pains, particularly in the larger joints- hips, knees- can occur in more than 40 % of people. People may also experience eye and skin problems, mouth, and rectal sores.

Other conditions that produce similar symptoms to ulcerative colitis include:

All of the symptoms above require medical attention, but symptoms alone are insufficient to diagnose ulcerative colitis. Nevertheless, once the diagnosis is established, changes in symptoms are a reliable way of determining whether the disease is active or not.

The most accurate way to diagnose ulcerative colitis is by examining the colon with a fiber-optic endoscope inserted into the rectum. Asigmoidoscopy examines the lower third of the colon and requires minimal preparation. Acolonoscopy examines the full colon and requires a thorough bowel cleansing to ensure complete visualization of the lining of the colon. When ulcerative colitis is present, the lining of the colon appears swollen and inflamed, with surface bleeding and ulcers (if severe enough) usually in a continuous pattern. Tiny samples (biopsies) of the lining of the colon are taken during the procedure, so that a pathologist may examine them under the microscope for inflammatory changes (histology). This combination of endoscopy and histology is the gold standard for diagnosis of ulcerative colitis. Nevertheless, in patients with signs of severe colitis, (a colonoscopy may be postponed, as the lining of the colon becomes very fragile and easy to damage with the endoscope, but a sigmoidoscopy would be done to assess the state of the disease).

Abdominal CT scans can detect thickening of the colonic lining, and identify the extent of involvement of the colon, but cannot distinguish between ulcerative colitis and other types of colitis (see above).

Examination of the stool under the microscope is important to exclude infections of the colon that can cause similar symptoms to ulcerative colitis. Even patients known to have ulcerative colitis can acquire these infections and develop worsening symptoms. Recognizing these infections is important, as the treatment for ulcerative colitis could worsen the infectious process.

In patients with diarrhea and abdominal pain, clues to the presence of ulcerative colitis in laboratory blood tests would include anemia (low Hemoglobin/Hgb and Hematocrit/HCT) and an elevation of inflammatory markers, Erythrocyte Sedimentation Rate (ESR) or C-Reactive Protein (CRP).

The majority of patients with ulcerative colitis respond to conventional medical therapy; less than 20% need surgery to remove their colon (colectomy). Most patients will experience improvement in symptoms with medications taken by mouth, although those with disease limited to the rectum often do better with topical agents (enemas, suppositories). Only 15% require admission to hospital for intravenous medications, and this most commonly occurs shortly after diagnosis. With treatment, about 50% of patients remain in remission for periods of months to years. Figure 2 highlights the main therapies used in ulcerative colitis. They are described in detail below.

5-ASA’s are medications used to treat mild to moderate ulcerative colitis. Although it is uncertain exactly how they work, the 5-ASAs appear to act topically on the GI tract (not by being absorbed into the blood stream)and exert an anti-inflammatory effect. There are a number of these agents available which can be delivered both orally or rectally. Depending on how each specific drug is designed, the active 5-ASA is released at various locations throughout the GI tract.

The original 5-aminosalicylate, known as sulfasalazine (Azulfidine), has been used to treat IBD for decades. It is most effective for mild to moderate Crohn’s disease, particularly when the disease affects the colon. The 5-ASA is bound to a compound called sulfapyridine, from which it detaches when it reaches the colon. Unfortunately, sulfasalazine has a number of side effects due to the part of the sulfapyridine molecule (moiety) to which it is attached, including symptoms such as nausea and headache, and up to 1/3 of patients cannot tolerate it over the long-term. Patients who have allergies to sulfa medications will also be intolerant of sulfasalazine. Patients who take Sulfasalazine must also take folic acid 1 mg daily, as the Sulfasalazine depletes folic acid stores.

Because many patients cannot tolerate sulfasalazine, other methods of delivering 5-ASA to the small intestine and colon have been developed that do not contain a sulfapyridine moiety. Almost all of the patients intolerant of sulfasalazine are able to take these other 5-ASA agents, which are designed to release 5-ASA at specific locations throughout the GI tract.

These medications include a free 5-ASA, known as mesalamine , which is enclosed within special capsules that release the active drug only when they reach the small intestine or colon. Asacol, Asacol HD, Apriso, and Lialda release the mesalamine in the terminal ileum and colon. Pentasa releases mesalamine throughout the small intestine and colon.

Other agents include 5-ASA bound to another 5-ASA molecule ( olsalazine , Dipentum) or a carrier molecule ( balsalazide , Colazal). These drugs release 5-ASA specifically to the colon.

One of the main issues with 5-ASA therapy is compliance. The pill burden can be substantial (4-12 pills per day). While the older drugs were designed to be taken three to four times a day, most physicians prescribe these medications twice a day to make it easier for patients to take, and this strategy appears to be just as effective. The newer 5-ASA’s, Lialda, and Apriso, are approved for ulcerative colitis for once daily dosing, with as few as four pills delivering 4.8g of mesalamine. Currently, other pharmaceutical companies are working on similar designs to make administration of this class of drugs as easy for patients as possible.

Mesalamine also comes in enema (Rowasa) and suppository (Canasa) forms, which is ideal for patients with disease limited to the lower third of the colon or rectum, respectively. These formulations are used quite commonly in patients with ulcerative colitis. They are actually more effective that oral 5-ASA. Often times the rectal therapies are used in conjunction with oral 5-ASA.

Side-effects from 5-ASA compounds are uncommon , but may include abdominal pain, gas, nausea, hair loss, headache, and dizziness. An important side effect for patients and physicians to recognize is a paradoxical worsening of diarrhea, which is due either to an allergic-type reaction or an increase in the secretion of water by the small bowel. If diarrhea worsens with initiation of these agents, this should be considered as a possible cause, and the drug should be stopped. There also are a number of rare but more serious side-effects from 5-ASA compounds, including allergic-type reactions in the pancreas, lungs, kidneys, skin, and bone marrow. Kidney function should be monitored annually in patients on 5-ASA. Reduced sperm counts have been noted in the majority of men on sulfasalazine (Azulfidine), so this should be kept in mind for male patients who are trying to conceive. Headache, nausea, loss of appetite, and vomiting are seen much more commonly with sulfasalazine therapy. Allergy to sulfa (rash, fever), a decreased red or white blood cell count, and abnormal liver tests can also be associated with sulfasalazine. Regular monitoring of blood counts and liver tests should be carried out in patients who are receiving this medication. The majority of these adverse effects are reversible once the drug is stopped.

Like sulfasalazine, corticosteroids (or “steroids”) have been used to treat IBD for decades and have become a mainstay of treatment for active flares. They are used to treat moderate-to-severe Crohn’s disease and when 5-aminosalicilates, and in some cases antibiotics, fail to control the disease. These drugs exert an anti-inflammatory and immunosuppressive effect and can be given by mouth, by rectum, or intravenously, depending on the location and severity of the disease.

Prednisone , the most commonly used oral steroid, produces consistent responses, and induces remission in about 70-80% of patients. Steroids also act quickly, with most patients noticing a response within one week.

Although steroids induce remission, they are not effective in the long-term to maintain remission. In addition, steroids are associated with a number of serious side-effects including low bone density (osteoporosis), diabetes, high blood pressure (hypertension), cataracts, psychosis, depression, increased risk of infections, acne, weight gain, difficulty sleeping (insomnia), and facial swelling. Steroids also cause the body’s adrenal glands to stop producing their own endogenous steroid (cortisol). If the administered steroids are tapered off too quickly, the body can go into a “steroid withdrawal” or adrenal crisis. Once started, steroids are usually slowly reduced in dose over a number of weeks to prevent a sudden flare of the disease or adrenal crisis.

Patients who are on steroids also need to be on adequate amounts of calcium (1200mg) and vitamin D (800 IU). Some patients, with underlying osteopenia or osteoporosis, or patients who remain on steroids for prolonged periods of time, may require additional drugs (bisphosphonates) to prevent further bone loss. Bisphosphonates (alendronate or risedronate) have been shown to be useful in this situation, particularly in postmenopausal females and in those patients on long-term steroids.

Although steroids are effective in quickly inducing remission, a number of patients are unable to reduce their steroids without a worsening of their symptoms, and essentially become steroid-dependent. These patients require further medical or surgical therapy in order to help get them off of the steroids. In fact, studies have shown that one year after starting steroids approximately 25% of patients are steroid dependent and 25% of patients have required surgery. Less than 1/2 of patients are in remission and off steroids at one year. Therefore, once steroids are utilized to induce remission, other drugs are needed to help wean patients off of steroids, avoid surgery, and maintain remission. The agents typically used in this situation are known as immunomodulators,which will be discussed in greater detail below.

In addition to oral and intravenous formulations, corticosteroids are also available as intravenous (IV) and rectal formulations. Intravenous corticosteroids (methylprednisolone, hydrocortisone, dexamethasone) are used in patients with severe disease that require hospitalization. Steroids also come in rectal form and can be given as enemas (Cortenema), hydrocortisone acetate foam (Cortifoam, ProctoFoam HC), or suppositories.

Immunomodulators, or immunosuppressants, alter the body’s immune response by inhibiting the inflammatory action of white blood cells. Since patients with ulcerative colitis are believed to have an overactive immune system as the cause of their uncontrolled GI inflammation, the use of a medication that tones down the immune response makes great sense. The immunomodulators used in the treatment of ulcerative colitis are azathioprine (Imuran) and 6-mercaptopurine (Purinethol).

These immunomodulators have a role in several circumstances. Most often they are used to maintain remission in those patients who initially required steroids, in those who have become steroid dependent, and in patients with perianal fistulae. In patients with milder symptoms, immunomodulators can also be used to induce remission. The reason that they are not used to induce remission in sicker patients is that they have a slow onset of action of up to three months before taking effect.

Azathioprine (AZA) is the pro-drug (precursor) of 6-mercaptopurine (6-MP) and breaks down to 6MP when it is absorbed into the bloodstream. These drugs may take six to 12 weeks to become effective. Over this time period, if patients are taking corticosteroids, the steroid dose is slowly reduced or tapered. These drugs appear to work to maintain remission in up to 2/3 of the patients. The dose of 6-MP/AZA is calculated based upon the patients’ weight. Typically, prior to starting these drugs, a special blood test is checked to make sure the patient isn’t at high risk for a low white blood count.

The most common side-effect of 6MP/AZA therapy is nausea. Interestingly, some patients who cannot tolerate 6MP due to nausea are able to tolerate AZA well, and vice-versa.

A small percentage of patients may be allergic to 6MP/AZA or develop inflammation of the pancreas known as pancreatitis. This occurs in 2% (2 out of 100 patients). The symptoms are an upper abdominal pain, and can be associated with nausea, and vomiting. If a patient develops this type of reaction to either drug, the other should not be used because the same reaction will develop. Once the medication is stopped, the pancreatitis usually quickly resolves.

Patients can also develop a low blood counts (typically white blood cells) or elevated liver tests (10% or 1 out of 10 patients) and therefore need frequent blood tests to monitor their blood cell counts and liver function. No matter how long one remains on the drug, these tests need to be continually monitored no less frequently than every three months, and more frequently at the initiation of therapy or after a dose change. There is now a test available that may identify those patients at greatest risk for developing a low white blood cell count. Also, it is now possible to measure the levels of the drug in the blood, known as metabolites. Assessing metabolite levels appears to be helpful in certain situations, such as assessing patients with suspected medication noncompliance, patients with abnormal liver tests, or patients who are not responding well to the 6MP/AZA.

Taking 6MP or AZA does put you at a slightly higher risk of both infection and lymphoma (a cancer of the lymph nodes. However, these potential risks are often outweighed by their benefits. Each individual considering these agents should discuss the pros and cons with their physician.

Cyclosporine (Neoral) is an oral medication used as “rescue therapy’ when patients with severe disease fail (do not respond to) steroids and are facing surgical removal of the colon. When patients require admission to hospital and intravenous steroids fail to improve their symptoms within a few days, intravenous cyclosporine has been shown to obtain short-term response rates of about 80%. It initially is given intravenously, and then orally, but is used as a bridge to more long term therapy (mercaptopurine). It is not used routinely in those with milder disease, as the side-effects of tremor, kidney damage, hypertension (high blood pressure), seizures, and infections are significant. However, it can get patients over the severe episode of colitis and allow them to consider continued medical treatments or planned (elective) surgery.

These drugs are specifically designed to bind to, and block the effects of TNF-, inflammatory protein or cytokine that is seen in high levels in patients with Crohn’s disease and ulcerative colitis. There are currently three anti-TNF agents approved for the treatment of Crohn’s disease, but only infliximab (Remicade), is approved for the treatment of moderate-to-severe ulcerative colitis.

Approximately 66% (2 out of 3) patients with ulcerative colitis will respond within the first two doses, and approximately 30-50% of those patients, will maintain response for up to one year.

Infliximab (Remicade) is a chimeric antibody, meaning that it is made up of material that is 25% mouse and 75% human. It is an antibody that binds to and blocks the effects of TNF — an inflammatory, protein (cytokine) that is seen in high levels in patients with inflammatory bowel disease. Infliximab has been in use to treat Crohn’s disease since 1998 and was approved for treatment of ulcerative colitis in 2005. Even some of the extra-intestinal manifestations of IBD (discussed above) may respond to infliximab therapy.

Infliximab is given intravenously. Administration typically takes place over two to three hours, and is usually well tolerated. After the initial infusion of infliximab, patients typically are given another IV dose two weeks and six weeks later, after which the drug is administered at consistent eight week intervals. This regimen of giving the drug more frequently at the beginning and then regularly thereafter has been shown to be more effective than receiving the drug just “on demand” when the patient has symptoms of a flare.

Although infliximab may prove highly effective in the initial stages of treatment, unfortunately some patients may lose response to infliximab over time. In such cases, the drug may need to be administered more frequently than every eight weeks or the dose may need to be increased. Patients can also develop reactions to the medication, which usually occur during the infusion. Most infusion reactions are mild and take the form of flushing, fevers, aches, and pains, but they can be more severe with associated chest pain, shortness of breath, hives, or a drop in blood pressure. Most of these reactions can be managed by slowing or stopping the infusion and giving intravenous fluids along with antihistamines, acetaminophen, or corticosteroids. Rarely the reactions can be delayed and occur a few days after the infusion. These types of reactions usually consist of joint pains, muscle aches, rash, and occasionally a fever. The vast majority of the infusion reactions are not true allergies. Hence, infusions can usually be completed and often do not preclude further use of the drug.

Although there are side effects associated with these medications, it is important to remember that anti-TNF therapy is both safe and extremely effective for the treatment of ulcerative colitis. There is a small increased risk of infections, including tuberculosis, as well as rare risks of heart failure, multiple sclerosis, lymphoma, autoimmunity (lupus-like reactions), and liver dysfunction, including reactivation of hepatitis B. These risks are relatively low, but should be considered.

Ongoing infection is an absolute contraindication to the treatment with any anti-TNF inhibitor. Prior to initiating treatment with infliximab or adalimumab, patients must be screened to make sure that they do not have an asymptomatic infection with tuberculosis. This is usually accomplished with a skin test (PPD test) and a chest x-ray. Patients who were born in countries where TB is more common may require treatment for TB before starting therapy with an anti-TNF agent. We recommend annual screening for TB while on anti-TNF therapy. We also recommend testing for previous exposure to hepatitis B virus prior to initiation of anti-TNF therapy.

When one considers that bacterial elements are a trigger for the initial inflammation in ulcerative colitis, then manipulating colonic bacteria as a therapy makes sense. However, antibiotics such as Ciprofloxacin (Cipro) and Flagyl (Metronidazole) have shown minimal clinical benefits in ulcerative colitis and are not routinely used. Ciprofloxacin is better tolerated than metronidazole, but still has rare side effects including headaches, nausea, and sun-sensitivity. There is also a very rare risk of tendon rupture. Patients on Ciprofloxacin are also at increased risk for clostridium difficile colitis, a type of antibiotic-induced colitis that can be severe and requires specific therapy with metronidazole or vancomycin, another antibiotic.

Side effects with metronidazole are not uncommon, especially at higher doses. Side effects include nausea, loss of appetite, metallic taste, diarrhea, dizziness, headaches, and dark urine. Numbness or tingling of the hands (peripheral neuropathy) is rare, but may be irreversible. If this occurs, the drug must be discontinued. Metronidazole can also react with alcohol and cause a rare, severe reaction (antabuse-like) of nausea, vomiting, and shortness of breath. As a result, most patients on short courses of metronidazole are cautioned to avoid alcohol.

There is some emerging evidence that Rifaximin (Xifaxan), a nonabsorbed antibiotic, is effective for the treatment of bacterial overgrowth and in small studies it has been shown to be effective in ulcerative colitis. It is a non-absorbed antibiotic that works by temporarily changing the mix of bacteria in the colon. There are no major side-effects, but it is unclear whether resistance by bacteria would become an issue in the long-term.

The agents listed above (except for antibiotics) are considered standard medical treatments for ulcerative colitis. Additionally, a number of complementary therapies are used by patients although very few have actually been studied in clinical trials. Clinical trials have found some benefits in a few complementary therapies. They can be considered in mildly active disease if an alternative or addition to 5-ASA is desirable. Patients taking any complementary therapies should let their physicians know.

Probiotics are organisms, either bacteria or fungus, that promote beneficial effects in the colon. Lactobacillus, Bifidobacteria, Saccharomyces and Streptobacillus are considered to have such protective properties. Probiotics are not uncommonly used by patients with IBD. The normal colon contains billions of bacteria, which compete with other detrimental organisms for survival in the “pea soup” of the normal colonic flora [5]. Single strains or combination of strains of some high-dose probiotics have been shown to produce similar results to mesalamine in inducing and maintaining a response in active ulcerative colitis. E.coli Nissle 1917, Bifidobacteria, Saccharomyces boulardii and a high-dose mix of Bifidobacteria, Lactobacilli and Streptococcus (“VSL3”) had beneficial effects in clinical studies. However, many of the probiotics sold in stores and over the Internet have not been tested in ulcerative colitis, and may be at lower concentrations than those used in clinical studies.

Both germinated barley foodstuff and psyllium (Metamucil, Fybogel) stimulate the growth of beneficial colonic bacteria, and have been reported to improve symptoms in mildly active disease. Aloe vera capsules and curcumin were also shown in one study each to be better than placebo (dummy pill) in improving symptoms in mild ulcerative colitis. Other agents that may improve symptoms of ulcerative colitis include wheat grass juice, Jian Pi Ling tablets, Kui jie qing enemas, acupuncture with moxibustion, and bovine colostrum enemas [6]. In addition, some patients report benefits with a restricted carbohydrate diet, known as the “Specific Carbohydrate Diet”. Most of these treatments have not been compared to placebo in measuring objective outcomes like colonic healing, which is considered the benchmark to assess any therapy. Investigational treatments

Novel treatments for ulcerative colitis are currently under development or in clinical trials . The novel treatments include:

Access to these therapies is currently only available through clinical trials as they are not F.D.A. approved for ulcerative colitis.

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Ulcerative Colitis | Beth Israel Deaconess Medical Center

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