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Concern of primary sclerosing cholangitis 4 (content expertise) Edit entry summary (PSC) is a cholestasis syndrome, characterized by intrahepatic, extrahepatic bile duct stenosis due to fibrosis and inflammation gradually, and eventually lead to complete blocking the development of cirrhosis.
Edit Summary List - [hide] 1 Over disease, clinical manifestations of disease etiology 3 4 5 diagnosis to treat the symptoms of natural disease 6 7 8 surgical treatment 9 10 prognosis drug therapy treatment efficacy evaluation Edit this paragraph 11 | Back to the top of the disease over
Primary sclerosing cholangitis is a rare progressive bile duct lesions. The progression of the disease eventually lead to biliary obstruction and severe obstructive jaundice, the prognosis is poor. Currently the etiology and pathogenesis of it is not yet understood, infection and autoimmune disease may

be related to this. The disease-prone adults, more men than women, children occasionally. According to statistics, obtained after diagnosis to death from the average survival time for six years. The disease is often accompanied by some systemic diseases such as chronic pancreatitis, thyroiditis, retroperitoneal fibrosis, mediastinal fibrosis, ulcerative colitis, enteritis limitations, orbital pseudotumor, vasculitis, and immune deficiency diseases. Treatment of this disease is mainly to improve the drainage of bile, to prevent or reverse hardening of the factors that lead to inflammation or symptomatic treatment. Although surgical treatment may improve bile drainage, relieve clinical symptoms, but many patients lesions of the liver bile duct and was often sexual, and ultimately the development of biliary cirrhosis, portal hypertension and liver failure, gastrointestinal bleeding, or death.
Primary sclerosing cholangitis, also known as stenosing cholangitis is essentially not a suppurative disease. Is an unknown etiology of liver fibrosis in chronic bile duct stenosis and occlusion of its rare clinical features. It is different from bile duct stones, tumors or bile duct injury secondary to sclerosing cholangitis (also called secondary bile duct stenosis), primary sclerosing cho
1, the infection causes still unknown factors in PSC, the earlier the infection factor is one of the points. Found in inflammatory bowel disease often accompanied by PSC (infiamma-(toryboweldisease, IBD), generally reported in about 70%, of which ulcerative colitis (ulcerativecolitis, UC) the most common, less Crohn's disease, that bacteria and their toxins through the intestinal inflammation around the bile duct and portal vein to the disease. However, some evidence does not support the bacterial hypothesis: PSC has never been observed in the typical performance of bacterial inflammation of portal vein; rare hepatic portal area neutrophil infiltration; not found in bacterial liver abscess; UC accounted for only 5% of PSC occurred; a lot of PSC with UC were diagnosed with PSC in a few years after UC; PSC lesion is not due to UC-line colorectal resection to cure and stop. In immunocompromised persons, Giant cell disease (cytomegalovirus, CMV) can cause sclerosing cholangitis, the Mehal-sensitive applications such as PCR, liver tissue, has been negative CMV is the cause of PSC.
2 toxin absorption factor as described above, PSC and IBD is closely related to inflammatory bowel disease as potential risk factors has attracted attention. Speculated that inflammation increases the permeability of intestinal mucosa, bacterial endotoxin, increased absorption of toxic bile acids to activate the liver Kupffer cells to tumor necrosis factor (TNF) have increased, leading to pathological changes similar to PSC bile duct damage and proliferation. In animal studies, many drugs such as antibiotics, antibodies and bacterial cell wall components can block tumor necrosis factor inhibitors PSC pathological changes in experimental animals. For the IBD incidence, time of onset, disease severity and PSC in time inconsistency problems, such as: 25% PSC in patients with normal colon, PSC disease occurred in the colon before the PSC after colon resection did not influence the course, some scholars have recently proposed some lymphocytes in the immune response with memory function, early activation still down, after the disease started when stimulated Zai Yu. Although this could explain the relationship between the part of the paradox, there is no direct evidence to prove a direct cause of IBD is the PSC, the most reasonable explanation is that two different organs of the common pathological causes of differences in physiological responses.
3, genetic factors PSC incidence in family members focused on closely related phenomena and the fact that HLA genetic factors suggest an important role in the pathogenesis of PSC. PSC-related HLA alleles with large, they occur in the PSC, may play a different role in the development. HLA-B8 found in 60% to 80% of PSC patients, HLA-DRB1 and DRw52a may determine the genetic susceptibility to PSC, and the presence of DR4 is a sign of rapidly deteriorating condition. PSC has been reported with TNF- receptor gene polymorphism related to, TNF- gene 308 base G replacing A on the susceptibility correlated with the PSC. Matrix metalloproteinase (MMP-3) of the polymorphism may also affect the disease susceptibility and disease development. Another literature shows that MICA-002 base can significantly reduce the risk of occurrence of PSC and the MICA-008 can increase the risk of occurrence of PSC. The fact that many of the tips above the occurrence and development of PSC has its inherent genetic basis.
4, immune factors present more attention to the immune mechanism in cellular immunity, we found hepatic portal area and inflammatory cells around the bile duct are mainly T lymphocytes, the majority of the portal area is a function of the immune helper-inducer T-lymphocyte subtypes CD4, mainly around the bile duct together with suppression of the immune and the other subtypes of cytotoxic CD8 cells. Chosen by normal biliary epithelial expression of HLA- antigen level, researchers found that PSC patients with bile duct epithelial antigen by the HLA- -DR expression level, but in some primary biliary cirrhosis (primarybiliarycirrhosis, PBC) and various cause of extrahepatic bile duct due to obstruction, bile duct epithelium have the same abnormalities were found, bile duct epithelial HLA-DR and the PSC particles pathogenesis is unclear. Evidence of humoral immunity and more non-specific: PSC blood of patients with different degrees of immune globulin levels increased; anti-nuclear factor and anti-smooth muscle antibodies; blood and bile and increased levels of immune complex clearance impaired; blood found in many anti-neutrophil cytoplasmic antibodies (, ANCA). Studies have found that a table only the extrahepatic bile duct epithelium and in colonic epithelial peptide, in 16 cases of PSC in about 2 / 3 of the serum test was positive, while other liver diseases and secondary detection of extrahepatic bile duct stenosis were negative, its pathophysiologic role is unclear.
5, bile duct ischemia and ischemic factors that can cause ischemic necrosis, leading to biliary fibrosis and sclerosis, and the PSC, there Imageology cholestatic and histological changes, often seen in the interventional chemotherapy, liver transplantation and cholecystectomy. Strictly speaking sclerosing cholangitis due to bile duct ischemia is not a PSC areas. Although various pathogenic factors are likely to play a role in the pathogenesis of PSC, but the different stages of one or more factors may play a major role. Edit this section | Back to the top of the clinical manifestations
Primary sclerosing cholangitis prevalent in young males, often with inflammatory bowel disease, particularly ulcerative colitis related. The onset was usually concealed, can have progressive worsening fatigue, itching and jaundice. The right upper quadrant pain and fever for the performance of the cholangitis attack is not common. Some patients may have hepatosplenomegaly or cirrhosis of the performance. Late disease was hypertension, ascites, liver failure, cirrhosis of such performance.
Mainly obstructive jaundice, the slow process was progressive. No history of abdominal colic general, only upper abdominal discomfort and use pain, accompanied by marked pruritus, there is loss of appetite, nausea and fatigue in a small number of patients can chills and fever. Leukocyte examination showed increased lymphocytes and eosinophils, serum bilirubin, alkaline phospholipase r-glutamine, and GGT values were increased slightly elevated ALT, IgM higher than normal. Part of the patient's anti-nuclear antibody and smooth muscle antibody positive, anti-mitochondrial antibody was negative, liver and urinary copper content increased. Edit this section | Back to the top of the disease diagnosis
Prevalence of PSC is unknown to many men (male to female ratio of about 2:1), with a median age of onset less than 40 years of age. Typical symptoms include jaundice and itching, and non-specific symptoms such as fatigue, anorexia, nausea, weight loss. Many patients have no symptoms at diagnosis, but will appear later, late stage cirrhosis, liver failure, portal hypertension and other symptoms. Most patients associated with inflammatory bowel disease (IBD), ulcerative colitis, of which more common.
1, blood tests of liver function tests in most patients showed bile stasis, AKP increased and slightly elevated transaminases. As the disease progress, gradually increased serum bilirubin, serum albumin decreased, increased serum ceruloplasmin, high hypergammaglobulinemia, which increased as much IgM autoantibody titers also increased. Was that the nucleus type anti-neutrophil cytoplasmic antibodies (p ~ ANCA) are valuable in the diagnosis of PSC, but found in other liver diseases, such as autoimmune hepatitis, primary biliary cirrhosis patients with positive rate of more high.
2, histological changes in liver histology in most patients non-specific, so the diagnostic value of liver biopsy is not on the PSC, but can prompt credit of PSC and their organizations. Histological changes of the disease include: bile duct fibrosis, portal area of inflammation, periportal hepatitis and liver parenchyma around the change. With disease progression, increase in portal area fibrosis. Interlobular bile duct decreased the formation of septal formation and ultimately the performance of biliary cirrhosis. According to abnormal levels, histology can be divided into ~ period. Stage as cholestasis cirrhosis.
3, radiological diagnosis of PSC ERCP is the best way. Percutaneous transhepatic cholangiography (PTC) are generally used for endoscopy losers. Magnetic resonance cholangiography (MRCP) is a potential check, but needs to improve its image quality. PSC characteristic bile duct radiology showed irregular narrowing and expansion of multiple local, diffuse biliary stenosis and normal expansion of the formation of a typical section of the "string of beads" to change. Recent medical centers in Europe five patients studied 394 patients, of which 73% involved the intrahepatic and extrahepatic bile ducts, intrahepatic bile duct changes were only less than 1% of extrahepatic bile duct changes were only 20%. One is called "small duct" PSC, the diagnosis is difficult because of small bile duct involved, as well as the abnormal ERCP can not be displayed. The patient associated with IBD, liver function tests showed the performance of biliary stasis; liver biopsy and is usually similar to PSC. Child PSC diagnosis difficult, as many more as the performance of autoimmune hepatitis, with the latter identification, ERCP should be more checks, especially those with IBD. Edit this section | Back to the top of the natural history
1, asymptomatic and symptomatic endoscopic technology to be more and more diagnosis of asymptomatic cases, PSC and IBD led a strong correlation between abnormal liver function physicians to screen patients with IBD, so that more and more and more patients are diagnosed early.
The latest reported 45% of asymptomatic PSC patients, with early reports of 10% to 25% in difference. Overall, the PSC symptomatic and asymptomatic patients with IBD incidence rate, the average age of onset and there was no difference between men and women ratio. However, Broome and so 34 171 asymptomatic patients and symptomatic patients was compared with that, the former is relatively young, more common in men with IBD more closely, less involvement of extrahepatic bile duct.
2, recurrent PSC in patients with recurrent PSC after transplantation is a recognized complication rate was 6% to 37%. Giant cell hepatitis, male, colon not involved by P donor sex mismatch, the use of mouse monoclonal antibodies 2CD3 and steroid-resistant rejection was positively correlated with recurrence. Although their risk factors remains controversial, but the following conditions should be suspected PSC recurrence: 90d after transplantation of non-agreement of significant stenosis, with AKP has been higher than 2 times upper limit of normal, excluding ABO blood group incompatibility, hepatic artery thrombosis or narrow circumstances.
3, small bile duct PSC about 5% to 10% of PSC patients showed isolated small bile duct lesions. Small bile duct PSC PSC with typical biochemical and histological changes, but cholangiography normal. The PSC good prognosis, but still is a progressive disease, the development of the ratio for the PSC bold tube remains unproved.
4, the overlap of autoimmune hepatitis (AIH) PSC AIH overlap in both the adult and pediatric reports. The incidence of very different (7.6% ~ 53.8%). Inhibitors of these patients may have on the immune response. Diagnosis is directly related to the treatment of choice.
The following clinical overlap syndrome may be considered. Prompt liver biopsy in young patients clear hepatitis plate boundary, significantly increased serum IgG, autoantibodies, elevated serum alkaline phosphatase but less than 2 times the upper limit of normal. Of course, you can not rely solely on the characteristics of these non-specific diagnosis of the merger AIH.
5, children 2 years of age despite the reported cases, but more than PSC was diagnosed in the early age of 20. Sick boys than girls, 50% to 80% combined with IBD, patients with recent 1P3 overlap AIH, in addition to the limiting plate of liver biopsy prompted hepatitis, these patients usually have high levels of IgG, autoantibodies. PSC lower the survival rate of children is usually required liver transplantation. Low platelet count, splenomegaly, older age was independently associated with low survival rates. Edit this section | Back to the top of the symptomatic treatment of
1, fatigue: fatigue in cholestatic liver disease in the cause is unknown, there is no particularly effective treatment methods, including UDCA. There is speculation it may be related to depression, but a fluvoxamine (a selective serotonin reuptake 52 inhibitors) randomized placebo-controlled trials of treatment after 6 weeks observation, found that their fatigue or quality of life index than good. Recently reported data, 93 patients with PSC weak points lower than the general population, suggesting that people may be over-emphasized the weakness of these patients symptoms.
2, itching: bile acid binding resin, to test the enamine of pruritus secondary to cholestasis is very effective, and less adverse reactions, should be treated as first-line treatment. Opioid antagonists can prevent excessive when cholestatic endogenous opioid agonist effect on cholestatic related pruritus effective. All opioid antagonists (nalmefene, naloxone, sodium bent one) will appear in the first use withdrawal reaction, but usually continue to disappear after administration of 2 ~ 3d. Ondansetron (52 serotonin receptor antagonist) could significantly improve the pruritus scores (visual analog scale), subject to the assessment of clinical practice. Rifampicin to relieve itching cholestatic liver disease an effective drug, its mode of action is mediated by microsomal enzymes of drug oxidizing system, promotion of endogenous metabolism itching; in the intestine has a direct anti-microbial effect, thus changing the secondary bile acid synthesis. However, the use of rifampicin in large part limited by serious allergic reaction and its high specificity as an enzyme inducer and the combination drug interactions.
3, osteoporosis: PSC patients with a variety of risk factors for osteoporosis; cirrhosis, cholestasis, and the use of corticosteroids. Researchers recommended that to the following bone mineral density in patients with chronic liver disease: clinical or histologic proof of cirrhosis of the liver; bilirubin greater than 3 times the upper limit of normal and continued for 6 months. Patients should also be correct in general habits, such as restrictions on alcohol consumption, regular weight-bearing exercise, smoking cessation, proper diet to prevent low body mass index, calcium and vitamin D and so on. In addition, if the hip or spine T2scores <2.5, should be held in postmenopausal women hormone replacement therapy on gonadal function of male hypothyroidism should be considered by the skin using testosterone. Bisphosphonates and hormone replacement therapy can be applied at the same time, it can be used as gonadal dysfunction in patients with non-medication options. These methods only for the treatment of primary biliary cirrhosis (PBC), the extrapolation of experience, there is no evidence-based support.
4, the lack of fat-soluble vitamins: fat-soluble vitamin deficiency in cholestatic liver disease of concern, but their clinical significance remains controversial. MayoClinic attend his trial in 1995 patients evaluated, found that vitamin A, D, E deficiency accounted for 40%, 14%, 2%. Another test on 72 patients transplanted before the PSC to assess the extent of their more serious vitamin deficiency (vitamin A, D, E, respectively 82%, 57%, 43%). Therefore, physicians should pay attention to the lack of fat-soluble vitamins in patients with PSC, and be appropriate to add. Edit this section | Back to the top of the treatment
There is currently a lack of treatment effects. The purpose of surgical treatment is drainage of bile, the bile duct decompression, to reduce liver damage. When the bile duct surgical exploration, subject to the bile duct and liver biopsy, and for cholangiography and bile of aerobic and anaerobic training. On the narrowest possible limits stenosis expansion into the T-shaped tube, catheter or plastic drainage tube and stays, the drainage pipe can be cut from the bile duct or liver surface leads. Indwelling drainage tube preferably more than 1 year, it was suggested that long-term retention, or even a lifetime reserved.
Extrahepatic bile duct lumen is sometimes too small catheter drainage difficulties and failures can occur. Although advocates for the narrow bile duct on the intestinal drainage, but more due to technical difficulties, decompression is not satisfactory, rarely been used. Generally believed that if the patient improved after treatment by medical drugs or development of biliary cirrhosis, are not suitable for surgery. If there is that associated with active ulcerative colitis patients, the for colectomy may stabilize the condition of primary sclerosing cholangitis have some help. In recent years, has been adopted by endoscopic or percutaneous approach for intubation and balloon dilatation for bile duct, but the success rate is not high. Medical treatment is mainly long-term use of steroid hormone drugs can relieve symptoms, but generally do not change the course of the disease. Early is better, the latter is not ideal. Broad-spectrum antibiotics to control the onset of acute inflammation of bile duct, in combination with hormones. It was also used immunosuppressants such as azathioprine and other treatment, but the effects are uncertain. Edit this section | Back to the top of the surgical treatment
Incision of bile duct stone is often used, expanding exploration and T-tube or U-shaped tube drainage, resection or removal of the gallbladder narrow - intestinal anastomosis, ease of portal hypertension of various surgical procedures and so on. Surgical therapy remains the main bile duct to relieve obstruction and infection and to stop bleeding caused by portal hypertension an effective measure. However, many drawbacks: difficult to lift the wide range of high bile duct stricture and its infectious complications; infectious complications after surgery than those who are not high, especially in the biliary enteric anastomosis and the U-shaped tube drainage after surgery, recurrent cholangitis more common; surgery will also affect the liver transplant operation and postoperative effects, patients undergo routine surgery or more times more complex, more difficult liver transplant operation and effect worse. Martin and other reports PSC178 cases, 233 cases were subjected to routine surgery times, after the majority of patients (75%) of symptom relief, but a higher complication rate and mortality, 103 patients who died in the 75 cases (73%) died liver failure, bleeding or infection, which killed portosystemic shunt in 14 cases, 13 cases of death were complications with the surgery. For liver transplantation in 16 cases, 8 patients died, most of them had received extensive prior surgery. Therefore, many advocate the use of the current endoscopic treatment of bile duct obstruction and infection, as far as possible to avoid surgery, in order to create favorable conditions for liver transplantation. Edit this section | Back to the top of the drug treatment
1, ursodeoxycholic acid: UDCA is a hydrophilic dihydroxy bile acid, as early as 1990 to be used for the treatment of PSC. In addition to the hydrophobic bile acid substitution outside, UDCA also regulate apoptosis-specific threshold, ie by activating the epidermal growth factor receptor and mitogen-activated protein to liver cell survival mediated signal transduction. In addition, UDCA can protect mitochondria from interference, thereby inhibiting apoptosis. Recent studies show that, UDCA to prevent the merger of the colon in patients with IBD have an important role in generating new biological. Deoxycholic acid combined colorectal cancer in ulcerative colitis P dysplasia in patients with higher levels of serum and feces, it will stimulate the animal colorectal epithelial hyperplasia, may also promote human colorectal tumorigenesis. The UDCA can regulate mitochondrial membrane potential and reactive oxygen transport free radicals, inhibition of deoxyribonucleic acid-mediated apoptosis. Under normal physiological conditions, UDCA accounts for about 3% of bile acid composition, the content along with the increase of dosage, the dose of 22 ~ 25mgPkg reached the platform. UDCA is usually administered twice a day, but compared with administration once a day, both in content and improve the liver function of bile there was no difference. Treatment of PSC, there is no uniform standard dose, usually 10 ~ 23mgPkg · d range. Some people use the 20 ~ 25mgPkg · d dose tested, the results showed biochemical and histological bile duct fibrosis contrast with the performance levels were significantly improved.
2, corticosteroids: some small sample test indicated that the hormone treatment is effective, but no large-scale test reports. Mayo 2000, such as the use of budesonide 9mgPd the program, the PSC patients 1 year of treatment, the results failed to obtain significant clinical efficacy, endpoint in the treatment of patients with femoral neck and lumbar spine bone mass with severely reduced. Another three small-scale studies have shown that, in endoscopic retrograde cholangiopancreatography (ERCP) biliary drainage after topical nasal corticosteroids may be effective, but the Royal Hospital, a controlled trial found that the treatment is not only ineffective, but bile colonies positive rate is high.
3, immunosuppressive agents: Schramm and other joint with UDCA500 ~ 700mgPd 1mgPkg · d prednisolone and azathioprine 1 ~ 1.5mgPkg · d treatment of 15 patients with PSC, of which 13 were well tolerated; received during follow-up liver biopsy 10 people, 6 histological improvement, 1 worse; biochemical improvement in all patients, including seven pairs of UDCA alone in patients with ineffective treatment. These results suggest that although corticosteroids on the role of cholestatic liver disease is still holding off state, but UDCA may be effective in combined immunosuppressive therapy. An open trial reported that methotrexate treatment of PSC is expected to become effective drugs, but then double-blind placebo-controlled trials show only methotrexate group an improvement in biochemical, and liver histology and ERCP image Results good. Similarly, compared with UDCA alone, not combined with methotrexate for better efficacy, but also appears interstitial pneumonia, liver toxicity and other adverse reactions. Therefore, PSC does not apply to the treatment of methotrexate. Other drugs are in early stage clinical trials, including cladribine (an anti-lymphocyte nucleoside analogues), pentoxifylline and etanercept, the latter two as TNF2 antagonists, but are not PSC good clinical efficacy.
4, antibiotics: Some people think that PSC and the bacteria from the gastrointestinal tract or product related to the use of antibiotics which inhibit the activity of intestinal bacteria may be a method of treatment. A study using metronidazole UDCA, showed that at least in terms of its efficacy is superior to biochemical alone UDCA. Minocycline is used for clinical assessment, but some people think their produce inducible nitric oxide synthase (a type of inflammatory mediators) was more effective than antibacterial effect, not for the treatment of PSC.
5, anti-fibrosis drugs: toluene pyridone is the only proven a specific anti-fibrosis drugs. Under other conditions the drug can be reversed as a result of fibrosis of peritoneal dialysis; However, a small, preliminary study on the PSC does not show its effective treatment, but serious adverse events occurred. Colchicine in PBC have been considered anti-fibrosis, but in 1995 a large-scale trial showed the drug to the PSC is invalid, and found the drug in the long-term research on the role of PBC has not yet sure. Silymarin is a liver disease for the majority of patients taking the medicine, has anti-fibrosis and the dual role of TNF inhibition is expected to become the treatment of PSC medication. Edit this section | Back to the top of the prognosis of treatment
Primary sclerosing cholangitis a poor prognosis. Some people think that this disease will eventually develop into cholangiocarcinoma. Most of the final result of secondary biliary cirrhosis, portal hypertension. Most patients died of liver failure, hepatic coma, but died of esophageal variceal bleeding were rare. Most people can only ease after diagnosis 5 to 10 years, an average of 6 to 7 years, ulcerative colitis associated with a worse prognosis.
Some cases may be asymptomatic for many years, these patients need follow-up observation (such as the conventional twice a year and liver biochemical tests.) Under normal circumstances, the disease showed a progressive increase. Of chronic cholestasis and complicated treatment of patients with cirrhosis should be supported. Patients with recurrent bacterial cholangitis patients should be treated with antibiotics. Bile duct stricture may be a significant hepatic or endoscopic dilation therapy can also be placed stent. Of ulcerative colitis patients Proctocolectomy for primary sclerosing cholangitis is no effect. Corticosteroids, azathioprine, penicillamine, methotrexate efficacy of different, and have significant side effects. Ursodeoxycholic acid can reduce itching and improve the biochemical index, but not shown to alter the natural course of the disease. Liver transplantation is clearly the only way to cure this disease. 7% to 10% of primary sclerosing cholangitis can occur in patients with cholangiocarcinoma. Underwent liver transplantation to prevent this complication is not the best time to clear. Edit this section | Back to the top of the efficacy evaluation
1, the cure: treatment by medication or surgery, symptoms and signs disappeared, bile duct wall to restore flexibility, without complications.
2, the improvement: treatment by medication or surgery, the patient decreased jaundice, liver function improved.
3, healed: treatment by medication or surgery, the pa
Unknown etiology of the disease, drug treatment is not ideal. If a patient with secondary cholangitis due to bile duct obstruction, they should immediately go to the hospital, under the guidance of doctors use anti-inflammatory, choleretic, immunosuppressive agents such as drug treatment; severe cases of extrahepatic biliary obstruction, surgical treatment, the establishment within or outside the biliary tract drainage channel. If the merger biliary cirrhosis, severe liver damage, liver transplant should be done. The current long-term survival of liver transplant may have cured the disease hope. Edit entry Open Category:
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Cindycinderella
2011/08/25 05:35
giljaca v, poropat g, stimac d, gluud c. glucocorticosteroids for primary sclerosing cholangitis. cochrane database of systematic reviews 2010, issue 1. art.
Colin
2011/09/09 16:03
glucocorticosteroids for primary sclerosing cholangitis
Louis
2011/09/13 10:15
welcome to psc support ~ the uk support group for persons suffering from primary sclerosing cholangitis.
Emily
2011/09/17 08:32
psc support
Irene
2011/09/21 01:43
with primary sclerosing cholangitis. click here to donate for research, education on psc! . of our members and contact the moderators at psc-support-owner@yahoogroups.com .
Salome
2011/10/02 19:52
psc-support : psc-support
Derek
2011/10/03 09:33
primary sclerosing cholangitis (psc) is a form of cholangitis due to an autoimmune reaction. a cholangitis is an inflammation of the bile ducts of the liver.
Jill
2011/10/17 08:24
primary sclerosing cholangitis psc
Gaby
2011/10/18 03:21
the european association for the study of the liver (easl) held a monothematic conference on "primary sclerosing cholangitis" in oslo, norway june 21-23, 2009.
Lawrence
2011/10/20 01:03
primary sclerosing cholangitis literature and psc partners .
Georgia
2011/10/20 17:04
primary sclerosing cholangitis. williams lf jr, schoetz dj jr. in spite of an improved . etiology of primary sclerosing cholangitis, which supports the use of .
Noel
2011/11/05 02:45
primary sclerosing cholangitis.
Vivien
2011/11/13 10:03
there is also a parent's support group, especially necessary . primary sclerosing cholangitis (psc) is a chronic. disease of the bile ducts both inside .
Arvin
2011/11/24 23:53
"diagnosing psc"
Belle
2011/12/20 15:03
overview: primary sclerosing cholangitis (psc) is a chronic cholestatic liver disease of unknown etiology that is recognized increasingly in children.
Charlotte
2012/01/09 16:10
primary sclerosing cholangitis: emedicine pediatrics: general .
Ignace
2012/01/17 09:03
the primary sclerosing cholangitis (psc) trust is dedicated to discovering the cause and cure of psc and related conditions.
Sebastian
2012/01/24 02:27
primary sclerosing cholangitis (psc)trust
Francis
2012/02/01 06:45
primary sclerosing cholangitis (psc) is a chronic progressive disorder of unknown etiology that is characterized by inflammation, fibrosis, and stricturing .
Eudora
2012/02/18 01:13
treatment of primary sclerosing cholangitis
Florence
2012/02/23 06:46
. psctrust.com the trust's vision is to discover the cause and cure for primary sclerosing cholangitis (psc) and their mission to support the work of .
Geoffrey
2012/03/04 06:42
primary sclerosing cholangitis trust | support | patient uk
Lynn
2012/03/05 05:13
treatment for primary sclerosing cholangitis (psc), which leads to bile duct cancer, at mayo clinic.
Stuart
2012/03/09 02:13
primary sclerosing cholangitis - diagnosis and treatment .
Winnie
2012/03/23 17:50
can you recommend a short article describing primary sclerosing cholangitis (psc) . please visit primary sclerosing cholangitis support (yahoo groups: .
Glendon
2012/04/06 22:18
frequently asked questions (faq), primary sclerosing .
Rachel
2012/04/08 02:45
primary sclerosing cholangitis (psc) - this is a chronic cholestatic liver disease with obliterative inflammatory fibrosis of the bile ducts.
Aaron
2012/04/26 21:02
primary sclerosing cholangitis (psc) | doctor | patient uk
Quinn
2012/04/26 22:11
primary sclerosing cholangitis - network of care - behavioral health lake - community-based resources and tools for individuals, families and agencies concerned with .
Zoe
2012/04/30 23:13
primary sclerosing cholangitis - network of care - behavioral .
Baird
2012/05/02 02:31
klingenberg sl, chen w. d-penicillamine for primary sclerosing cholangitis. cochrane database of systematic reviews 2006, issue 1. art. no.: cd004182.
Moses
2012/05/03 13:21
d-penicillamine for primary sclerosing cholangitis
Garbo
2012/05/11 04:02
share this site with others using one of these sharing tools. primary biliary cirrhosis, primary sclerosing cholangitis, alcoholic liver disease/nonalcoholic fatty liver .
Astaire
2012/05/13 14:31
primary sclerosing cholangitis treatment - mayo clinic
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