Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a 31 year old man who had been intravenous drug abuser for years is reported. He was studied because of abdominal pain, jaundice, a weight loss of 10 kg, and the presence of a subclavicular mass. Biopsy of the mass demonstrated a high-grade B-cell non-Hodgkin's lymphoma, and the patient was classified in group IV-D of the human immunodeficiency virus infection because he had HIV serum antibodies and a reduced CD4/CD8 lymphocyte ratio. Although lymphoma had a good response to chemotherapy, persistent cholestasis led to liver and biliary evaluation. Sclerosing cholangitis and papillary stenosis were found. He has been followed for two years, without evidence of any secondary infectious disease associated to the acquired immunodeficiency syndrome.
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PMID:[Sclerosing cholangitis, papillary stenosis and B-cell lymphoma in a patient with acquired immunodeficiency syndrome]. 189 85

A 22 year old man developed sclerosing cholangitis within two months of documented HIV-1 seroconversion. Sclerosing cholangitis should be included in the differential diagnosis of causes of abdominal pain and raised alkaline phosphatase enzyme levels in HIV-1 antibody positive patients without established CDC stage IV disease.
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PMID:Sclerosing cholangitis rapidly following anti-HIV-1 seroconversion. 207 Nov 28

An 11-year-old male presented with abdominal pain and emesis. Serum chemistries revealed cholestasis and an ERCP demonstrated sclerosing cholangitis. Secondary causes of this disease process were excluded. Sclerosing cholangitis is distinctly uncommon in the pediatric age group, but it should be considered in evaluation of patients of any age with cholestasis. It appears in some cases that there may be subtle histologic and radiographic features which separate the pediatric and adult forms of the disease.
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PMID:Pediatric primary sclerosing cholangitis. 372 Apr 73

Described is a 15-year-old boy who presented with an ulcerative destructive soft palate lesion, skin lesions, and prolonged history of weakness and abdominal pain associated with abnormal liver functions. A midline destructive lesion was considered. However biopsies revealed chronic inflammation. After thorough investigation including colon, liver, skin and uvular biopsies a diagnosis of Inflammatory Bowel Disease in association of Autoimmune Sclerosing Cholangitis was made. Treatment with steroids improved his symptoms, normalized liver functions and enhanced healing of the skin and palatal lesions. This case demonstrates the involvement of the palate in a rare systemic disease and to our knowledge is the first description of Sclerosing Cholangitis presenting as an ulcerative lesion of the soft palate.
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PMID:Inflammatory bowel disease and sclerosing cholangitis with ulcerative lesions on skin and soft palate. 1536 9

Autoimmune liver diseases in childhood includes Autoimmune Hepatitis (AIH) and Primary (Autoimmune) Sclerosing Cholangitis (P(A)SC). Both diseases are characterized by a chronic, immune-mediated liver inflammation involving mainly hepatocytes in AIH and bile ducts in PSC. Both diseases, if untreated, lead to liver cirrhosis. AIH could be classified, according to the autoantibodies pattern, into two subtypes: AIH type 1 presents at any age as a chronic liver disease with recurrent flares occasionally leading to liver cirrhosis and liver failure. Characterizing autoantibodies are anti-nuclear (ANA) and anti-smooth muscle (SMA), usually at high titer (>1:100). These autoantibodies are not specific and probably do not play a pathogenic role. AIH type 2 shows a peak of incidence in younger children, however with a fluctuating course. The onset is often as an acute liver failure. Anti-liver kidney microsome autoantibodies type 1 (LKM1) and/or anti-liver cytosol autoantibody (LC1) are typically found in AIH type 2 and these autoantibodies are accounted to have a potential pathogenic role. Diagnosis of AIH is supported by the histological finding of interface hepatitis with massive portal infiltration of mononuclear cells and plasmocytes. Inflammatory bile duct lesions are not unusual and may suggest features of ''overlap'' with P(A)SC. A diagnostic scoring system has been developed mainly for scientific purposes, but his diagnostic role in pediatric age is debated. Conventional treatment with steroids and azathioprine is the milestone of therapy and it is proved effective. Treatment withdrawal however should be attempted only after several years. Cyclosporin A is the alternative drug currently used for AIH and it is effective as steroids. P(A)SC exhibit a peak of incidence in the older child, typically in pre-pubertal age with a slight predominance of male gender. Small bile ducts are always concerned and the histological picture shows either acute cholangitis (bile duct infiltration and destruction) and/or lesions suggesting chronic cholangitis as well (bile duct paucity and/or proliferation, periductal sclerosis). Small bile ducts damage may be associated, at onset or in the following years, with lesions of larger bile ducts with duct wall irregularities, strictures, dilations, and beading resulting in the characteristic ''bead-on-a-string'' appearance. The ''small duct'' (autoimmune) sclerosing cholangitis is also called autoimmune cholangitis. PSC is strictly associated to a particular form of inflammatory bowel disease (IBD) which shows features not typical of ulcerative colitis neither of Crohn's disease. Symptoms related to IBD often are present at onset (abdominal pain, weight loss, bloody stools) but the liver disease is frequently asymptomatic and it may be discovered fortuitously. Treatment of PSC is particularly challenging. In case of ''small duct'' SC or in case of evidence active inflammation on liver biopsy, immunosuppressive treatment is probably useful while in case of large bile ducts non inflammatory sclerosis, immunosuppression is probably uneffective. Ursodeoxycholic acid, however, may leads to an improvement of liver biochemistry even if there's no evidence that it may alter the course of disease. Thus, liver transplantation, is often necessary in the long term follow-up, even with a risk of disease recurrence. In adjunction to these two main disorders, many patients show an''overlap'' disease with features of both AIH and PSC. In such disorders the immune-mediated damage concerns both the hepatocyte and the cholangiocyte with a continuous clinical spectrum from AIH with minimal bile ducts lesions and PSC with portal inflammation and active inflammatory liver damage.
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PMID:Autoimmune diseases of the liver and biliary tract and overlap syndromes in childhood. 1921 8