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)

A 16-year-old girl was admitted to our hospital because of high fever, abdominal pain, and jaundice. Abnormal lymphocytes and hemophagocytic cells had infiltrated the bone marrow. Laboratory data revealed a severe type of hemophagocytic syndrome accompanied by an initial Epstein-Barr virus (EBV) infection. Persistent EBV infection was identified by polymerase chain reaction (PCR) detection of EBV-DNA in peripheral blood and bone marrow mononuclear cells. The limited efficacy of initial treatment with high-dose gamma-globulin, plasmapheresis, and high-dose methylprednisolone prompted us to administration of T-COP-E (VP-16). Two courses of T-COP-E improved the patient's clinical symptoms and laboratory data; however, marked splenomegaly remained. In addition, fever and serum increase of lactate dehydrogenase (LDH) and cytokines such as gamma-interferon recurred shortly after chemotherapy. On day 53 after diagnosis, the patient underwent laparoscopic splenectomy. The resected spleen weighted 420 g and abnormal lymphocytes in the spleen were positive for CD 8 and negative for CD 56. In situ hybridization revealed EBV-encoded small RNAs (EBERs) in the abnormal lymphocytes. Clinical symptoms including high fever disappeared shortly after the splenectomy, and laboratory data returned to normal. Lymphocytosis after the splenectomy was not observed. We continued out patient monitoring of the case, and 16 months after diagnosis, EBV-DNA in peripheral blood mononuclear cells was not detected, even by PCR.
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PMID:[Severe type of Epstein-Barr virus associated hemophagocytic syndrome successfully treated with T-COP-E and splenectomy]. 1276 Jan 5

Carcinoid tumors are rare forms of gastrointestinal tumors, although lately they have been found with increasing frequency. We report here the combined diagnosis of an intestinal metastasized carcinoid tumor. A 67-year-old patient was followed up during a nine-year period. In 1990 the patient was diagnosed with carcinoid tumor of intestinal origin with multiple liver metastases. Initial treatment consisted of partial resection of the intestine and resection of the liver. Since multiple liver metastases were found, chemoembolization was also performed. After this therapy the patient was free of complaints until 1996. That year the patient reported upper abdominal pain with occasional diarrhea. Given his past medical history and multiple hepatic metastases proven by three-dimensional ultrasonography, combined octreotide and interferon therapy was started following octreoscan scintigraphy. During a three-year period the patient was without complaints and the tumor marker value decreased to almost normal. In 1998 the patient at a regular follow-up visit complained about colic abdominal pain around the umbilical region. Abdominal ultrasonography showed a local wall thickening in the intestinal region. The computed tomography and selective enterography were positive as well. The surgical treatment and histology demonstrated intestinal recurrence of the tumor in the ileal region. After the operation we started a long-acting sandostatin and interferon treatment. We conclude that an ultrasound with a high index of clinical suspicion is a useful test for the diagnosis of carcinoid tumor in detection and in follow-up examinations.
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PMID:The importance of follow-up examinations in patients with carcinoid tumor. 1457 61

Systemic mastocytosis (SM), as opposed to cutaneous-only mastocytosis, implies the presence of neoplastic mast cell infiltration in extracutaneous tissue. Mast cell disease in adults is often systemic and often involves the bone marrow. Typical clinical and laboratory features of SM include urticaria pigmentosa, mast cell mediator symptoms (eg, headache, flushing, lightheadedness, urticaria and pruritus, nausea, diarrhea, abdominal pain, and vasodilatory shock), bone pain (eg, osteoporosis, lytic bone lesions, and fractures), hepatosplenomegaly, cytopenia, eosinophilia, elevated serum tryptase and histamine, and bone marrow fibrosis and angiogenesis. SM may be indolent (no evidence of organ dysfunction), aggressive (presence of organ dysfunction), associated with another often chronic myeloid hematologic disease (SM-AHD), or present as mast cell leukemia or sarcoma. Mast cell-mediator symptoms are treated with histamine antagonists and cromolyn sodium. Indolent SM does not require cytoreductive therapy. Aggressive SM and SM-AHD are managed based on their molecular profile. Recent information suggests that FIP1-like-1-platelet-derived growth factor receptor-alpha(+) SM responds well to imatinib mesylate, whereas interferon-alpha should be considered as a first-line treatment in all of the other cases, including patients with Asp816Val(+) SM. Cladribine has been shown to be effective in patients who develop resistance to interferon treatment.
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PMID:Systemic mastocytosis: current concepts and treatment advances. 1508 68

The case report of a young female patient with personal history of primary thrombocythaemia, treated with interferon alpha, admitted to our medical department for severe abdominal pain, hepatomegaly, ascites and alteration of hepatic function is presented. Magnetic resonance imaging showed the picture typical for Budd-Chiari syndrome caused by external obstruction of the intrahepatal portion of inferior vena cava. The cause of the syndrome remains uncertain, possibility of the haematogenic infiltration of the liver or venal thrombosis within primary or secondary (interferon-induced) antiphospholipid syndrome is discussed. Liver biopsy could elucidate the exact cause, but it was not performed for technical problems.
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PMID:[The Budd-Chiari syndrome in a patient with primary thrombocythemia treated with interferon alfa and transjugular portosystemic shunt]. 1513 42

A 57-year old woman received interferon alfa-2b and ribavirin combination treatment for chronic hepatitis C. High fever and lower abdominal pain developed 10 months after the start of treatment. Antibiotic drugs were not effective. After two weeks, colonoscopic findings revealed a periappendiceal abscess. After colonoscopy study, fever decreased. We have to suspect abscess formation too as appearing a high fever during interferon and ribavirin combination treatment.
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PMID:[A periappendiceal abscess during combination interferon and ribavirin treatment for chronic hepatitis C]. 1798 12

Interferon therapy is indicated for the treatment of chronic hepatitis C and prevention of hepatocellular carcinoma. We describe the case of a 66-year-old Italian woman who received pegylated interferon alpha-2a plus ribavirin combined therapy for HCV-related chronic liver disease. Preliminary hematochemical, ultrasound and bioptic investigations did not show liver cirrhosis or hepatocarcinoma. After 24 weeks of treatment transaminase serum levels were in the normal range and circulating HCVRNA was undetectable by PCR qualitative assay. On week 46 a serious adverse event occurred, with rapid transaminase increase, severe hyperpyrexia, and abdominal pain, leading to interruption of interferon and ribavirin. Liver biopsy was repeated and it revealed poorly differentiated hepatocellular carcinoma. Only palliative care could be performed and the patient died of liver failure within 2 months. The present case underlines that hepatocellular carcinoma can be misdiagnosed in spite of laboratory and instrumental follow-up. More sensitive tools are needed for tumor detection, to avoid IFN impairment of the liver, even though it eradicates HCV.
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PMID:Occurrence of diffuse, poorly differentiated hepatocellular carcinoma during pegylated interferon plus ribavirin combination therapy for chronic hepatitis C. 1860 96

A58-year-old man with upper abdominal pain had a duodenal perforation and a huge hepatocellular carcinoma (BCC). Atumor embolism in the main portal vein was also seen. Extended right lobectomy against a huge tumor in right lobe and ethanol injection to a tumor in the lateral segment were performed. In addition, fluorouracil arterial infusion and interferon therapy(FAIT)were carried out. He has been for 4 years and 6 months without recurrence. Although prognosis of patients with a huge BCC is miserable even if curative hepatic resection is performed, it may be possible for adjuvant FAIT to suppress the recurrence after hepatic resection for huge BCC.
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PMID:[A resected case of huge advanced hepatocellular carcinoma(BCC)treated with intra-arterial infusion chemotherapy combined with interferon-alpha]. 1893 83

We report a case of classic polyarteritis nodosa complicated with renal infarction. A 14-year-old boy manifested fever, abdominal pain, watery and bloody diarrhea, and weight loss. Laboratory findings indicated anemia, increased levels of C-reactive protein, and erythrocyte sedimentation rate. Lower gastrointestinal endoscopic examination revealed multiple colorectal ulcerations, and histopathological findings were non-specific, suggesting gastrointestinal involvement of Behcet disease. The patient was referred to our hospital, and suspected to have vasculitis syndrome since the abnormal laboratory findings included persistently increased levels of FDP-E/fibrin monomer as well as inflammatory markers, and the extraordinary high excretion of beta 2-microglobulin, which indicated abrupt and massive expression of HLA class I molecule on endothelial cells due to interferon-gammanemia. To examine the site of vasculitis, 3D-CT angiography was applied to demonstrate bilateral renal infarction and renal artery microaneurysms. Together with the clinical, laboratory, and 3D-CT angiographic findings, he was finally diagnosed as having classic polyarteritis nodosa. After 12 month-course of intravenous cyclophosphamide pulses and prednisolone/azatioprine therapy, complete disappearances of inflammatory manifestations, and renal infarction and microaneurysms were documented. The diagnosis of classic polyarteritis nodosa is frequently delayed because both clinical symptoms and signs, and laboratory findings are not disease-specific, but early diagnosis and treatment are necessary to prevent serious organ damage. In addition to the precise estimation of laboratory findings such as inflammatory markers, and FDP-E/D-dimer/fibrin monomer, the newly developed 3D-CT angiography, a less invasive imaging technique, will be helpful to diagnose patients with classic polyarteritis nodosa, and intervene the disease progression with early and active treatment.
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PMID:[Gastrointestinal involvement and renal infarction in a boy with classic polyarteritis nodosa diagnosed with 3D-computed tomography angiography]. 1897 26

Hepatitis C is caused by the hepatitis C virus (HCV) infection. According to World Health Organization data, 3% of the world population (approximately 170 million people) is infected with HCV; in Poland there are over 700,000. Over 70% of those infected manifest no symptoms in the acute phase of the disease, and in about 70-80% the acute phase progresses into a chronic form. Patients with symptoms in the acute phase of HCV infection most commonly present with unspecific signs and symptoms that may develop in other viral liver infections, e.g. malaise, fatigue, abdominal pain, mild hepato- and splenomegaly and arthralgia. These symptoms usually persist for 2 to 12 weeks. In the chronic phase a subset of patients complain of malaise, nausea, abdominal pain and itching. With time, chronic hepatitis C may develop into liver cirrhosis. The basic diagnostic methods in HCV infection involve determination of anti-HCV antibodies using the ELISA immunoassay and examination of HCV-RNA with the RT-PCR method. The current treatment of HCV infection involves administration of pegylated interferon a and ribavirin over a period of 48 weeks in HCV-1 genotype infection, and 24 weeks for HCV-2 and 3 genotypes. Effectiveness of therapy depends on the HCV genotype. HCV elimination can be achieved in 78% of patients with HCV-2 and 3 genotypes, and in 55% of patients with HCV-1 genotype.
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PMID:Viral hepatitis C. 1920 52

Although an estimated 1 million persons in the United States are chronically infected with hepatitis B virus, the prevalence of hepatitis B has declined since the implementation of a national vaccination program. Hepatitis B virus is transmitted in blood and secretions. Acute infection may cause nonspecific symptoms, such as fatigue, poor appetite, nausea, vomiting, abdominal pain, low-grade fever, jaundice, and dark urine; and clinical signs, such as hepatomegaly and splenomegaly. Fewer than 5 percent of adults acutely infected with hepatitis B virus progress to chronic infection. The diagnosis of hepatitis B virus infection requires the evaluation of the patient's blood for hepatitis B surface antigen, hepatitis B surface antibody, and hepatitis B core antibody. The goals of treatment for chronic hepatitis B virus infection are to reduce inflammation of the liver and to prevent complications by suppressing viral replication. Treatment options include pegylated interferon alfa-2a administered subcutaneously or oral antiviral agents (nucleotide reverse transcriptase inhibitors). Persons with chronic hepatitis B virus infection should be monitored for disease activity with liver enzyme tests and hepatitis B virus DNA levels; considered for liver biopsy; and entered into a surveillance program for hepatocellular carcinoma.
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PMID:Hepatitis B: diagnosis and treatment. 2038 72


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