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)

In a patient with liver cirrhosis and severe hypersplenism resistent to corticosteroids splenectomy was attempted but proved impossible. Embolisation of the splenic artery with tiny fragments of absorbable gelatin sponge induced gradual restitution of haematological function to normal after 6 wk. Abdominal pain, paralytic ileus of short duration, transient pyrexia, and pleural effusion ensued but were well tolerated. The patient has remained well, 2 1/2 mo later. It is suggested that this simple method may prove rewarding and could safely be used, if necessary, more than once in patients for whom other treatments are unsuitable or have failed.
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PMID:Treatment of hypersplenism by embolus placement in the splenic artery. 6 45

Wandering spleen may result from congenital failure of splenic attachments or acquired laxity of attachments due to stretching. The wandering spleen is quite vulnerable to the complication of torsion, which is seen most often as an acute abdominal emergency due to splenic infarction. A more unusual variant is chronic torsion which causes intermittent mild to moderate abdominal pain, gastrointestinal disturbances and, in one case, hypersplenism. A mass has been present in most cases and may be anywhere in the abdomen or pelvis. Splenectomy should be performed for all cases of wandering spleen with or without torsion.
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PMID:Chronic torsion of the spleen. 93 48

It is reported about 6 patients suffering from sarcoidosis with splenomegaly. In these cases indication for splenectomy was given by symptoms of hypersplenism, abdominal pain and ineffective cortisone therapy. In general after operation activity of sarcoidosis is unchanged. Different markers of activity were used after a time interval of 2-11 years. In one case it has to be discussed an overwhelming postsplenectomy infection (OPSI).
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PMID:[Splenectomy in sarcoidosis]. 180 52

Five patients with hypersplenism associated with liver cirrhosis were treated by PSE and the changes of peripheral blood cells and liver function tests were observed. After PSE, all patients had a high fever and abdominal pain continued for a few weeks without severe complications. Peripheral blood cell counts improved soon after PSE and liver function tests (hepaplastin test and ICGR15) grew transiently worse, but they also improved within two months. During 4.5 to 10 months, the levels of albumin and total cholesterol of three patients increased, although the changes of bilirubin level and HPT were not shown. For other two patients, it was difficult to estimate the effect of PSE, because one patient was treated at the same time with lipiodol chemoembolization for HCC and another patient had a progress of nephrotic syndrome. On the other hand, ICG levels were stable after PSE but RI-uptake on liver scintigram increased in the liver. These results suggest that PSE may be able to improve not only hypersplenism but also liver function in the patients with compensated liver cirrhosis without severe complication.
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PMID:[The effect of partial splenic embolization (PSE) on liver function test in patients with liver cirrhosis]. 206 49

A case of hepatoma with cirrhosis for whom hepatectomy was impossible because of a severe complication is reported. The case has been treated with various treatments, so long survival has been obtained. The patient is a 56-year-old female with hepatoma with cirrhosis. The initial symptom was bleeding from esophageal varices. Her condition was not suitable for hepatectomy because of hypersplenism and remarkable hepatic disorder. Consequently, she was given endoscopic sclerotherapy for esophageal varices, partial splenic embolization for hypersplenism, and transarterial embolization with ADM, Lipiodol and Spongel powder for hepatoma. Although abdominal pain, pleural effusion and bleeding from gastric ulcer appeared after embolization, esophageal varices and hypersplenism were significantly improved; reduction of 75% of hepatoma was observed and AFP decreased from 18.7 ng to 3 ng. At 12 months after the embolization, there is no sign of hepatoma growth, rupture of esophageal varices or hypersplenism.
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PMID:[Transarterial embolization in the treatment of hepatoma complicated with cirrhosis, esophageal varices and hypersplenism]. 284 16

Eleven cases with hypersplenism, one with liver cirrhosis and ten with hepatocellular carcinoma (HCC) associated with liver cirrhosis, underwent transcatheter partial splenic arterial embolization. In four of ten HCC cases, the spleen was accidentally infarcted during the procedure of transcatheter hepatic arterial embolization (TAE). The mean infarcted area of the spleen was 55.7%. An increase in the peripheral platelet count was particularly remarkable and continued over one year after the embolization. High fever and abdominal pain were observed in all cases. The fever was seen for 18.0 days and pain was noted for an average of 12.8 days after the embolization. Other adverse effects such as pleural effusion and ascites were transitorily observed. Splenic embolization is an effective supporting therapy for hypersplenism in patients with cirrhosis or HCC.
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PMID:Transcatheter partial splenic arterial embolization in patients with hypersplenism: a clinical evaluation as supporting therapy for hepatocellular carcinoma and liver cirrhosis. 301 29

High risk splenectomy is often encountered in cases of hypersplenism with massive splenomegaly (10 times usual weight of 150-200 g) resulting from myelophthisic processes. Intra-operative ligation of the splenic artery through the lesser sac is a technically useful method of gaining vascular control prior to mobilizing the challenging spleen. However, a massive or inaccessible spleen imposes mechanical limitations during surgery and may be complicated by torrential intra-operative hemorrhage in the setting of severe thrombocytopenia refractile to platelet transfusions. The authors describe pre-operative intravascular proximal splenic artery control in four adult patients (3 men, 1 woman) with extreme splenomegaly (2,250-10,000 g). The massive splenomegaly in this group resulted from chronic myelogenous leukemia (n = 2), isolated splenic lymphoma (n = 1), and agnogenic myeloid metaplasia (n = 1). Chief symptom manifestations included left upper quadrant abdominal pain, early satiety, post-prandial emesis, dyspnea, petechiae, and associated easy bruising. Prior to surgery, all the patients were taken to the radiology suite where either detachable silastic balloons or stainless steel coils were placed selectively into the splenic artery under fluoroscopic guidance requiring approximately 35 minutes. Splenic artery occlusion aided normalization of thrombocytopenia (average increases 19,000/microliter to 215,000/microliter) with prolongation in survival of platelets. Successful splenectomy was subsequently performed with no additional transfusion requirements and was made technically easier by reducing splenic bulk. There were no adverse consequences of intravascular occlusion and no peri-operative morbidity or mortality. Preoperative intravascular selective splenic artery occlusion, used as an important potential adjunct to anticipated high risk splenectomy, is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preoperative splenic artery occlusion as an adjunct for high risk splenectomy. 317 46

Gaucher's disease involves the liver, the spleen, and the bone. Liver-spleen and bone scintigraphy were used during an 8-yr period to evaluate changes caused by this disease. Patients were investigated with a liver-spleen scan for abdominal pain, mechanical discomfort, enlarged liver or spleen on physical examination, abdominal mass, abnormal liver function tests, and symptoms of hypersplenism. Fourteen liver-spleen scans were performed in nine patients. Liver scintigraphy showed various degrees of enlargement and inhomogeneous uptake. In two patients focal defects were detected. In one, focal defects were due to liver involvement with Gaucher's disease, but in the other they were caused by metastatic pancreatic carcinoma. The study was also useful in detecting splenic infarction and in following enlargement of the spleen after partial splenectomy. The main indication for bone scintigraphy in six patients was bone pain. This was found to be caused by either aseptic necrosis of the head of the femur, bone infarction, pathological fractures, or osteomyelitis. Loosening after total hip replacement was ruled out in three patients and missed in one patient. Scintigraphy appears to be a simple, sensitive test for evaluation of the liver, spleen, and bony skeleton in patients with symptomatic Gaucher's disease.
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PMID:Scintigraphic findings in Gaucher's disease. 376 Sep 80

An unusual hepatic disease developed in 3 patients with a well-functioning kidney graft 16-24 months after transplantation. Vague abdominal pain, increased bleeding tendency and edema were initial complaints, and hepato- or splenomegaly and ascites were found as well. Liver function tests were not or only mildly disturbed; hemolysis and pancytopenia were always present. Colloid uptake was absent at liver scintigraphy and the hepatic venous wedge pressure was increased. Esophageal varices were demonstrated. Liver biopsy showed extensive midzonal and pericentral sinusoidal dilatation. After discontinuation of azathioprine the symptoms and the extent of sinusoidal dilatation disappeared gradually, but after 1-3 years fibrosis or micronodular cirrhosis had developed and splenomegaly with hypersplenism remained. These observations strongly suggest an association between chronic use of azathioprine and the development of venous congestion of the liver with sinusoidal dilatation, eventually resulting in chronic liver disease.
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PMID:Hepatic sinusoidal dilatation with portal hypertension during azathioprine treatment after kidney transplantation. 390 52

We analyzed the clinical and bacteriologic features of 12 episodes of spontaneous bacterial peritonitis (SBP) in 11 children (four boys, median age 5.5 years) with chronic liver disease. All patients had cirrhosis and ascites; four had hypersplenism, and one was asplenic. Symptoms included increasing abdominal distention, pyrexia, abdominal pain, gastrointestinal disturbance, and encephalopathy. Nine had rebound tenderness on abdominal palpation, and 12 had reduced bowel sounds. The most frequent organisms isolated from culture of ascitic fluid were Streptococcus pneumoniae (nine). Klebsiella (two), and Haemophilus influenzae (one); blood cultures grew identical organisms in nine. Seven patients died despite intensive antibiotic therapy. In the 3 months prior to onset of SBP, defective yeast opsonization and reduced serum concentration of C4 were found in all nine children tested; eight had reduced concentration of C3. Functional deficiency of all complement components was present in four tested within 1 to 5 months of the onset. In contrast, only eight of 59 cirrhotic children without SBP had low C3, and eight had defective yeast opsonization, although 35 had low C4 values. Four of the patients with SBP and low C3 and C4 concentrations had normal concentrations at the time of diagnosis of liver disease 2 to 5 years previously. Opsonization of type III pneumococci was reduced in sera from three patients who subsequently developed pneumococcal peritonitis. The incidence of SBP in children with chronic liver disease is similar to that in adults, as are the clinical features. Our observations suggest that complement deficiency induced by chronic liver disease may be important in the pathogenesis of SBP.
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PMID:Spontaneous bacterial peritonitis in children with chronic liver disease: clinical features and etiologic factors. 399 46


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