Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenic artery ligation, a simple surgical procedure expected to decrease splenic flow and portal pressure in patients with cirrhosis of the liver, was performed concomitantly with a distal splenorenal shunt procedure in six patients and as the main surgical procedure in two patients. Immediate cessation of bleeding was achieved in the four patients in whom the splenic artery was ligated to reduce intraoperative bleeding. However, three of the seven patients with previous gastroesophageal hemorrhage rebled from various postoperatively. Symptoms of splenic infarction were observed in six patients, resulting in thrombosis of the splenic vein and/or of the distal splenorenal shunt in four patients and necessitating splenectomy in one. This incidence of thrombosis of the distal splenorenal shunt is much higher than the overall incidence of 5 per cent observed at our institution. It is thus concluded that the splenic artery should not be ligated in cirrhotic patients with patent distal splenorenal shunts, since splenic arterial collateral vessels have already been reduced by the gastric devascularization, an integral component of the distal splenorenal shunt.
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PMID:Splenic artery ligation in distal splenorenal shunts. 56 93

The effects of splenic artery ligation were studied in Sprague-Dawley rats and in eight selected symptomatic patients with hepatic cirrhosis. In rats, this maneuver induced splenic infarction, reduced functional splenic mass, transiently raised platelet and reticulocyte counts and was without local complications. In seven selected patients with cirrhosis and prominent splenomegaly, the splenic artery was markedly enlarged, splenic arterial flow was greatly increased and splenic artery ligation partially lowered portal pressure. In three patients with varying cytopenias secondary to hypersplenism splenic artery ligation uniformly improved peripheral blood elements, although varying degrees of hypersplenism later recurred necessitating splenectomy in one. In five other patients, splenic artery ligation in conjunction with coronary vein ligation in four was performed for bleeding esophageal varices. Two patients later required portacaval shunting, and one other in whom operation was undertaken in desperation died of hepatic failure. Celiac-mesenteric arterioportography, operative portography, hemodynamic measurements and examination of peripheral blood elements in these eight patients suggests that splenic artery ligation in conjunction, where appropriate, with coronary vein ligation has several potentially beneficial effects. Hypersplenism may be sufficiently controlled to alleviate clinical symptoms. Arterial inflow into the portal system is reduced tending to lower portal pressure. Transheptic portal flow from the mesenteric bed is preserved. Venous anastomotic channels still functioning around the splenic pedicle and no longer draining a hyperdynamic splenic circuit may be converted into an escape route for mesenteric venous blood entering the portal system under high pressure. Nonetheless, each of these effects and their interrelationships require further study before this operation assumes a larger role in the treatment of complications of portal hypertension.
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PMID:Splenic artery ligation in selected patients with hepatic cirrhosis and in Sprague-Dawley rats. 108 42

Splenectomy for massive splenomegaly and hypersplenism carries a significant morbidity and mortality. We have used partial splenic embolization (PSE) as an effective alternative to splenectomy. Ten PSE procedures were performed on nine patients without mortality and with minimal morbidity. The age of the patients ranged from 8 months to 32 years (mean 14 years). The causes of splenomegaly and hypersplenism included cystic fibrosis with cirrhosis (2), tyrosinemia and cirrhosis (1); thalassemia (1), hemophilia with Human Immune Deficiency Virus infection (2), chronic hepatitis with portal hypertension (1), malignant histiocytosis (1), and Wiskott-Aldrich Syndrome (1). All procedures were performed under local anesthesia with sedation. A percutaneous femoral artery approach to the splenic artery was used to deliver Ivalon sponge particles (280-800 microns) into the spleen. Splenic infarction was assessed by postembolization angiograms. All of the patients except one demonstrated improvement of hematologic parameters. In one patient, however, cytopenia improved only after a second embolization. In the total series, there was an early mean rise of 8,600/mm3 in the leukocyte count (range 2,900-14,900) and 212,000/mm3 in the platelet count (range 30,000-718,000). Follow-up ranged from 4 months to 7 years. Improvement of the blood picture has been persistent in seven of the eight patients who showed initial improvement. Transient procedural complications included fever (5), pleural effusion (2), pneumonia (1), and splenic abscess (1). One patient had paralytic ileus lasting for 10 days and one patient developed a streptococcal peritonitis 3 weeks after embolization. No patient developed pancreatitis or vascular compromise of other abdominal viscera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial splenic embolization. An effective alternative to splenectomy for hypersplenism. 226 5

We performed a partial splenic arterial embolization in 22 patients with cirrhosis associated with thrombocytopenia and then evaluated the changes in platelet kinetics after undergoing the procedure using 111In-tropolone-labeled platelets. The controls consisted of eight chronic hepatitis patients who showed a normal platelet count and normal spleen size. The mean splenic infarction ratio after the procedure was 54.9%. A platelet kinetics study was performed before and 2 months after the procedure. Before the procedure, the cirrhotic patients showed increases in the splenic volume and the spleen/liver uptake ratio of the 111In-labeled platelets on both the third and seventh days, and a decrease in the platelet recovery compared with the controls, which suggested an increased platelet pool in the spleen. In addition, the platelet survival time in cirrhotic patients was shortened, whereas the platelet-associated immunoglobulin G (PA-IgG) was higher than that of the controls, which suggested the involvement of immunologic mechanisms in the thrombocytopenia. With an increase of the platelet count after a partial splenic arterial embolization, the spleen/liver uptake ratio of the 111In-labeled platelets decreased, whereas the platelet recovery increased. Furthermore, the platelet survival time was prolonged, whereas the PA-IgG decreased. The platelet count showed a positive correlation with the platelet survival time and a negative correlation with PA-IgG before and after the procedure. These results suggest that a transcatheter splenic arterial embolization not only may reduce the increased platelet pool in the spleen but also may improve the thrombocytopenia induced by immunologic mechanisms in patients with cirrhosis.
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PMID:Changes in platelet kinetics after a partial splenic arterial embolization in cirrhotic patients with hypersplenism. 748 74

Splenic infarction is rare in cirrhotic patients. The diagnosis of the condition is based on clinical findings and splenic imaging. In recent years, ultrasonography and computed tomographic scan have gained popularity over the more classical scintigraphy as the preferred investigations for the diagnosis of splenic infarction. We report three cases of splenic infarction in patients with cirrhosis and portal hypertension. Computed tomographic scan, angiography and ultrasonography failed to identify the lesions and the diagnoses were finally made with the aid of liver--spleen scintigraphy. We suggest that scintigraphy is the investigation of choice if splenic infarction is suspected in patients with congestive splenomegaly secondary to liver cirrhosis.
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PMID:Liver/spleen scintigraphy for diagnosis of splenic infarction in cirrhotic patients. 825 38

The authors describe for the first time a case of splenic infarction in a 7-year-old boy with portal hypertension and biliary cirrhosis secondary to biliary atresia. This rare complication may cause serious acceleration of chronic liver failure.
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PMID:Splenic infarction in a child with portal hypertension secondary to biliary atresia. 912 79

An autopsy case of systemic mast cell disease (SMCD) without primary skin lesions in a 57-year-old Japanese male is described. Initially the patient was suspected of having liver cirrhosis or malignant lymphoma because of hepatomegaly and lymph node enlargement on admission. However, a lymph node biopsy and bone marrow aspiration conducted on his third admission indicated a SMCD because of the existence of metachromatic cell aggregates stained with toluidine blue. At autopsy, the diagnosis was confirmed because the proliferating cells were histochemically proven to be mast cells by naphthol AS.D chloroacetate esterase, Giemsa and alcian blue, in addition to toluidine blue staining. The intra-abdominal and retroperitoneal lymph nodes were replaced by mast cell aggregates, which caused the splenic infarction and bilateral hydronephrosis, with infiltration of mast cells into the spleen and kidneys also being apparent. Mast cell infiltration was similarly found in the bone marrow, liver, ileum and ascending colon. Immunohistochemically, the mast cells were positive for antibodies of alpha 1-antichymotrypsin, CD45 (LCA), CD43 (MT-1), CD45R (MB-1) and the oncoprotein c-kit. Electron microscopic examination using formalin-fixed tissue gave supportive evidence of a mast cell origin for the lesions.
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PMID:Systemic mast cell disease with splenic infarction: a case report. 970 48

Splenic infarct is a rare complication of portal hypertension. It has been reported as an early complication after successful liver transplantation when portal pressure returns to normal and the splenic size progressively declines. It has not been reported as a late complication of liver transplantation. We describe the case of a 19-year-old patient with a splenic infarct which occurred 11 months after successful orthotopic liver transplantation for decompensated cryptogenic liver cirrhosis. Following transplantation, the patient was in excellent general health, liver function tests were normal, there was no clinical evidence of portal hypertension and the splenic size had decreased significantly compared to the pre-transplantation period, although it remained increased. The patient presented with high fever, left pleuritic pain and vomiting. The splenic size had not changed and left pleuritic exudate fluid collection was detected. A hypoechoic region of the spleen was demonstrated in the ultrasound examination corresponding to a hypodense lesion in the computerized tomography scanning. The patient recovered completely, with the disappearance of the infarct in the imaging studies in 2 months time. This case report indicates that a symptomatic splenic infarct can occur late following successful liver transplantation for liver cirrhosis despite lack of any evidence of residual portal hypertension at a time that splenomegaly has not yet regressed. The differential diagnosis from a splenic abscess in transplanted patients can be difficult but the final prognosis seems to be good.
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PMID:Splenic infarct as a late complication of liver transplantation. 983 Dec 79

Terminal liver cirrhosis is associated with marked severe portal hypertension, which increases the risk of intraoperative hemorrhage and graft hyper-perfusion, especially, in small-for-size graft. In cases with developed collateral vessels, we often face difficulties in perihepatic dissection with blood stanching against bleeding during recipient hepatectomy. For aseptic preoperative portal decompression, we established the proximal splenic artery embolization (PSAE) technique. Sixty adult living donor liver transplantation recipients with viral/alcoholic hepatic failure were divided into two groups; PSAE group (n = 30) and non-PSAE (n = 30). In the PSAE group, the splenic artery was embolized proximal to the splenic hilum 12-18 h before surgery. PSAE enabled shortening of operating time, reduced blood loss, led to less need for transfusion, and significantly reduced the post-transplant portal venous velocity and ascites. PSAE was not associated with complications, e.g., splenic infarction, abscess, or portal thrombosis. Six of the non-PSAE patients required additional surgical intervention to resolve postoperative hemorrhage and three patients required secondary PSAE for arterial-steal-syndrome. The hospital mortality rate of PSAE patients (3.3%) was significantly better than that of the PSAE group (13.3%, P < 0.05). Preoperative noninvasive PSAE makes more efficient use of portal decompression; thus, it can potentially contribute to improvement of outcome.
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PMID:Preoperative proximal splenic artery embolization: a safe and efficacious portal decompression technique that improves the outcome of live donor liver transplantation. 1761 80

Spontaneous splenic infarction has been seen rarely in cirrhosis and portal hypertension. The clinical presentation can mimic other causes of acute abdominal pain. The diagnosis of the condition is based on clinical findings and splenic imaging. In recent years, ultrasonography and computed tomographic scan have gained in popularity for the diagnosis of splenic infarction. Most reported cases are of focal infarction, and treatment is mostly conservative. Herein, we describe a rare case of spontaneous splenic infarction in an elderly cirrhotic patient with portal hypertension who also had comorbidities. A 72-year-old female previously diagnosed with cirrhosis was admitted for left upper quadrant abdominal pain for two days. Her medical history included cryptogenic cirrhosis, congestive heart failure, chronic obstructive pulmonary disease, and hypertension. Physical examination on admission revealed a palpable splenomegaly. Abdominal ultrasonography revealed splenomegaly and a hypoechoic area with lobulated contours measuring 62 x 35 mm extending from the subcapsular area to the hilus in the middle section of the spleen. Abdominal computed tomographic showed a subcapsular hypodense lesion of the spleen measuring 64 x 58 mm. Doppler ultrasound revealed a wedge-shaped heterogeneous hypoechoic avascular area extending from the central zone to the lateral zone of the spleen. In our case, diagnosis of splenic infarction was made by computed tomographic and Doppler ultrasonography. Our patient received conservative treatment for the underlying diseases. Spontaneous splenic infarction must be kept in mind in cirrhotic patients with underlying comorbidities presenting with left upper quadrant pain.
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PMID:Spontaneous splenic infarction in an elderly cirrhotic patient with multiple comorbidities. 2316 8


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