Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a population-based study of 402 cases of colorectal cancer in Auckland, 72 patients (18%) demonstrated liver metastases either at presentation or at initial surgery. The findings of pre-operative weight loss, hepatomegaly and elevated alkaline phosphatase were significantly associated with heptic metastases. Individually these factors were insensitive indicators of the presence of liver metastases. Two or more of these risk factors were demonstrated by 54% of the patients with liver secondaries compared to 19% in the series without liver metastases. Continuing surveillance of the latter group of patients will show whether they are also at risk of developing liver secondaries. The median survival for the 69 patients who were diagnosed before death was 6.0 months. When the primary lesion was resected and the patient survived the post-operative period the median survival was 11.0 months.
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PMID:Colorectal cancer in Auckland 1981-1982: patients with liver metastases. 386 34

The use of radiocolloid liver scanning as a routine diagnostic procedure to detect liver metastases has been declining as the most effective uses of this test have become better appreciated. Liver scanning to detect hepatic metastases appears to have the greatest efficacy in two circumstances. The first is as a staging procedure in malignancies that metastasize to the liver early, before being suspected clinically or liver function parameters alter. Such malignancies include gastric carcinoma, Wilms' tumor, small cell carcinoma of the lung, and rhabdomyosarcoma. The second effective use of liver scanning is as a confirmatory test in patients with known malignancy who develop abnormal levels of serum liver enzymes, carcinoembryonic antigen titer, hepatomegaly, ascites, or jaundice.
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PMID:Efficacy of liver scanning in malignant diseases. 609 64

Two children being treated with combination chemotherapy and irradiation for localized, rightsided Wilms' tumor developed sudden enlargement of the liver with defects on liver scintigram resembling liver metastases. One child also developed pancytopenia. When chemotherapy was temporarily withheld in both children, hepatomegaly and scintigram abnormalities resolved. The planned courses of chemotherapy were subsequently completed without complications. The clinical course in our patients is compared to previously published experiences. Awareness of this complication could prevent the mistaken diagnosis of metastatic disease and emphasizes the care necessary when administering cytotoxic drugs to children receiving irradiation to all or a portion of the liver.
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PMID:Hepatopathy following irradiation and chemotherapy for Wilms' tumor. 628 75

Arterial embolisation is performed in order to interfere with the blood supply and growth of tumours and also to palliate the pain produced by them. In the present study 5 patients with liver metastases, 6 patients with renal tumours and 1 patient with bleeding from the rectum were treated by arterial embolisation with gelatin (Gelfoam). Before embolisation angiography was performed in all and computerized tomography in some of the patients. The control examinations and repetitive procedures were performed 2-4 weeks afterwards and there after according to the response. The effectiveness of the embolisation was assessed by angiography as good in 70% of the cases. Out of 5 patients examined with CT in 4 the tumour was found to have become smaller. The procedure eliminated pain caused by the enlarged liver in all 5 patients, stopped the rectal bleeding, and the subjective condition of all patients improved. Pain produced by the postembolisation syndrome occurred in all cases, but repeated embolisations did not result in further pain. Serious complications did not occur.
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PMID:Arterial embolisation in the treatment of malignant tumours. 697 72

The median survival of all patients with hepatic metastases from colorectal cancer referred to the Sidney Farber Cancer Institute during a five-year period was 12.5 months. Two major factors influenced survival. The first was extent of disease at presentation. The second was the histologic grade of the cancer. The median survival of patients presenting with the least disease, characterized by less than four liver nodules visible on liver scan (n = 38), normal liver size on physical examination (n = 60), normal liver function test results (n = 30), and normal performance status (n = 91), was between 18 and 24 months, regardless of treatment. The median survival of those few patients (n = 13) who had objective responses to a variety of treatments, most of whom also had minimal disease at presentation, was also 24 months. Patients whose tumors were poorly differentiated or who had abnormal performance status or weight loss of greater than 10 per cent at presentation survived only six months (median). Those with four or more liver nodules, hepatomegaly (greater than 16-cm vertical span on physical examination), or abnormal liver function test results, survived ten, eight, and 12 months (median), respectively. It is concluded that a significant group of patients survived longer than would have been predicted by earlier literature surveys after the diagnosis of colorectal cancer metastatic to the liver. It is suggested that future therapeutic trials, using survival as a measure of response of patients with liver metastases from colorectal cancer, must be prospectively controlled before selection factors can be differentiated from significant therapy effect.
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PMID:Factors influencing survival in patients with hepatic metastases from adenocarcinoma of the colon or rectum. 717 42

The survival probability is 79% for patients with neuroblastoma stage 4S treated according to the German Society for Pediatric Oncology and Hematology (GPOH) treatment studies. Most of these patients (80%) have liver metastases. Patients are grouped according to their condition at diagnosis and tumour resectability to different risk groups (A, B, C). Chemotherapy is provided for patients who are initially diagnosed as critically ill, caused for example by excessive hepatomegaly due to liver metastases. The aim of this study is to clarify whether liver infiltration is associated with liver dysfunction and whether chemotherapy plays a role in this process. Hepatopathy was diagnosed when clinical signs were present and/or liver function tests revealed pathologic results. The charts of 48 patients (22 boys, 26 girls) diagnosed between 1990 and 1994 from the ongoing NB-90 treatment study were evaluated retrospectively. Median age at diagnosis was 52 days (range: 1-328). 41 patients (85%) had liver infiltration, 26 patients (54%) had bone marrow involvement and in nine patients (19%) skin metastases were found. 12 patients were in poor general condition at diagnosis (risk group C). 36 of 48 patients (75%) received chemotherapy, three children were treated with radiotherapy additionally, due to massive liver enlargement. 15 patients (31%) had signs of hepatic dysfunction at diagnosis or during their illness, 14 of these had liver metastases. All these 15 patients were treated with chemotherapy. 12 of 15 patients with hepatopathy were younger than two months at diagnosis. Five patients with liver dysfunction were not critically ill at diagnosis. Hepatomegaly > or = 6 cm was present in 10 of 15 patients with liver dysfunction. Hepatopathy was transient in eight patients, four patients died soon of multiorgan failure during progression of disease. Three children developed liver fibrosis with conversion to cirrhosis. Hepatopathy was correlated with distribution to risk groups (A and B (5/36) vs. C (10/12), p < 0.001). The appearance of hepatic dysfunction in patients with neuroblastoma stage 4S remains a serious problem especially for young children with excessive hepatic infiltration. Liver dysfunction was of short duration and reversible in most patients, however, even with age-adapted dosages of chemotherapy long-standing cases of hepatopathy were observed. A general recommendation for treatment strategy in this heterogeneous patient group is difficult. Attention should be given to for this complication.
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PMID:[Hepatopathy in patients with stage 4S neuroblastoma]. 892 87

In a group of 97 patients aged from 6 months to 12 years, all with suspected or proven neural crest tumours, metaiodobenzylguanidine (MIBG) scintigraphy was performed at the time of diagnosis and, in some instances, after induction chemotherapy. All the patients underwent a tumour biopsy with cytological and histological analysis, in addition to imaging examinations such as X-rays, ultrasound, computed tomography and magnetic resonance, within a short period before or after scintigraphy. In 82 of 97 cases MIBG was effective in detecting the primary tumour, hence the technique's sensitivity was 84%. A significant different of sensitivity between [131I]MIBG and [123I]MIBG was not demonstrated. As regards metastatic locations, MIBG scans revealed one or more bone metastases in 12 cases, bone marrow involvement (assumed to be present when diffuse and symmetric uptake in the spine, pelvis and possibly other skeletal sites were visualized) in 9 cases, and focal liver metastases or hepatomegaly in 4 cases. Probably owing to the restrictive diagnostic criterion adopted or to the early phase of the bone marrow involvement, the last was found by biopsy but missed by MIBG in 25 cases. The overall sensitivity in detecting metastases was low (48%), but it was much higher if only bone metastases were considered (81%). Twenty-nine patients who had positive scans at diagnosis were checked following 1-2 courses of induction chemotherapy (IC). MIBG scans remained positive in 22 primary tumours, while 7 primary masses were no longer detected. Out of 12 cases showing metastases at diagnosis, two cases with liver lesions became normal and in one case some, but not all, of the bone lesions were not detectable; 4 cases remained abnormal, while in 5 cases bone marrow involvement was not confirmed. Three cases were confirmed to be true negatives; in 4 other cases bone marrow involved not showing at diagnosis was revealed and confirmed by biopsy; 3 cases in which bone marrow involvement was not revealed by MIBG at diagnosis, had normal MIBG and biopsy results after IC; finally, 2 false negative bone marrow cases and 5 true negative cases at diagnosis remained unchanged, but were not checked by biopsy. Performing total body MIBG scintigraphy in childhood neuroblastoma at diagnosis is useful: 1) to predict the nature of the masses detected by other imaging techniques, when biopsy has not yet been performed; 2) for more accurate tumour staging, in addition to standard imaging investigations, MDP scintigraphy and bone marrow aspiration biopsy, thanks to its ability to detect metastatic lesions; 3) to anticipate the decrease in sensitivity of the technique in detecting both the primary mass and the metastases following induction chemotherapy.
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PMID:Radioiodinated meta-iodobenzylguanidine in the diagnosis of childhood neuroblastoma. 900 44

The case of a patient with sudden onset of abdominal pain, hepatomegaly and laboratory findings which indicated necrosis of a parenchymal organ is reported. Patient died soon after the admission to hospital after fulminant disease development. At the time of admission diagnosis of hepatic vein occlusion, i.e., Budd-Chiari syndrome was made based on ultrasonographic finding. Obduction confirmed this finding showing lung adenocarcinoma with liver metastases as well as occlusion of all hepatic vein branches with thrombi. This report emphasizes the role of ultrasonographic diagnostics in the early diagnosis of Budd-Chiari syndrome.
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PMID:[The Budd-Chiari syndrome--case report of a patient with hepatic vein occlusion and adenocarcinoma of the lung]. 937 21

Carcinoids are neuroendocrine tumours of the gut which may also be found in the bronchus, pancreatic islets and retroperitoneum. They probably arise from gastrointestinal or bronchopulmonary pluripotential stem cells. Carcinoid tumours derived from these cells are potentially malignant; the strength of the tendency for aggressive growth correlates with the site of origin, depth of local penetration and the size of the tumour. Carcinoids occur sporadically or result from specific hereditary tumour syndromes. Mutations and/or aberrant expression of specific genes induce and promote tumour growth. Clinical features include local symptoms due to angulation or obstruction and hepatomegaly due to liver metastases. The carcinoid syndrome commonly involves flushing, diarrhoea, bronchospasm and hypotension. Other distinct syndromes may be caused by tumour release of products that may also be used as biochemical markers in diagnosis and follow-up. Scanning using radiolabelled octreotide, an analogue of somatostatin, sensitively identifies occult primary and metastatic deposits. Localized carcinoid tumours should be resected. Some patients benefit from hepatic resection. Palliation of symptoms is best achieved with octreotide. Hepatic artery chemoembolization may produce long-acting palliation. Further genetic characterization of the different types and stages of carcinoid development as well as assessment of gene expression profiles may improve differential diagnosis, prognosis and treatment.
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PMID:The spectrum of carcinoid tumours and carcinoid syndromes. 1462 99

A 68 year old Ecuadorian man was investigated for polyuria, polydipsia and weight loss of 3 kg during the previous two months. Insulin dependent diabetes mellitus was diagnosed 10 year before admission and treated with appropriate diet and insulin (35 U/d). 18 months before was diagnosed in El Ecuador of "multiple liver nodes non-suggestive of malignancy". Physical examination showed a large multinodular petrous hepatomegaly. There was no evidence of skin lesions. Results of laboratory studies included a basal plasma glucose level that ranged between 275-367 mg/dl (N=60-100), glycosylated haemoglobin of 8.9% (N<5) and a serum albumin of 2.8 gr./dl (N=3.4-4.8). At admission non-other laboratory alterations were detected. Computed tomography showed a mass on the head of the pancreas with loco-regional lymph nodes and liver metastases. Tumor markers were normal. Fine-needle aspiration cytology of the liver masses revealed the presence of liver metastases of a non-differentiated malignant tumor. A 111In-DTPAOC scintigraphy revealed the presence of somatostatin receptors in the liver metastases, also detecting the presence of multiple bone metastases in the axial and appendicular skeleton. Plasma glucagon level was 678 pg/ml (N<250). A diagnosis of metastatic glucagonoma was established and therapy with streptozocin, 5-FU, insulin and synthetic somatostatin analogs was initiated. Three months after the therapy initiation the patient was symptom free. Some weeks after the patient suffered from left hip pain, and a control 111In-DTPA scintigraphy showed progression of his bone metastases. In conclusion, glucagonoma must be suspected in all diabetic patients with metastatic liver, even in absence of necrotic migratory erythema. In these circumstances, plasmatic glucagon level and somatostatin receptors scintigraphy will be a useful tool for establishing the final diagnosis.
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PMID:[Diabetes mellitus and pancreatic tumor]. 1471 49


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