Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method to prepare cisplatin suspended in an oily lymphographic agent, Lipiodol (LPS), has been established to deliver cisplatin to hepatocellular carcinoma (HCC) by the hepatic artery. Seventy-one patients, one Stage I, 16 Stage II, 16 Stage III, and 38 Stage IV, were treated with LPS therapy. A partial response was obtained in 33 cases (46.5%), a minor response in 20 cases (28.2%), and no change in 18 cases (25.3%). In 34 patients whose serum alpha-fetoprotein (AFP) levels were greater than 400 ng/ml, the serum AFP levels decreased in 31 patients (91.2%). The AFP decreased by more than 50% in 25 cases (73.5%) and more than 75% in 19 cases (55.9%). The plasma des-gamma-carboxy prothrombin (DCP) levels decreased in all of the 26 DCP-positive patients. The survival rate was 77% at 6 months and the 1-year survival rate was estimated to be 55%. The patients treated with LPS therapy survived longer compared with patients given Lipiodol containing neocarzinostatin by the hepatic artery. Complications such as acute gastroduodenal mucosal lesions (24%), cholecystitis (2.8%), pancreatitis (7%), delayed jaundice (7%), and hepatic encephalopathy (4.2%) were observed after therapy. The peak plasma platinum (Pt) concentrations determined as ultrafilterable Pt occurred 5 to 20 minutes, and 5 to 60 minutes as total Pt after the end of LPS injection. The Pt concentrations in the tumor tissues were 42 times higher in four operated cases and 7.1 times higher in six autopsy cases than those in the nontumorous tissue. These results suggest that LPS selectively accumulates in the HCC, is long-lasting and gradually releases the drug. In addition it is effective as a new anti-cancer therapy for hepatocellular carcinoma.
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PMID:Hepatic arterial injection chemotherapy with cisplatin suspended in an oily lymphographic agent for hepatocellular carcinoma. 247 31

The ductular accumulation of "abnormal mucus" is the key histologic feature in cystic fibrosis. This material is periodic acid-Schiff positive and diastase resistant, suggesting that it is glycoprotein in nature. We used the avidin-biotin-peroxidase method to identify this material using antibodies to the serum glycoproteins carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein on paraffin sections of pancreas obtained from a total of 21 patients: 9 with cystic fibrosis, 5 with chronic pancreatitis, and 7 controls. The control patients had normal pancreatic histologic findings, no alpha 1-antitrypsin or alpha-fetoprotein was demonstrated, and only the ductular epithelium reacted weakly for carcinoembryonic antigen. The pancreas in pancreatitis showed fibrosis, acinar atrophy, and ectasia of the ducts that contained only a small amount of periodic acid-Schiff-positive material. This material reacted weakly for carcinoembryonic antigen and alpha 1-antitrypsin. The appearance of the pancreas in cystic fibrosis was similar to that in chronic pancreatitis. However, the ducts contained a greater amount of periodic acid-Schiff-positive material, mostly in the form of globules that reacted strongly for carcinoembryonic antigen and alpha 1-antitrypsin and weakly for alpha-fetoprotein, as did the ductular epithelium. This study shows that the periodic acid-Schiff-positive material in cystic fibrosis contains at least the three serum glycoproteins and that the accumulation may represent a possible defect in cellular synthesis, assembly, or transport of glycoproteins in the ducts.
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PMID:Carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein in the pancreas of patients with cystic fibrosis. 247 7

A large number of ascitic fluid tests, e.g., fibronectin and cholesterol, have been proposed as helpful in detecting malignancy as the cause of ascites. Unfortunately, these "humoral tests of malignancy" are nonspecific. Although the ascitic fluid concentrations of these proteins or protein-bound substances tend to be quite high in patients with peritoneal carcinomatosis and low in the setting of cirrhotic ascites, the problem is that patients with tuberculous peritonitis, cardiac ascites, pancreatitis ascites, etc. usually have values in the malignancy range, i.e., false-positive results. This can lead to an extensive search for a nonexistent tumor, with confusion and anxiety for patient and physician. The cytology is the single best test to order when peritoneal carcinomatosis is suspected; its sensitivity approaches 100%. However, peritoneal carcinomatosis is only one of several mechanisms by which tumors can cause ascites. No one test can be expected to detect tumors as the cause of these diverse mechanisms of ascites formation. The serum-ascites albumin gradient is a helpful test in classifying ascitic fluid specimens into portal-hypertension-related and non-portal-hypertension-related categories. An elevated serum alpha-fetoprotein test can be useful in raising suspicion of hepatocellular carcinoma. Careful analysis of ascitic fluid, without measurement of "humoral tests of malignancy," combined with information obtained from the history and physical examination, usually lead to an accurate diagnosis of the cause of ascites.
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PMID:Malignancy-related ascites and ascitic fluid "humoral tests of malignancy". 818 30

Yolk sac tumor is a rare and highly malignant germ cell tumor. We report a case of yolk sac tumor primarily in the pancreas in a 32-year-old man. He presented with pancreatitis at presentation with significantly increased serum alpha-fetoprotein (AFP). F-FDG PET/CT revealed diffuse enlargement of the pancreas in the neck, body, and tail portion with homogeneously increased FDG uptake, similar to the change of pancreatitis. The lesion progressively developed to a huge pancreatic mass in the follow-up images, and endoscopic ultrasonography-guided aspiration biopsy of the pancreatic mass confirmed the diagnosis of yolk sac tumor.
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PMID:Primary Pancreatic Yolk Sac Tumor Presenting as Diffusely Enlarged Pancreas in Initial 18F-FDG PET/CT. 3233 17