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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a retrospective review of 233 patients who had surgical exploration for proven or suspected malignant lesions of the exocrine pancreas and periampullary structures. There were 24 patients with carcinoma of the ampulla or duodenum, 12 with carcinoma of the bile duct, and 197 with lesions of the pancreas. Among the latter group, 128 patients had carcinoma diagnosed at initial operation (31 by duodenopancreatectomy, 33 by liver, and 64 by other biopsies), and 69 patients had suspected carcinoma of the pancreas without histological proof. History of jaundice, pruritus, nausea/vomiting, total weight loss, duration of pain, and values of blood urea nitrogen, bilirubin, alkaline phosphatase, and albumin were significantly different among the various groups. Patients who had resection of carcinoma of the duodenum or ampulla had the best 5-year survival rate (39 +/- 12%). Among patients with resectable or nonresectable carcinoma of the pancreas, some of the symptoms and laboratory tests studied had prognostic significance.
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PMID:Clinical and laboratory findings of carcinoma of the pancreas and periampullary structures. 669 85

Acute pancreatitis in a patient on oral contraceptive therapy is reported, and the relationship of estrogen administration to hyperlipemia and pancreatitis is discussed. A 23-year-old white woman was admitted to a hospital with epigastric pain, nausea, and vomiting. Three previous episodes of abdominal pain had been diagnosed as acute pancreatitis. On the present and previous admissions, she had just completed a cycle on her combination norethindrone 1 mg, mestranol 8 micrograms contraceptive. Laboratory results showed mild leukocytosis and elevated concentrations of blood glucose, alkaline phosphatase, serum amylase, and urine amylase. Serum cholesterol and triglycerides were elevated, and lipoprotein electrophoresis showed a type IV pattern. Abdominal sonogram revealed a normal pancreas, and all other test results were normal. The patient was treated with i.v. fluid replacement, dimenhydrinate, and meperidine hydrochloride. Within 72 hours she was asymptomatic, and serum amylase, triglyceride, and cholesterol concentrations had decreased. She was discharged with a diagnosis of acute pancreatitis secondary to oral-contraceptive-induced hyperlipidemia. Oral contraceptive therapy was not resumed. Predisposing factors, symptoms, and laboratory findings associated with estrogen-induced acute pancreatitis are presented, and the mechanisms through which serum lipid elevations and subsequent pancreatitis occur are discussed. Monitoring serum lipid concentrations before and during estrogen therapy is recommended. Research suggests that patients who are over 40 years old or have family histories of hyperlipemia are at particular risk, and that estrogen therapy should be discontinued if pancreatitis occurs.
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PMID:Estrogen-induced pancreatitis. 688 34

Alpha-methyldopa-induced histologic alterations were investigated in 21 patients with hepatic injury after short- and long-term exposure. Seven patients developed liver injury within 6 months and 24 after several years (mean, 5 years) of exposure. Histologic findings and clinical and biochemical data differed significantly in the two groups. Morphologic analysis of the short-term-treated group revealed marked parenchymatous degeneration, focal, confluent and massive necrosis, and inflammation. Fatty accumulation and increased fibrous trabeculae were characteristic for the patients treated for long term. All patients in the short-term-exposed group had acute and severe hepatitis. Four of them had icterus. Two patients died of hepatic coma. Patients in the long-term-treated group had for several months initially mild but increasing discomfort, dyspepsia, nausea, and colics. Liver function tests in these groups revealed differences in serum albumin, bilirubin, and transferase levels. No changes were observed in alkaline phosphatase and Thrombotest. Fat accumulation and fibrous trabeculae suggest that the alterations precede the clinical symptoms and biochemical signs of hepatitis. The findings show that alpha-methyldopa may induce hepatocellular injury after short- and long-term exposure.
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PMID:Morphologic alterations in patients with alpha-methyldopa-induced liver damage after short- and long-term exposure. 732 15

Piroxantrone, a synthetic intercalating agent, was studied in patients with advanced, measurable gastric adenocarcinoma who had not received prior chemotherapy. The starting piroxantrone dose was 150 mg/m2 given intravenously over 1 hour on day 1 and repeated every 21 days. Response and toxicity could be evaluated in 15 patients. No complete, partial, or minor responses were observed. Toxic effects included granulocytopenia, anemia, vomiting, nausea, anorexia, fatigue, stomatitis, alopecia, hyperbilirubinemia, and increased alkaline phosphatase levels. At the stated dose and schedule, piroxantrone does not possess significant activity against advanced gastric cancer.
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PMID:Phase II trial of piroxantrone in metastatic gastric adenocarcinoma. 789 47

The objective of this study was to test the efficacy and safety of salmon calcitonin (sCT) suppository in post-menopausal women with previous hip fractures as an inhibitory agent of bone loss. The study was a single blind, randomized, and placebo-controlled trial comparing three parallel groups of patients. Fifty-four healthy women were randomly allocated to 1 year's treatment with either sCT 100 IU/6 times a week, 200 IU/3 times a week, or placebo/6 times a week. All groups received a calcium supplement of 500 mg daily. Fifteen patients left the study before its end, six of those due to adverse events, such as abdominal and rectal pain, nausea, headache, and diarrhea. Bone mineral density of the spine and the femoral neck was measured every 26 weeks, and biochemical markers of bone turnover were measured at baseline and week 12, 26, and 52. There were no significant changes in bone mineral density in the spine and in the hip in any of the treatment groups. No significant changes were observed in serum alkaline phosphatase, serum osteocalcin, urine hydroxyproline, and urine pyridinoline or deoxypyridinoline. Conclusively, we did not observe any significant effect on bone metabolism in women with postmenopausal osteoporosis after 1 year of treatment with sCT suppositories at the doses used.
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PMID:Effects of salmon calcitonin suppositories on bone mass and turnover in established osteoporosis. 811 46

We present a case of unknown fever and abnormal liver functions which developed during the course of pain management for herpes zoster with repeated epidural blocks with 0.5% lidocaine 10 ml. The patient was a 67 year old woman. At her first admission to dermatology, there were no abnormal findings in her blood examinations. She complained of severe pain from herpes zoster. She was admitted to the pain clinic. She received thoracic epidural blocks with 0.5% lidocaine 10 ml repeatedly three or four times a week. Two weeks later, she developed general fatigue, appetite loss, nausea and a high fever. Blood examinations revealed the elevation of glutamic oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), alkaline phosphatase (ALP), and gamma glutamyltrans peptidase (gamma-GTP), C reactive protein (CRP), and blood sedimentation rate (BSR). Many examinations including abdominal and thoracic computer tomography and abdominal echograph could not reveal the cause of high fever and abnormal blood examinations. We continued the thoracic epidural block for her herpes zoster pain. GOT, GPT, ALP, and gamma-GTP gradually went down to normal values in next two weeks, though fever still persisted. At this time, lymphocyte cell simulation test with 0.5 % lidocaine was positive and eosinophylic cell had increased to 5%. After ceasing the epidural block, fever resolved and blood examinations returned to normal values. These findings suggest strongly that 0.5% lidocaine induced fever and hepatitis.
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PMID:[Unknown fever and abnormal liver functions after repeated epidural blocks with lidocaine for management of herpes zoster pain]. 818 88

A 56-year-old white man was referred for evaluation of severe hypercalcemia following a three-week history of progressive weakness, nausea, and depression. Initial laboratory results showed serum total and ionized calcium (Ca++) values of 5.3 and 2.6 mmol/l, respectively. A short intact PTH assay was immediately performed and an extremely high value was obtained in just 30 min (1315 ng/l, normal values 6.4-70.4). The patient was therefore treated with saline solution and with salmon calcitonin (1200 IU/day, half by continuous i.v. infusion and half by i.m. route) for 10 days. There was a sudden decrease of both Ca++ and intact PTH during the first six days; then there was a trend to reach a steady-state until parathyroidectomy was performed. After withdrawal of calcitonin therapy it was possible to observe a positive uncoupling between bone formation (serum alkaline phosphatase and osteocalcin) and resorption (serum tartrate-resistant acid phosphatase) markers. On day 35 the patient underwent neck exploration, and an enlarged lower left parathyroid gland was removed that on macroscopic examination revealed the presence of a haemorrhagic cyst; microscopic appearance was suggestive of a previous glandular infarction. This is the first time the daily clinical course of a parathyroid crisis has been documented. Furthermore, changes of biomarkers of bone turnover following calcitonin therapy show that high doses of the hormone may cause a prolonged positive uncoupling of the two processes of bone remodeling.
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PMID:Parathyroid storm: immediate recognition and pathophysiological considerations. 826 42

Continuous regional delivery of chemotherapeutic agents offers the prospect of maximising dose intensity at the site of localised disease, while minimising systemic toxicity. This prospective phase II study evaluates the efficacy and toxicity of hepatic arterial infusion of 5-Fluorouracil (5-FU) via an implantable Infusaid pump in previously untreated patients with localised but unresectable hepatic metastases from colorectal cancer. In 25 patients the response rate was 56% and median survival was 15 months, comparable to previous reports utilising fluorodeoxyuridine (FUDR). Twenty per cent of patients (all responders) survived longer than three years. Systemic toxicity was trivial, and the practice of reducing the intensity of therapy when nausea or a rise in alkaline phosphatase occurred avoided the previously described local toxicity of biliary sclerosis seen frequently with FUDR. In selected patients, particularly those with more limited disease, this form of therapy is effective and well tolerated and warrants further evaluation as an alternative to FUDR.
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PMID:Continuous hepatic artery infusion of 5-fluorouracil for metastatic colorectal cancer localised to the liver. 846 Sep 71

Merbarone, NSC 336628, is an investigational anticancer drug with activity against experimental animal tumors including melanoma. This paper presents results of a Phase II clinical study of merbarone in patients with biopsy proven stage IV malignant melanoma without prior chemotherapy and with no evidence of CNS involvement. Thirty-five patients with median age 58 (range 27-81), with performance status 0-2 were treated with merbarone 1000 mg/m2/day for five days by intravenous continuous infusion repeated every 3 weeks. All patients (21 males and 14 females) were evaluable for toxicity. Two patients were not evaluable for response having been removed from protocol treatment due to toxicity and received other treatment during the first course of chemotherapy. Among the evaluable patients there was one complete response in a supraclavicular lymph node lasting four months and one partial liver response lasting three months. The remaining thirty-one patients were non-responders. Of these one had a stable disease lasting 21 months. The overall objective response rate was 6% (2/35) with a 95% confidence interval of 1%-19%. Twenty-six of the 35 patients have died. The estimated median survival of the entire group was 9 months with a 95% confidence interval six to eleven months. Renal toxicity was dose-limiting and manifested as increasing serum creatinine (54% of patients), proteinuria (51%) and hematuria (9%). One patient experienced grade 4 creatinine increase, proteinuria and acute renal failure. Other toxicities included nausea (71%), vomiting (51%0, malaise (23%), weakness (20%), alopecia (17%), diarrhea (17), anorexia (14%) transaminase (SGOT, SGPT) increase (14%), constipation (14%), alkaline phosphatase or 5'nucleotidase increase (9%), and fever (9%). Hematologic toxicity (granulocytopenia, leukopenia, and anemia) was generally mild and infrequent (29%, only one patient had grade 4 granulocytopenia). Overall 9 patients (26%) had at least one grade 3 toxicity. We conclude that merbarone at this dose and schedule has detectable but minimal activity in the treatment of metastatic malignant melanoma and given the significant renal toxicity this schedule does not merit further evaluation in this disease.
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PMID:Evaluation of merbarone (NSC 336628) in disseminated malignant melanoma. A Southwest Oncology Group study. 861 77

In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
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PMID:Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes. 898 49


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