Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of lung cancer producing CA19-9 and amylase. A 58-year-old woman was admitted with dry cough and right chest pain. Chest X-ray and CT showed a mass shadow in the right lung field and right pleural effusion. Histological examination of a lung specimen obtained by TBLB and cytological examination of pleural effusion showed adenocarcinoma. The diagnosis of lung adenocarcinoma was made. CA19-9 values in serum and pleural effusion were very high. Amylase value was high in pleural effusion, but that in serum was normal. The amylase isozyme pattern was salivary-type. No abnormality was detected on abdominal CT and ultrasonography. In spite of treatment of the pleural effusion, the patient's condition gradually deteriorated and she died of respiratory failure. Histological examination of lung specimens obtained at necropsy showed moderately differentiated papillary type adenocarcinoma. Immunohistochemically, the tumor cells stained positively for both CA19-9 and amylase. We conclude that the lung cancer produced both CA19-9 and amylase.
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PMID:[A case of lung cancer producing CA19-9 and amylase]. 768 38

The patient was a 72-year-old man, who was admitted to our hospital because of cough. Chest X-rays showed a mass shadow in the right lower lung field. Amylase activities in serum and urine were extremely high. Amylase isozyme pattern identified salivary type amylase. Cytological examination of the sputum suggested adenocarcinoma. Amylase activities in serum and urine gradually decreased with the administration of chemotherapy. Afterwards, pleural effusion increased, and the amylase activity in pleural fluid was also extremely high. Pleural fluid also showed adenocarcinoma. Enzyme-labeled antibody method (PAP) on this specimen from pleural fluid proved that tumor cells were producing amylase ectopically.
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PMID:[A case of amylase producing lung cancer]. 768 22

A previously healthy 2-year-old boy was admitted because of shortness of breath, cough, and fever; there was minimal abdominal pain. He had recurrent right, followed by left pleural effusions, which contained markedly elevated amylase levels and high protein content. The pleural fluid amylase levels were disproportionately higher than the serum amylase levels. His abdominal signs were minimal. Surgical exploration showed a disruption of the proximal pancreatic duct. Distal pancreatectomy and Roux-en-Y pancreatico-jejunostomy were performed. After a complicated postoperative course he was discharged well and has remained so for more than 2 years.
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PMID:Pancreatic pleural effusion: an indication for emergency distal pancreatectomy and Roux-en-Y pancreatico-jejunostomy. 858 42

Swainsonine, an alpha-mannosidase inhibitor which blocks Golgi oligosaccharide processing, represents a new class of compounds that inhibit both rate of tumor growth, and metastasis, in murine experimental tumor models. In this first phase I study, the quantitative and qualitative toxicities of swainsonine have been studied in patients given a continuous i.v. infusion over 5 days, repeated at 28-day intervals. Dose levels were escalated in increments of 100 micrograms/kg/day from 50-550 micrograms/kg/day. Nineteen patients with both solid tumor and hematological malignancies were given a total of 31 courses. Hepatotoxicity, particularly in patients with liver metastases, was the dose-limiting toxicity. The maximum tolerated dose (MTD) and the recommended starting dose (MTD -1 level) were 550 and 450 micrograms/kg/day, respectively. Common side effects included edema, mild liver dysfunction, a rise in serum amylase, and decreased serum retinol. Acute respiratory distress syndrome possibly precipitated by swainsonine resulted in a treatment-related death in a patient with significant pretreatment hepatic dysfunction. One patient with head and neck cancer showed > 50% shrinkage of tumor mass for 6 weeks after treatment. Two patients with lymphangitis carcinomatosis on chest X-ray noted improvement in cough and shortness of breath during the infusion of swainsonine and for 1 week thereafter. Clearance and serum half-life for swainsonine were determined to be approximately 2 ml/h/kg, and 0.5 day, respectively. Golgi oligosaccharide processing, a putative anticancer target for swainsonine was inhibited in peripheral blood lymphocytes as evidenced by a marked decrease in leukoagglutinin binding after 5 days of treatment. Oligomannosides in patient urine increased 5-to 10-fold over the 5 days of treatment, indicating that tissue lysosomal alpha-mannosidases were also blocked by swainsonine. Urine oligomannoside accumulation reached steady state at 3 days, approximately 1 day after serum drug levels reached steady state. The fraction of HLA-DR-positive cells in peripheral blood lymphocytes increased following 5 days of swainsonine treatment, an effect similar to that observed for peripheral blood lymphocytes from normal subjects cultured with swainsonine. No significant changes in CD3, CD4, CD8, CD16, and CD25 were observed. Swainsonine produces minimal toxicity when administered i.v. to cancer patients at dosages that inhibit both Golgi alpha-mannosidase II and lysosomal alpha-mannosidases. Detection of hepatic metastases or liver enzyme abnormalities prior to treatment predict for more significant toxicity.
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PMID:A phase I study of swainsonine in patients with advanced malignancies. 813 47

A 22-year-old woman began to have the symptoms of anorexia, high fever, cough and general fatigue from June of 1997. She was admitted in our hospital on Aug. 8th, 1997 for the further detail examination because of pancytopenia and positive antinuclear antibody (ANA). Her laboratory findings and clinical symptoms were compatible with systemic lupus erythematosus (SLE) such as leukopenia, proteinuria, hypocomplementemia, positive ANA, elevated titer of autoantibodies including anti-DNA, anti-Sm, anti-RNP antibodies, polyarthralgia and photosensitivity. The administration of oral prednisolone (40 mg/day) was started on Aug. 15th, 1997 under the diagnosis of SLE. However, she had severe abdominal pain in epigastrium with elevated serum amylase, ascites and dull shape of pancreas tail by CT scan compatible with acute pancreatitis. On Aug. 18th, her general condition was worsening with fever, epigastralgia, abdominal distension, anemia, weak palpation of radial artery, hypotension, tachycardia, shallow breathing and cold sensation on both extremities as shock. In spite of steroid pulse therapy with nafamostat mesilate intraarterial infusion, her condition was not improved. The dose of 50 mg/day of cyclophosphamide was added to the regimen on Aug. 22nd. Then, gradually her condition started to be restored. Anemia, leukopenia, hypocomplementemia continued. Second steroid pulse therapy was done on Sep. 5th. After then, she became better in her clinical symptoms and laboratory data. The dose of PSL was tapered to 15 mg/day and 7.5 mg/day update of Oct. 1998 without the pseudcysts found after pancreatitis. She is a rare case who recovered from severe acute pancreatitis due to SLE itself.
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PMID:[A case of systemic lupus erythematosus associated with severe acute pancreatitis]. 1043 57

In recent years, chronic massive pleural effusions have been increasingly recognized as a serious complication of pancreatitis. We describe the third reported case of a pancreatic pleural effusion accompanied by bronchopleural fistula. A 49-year-old man suffering from chronic alcohol-related pancreatitis was admitted to our hospital complaining of cough and shortness of breath. A chest x-ray film disclosed a large right pleural effusion with an air-fluid level. Ultrasonography and computed tomography of the upper abdomen demonstrated a giant pancreatic pseudocyst in the pancreatic tail and a fistulous tract reaching into the posterior mediastinum via the esophageal hiatus. Thoracentesis revealed sterile hemorrhagic fluid with markedly elevated amylase activity of 20,955 IU/l (pancreatic isozyme, 100%) and no malignant cells. A diagnosis of pancreatic pleural effusion was made. The therapy for pancreatic internal fistula is somewhat controversial. We employed conservative therapy, including hyperalimentation and chest tube drainage that successfully decreased the pleural effusion and closed the fistulous tract. Nonetheless, we were still troubled by a continuous air-leak via the drainage tube. Pleurodesis confirmed the tentative diagnosis of bronchopleural fistula and successfully stopped the air-leak. No re-accumulation of pleural effusion has been seen for 2 years. We concluded that pancreatic enzyme-rich effusions, if long-standing, may be complicated by bronchopleural fistula, thus underscoring the need for urgent drainage and initially conservative management.
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PMID:[Pancreatic pleural effusion accompanied by bronchopleural fistula]. 1049 9

We report two patients who were long-time habitual consumers of alcohol and suffered from thoracopancreatic fistula. The first patient, a 52-year-old man with no symptoms, underwent chest CT scan for a medical check-up and was revealed to have left small pleural effusion. A month later, he suddenly experienced severe cough and back pain. The immediate CT scan showed massive pleural effusion and mediastinal pseudocyst, and the amylase level in the aspirated pleural effusion proved to be elevated. He was successfully treated with medication and drainage of the effusion. The second patient, a 39-year-old woman, underwent CT scan for a medical check-up, and it disclosed that she had a small pleural effusion in the left lower thorax. Follow-up CT two months later revealed the pleural effusion to be resolved, however, it demonstrated that a narrow tract derived from the pancreatic secretion located just posterior to the pancreatic tail extended to the mediastinum along the left hemidiaphragmatic crus. She experienced severe cough and sputum four months later. CT scan showed massive pleural effusion in the left thorax and revealed that the pancreaticopleural fistula was located in the same position as the small tract that had been detected by the previous CT scan. The patient received conservative treatment and eventually recovered from the severe chest complications. We consider that asymptomatic left small pleural effusion in these patients who were habitual drinkers is a potential precursor to symptomatic pancreatitis. The patients developed mediastinal pseudocyst and pancreaticopleural fistula in association with chronic pancreatitis within a few months, and therefore intensive follow-up should be undertaken to minimize or prevent chest complications in association with the subsequent symptomatic pancreatitis.
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PMID:Two cases of thoracopancreatic fistula in alcoholic pancreatitis: clinical and CT findings. 1229 38

In three patients, a 44-year-old schizophrenic woman and two men aged 54 and 42, who presented with dyspnoea, a pancreaticopleural fistula was diagnosed as a complication of pancreatitis, i.e. a fistulous tract between the pancreas and the pleural cavity. In general, these fistulas have a good prognosis; however, delay in finding the correct diagnosis influences the prognosis. This is often due to unfamiliarity with the disease and the non-specific presentation of patients with pleural effusion. The initial presentation usually comprises respiratory (dyspnoea, coughing due to pleural effusion) and occasional abdominal symptoms (epigastric pain). A definitive diagnosis is made when elevated pleural effusion amylase levels are demonstrated. Surgical treatment is only indicated if conservative or endoscopic treatment fails, and consists of resection of the fistula and drainage of the pancreatic duct via a lateral pancreaticojejunostomy or resection of the part of the pancreas where the fistula originates. In the first patient, surgical drainage of the fluid accumulation was applied, but she died of aspiration pneumonia after she had removed the feeding tube and had refused further treatment. Pancreatic resection resulted in recovery in the two men.
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PMID:[Pleural fluid in chronic pancreatitis]. 1290 43

Inhalation of dust from different enzymes can be the cause of occupational asthma in exposed workers. Enzymes from different sources are being increasingly used in food. Few cases of food allergy to alpha-amylase induced by eating bread have been reported. Those cases were reported in bakery-related patients and in a pharmaceutical-industry worker. A 25-year-old farmer suffered sneezing, rhinorrhea, oropharyngeal itching, hoarseness, cough, and non-wheezy dyspnea after eating white bread. Skin prick tests (SPT) with common aeroallergens and food allergens revealed only sensitization to Olea europaea pollen. SPT response was positive to Aspergillus oryzae alpha-amylase. Specific IgE against alpha-amylase was positive. A double-blind placebo-controlled challenge with 5 mg of uncooked -amylase induced sneezing, cough, oral angioedema within 10 minutes. The provocation test with 50 g of white bread gave similar findings. This case indicates that alpha-amylase contained in bread may provoke IgE-mediated food allergy. It is worth noting that in this case, the only source of alpha-amylases sensitization was bread.
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PMID:Bread eating induced oral angioedema due to alpha-amylase allergy. 1573 22

Glucantime is the firstline treatment for cutaneous leishmaniasis in Tunisia. Adverse effects related to systemic administration of Glucantime are frequent. The purpose of this retrospective study was to review the files of 53 patients who were treated for cutaneous leishmaniasis using meglumine antimoniate at a dose of 60 mg/kg/day for 15 days during the period between 1998 and 2007. Adverse effects were observed in 5 men and 4 women with an average age of 40.8 years. Antimony intolerance occurred in 8 patients and stibio-intoxication occurred in 4. Glucantime was considered as the most likely cause of adverse effects in 6 patients and as the plausible cause in 3 patients. Fever was the most frequent complication of antimony intolerance followed by cough, myalgia, and cutaneous lesions. Hepatic cytolysis was the most frequent sign of stibio-intoxication. Asymptomatic elevation of amylase level to 108 UI/l was observed in one case. The most serious complication was acute toxic kidney failure on the 15th day of treatment. The incidence of adverse events to Glucantime ranges from 16% to 59%. The most severe complication is acute renal failure on the 15th day of treatment, as observed in one patient in this series. Patient status must be monitored by performing laboratory tests at the beginning and end of the treatment. Since cutaneous leishmaniasis observed in Tunisia is a self-healing dermatosis that never results in sequels, treatment with Glucantime should be discontinued in any patient who develops suspicious symptoms.
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PMID:[Adverse events related to systemic treatment using Glucantime for cutaneous leishmaniasis: a report from Tunisia]. 1906 83


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