Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate geographical differences in the liver pathology of ducks infected with duck hepatitis B virus (DHBV), ducks in Chiba and Shimane, Japan, and Shanghai, China, were investigated. The numbers (DHBV positive/negative) and the maximum age of the ducks examined were 18/10 at 19 mo, 15/1 at 3 yr 4 mo, and 72/27 at 18 mo, respectively. DHBV infection was induced experimentally in ducks from Chiba and Shimane but was present congenitally in those from Shanghai. Ducks were examined regarding liver function tests, conventional histology, immunohistology, electron microscopy, and molecular hybridization for DHBV DNA in the serum and liver. There was no significant difference between DHBV-positive and -negative ducks in bilirubin and transaminase and alkaline phosphatase activities in the sera. Histologically, while the livers of ducks from Chiba and Shimane did not show necroinflammatory (hepatitis) activity, those from Shanghai frequently did (52.5%). Necroinflammatory activity of the Shanghai ducks was present almost equally in both DHBV-positive and -negative livers. The livers of Shanghai ducks but not the other two areas often (8.3%) had ground-glass inclusions which corresponded ultrastructurally to numerous virus particles in the dilated cisternae of the proliferated endoplasmic reticulum. No advanced liver disease, such as cirrhosis or hepatocellular carcinoma, was observed. There was no significant difference in the amount of DHBV DNA in the sera or in its pattern in the liver tissue among ducks of the three areas. In addition, the livers of Chiba ducks frequently had amyloidosis, while those of Shanghai ducks were contaminated with parasites. In conclusion, DHBV infection did not appear to provoke significant hepatitis activity or advanced liver disease in the examined ducks of all three areas, and the DHBV-positive livers from Shanghai ducks showed a different morphological appearance from those of the other two areas. This variation might reflect the difference in the strain of ducks, subtypes of DHBV, environmental factors, or a combination of these influences.
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PMID:Geographical pathology of duck livers infected with duck hepatitis B virus from Chiba and Shimane in Japan and Shanghai in China. 334 10

I treated a patient who had amyloidosis with predominantly hepatic involvement and portal hypertension. The main clinical features were hepatomegaly, gross ascites, proteinuria, and elevated alkaline phosphatase levels. Despite permanganate-sensitive AA protein being present in the biopsy specimen, none of the recognized disease entities associated with secondary amyloidosis were found. A review of the literature and the mechanism of portal hypertension in amyloidosis is given. It is suggested that elevated portal pressures may be of greater importance in the pathogenesis of ascites in amyloidosis than has been appreciated.
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PMID:Hepatic amyloidosis. An unusual cause of ascites and portal hypertension. 649 30

Secondary amyloidosis was diagnosed in five Rhesus monkeys with chronic indwelling venous catheters. Diagnostic enzymology demonstrated normal serum alanine aminotransferase concentration and consistently elevated serum alkaline phosphatase. Serum protein electrophoresis on all five animals showed a typical pattern of decreased albumin and increased gamma globulin. Necropsy or biopsy specimens verified the presence of amyloid deposits in all animals. The diagnostic usefulness of clinical enzymology, serum protein electrophoresis and liver biopsy were demonstrated and the importance of considering amyloidosis as a differential diagnosis in monkeys with indwelling vascular catheters is emphasized.
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PMID:Secondary amyloidosis in rhesus monkeys with chronic indwelling venous catheters. 651 13

A 37-year-old woman with amyloidosis derived from light chain immunoglobulin had hepatosplenomegaly, elevated serum alkaline phosphatase values, and progressively destructive bony lesions. A 44-month intermittent course of chemotherapy with melphalan and prednisone resulted in regression, confirming the occasional efficacy of cytotoxic chemotherapy in this disease.
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PMID:Objective response in amyloidosis treated with intermittent chemotherapy. 672 58

Fifteen patients on regular dialytic treatment for more than 15 years were given X-rays of the skull, spine, shoulders, wrists, pelvis and knees with the purpose of studying the principal skeletal and articular alterations due or not due to the uraemic status. Serum calcium, phosphorus, parathyroid hormone, alkaline phosphatase and basal aluminium were recorded. Osteopenia was evident in all the patients. Ten of whom (67%) showed alterations due to hyperparathyroidism. Nine patients presented the marks of dialysis spondyloarthropathy; in 14/15 cases geodes were present in the wrists, humeral heads or hip-joints; in ten patients there were multiple amyloid lesions. Two patients with serum basal aluminum above 100 micrograms/L showed the typical radiographic marks of osteomalacia. The majority of the long-term survivors showed multifactorial osteo-articular alterations resulting mainly from the combination of hyperparathyroidism and dialysis-related amyloidosis. The less frequent joint alterations were represented by arthrosis, enthesopathy and chondrocalcinosis. Disability and decreased articular mobility resulted in being mainly due to amyloid osteo-arthropathy.
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PMID:Clinical and radiological features of bone disease in long-term (15 or more years) hemodialysis patients. 812 16

Systemic amyloidosis presenting with jaundice is rare. A case of primary amyloidosis presenting with severe intrahepatic cholestasis is reported. The patient had hepatomegaly, ascites, and a markedly elevated serum alkaline phosphatase level. He had a rapid downhill course resulting in death. Autopsy showed evidence of amyloidosis involving multiple organs, including the liver, kidney, and heart.
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PMID:Hepatic amyloidosis presenting with severe intrahepatic cholestasis. 925 70

Large tendon rupture is a rare catastrophic occurrence in dialysis patients. Pathogenesis of this has been variably thought to be due to malnutrition, insufficient dialysis, amyloidosis, chronic acidosis, or hyperparathyroidism. We investigated contributory causes and timing of this complication in 44 dialysis patients (42 hemodialysis and two peritoneal dialysis patients). Five cases were our own; the other 39 were reported in the literature during the last two decades. Data were compared with a hospital database of 916 patients. The patients who experienced tendon ruptures had been on dialysis longer (mean duration, 7.6 years v 4.0 years; P = 0.001), were younger (mean age, 39.7 years v 48.4 years; P = 0.0001), had much higher parathyroid hormone levels (1,802 pg/mL v 202 pg/mL; P = 0.0001), had a higher phosphate level (6.8 mg/dL v 5.9 mg/dL; P = 0.001), had a slightly higher calcium level (9.2 mg/dL v 8.8 mg/dL; P = 0.038), and had a higher alkaline phosphatase level (649 IU/L v 109 IU/L; P = 0.0001) than control patients. Patients with tendon ruptures had no evidence of malnutrition (albumin 3.7 g/dL v 3.8 g/dL; P = 0.237) and had the same acidosis (bicarbonate 22.2 mEq/L v 22.0 mEq/L; P = 0.180). The time on dialysis to rupture was inversely related to the patient's age (r = 0.47, P = 0.004). Most patients had evidence of years of poorly controlled hyperparathyroidism with high and increasing levels of parathyroid hormone and alkaline phosphatase. Previous steroid use was also much more common in patients with tendon ruptures, as was radiographic evidence of osteitis fibrosa. The disease led to long hospitalization and prolonged morbidity, with mobility limitations in several patients. Spontaneous large tendon rupture in patients is secondary to hyperparathyroidism; is more common in young patients, particularly if exposed to corticosteroids; leads to long-lasting morbidity; and should be preventable by better supervision and treatment of hyperparathyroidism.
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PMID:Spontaneous tendon ruptures in patients on chronic dialysis. 918 88

The purpose of this study was to assess prognostic factors and survival in patients with liver involvement in immunoglobulin light-chain amyloidosis. Comparisons were made with other patients with immunoglobulin light-chain amyloidosis who did not have liver involvement. A total of 77 consecutively seen patients were evaluated: 19 had hepatic amyloidosis and 58 had amyloidosis without liver involvement. Eighteen of 19 patients with liver amyloidosis could be histologically diagnosed without needle biopsy of the liver. All but 2 had a detectable free light chain in the serum or urine, distinguishing this from other infiltrative liver processes. Patients with liver amyloid had significantly higher alkaline phosphatase levels and C-reactive protein levels compared with patients without hepatic amyloid. The majority of patients had extrahepatic involvement predominantly in the kidney (47%) or heart (42%). The presence of hyposplenism was not a good screening test for the presence of hepatic amyloid. Seven of 19 patients responded to chemotherapy with objective regressions of the clinical manifestations of renal, hepatic, or cardiac involvement. We conclude that the survival of patients with liver involvement in amyloidosis is no different than other patients with amyloidosis. This results from the high proportion of patients having associated renal or cardiac involvement. Most patients can be diagnosed without a liver biopsy when a monoclonal protein is found in the serum or urine. Serum albumin and C-reactive protein levels appear to distinguish patients with liver involvement from those without.
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PMID:Hepatic amyloidosis: clinical appraisal in 77 patients. 898 76

Although the involvement of the liver is common in systemic amyloidosis (AL), clinical features of hepatic dysfunction and liver chemistry abnormalities are often mild or absent. A mild increase in the serum alkaline phosphatase value is the most common finding. Hypertransaminasemia, hyperbilirubinemia, and portal hypertension with ascites and gastroesophageal varices occur late in the course of the disease and predict a short survival. We describe the case of a 58-year-old woman with AL, whose dramatic and unusual clinical picture, consisting of giant hepatomegaly, hypertransaminasemia, increase in alkaline phosphatase, esophageal varices, and ascites, was rapidly complicated by severe obstructive cholestasis.
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PMID:Primary systemic amyloidosis with giant hepatomegaly and a swiftly progressive course. 917 38

We retrospectively investigated the feasibility and the toxicity of autologous stem cell transplantation (ASCT) in 21 cases of systemic amyloidosis (AL). The conditioning regimens consisted of high-dose melphalan (HDM) alone (n = 18) or in combination with 12 Gy total body irradiation (n = 3). Toxic death rate was high: 9/21 patients (43%) died within the first month following ASCT, and 10/12 surviving patients achieved a response. With a median follow-up of 14 months, the OS and the EFS rates at 4 years were 57.1% (+/-10.8) and 29.9% (+/-14.5) respectively for the whole group. The major prognostic factor for both response and survival was the number of clinical manifestations at the time of ASCT, of the following five criteria, i.e. creatinine clearance < 30 ml/min, nephrotic syndrome with urinary protein excretion > 3000 mg/24 h, congestive heart failure, neuropathy, or hepatomegaly associated with alkaline phosphatase level > 200 IU/l. For patients presenting with two or more clinical manifestations the 4-year OS and EFS were both 11.1% compared with 91.7% and 46.3% respectively in patients with fewer than two clinical manifestations at the time of ACST. We conclude that ASCT is feasible in AL in a subset of patients with fewer than two clinical manifestations at the time of ASCT. Given the severe extra-haematological toxicity, ASCT should not be considered in other cases.
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PMID:Prognostic factors for survival and response after high-dose therapy and autologous stem cell transplantation in systemic AL amyloidosis: a report on 21 patients. 967 53


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