Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative morphometric analyses of iliac crest biopsies from 20 epileptic patients receiving chronic anticonvulsant therapy have been performed before and after 4-8 months of vitamin D2 treatment with 9 000 U per day. Biochemical quantities, including serum 25-hydroxycholecalciferol (25-HCC) and serum parathyroid hormone (iPTH), were measured. The anticonvulsant osteomalacia found in the initial bone biopsies was characterized by an increased amount of ummineralized bone, an increased bone resorption and, contrary to vitamin D deficiency, an increased bone mineralization and bone formation. Bone resorption and bone formation were probably equally increased since the amount of cancellous bone was normal. Except for a slight increase in osteoidcovered surfaces and osteoclastic resorption surfaces, the bone changes were normalized after vitamin D2 treatment, leading to a mean serum level of 25-HCC 2.4 times above normal. Serum iPTH was normal before and unchanged during D2 therapy. The urinary calcium excretion remained decreased. The investigation characterizes anticonvulsant osteomalacia as a specific bone disease different from that of vitamin D deects of vitamin D metabolites on receptor cells.
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PMID:Effect of long-term vitamin D2 treatment on bone morphometry and biochemical values in anticonvulsant osteomalacia. 30 May 47

Serum 25-hydroxycholecalciferol (25-HCC) and serum parathyroid hormone (iPTH) were measured in 59 randomly selected adult epileptic outpatients receiving chronic anticonvulsant therapy. Quantitative morphometric analysis of iliac crest biopsies was performed. A mild degree of osteomalacia was found which was inversely correlated to dietary vitamin D intake. Serum 25-HCC was reduced in the epileptic patients compared to a control group, although dietary intake of vitamin D was higher than the mean daily intake in the Danish population. Serum 25-HCC was positively correlated to dietary vitamin D intake, but not correlated to the severity of bone changes, indicating that other factors than circulating 25-HCC are responsible for the development of anticonvulsant osteomalacia. Serum 25-HCG was inversely correlated to serum iPTH in patients with a low dietary calcium intake. The mean value of serum iPTH was not increased, and there was no correlation between serum iPTH and bone morphometry.
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PMID:The interrelationships between serum 25-hydroxycholecalciferol, serum parathyroid hormone and bone changes in anticonvulsant osteomalacia. 57 30

The seasonal variations in circulating 25-hydroxycholecalciferol (25-HCC) were studied in 102 alcoholics with fatty liver disease without histologic signs of cirrhosis and in 35 patients with alcoholic cirrhosis. The mean levels were compared with those of normal persons. Alcoholics had generally lower 25-HCC values than the controls, particularly in the summer. This was primarily explained by insufficient diet and reduced exposure to sunshine. The ability of the liver to hydroxylate in the 25-position was studied in three groups of alcoholics with 1) fatty liver disease without cirrhosis, 2) compensated cirrhosis, 3) severely incompensated liver cirrhosis. All three groups exhibited a significant increase in serum 25-HCC following the peroral administration of cholecalciferol at a dose of 1 200 U daily for 7 days. Similar rises were seen 7 days after a single injection of 10 000 U cholecalciferol. This indicates a normal intestinal absorption of vitamin D, even in advanced alcoholic liver disease, and is inconsistent with a severely damaged 25-hydroxylation capacity in these patients. Osteomalacia due to impaired liver hydroxylation of vitamin D can hardly explain the increased fracture rate and the decreased bone mass, which have been described in alcoholics.
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PMID:The hepatic conversion of vitamin D in alcoholics with varying degrees of liver affection. 91 Jun 39

A 61-year-old male with hepatocellular carcinoma (HCC) complicating liver cirrhosis presented hypophosphatemia progressing with HCC expansion and serum alpha-fetoprotein elevation. These changes were associated with an increased fractional excretion of phosphate and decreased theoretical phosphate threshold. There was increased nephrogenous cyclic adenosine monophosphate despite normal serum parathyroid hormone. Serum 1,25-dihydroxyvitamin D levels were markedly reduced with normal 25-hydroxyvitamin D levels. There were no symptoms of osteomalacia, however, a slightly increased osteoid seam was elicited on autopsy. The hypophosphatemia could be explained by presumed secretion from HCC of humoral factors which have a phosphaturic effect and also inhibit 25-hydroxyvitamin D-1 alpha-hydroxylase in renal tubular cells.
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PMID:Marked hypophosphatemia with decreased serum 1,25-dihydroxyvitamin D in a patient with hepatocellular carcinoma complicating liver cirrhosis. 171 78

Plasma levels of 25-hydroxycholecalciferol (25-HCC) were measured by a specific competitive protein-binding assay. Mean levels in both normal London adults and adolescent schoolchildren were 16 ng/ml and the mean level in a group of epileptic patients on high-dosage anticonvulsant therapy was 5 ng/ml, (difference from normals P < 0.001). Two further epileptic patients, with well-marked anticonvulsant osteomalacia, were treated with small doses of 25-HCC during full metabolic balance studies; rapid healing followed administration of 25-HCC by mouth in doses of 10-45 mug daily, which is well below the effective dose range of calciferol in this condition. These findings provided further evidence that anticonvulsant osteomalacia results from hepatic enzyme induction which, by increasing the metabolism of cholecalciferol to inactive compounds, lowers 25-HCC levels in patients whose dietary vitamin D intake and exposure to sunlight are otherwise adequate. Results also indicated that under certain circumstances 25-HCC may have considerably stronger antirachitic potency in man than has hitherto been recognized.
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PMID:Plasma levels and therapeutic effect of 25-hydroxycholecalciferol in epileptic patients taking anticonvulsant drugs. 434 60

Bone histology and its relationship with calcium metabolism was evaluated in adult patients with nephrotic syndrome: 29 had normal renal function (GFR 103 +/- 4 ml/min/1.73 m2) (group 1) and 20 had renal insufficiency (GFR 31 +/- 4 ml/min/1.73 m2) (group 2). In group 1, serum PTH, 1.25-HCC and 24.25-HCC levels were normal, while 25-HCC values were reduced. Bone histology was normal in 76% of the patients, while 17% had isolated osteomalacia and 7% an associated bone resorption. Group 2 showed a higher incidence of bone resorption when compared with a matched group of patients with renal failure and no proteinuria (40% vs. 13%) and a comparable frequency of isolated mineralization defect (25% vs. 34%). PTH levels were definitely increased and serum total calcium and all the vitamin D metabolites were reduced. A significant correlation between the apparent duration of the disease and the severity of osteodystrophy was found only in group 2. In conclusion, no constant derangement of calcium metabolism and bone histology is evident in patients with nephrotic syndrome and normal renal function, while patients with persistent proteinuria are at high risk of osteodystrophy even in the early phases of renal failure.
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PMID:Bone histology and calcium metabolism in patients with nephrotic syndrome and normal or reduced renal function. 673 66

Calcium metabolism was studied in 83 patients during eighteen months' rifampicin and isoniazid therapy for tuberculosis by measurements including calcium, alkaline phosphatase and 25-hydroxycholecalciferol (25-HCC). Five out of 52 Indian patients in the series were found to have osteomalacia, a prevalence probably no higher than in the Asian population in the UK at large. Moreover, osteomalacia responded to physiological supplementation with vitamin D. One European out of 31 had osteomalacia due to low vitamin D intake. Serum calcium was compared in 17 patients before and after six months of antituberculous chemotherapy but no significant difference was detected (P greater than 0.1). Two Indian patients were in positive calcium balance with low to normal plasma 25-HCC levels, indicating that an effect on 1,25 dihydroxyvitamin D activity during therapy was unlikely. It is concluded that rifampicin when combined with isoniazid has no significant effect on calcium metabolism over an eighteen-month treatment period.
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PMID:Calcium metabolism during rifampicin and isoniazid therapy for tuberculosis. 708 5

Adefovir-induced hypophosphatemic osteomalacia in the context of hepatocarcinoma is rare and needs to be differentiated from metastatic hepatocarcinoma. We here report a case of severe osteomalacia whose focal uptakes of radiotracer on the Tc-MDP SPECT/CT images mimicked that of metastatic hepatocarcinoma.
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PMID:Adefovir-Induced Hypophosphatemic Osteomalacia Mimicking Bone Metastases From Primary Hepatocarcinoma. 2871 45

A 68-year-old man with type 2 diabetes mellitus and chronic hepatitis B infection was referred to the nephrology department before planned surgery for hepatocellular carcinoma. He had been receiving low-dose adefovir dipivoxil (ADV) for 11 years. Laboratory findings revealed impaired re-absorption in the proximal renal tubules. He had been diagnosed with diabetic kidney disease and osteomalacia due to vitamin D deficiency; thus, ADV was not discontinued until he was referred to us. In this case, concomitant diabetes mellitus and vitamin D deficiency might have prevented the early diagnosis of ADV-induced Fanconi syndrome.
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PMID:Hypophosphatemic Osteomalacia Associated with Adefovir-induced Fanconi Syndrome Initially Diagnosed as Diabetic Kidney Disease and Vitamin D Deficiency. 3033 20