Polyamines in blood-cells as cancer markers.
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Adult↗
Biomedical subjects
M R Wills
Publications and source records attributed to M R Wills.
The response to 1,25-dihydroxycholecalciferol and to dihydrotachysterol in adult-onset hypophosphataemic osteomalacia.
The biochemical changes observed in a patient with adult-onset hypophosphataemic osteomalacia after three weeks treatment with 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) followed by dihydrotachysterol (DHT) are reported. The treatment with 1,25-(OH)2D3 resulted in restoration of intestinal phosphate absorption to normal with a small rise in plasma phosphate concentration; there was no significant change in tubular reabsorption of phosphate. The tubular reabsorption of bicarbonate, which was initially low, returned almost into the normal range with normalisation of plasma bicarbonate concentration. Aminoaciduria decreased. There were no changes in plasma or urinary calcium but immunoreactive parathyroid hormone (i-PTH) which was initially elevated fell but still remained above the normal range. These changes were maintained after replacing the 1,25-(OH)2D3 treatment with dihydrotachysterol (DHT).
Amino Acids↗
Intestinal absorption of cholecalciferol in alcoholic liver disease and primary biliary cirrhosis.
The intestinal absorption of (3H)cholecalciferol was studied in five patients with alcoholic liver disease, six patients with primary biliary cirrhosis, and 15 healthy subjects. The rate of appearance in plasma of (3H)cholecalciferol after oral ingestion and the subsequent appearance of (3H) polar metabolites in the alcoholic subjects were similar to those in the healthy subjects. In subjects with primary biliary cirrhosis the rate of appearance in plasma of (3H)cholecalciferol was significantly reduced. The rate of appearance of labelled polar metabolites of cholecalciferol was also lower in this group, suggesting that increased removal of labelled vitamin by conversion into more polar metabolites could not account for the reduced plasma (3H)cholecalciferol response. It is suggested that intestinal absorption of cholecalciferol is usually normal in alcoholic liver disease but impaired in primary biliary cirrhosis. Hepatic 25-hydroxylation is normal in alcoholic liver disease but may be defective in primary biliary cirrhosis.
Adult↗
Performance assessment of the GammafloTM automated radioimmunoassay system by assaying for digoxin.
We report an evaluation of the GammafloTM automated continuous-flow radioimmunoassay instrument in which we used a digoxin assay to assess system performance. System operation was based on combined continuous-flow and column-chromatographic techniques. No drift or carryover was detectable in 180 within-assay consecutive determinations performed at a rate of 42 determinations per hour (5 h of continuous operation). Within-assay and between-assay precision were less than 6% (coefficient of variation). The automated method correlated well (r = 0.960 and 0.952, respectively) with two established manual digoxin radioimmunoassay procedures. The data suggest this automated system offers a valid alternative to manual radioimmunoassay procedures in terms of overall precision, simplicity of operation, and sample throughout capacity.
Autoanalysis↗
Immunonephelometric assay for urinary total protein and albumin in mice.
A quantitative immunonephelometric assay for measuring total protein and albumin in mouse urine has been developed. Antisera to whole mouse sera or to mouse albumin was added to aliquots of urine and the antigen-antibody complexes formed were measured by laser nephelometry. Sample volumes were small (20 microliters) and the assay time was 90 minutes. The assays were sensitive to 10 mg/L and within-day and day-to-day precision studies demonstrated coefficients of variation of less than 15%. Average urinary total protein and albumin concentrations for random urine specimens in female C3H mice (age 80-150 days) were 42 and 24 mg/L respectively. Urinary total protein and albumin to creatinine ratios were also determined.
Albuminuria↗
Hypercalcemia associated with chronic lymphocytic leukemia.
A patient with chronic lymphocytic leukemia (CLL) is described in whom hypercalcemia occurred in association with elevation of the peripheral lymphocyte count and expansion of total tumor mass. Hypercalcemia was ameliorated with the institution of chemotherapy for the leukemic process and subsequent fall in WBC count and decrease in total tumor burden; hypercalcemia recurred with relapse of the leukemic process. The serum immunoreactive parathyroid hormone (iPTH) concentration, when measured, was inappropriately elevated for the degree of hypercalcemia. The hypercalcemia would appear to be a direct consequence of the leukemia, and possibly involved secretion of a parathyroid hormone-like polypeptide by the CLL cells. Although a possible role for either an osteoclast-activating substance or prostaglandins was not excluded, they would not account for the elevated serum iPTH levels observed.
Aged↗
Serum binding of aluminum.
The binding of aluminum in the serum of a normal male volunteer was examined using gel filtration chromatography and flameless atomic absorption spectrometry. The elution profile obtained with Sephacryl S-200 gel separated the aluminum into four major peaks. These peaks appear to be associated with a high molecular weight protein(s), albumin, and possibly some low molecular weight protein(s) and/or some inorganic anions. The elution profile for a renal dialysis patient gave similar results.
Adult↗
Phosphate metabolism in chronic liver disease.
Phosphate metabolism was investigated in 26 patients with a spectrum of liver diseases and mean fasting plasma phosphate concentrations were in the low normal range. A standard oral load of phosphate was used to test absorption and was subnormal in the majority of patients with large bile-duct obstruction and alcoholic liver disease. Subnormal results were also seen in patients with primary biliary cirrhosis and cirrhosis secondary to chronic active hepatitis. These abnormalities appeared to be related to vitamin-D deficiency. Tubular reabsorption of phosohate was markedly reduced in 3 of 14 patients. The therapeutic implications of phosphate status in liver disease are important.
Absorption↗
Formation of vitamin D metabolites from 3H- and 14C-radiolabelled vitamin D-3 in chronic liver diseases.
Four of the eight patients studied were vitamin D replete and 4 vitamin D depleted as judged by serum 25-hydroxy vitamin D (25-OHD) concentration. Three of the 4 vitamin D depleted patients (including 2 with histological osteomalacia) formed radioactive 1,25-dihydroxycholecalciferol. One of the four vitamin D replete patients formed 1,25-dihydroxycholecalciferol but all formed 24,25-dihydroxycholecalciferol. This study suggests that patients with liver disease form dihydroxy vitamin D metabolites in an appropriate manner.
Adult↗
Long-term effects of small doses of 1,25-dihydroxycholecalciferol in renal osteodystrophy.
An oral dose of 0.5 microgram of 1,25-dihydroxycholecalciferol (1,25-[OH]2D3) and 4 g of calcium carbonate was given daily to two dialysed patients and three undialysed patients in chronic renal failure with renal osteodystrophy. Treatment was given for 4-16 months. Intestinal calcium absorption became normal in all five patients. Plasma alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone were considerably reduced in all of the patients and in four of them these values were restored to normal. Bone histology was improved in all patients after treatment with 1,25-(OH)2D3. As well as a dramatic improvement in bone mineralisation, there was remodeling of trabecular architecture and a decrease in fibrosis in patients with initial parathyroid overactivity.
Administration, Oral↗
Plasma calcium and magnesium fractions in liver disease.
Plasma calcium and magnesium fractions were measured in 51 patients with either hepatocellular or biliary disease. The fractions were found to be only minimally deranged. Plasma albumin correlated with total calcium and with the protein bound and ionized fractions. Abnormalities of plasma calcium or magnesium fractions are unlikely to play a role in the pathogenesis of the osteomalacia seen in chronic biliary disease.
Adult↗
Parenteral 1,25-dihydroxycholecalciferol in hepatic osteomalacia.
Despite regular long-term parenteral vitamin D2 treatment, four patients with biliary cirrhosis had multiple symptoms of bone disease and bone biopsy specimens showed osteomalacia without osteoporosis. Three patients also had a proximal myopathy. Plasma calcium values (after correction for albumin), phosphorus, magnesium, and serum 25-hydroxy-vitamin D were within normal limits. Treatment with 1,25-dihydroxy-cholecalciferol (1,25-(OH)2D3) relieved symptoms in three of the four patients and improved those in the fourth. Histological examination of bone showed improvement in all four patients, but serum and urinary biochemical changes were not pronounced. We conclude that 1,25-(0H)2D3 treatment has a beneficial effect on bone and muscle in hepatic osteomalacia, either because vitamin D 1-hydroxylation fails in biliary cirrhosis or because hepatic osteomalacia is resistant to vitamin D2 metabolites.
Aged↗
Changes in ionized calcium and other plasma constituents associated with cardiopulmonary bypass.
Plasma concentrations of calcium fractions, proteins, phosphate and magnesium were measured before, during and after cardiopulmonary bypass in 15 patients undergoing cardiac surgery. When calcium chloride was added to a pump priming solution which contained little or no blood, the concentrations of all calcium fractions were significantly greater after bypass than before, with a mean ionized calcium concentration of 1.52 mmol litre-1 plasma water, 30 min after completion of bypass. This iatrogenic hypercalcaemia was increased significantly by the administration of more than 10 mg kg-1 calcium chloride in the first 30 min after bypass. Other plasma constituents showed the dilutional effect of the pump prime during bypass and only the magnesium concentration failed to return towards normal values after operation.
Adolescent↗
Clinical, biochemical, and histological studies of osteomalacia, osteoporosis, and parathyroid function in chronic liver disease.
Twenty of 32 patients with either chronic cholestatic or hepatocellular liver disease had bone pain or recent fractures. On bone biopsy five patients had normal bone, 15 had osteomalacia, five had osteoporosis, and seven had a combination of osteomalacia and osteoporosis. In the presence of osteoporosis, osteomalacia was minimal or absent. There was no biochemical, radiological, or histological evidence of excess parathyroid activity. No significant correlations were demonstrated between the plasma and urinary biochemical findings and the presence of either osteoporosis or osteomalacia and bone biopsy was essential for correct diagnosis. There was no statistical relationship between low serum 25-hydroxy vitamin D values and the presence of osteomalacia. Bone disease was not prevented by regular intramuscular vitamin D2, although biochemical changes were improved. Drugs such as corticosteroids and cholestyramine may be important aetiological factors in hepatic osteodystrophy.
Adult↗
Serum prolactin in liver disease and its relationship to gynaecomastia.
Serum immunoreactive prolactin was measured in 150 patients with liver disease of varying aetiology and severity and in 45 control subjects. The upper limit of the reference range for serum prolactin was 331 mU/l. Eighteen patients with liver disease (12%) had unexplained hyperprolactinaemia. No relationship existed between the prolactin value and the sex of the patient, the aetiology of the liver disease, the severity of the liver disease, or the presence of gynaecomastia. The cause of the hyperprolactinaemia in patients with liver disease and its clinical implications need further investigation.
Fatty Liver, Alcoholic↗
Hepatic osteodystrophy.
Hepatic osteodystrophy consists of three types: osteomalacia, osteoporosis, and periosteal reaction with new bone formation. Secondary hyperparathyroidism is very rare, if it occurs at all. The cause of osteomalacia appears to be vitamin D deficiency due to a lack of vitamin D substrate. In the presence of adequate substrates, 25-OHD and dihydroxy vitamin D metabolites are formed. The vitamin D deficiency results in osteomalacia and malabsorption of calcium and phosphorus. The osteomalacia can be treated successfully with vitamin D supplements. In some patients calcium, phosphorus, and magnesium supplements may be required. The aetiology and treatment of the osteoporosis and the periosteal reactions remain obscure.
Bone and Bones↗
Serum 25-hydroxyvitamin D assay. Evalution of chromatographic and non-chromatographic procedures.
A competitive protein binding assay for serum 25-hydroxyvitamin D is described in which normal human serum is used as the source of binding protein. A serum sample is extracted with diethyl ether/methanol and then chromatographed using silica gel. Validation of the method is reported. Silica gel chromatography is compared with LH20 chromatography. The method is also compared with extraction techniques using diethyl ether and ethanol without subsequent chromatography. It is concluded that chromatography with either silica gel or LH20 is essential. The non-chromatographic methods investigated, in addition to giving much higher values than chromatographic methods, did not meet validation requirements with respect to accuracy and behaviour of samples on dilution.
Chromatography, Gel↗