The role of government in preventive medicine.
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Environmental Health↗
Biomedical subjects
G A Rose
Publications and source records attributed to G A Rose.
Plasma oxalate and creatinine and oxalate/creatinine clearance ratios in normal subjects and in primary hyperoxaluria. Evidence for renal hyperoxaluria.
Plasma oxalate and creatinine were measured repeatedly in healthy individuals and in 12 patients with type 1 primary hyperoxaluria unresponsive to pyridoxine. The mean ratios were 0.025 (SD 0.006) and 0.120 (SD 0.048), respectively. One patient repeatedly had normal plasma oxalate despite markedly raised urinary oxalate and it seems unlikely that this excess oxalate could have come from the liver. Oxalate/creatinine clearance ratios in the normal group had an overall mean of 0.59 (SD 0.27) in 24 h urine collections and 0.741 (SD 0.297) in repeated short clearance periods. Both renal tubular absorption and secretion of oxalate apparently occurred on different days, but this did not depend upon urinary flow rate. Oxalate/creatinine clearance ratios in type 1 primary hyperoxaluria had a mean of 2.88 (SD 3.11). The raised oxalate/creatinine clearance ratios in the patients were not correlated with either plasma oxalate or creatinine. A few patients showed much higher clearance ratios and in some were sufficiently high to indicate that oxalate was generated and secreted in the kidneys.
Creatinine↗
Effects of oral pyridoxine upon plasma and 24-hour urinary oxalate levels in normal subjects and stone formers with idiopathic hypercalciuria.
The effect of pyridoxine hydrochloride, 200 mg/day (0.97 mmol/day) for 3 weeks, upon plasma and urinary oxalate has been determined in ten normal subjects and seven patients with idiopathic hypercalciuria while both groups were on low-oxalate diets. Patients had higher basal urinary oxalate levels than normal subjects. In normal subjects pyridoxine administration decreased plasma oxalate levels and raised urinary oxalate. The patients showed no change in either plasma or urinary oxalate.
Calcium↗
Excessive urinary oxalate excretion after combined renal and hepatic transplantation for correction of hyperoxaluria type 1.
A 4.5-year-old boy received a combined liver and kidney transplant for correction of hyperoxaluria type 1. Both organs were from the same donor and functioned primarily. Three months after transplantation, urine oxalate excretion reached a maximum of 10,500 mumol/24 h and remained above 2300 mumol/24 h for the next 2 months. Two months later, oxalate excretion decreased to about 565 mumol/24 h, indicating exhaustion of a large oxalate pool. Six months after transplantation plasma oxalate is near normal (4.9 mumol/l). With the exception of one episode of acute rejection of the renal transplant, both organs were tolerated well and continue to have a unimpaired function 9 months after transplantation. However, there is increased echogenity on renal ultrasound, indicating oxalate deposits in the grafted kidney. This case illustrates that successful combined transplantation of both liver and kidney can be performed in infants, resulting in cure of the metabolic defect. The prolonged or acute excretion of oxalate may lead to oxalate deposition in the grafted kidney without impaired graft function or early graft loss.
Child, Preschool↗
Liquid chromatographic studies of vitamin B6 metabolism in man.
The effects of increased intake of pyridoxine hydrochloride on plasma vitamin B6 metabolism within therapeutic limits (up to 800 mg/day) were investigated. Maximum plasma concentrations of pyridoxal phosphate were attained at relatively low intakes of pyridoxine hydrochloride. Two metabolism thought to be unidentified forms of vitamin B6 were present in subjects taking more than 200 mg of pyridoxine hydrochloride per day as have recently been described. We investigated the possibility that these were isomeric forms of vitamin B6. However, 'Peak 2' metabolite was shown to be probably 4-pyridoxolactone. The metabolism of isopyridoxal has not previously been investigated in man. We demonstrated that it is an active vitamer of the B6 complex in humans. The main fluorescent metabolite of isopyridoxal present in plasma and urine had a similar retention time to 'Peak 1' metabolite. Isopyridoxal was incapable of being directly phosphorylated in rat liver extract and it is therefore unlikely that peak 1 is isopyridoxal phosphate. Its nature remains unknown.
Animals↗
Fluoride therapy and parathyroid hormone activity in osteoporosis.
1. To determine the relationships between parathyroid hormone activity and long-term sodium fluoride therapy in osteoporosis, cytochemical bioassays (for biologically active parathyroid hormone) were performed in 22 osteoporotic control patients and in 18 patients after 15 +/- 10 months of treatment (60 mg of sodium fluoride daily). Ten patients were studied longitudinally by repeated metabolic balances and were therefore common to both groups. All patients were receiving mineral supplements. 2. Cross-sectional data showed a fourfold mean increase in biologically active parathyroid hormone on fluoride treatment (P less than 0.005) together with a 51% increase in serum alkaline phosphatase (P less than 0.005). Longitudinal data showed, in addition, a significant increase in the calcium balance of 2.4 +/- 1.2 (SEM) mmol daily (P less than 0.05) and the development of a positive phosphorus balance (P less than 0.02). 3. Fluoride-treated patients were then analysed in two groups according to the level of biologically active parathyroid hormone. Thirty-two per cent of values were above the upper limit of normal (18 pg/ml). The mean serum alkaline phosphatase level in this group showed no elevation above that of the control patients, the overall rise being accounted for entirely by patients with normal levels of biologically active parathyroid hormone. High levels of biologically active parathyroid hormone were also associated with relative hypophosphataemia (P less than 0.01), relative hypercalciuria (P less than 0.05) and an increased urine/faecal calcium ratio (P less than 0.025). 4. Results show that long-term fluoride and calcium therapy increase biologically active parathyroid hormone in osteoporosis and that excessive parathyroid hormone activity may account for certain features of the refractory state.
Adult↗
Experience with a transfusion recipient education program about hepatitis C.
Shortly after test kits for antibodies to the hepatitis C virus (HCV) were licensed in May of 1990, our medical community undertook a public education program encouraging previous transfusion recipients to see their physicians about the wisdom of being tested for anti-HCV. In response, 1034 samples were received for testing. All samples repeatably reactive (RR) with anti-HCV enzyme-linked immunoassay (EIA) were tested further with a research recombinant immunoblot assay (RIBA). Overall, 76 of the 1034 (7.4%) recipient samples were RR and 64 of these (84.2%) were reactive with RIBA. Recipients transfused prior to surrogate testing (alanine aminotransferase [ALT] and anti-hepatitis B core [anti-HBc]) in 1986 showed a 8.6 percent reactivity with RIBA and those transfused after surrogate testing showed a 4.8 percent reactivity, a 44 percent reduction. Of the 57 recipient samples reactive with RIBA and suitable for assay, 11 (19.3%) had an elevated ALT. Among 76 randomly selected blood donors with RR EIAs studied for comparison with recipients, 20 (26.3%) were reactive with RIBA, 9 of which had an abnormal surrogate test that would have disqualified them. ALT concentrations were abnormal in 6 (30%) of the donors who were reactive on RIBA. We conclude that an education program that encourages previous transfusion recipients to seek medical advice about anti-HCV testing is practical from the standpoint of the blood center. We believe more widespread implementation of similar programs should be considered.(ABSTRACT TRUNCATED AT 250 WORDS)
Antibodies, Viral↗
Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions.
The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.
Adult↗
Chronic dehydration stone disease.
A study was made of 819 patients attending a metabolic stone clinic. A firm diagnosis was made in 708 (86%) and in 132 of these (19%) the diagnosis was thought to be chronic dehydration. The records were available for study for 87 males and 11 females in the chronic dehydration group. The mean age at presentation was 43 years. The causes of chronic dehydration were hot climate (62%), with hot occupation and low water intake almost equal in second place. In patients with a single cause of chronic dehydration, 57% also had a dietary risk factor for urolithiasis and this was most commonly high oxalate intake. Following dietary advice, the mean urinary volume increased from 1720 to 2475 ml/24 h. This was accompanied by a rise in mean urinary calcium from 6.02 to 6.96 mmol/24 h, presumably due to the calcium in the additional water drunk. Urinary oxalate did not change significantly. The mean follow-up time was 4.85 years and the stone recurrence rate was low. It was concluded that chronic dehydration is a common cause of urolithiasis; this can be treated satisfactorily by increasing water intake plus dietary advice in certain cases.
Adult↗
Chemical measurement of calcium oxalate crystalluria: results in various causes of calcium urolithiasis.
Calcium oxalate and calcium phosphate crystalluria have been measured chemically in 1,173 urine samples whose chemical compositions were also analysed. The importance of urinary oxalate as a determinant for calcium oxalate crystalluria was confirmed. Significant concentrations of calcium oxalate crystals may be present in urine even though the crystals are too small for detection by light microscopy or by many particle-counting methods. Calcium phosphate crystals in urine always contain a small proportion of calcium oxalate. Results in various clinical situations are reviewed.
Calcium Oxalate↗
Seizure induction by alcohol in patients with epilepsy.
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Alcohol Drinking↗
Salt and blood pressure in Rio Grande do Sul, Brazil.
A 1978 survey of 4,565 people in Rio Grande do Sul obtained interview and blood pressure data as well as casual urine specimens for subsequent sodium and creatinine titrations. Data derived from this survey have demonstrated a variety of complex relationships between blood pressure and sodium, a number of which are examined here. The main conclusion is that observed blood pressure differentials could reflect the kidney's ability to handle sodium, an ability subject to the influences of age, heredity, and the environment. As a consequence, it is suggested that the adoption of salt restriction by populations could bring them large health benefits.
Adult↗
Risk factors for urinary calcium oxalate crystals as revealed by their specific enzymatic assay.
Calcium oxalate crystal concentrations were assayed by a new highly specific enzymatic method in 1200 urine samples from normal subjects and stone formers. Examination of the crystals was also carried out by light microscopy and urines were analysed for oxalate, calcium, magnesium, citrate, urate, pH and osmolality. A striking positive correlation was established between urinary oxalate concentration and calcium oxalate crystal concentration as well as incidence of calcium oxalate crystals and aggregates seen by microscopy. A less striking relationship, also supported by light microscopy, was found between calcium oxalate crystal concentration and urinary calcium concentration. A small rise in calcium oxalate crystalluria was seen with increasing osmolality, but no relationship found between concentration or urinary urate, citrate or magnesium and that of calcium oxalate crystals. Higher levels of calcium oxalate crystal concentration appeared in alkaline urines in association with calcium phosphates. The dominance of urinary oxalate as a risk factor for calcium oxalate crystalluria is confirmed.
Calcium↗
Measurement of calcium phosphate crystalluria: influence of pH and osmolality and invariable presence of oxalate.
Calcium phosphate and calcium oxalate urinary crystal concentrations in normal and stone-forming subjects were measured. The urinary crystals were examined by light microscopy and urine samples were analysed for oxalate, pH and osmolality. Calcium phosphate crystal concentrations were clearly related to urine pH but unrelated to urine osmolality. An unexpected finding was co-precipitation of oxalate with calcium phosphate. Consequently, precipitated invariable oxalate increased with rising urinary pH. Possible explanations and implications are discussed.
Calcium Oxalate↗
Failure of allopurinol to modify urinary composition in enteric hyperoxaluria.
Conventional treatment of enteric hyperoxaluria (EHO) consists of dietary restriction of oxalate and fat and correction of its underlying cause whenever possible. Recent work suggests that allopurinol reduces the incidence of urolithiasis and the urinary excretion of both oxalate and uric acid in patients without intestinal disease. We have assessed the effect of allopurinol, 300 mg daily for 2 weeks, on urine biochemistry in patients with EHO due to small bowel Crohn's disease and/or resections. Compliance with treatment was confirmed by a fall in plasma uric acid in every patient. Allopurinol failed to alter 24 h urinary oxalate excretion or oxalate concentration. There were also no significant changes in the urinary excretion of glycollate (like oxalate, a breakdown product of glyoxylate), citrate, magnesium or calcium, each of which was at the lower end of the normal range before and during treatment with allopurinol. It appears unlikely that allopurinol will prove useful in the prevention of urolithiasis in patients with EHO.
Adult↗
The automated enzymic assay of D-isocitrate in human urine.
A simple, automated, enzymic assay for the analysis of D-isocitrate in urine is described. The method detects D-isocitrate in the range 0.05-1.00 mmol/L, producing within-batch and between-batch coefficients of variation of 1.8-3.2% and 2.7-3.0% respectively. The assay was also shown to be robust, tolerating extremes of sample pH. Of a wide range of substances tested, only Fe3+ ions interfered, but only at levels considerably in excess of those encountered in urine. D-isocitrate was stable in urine for up to one week at room temperature or at 4 degrees C, with or without preservatives.
Autoanalysis↗
Determination of plasma pyridoxal phosphate levels using a modified apotryptophanase assay.
The development of a simple non-isotopic enzymatic assay for plasma pyridoxal phosphate (PLP) using a modified apotryptophanase procedure is reported. Recovery of added PLP from plasma was 86% and the within-run precision of the assay was 6.5%. Between-run precision was 7.5%. Concentrations of cupric ions as low as 20 mumol/L severely inhibited apotryptophanase activity and this effect of copper was almost completely prevented by the addition of EDTA. The reference plasma PLP range obtained by the apotryptophanase method was found to be between 5 and 50 micrograms/L plasma, with a mean of 17 +/- 10 micrograms/L plasma. The assay requires minimum technical skill and, with the aid of a multisample reaction rate analyser, more than 50 samples could easily be handled within a working day.
Apoenzymes↗
A simple liquid-chromatographic method for measuring vitamin B6 compounds in plasma.
This relatively simple high-performance liquid chromatographic (HPLC) method for measuring all seven known forms of vitamin B6 in plasma from individuals supplemented with pyridoxine hydrochloride shows good analytical recovery (85-98%) and precision. Within-run and between-run CVs for plasmas supplemented with standards were 4% and 7%, respectively. The major forms of B6 found in unsupplemented plasma from normal subjects were pyridoxal phosphate and 4-pyridoxic acid, with pyridoxal just detectable. The HPLC procedure correlated well (r = 0.94) with a modification of an enzymatic method involving apotryptophanase (Anal Biochem 1972;45:567-76) for measuring plasma pyridoxal phosphate, and also (r = 0.94) with a routine method for determining 4-pyridoxic acid in urine (Clin Chem 1964;10:479-89). Elimination of pyridoxine from the plasma of both normal and hyperoxaluric individuals was shown to be very rapid, with half-lives (t1/2) of 45 and 40 min, respectively. Finally, we present evidence for the existence of two other forms of B6 and discuss the possibility of a new metabolic pathway in vitamin B6 metabolism.
Chromatography, High Pressure Liquid↗