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D M Wilson

Publications and source records attributed to D M Wilson.

At least 109 records · Page 6Linked to original sources
PubMed1996

Is testing for growth hormone release necessary?

The question of if testing for growth hormone release is necessary in patients with chronic renal failure (CRF) is part of a greater debate. The question of what constitutes growth hormone deficiency (GHD) has become more controversial over the past few years. In some ways, the question has been replaced by the question, "Who will have a meaningful response to growth hormone (GH) therapy?" Since children with CRF generally respond to GH therapy, the question should be recast as, "When is testing for growth hormone release necessary in patients with CRF?" Why is the diagnosis of GHD important? A clear diagnosis of class GHD has many important implications for a patient. GHD is an easily treated cause of neonatal hypoglycemia. The diagnosis alerts the clinician to search for etiologies of GHD such as intracranial tumors and should stimulate a search for other pituitary deficiencies. Another important claim is that patients with classic GHD have a better long-term response to GH therapy. Children in other diagnostic categories, such as renal failure and Turner syndrome, also respond to GH therapy. Do diagnostic studies use to determine the function of the growth hormone-insulin-like growth factor (GH-IGF) axis help in the management of these children? Recently, experts have become increasingly interested in what constitutes a useful diagnostic test. To be a "good" diagnostic test, a procedure should have the following properties: (1.) have a rational connection to the disorder; (2.) good concordance with the diagnosis/outcome; (3.) accurate; and (4.) reproducible. Among tests that share these properties, the best test is generally the easiest and/or the least expensive. Many different tests can be used to evaluate the GH-IGF axis. These include GH stimulation tests, 24-hour GH profiles, IGF-I, and insulin-like growth factor binding protein 3 (IGFBP-3). High quality determinations of IGF-I and IGFBP-3 can be used to evaluate the GH-IGF axis.

Child↗
PubMed1995

Trans-complementation by human apurinic endonuclease (Ape) of hypersensitivity to DNA damage and spontaneous mutator phenotype in apn1-yeast.

Abasic (AP) sites in DNA are potentially lethal and mutagenic. 'Class II' AP endonucleases initiate the repair of these and other DNA lesions. In yeast, the predominant enzyme of this type is Apn1, and its elimination sensitizes the cells to killing by simple alkylating agents or oxidants, and raises the rate of spontaneous mutation. We investigated the ability of the major human class II AP endonuclease, Ape, which is structurally unrelated to Apn1, to replace the yeast enzyme in vivo. Confocal immunomicroscopy studies indicate that approximately 25% of the Ape expressed in yeast is present in the nucleus. High-level Ape expression corresponding to approximately 7000 molecules per nucleus, equal to the normal Apn1 copy number, restored resistance to methyl methanesulfonate to near wild-type levels in Apn1-deficient (apn1-) yeast. Ape expression in apn1- yeast provided little protection against H2O2 challenges, consistent with the weak 3'-repair diesterase activity of the human enzyme. Ape expression at approximately 2000 molecules per nucleus reduced the spontaneous mutation rate of apn1- yeast to that seen for wild-type cells. Because Ape has a powerful AP endonuclease but weak 3'-diesterase activity, these findings indicate that endogenously generated AP sites can drive spontaneous mutagenesis.

DNA Damage↗
PubMed1995

Polymerization of microtubule-associated protein tau under near-physiological conditions.

Neurofibrillary tangles, which form in certain degenerating neurons in the brains of patients with Alzheimer's disease, are amassed from filaments having a straight or paired helical morphology. Solubilization of these filaments reveals that they are composed of the microtubule-associated protein tau. It has not previously been shown, however, that tau will assemble to form filaments of similar morphology under conditions representative of the intracellular environment. We have succeeded in forming such filaments using tau purified from porcine or rat microtubules. The filaments are relatively straight with narrowing at irregular intervals, and are about 10 nm wide, a morphology similar to that of straight filaments seen in Alzheimer's disease neurofibrillary tangles. At tau concentrations of 1-10 microM, in vitro assembly occurs at physiological pH, ionic strength, temperature, and reducing potential, and each one of these factors modulates the reaction. Assembly is judged to be only slowly reversible by the exponential rather than normal distribution of filament lengths, and by the limited disassembly observed under conditions which inhibit polymerization. Tau purified directly from whole brain tissue rather than from microtubules does not polymerize under conditions described in this report.

Animals↗
PubMed1995

Incision activity of human apurinic endonuclease (Ape) at abasic site analogs in DNA.

The major apurinic/apyrimidinic (AP) endonuclease of human cells, the Ape protein, incises DNA adjacent to abasic sites to initiate DNA repair and counteract the cytotoxic and mutagenic effects of AP sites. Here we address the determinants of Ape AP endonuclease activity using duplex DNA substrates that contain synthetic analogs of AP sites: tetrahydrofuranyl (F), propanediol (P), ethanediol (E), or 2-(aminobutyl)-1,3-propanediol (Q). The last of these, a branched abasic structure, was a poor substrate for which Ape had kcat > 1000-fold lower than for F. In contrast, the specificity constant (kcat/Km) for E or P of Ape purified from HeLa cells was only 5-8-fold lower than for F. Positioning a phosphorothioate ester immediately 5' to F inhibited Ape incision activity 20-fold (Rp isomer) or > 10,000-fold (Sp isomer). Although Ape did not have detectable endonuclease activity toward single-stranded substrates or unmodified double-stranded DNA, the enzyme displayed a low level of 3'-exonuclease activity for duplex DNA (< 0.03% of its AP endonuclease activity), which was influenced by the reaction conditions. The base positioned opposite F did not dramatically affect the cleavage efficiency of Ape, but an F:F arrangement was cleaved at approximately one-third of the efficiency of F:C. A 3'-mismatch diminished P and E cleavage only slightly and F not at all. A 5'-mismatch reduced the Ape cleavage rate 4-10-fold for F and approximately 100-fold for P and E. A series of substrates with F at different positions along the oligonucleotide showed that Ape requires > or = 4 base pairs 5' to the abasic site and > or = 3 base pairs on the 3'-side. The implications of these results for substrate recognition by Ape are discussed.

Base Sequence↗
PubMed1995

A quantitative assay for IGF-I and IGF binding protein mRNAs: expression in malignant melanoma cells.

The quantification of messenger RNA is central in studies of gene expression. We describe a quantitative assay for specific mRNAs (QASM) that measures mRNAs for insulin-like growth factor-I, IGF binding proteins (IGFBPs) -2, -3, -4, and -5, and beta-actin. The assay utilizes reverse transcription and polymerase chain reaction, followed by an ELISA based DNA assay technique. The use of internal (competitive) quantification standards gave poorly linear results, while external standards gave linear and reproducible results. QASM results correlated with IGFBP protein concentrations in conditioned medium and with mRNA levels determined by Northern blotting. QASM was used to study IGFBP expression in human malignant melanoma cells. Messenger RNA for IGFBP-2, -3, and -5 were present, while IGF-I and IGFBP-4 mRNAs were not detected. IGFBP-2 and -3 expression was increased in a dose dependent manner by treatment with IGF-I. Protein concentrations in conditioned media paralleled mRNA levels. QASM is a sensitive, specific, and reproducible approach to determining mRNA levels.

Actins↗
PubMed1995

GLY113-->ASP can restore activity to the ASP51-->SER mutant in the melibiose carrier of Escherichia coli.

ASP51 in the putative membrane-spanning helix 2 of the melibiose carrier of Escherichia coli was replaced by SER. This mutation caused failure of the cell to transport melibiose and failure to ferment melibiose on indicator plates. A melibiose-positive revertant was isolated from these plates and was found to have two additional mutations, GLY113-->ASP (in helix 4) and PHE16-->LEU (in helix 1). The double mutant ASP51-->SER/GLY113-->ASP was constructed and showed accumulation of melibiose. On the other hand ASP51-->SER/PHE16-->LEU showed no activity. It is concluded that the new carboxyl group at position 113 compensates for the loss of the carboxyl group at position 51.

Amino Acid Sequence↗
PubMed1995

Problem drinkers: can we identify and help them?

Most people who have a drinking problem are not alcoholics. Even though problem drinkers tend to drink less than alcoholics and to have a shorter history of heavy drinking they are still at increased risk of health problems. To significantly reduce the burden of alcohol-related problems on society, priority should be given to reducing the number of problem drinkers. Because physicians are exposed to a large adult population, and because they have credibility in diagnosing problems, they have an important role to play in encouraging moderation in the use of alcohol. Although the potential for physicians to make a difference is commonly viewed with scepticism, studies have demonstrated that physician interventions can be effective. By working in partnership with other professionals and making use of the community and other resources that are now available, physicians can optimize the effectiveness of their interventions with problem drinkers.

Alcohol Drinking↗
PubMed1995

Characterization of the promoter region of the human apurinic endonuclease gene (APE).

Apurinic/apyrimidinic (AP) sites are mutagenic and block DNA synthesis in vitro. Repair of AP sites is initiated by AP endonucleases that cleave just 5' to the damage. We linked a 4.1-kilobase pair HindIII DNA fragment from the region upstream of the human AP endonuclease gene (APE) to the chloramphenicol acetyltransferase (CAT) gene. Deletions generated constructs containing 1.9 kilobase pairs to 50 base pairs (bp) of the APE upstream region. Transient transfection studies in HeLa cells established that the basal APE promoter is contained within a 500-bp fragment. The major transcriptional start site in HeLa, hepatoma (HepG2), and myeloid leukemic (K562) cells was mapped to a cluster of sites approximately 130 bp downstream of a putative "CCAAT box," approximately 130 bp 5' of the first splice junction in APE. Deletion of 5' sequences to within 10 bp of the CCAAT box reduced the CAT activity by only about half, and removal of the CCAAT box region left a residual promotor activity approximately 9%. Deletion to 31 bp upstream of the transcriptional start site abolished APE promoter activity. DNA sequence analysis revealed potential transcription factor recognition sites in the APE promoter. Gel mobility-shift assays showed that both human upstream factor and Sp1 can bind their respective sites in the APE promoter. However, DNase I footprinting using HeLa nuclear extract showed that the binding of Sp1 and upstream factor is blocked by the binding of other proteins to the nearby CCAAT box region.

Animals↗
PubMed1995

Normal ranges for immunochemiluminometric gonadotropin assays.

OBJECTIVE: We sought to establish normative data for spontaneous and gonadotropin-releasing hormone (GnRH)-stimulated serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels measured by new immunochemiluminometric assays (ICMA) in children and adolescents. METHODS: Random serum samples were obtained from 375 normal subjects (0.1 to 17.7 years, 230 female subjects). Intravenous GnRH stimulation tests were performed in 41 normal subjects (4.8 to 18 years, 20 female subjects). Normal ranges were calculated by age and Tanner stage. Immunochemiluminometric assays of LH and FSH concentrations were compared with levels obtained by a sensitive immunofluorometric assay and a less sensitive radioimmunoassay. RESULTS: Random gonadotropin concentrations in normal children followed the pattern of transient elevation in infancy, low but measurable prepubertal levels, and markedly increased values at puberty. Spontaneous LH levels were higher in male infants but were not statistically different in boys and girls after infancy. Mean prepubertal LH was 0.04 +/- 0.04 IU/L (n = 66), rising 100-fold during puberty. Spontaneous FSH levels were much higher than LH values, were higher in female infants, and rose threefold at puberty. Peak GnRH-stimulated LH was identical in prepubertal boys and girls (1.8 +/- 1.3 IU/L, n = 17) and increased 20-fold at puberty. Mean peak GnRH-stimulated FSH was highest in prepubertal female subjects. Luteinizing hormone values measured by ICMA and immunofluorometric assay were highly correlated, but radioimmunoassay levels diverged markedly from ICMA levels at lower concentrations. Because absolute levels were higher, FSH values correlated adequately in the three assays throughout the normal physiologic range. CONCLUSIONS: Measurement of LH by ICMA is much more sensitive than older assay methods. Spontaneous LH can be accurately measured by ICMA to the very low levels present in normal prepubertal children, providing a potentially important biochemical discriminator of pubertal status. An ICMA GnRH-stimulated LH level greater than 5 IU/L is suggestive of maturing gonadotropin secretion. The ICMA LH assays provide significant enhancement in sensitivity; these assays should be used when levels may be low, and by their accuracy may reduce the time and expense of testing procedures.

Adolescent↗
PubMed1995

Spontaneous serum gonadotropin concentrations in the evaluation of precocious puberty.

OBJECTIVE: We assessed the utility of spontaneous and gonadotropin-releasing hormone (GnRH)-stimulated serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels measured by new immunochemiluminometric assays in the evaluation and monitoring of precocious puberty. METHODS: We evaluated serum gonadotropin values from intravenous GnRH stimulation tests in 49 girls with clinical signs suggesting central precocious puberty (CPP). Because GnRH-stimulated LH has been considered the standard for diagnosing CPP, we used it as the basis for comparison with GnRH-stimulated FSH levels and spontaneous LH and FSH measured by immunochemiluminometric assay. RESULTS: Twenty-six patients had a peak serum LH value above the +2 SD threshold for normal prepubertal female subjects (LH > 5 IU/L). The GnRH-stimulated FSH values had a narrow range and did not discriminate patients with CPP. In contrast, elevations in spontaneous LH and FSH were found to be specific for CPP. Spontaneous LH levels correlated strongly with peak stimulated LH levels in subjects with precocious puberty (r = 0.79) or in control subjects (r = 0.93, both p (0.0001). Spontaneous LH levels in excess of 0.1 IU/L detected true puberty with 94% sensitivity and 88% specificity. Random LH levels in excess of 0.3 IU/L had 100% specificity for CPP. CONCLUSIONS: The GnRH-stimulated FSH levels do not adequately differentiate children with and without CPP and have limited utility in the evaluation of precocious puberty. Spontaneous FSH levels are elevated in CPP with fair sensitivity and marked specificity. Elevated random LH, measured by third-generation assay such as immunochemiluminometric assay, is strongly correlated with and highly predictive of elevated peak GnRH-stimulated LH, and is a useful screening tool for CPP.

Adolescent↗
PubMed1995

Osteomalacia associated with adult Fanconi's syndrome: clinical and diagnostic features.

OBJECTIVE: Osteomalacia associated with adult acquired Fanconi's syndrome is thought to result from hypophosphataemia and relative 1,25-dihydroxyvitamin D deficiency. We have followed the clinical and diagnostic features of patients with osteomalacia associated with adult Fanconi's syndrome, with particular emphasis on their responses to treatment with calcium, phosphate and vitamin D. DESIGN: Retrospective Mayo Clinic case-note review from 1975 to 1994 and prospective follow-up study, combined with literature review. PATIENTS: Eleven patients (7 male, 4 female) were identified who satisfied criteria for diagnosis of osteomalacia and adult Fanconi's syndrome. Twenty-five additional patients were identified in a literature review from 1954 to the present. METHODS: Clinical history and physical examination, serum and urine bone and mineral parameter, X-ray radiography and iliac crest bone histomorphometry. RESULTS: All patients presented with typical symptoms of osteomalacia, including lower extremity or low back bone pain, and all had fractures, pseudofractures, and/or bone demineralization on X-ray radiography. Osteomalacia and Fanconi's syndrome were diagnosed concurrently in 10 patients, whereas osteomalacia preceded diagnosis of Fanconi's syndrome by 5 years in one patient. Pre-treatment bone biopsies in 9 of the 11 patients demonstrated increased osteoid surface, volume and width. In the one patient labelled with tetracycline prior to biopsy, mineralization lag time was prolonged at 111 days (normal 19.2 +/- 1.0 days). Hypophosphataemia, inappropriately low 1,25-dihydroxyvitamin D levels, renal insufficiency, and chronic acidosis due to bicarbonate leak and uraemia, contributed to the osteomalacia in these patients. Secondary hyperparathyroidism was present in two patients. Eight of the 11 patients with osteomalacia associated with Fanconi's syndrome had monoclonal disorders, including multiple myeloma or lymphoma, many of them manifest by light-chain proteinuria. Over a mean patient follow-up period of 46 months (range 1-239 months), patients responded symptomatically to calcium, phosphate, and vitamin D replacement typically within 1-6 months. In 8 patients in whom follow-up data were available, post-treatment serum phosphate and 1,25-dihydroxyvitamin D levels improved in the setting of stable mild renal insufficiency; only one patient developed end-stage renal failure after 20 years, suggesting that these patients do not invariably progress rapidly to renal failure. CONCLUSIONS: Regardless of the underlying cause, osteomalacia associated with adult acquired Fanconi's syndrome appears to respond well to calcium, phosphate, and vitamin D replacement. These patients do not appear to necessarily require 1,25-dihydroxyvitamin D replacement.

Adult↗
PubMed1995

Mechanism of renal calcium conservation with estrogen replacement therapy in women in early postmenopause--a clinical research center study.

To assess the mechanism by which estrogen replacement therapy (ERT) enhances renal calcium conservation in perimenopausal women, we studied 18 normal women in early postmenopause before and after 6 months of ERT (cyclic treatment with transdermal estradiol at 100 micrograms/day and medroxyprogesterone acetate at 10 mg/day for the first 12 days of each cycle). The changes after ERT were: serum ionized calcium and ultrafiltrable calcium, no change; serum intact PTH, 38.2% increase (P < 0.0001); serum 1,25-dihydroxyvitamin D, 23.8% increase (P < 0.0001); urinary calcium excretion, 33.3% decrease (P < 0.001); and deoxypyridinoline (a marker for bone resorption), 19.5% decrease (P < 0.0001). Also, ERT increased tubular reabsorption of calcium (TRCa; 97.6% +/- 0.2% to 98.7% +/- 0.1%; P < 0.0001), and this increase correlated with that in serum PTH (r = 0.49; P < 0.05). After the infusion of human PTH-(1-34), the TRCa maximum was greater after ERT than at baseline (99.4% +/- 0.1% vs. 99.0% +/- 0.1%; P < 0.0001), resulting in decreased calcium excretion (0.9 +/- 0.20 vs. 1.43 +/- 0.20 mumol/dL glomerular filtrate; P < 0.001). Thus, in early postmenopause, the major mechanism of increased renal calcium conservation after ERT is an increase in TRCa due to an increase in serum PTH because of estrogen-induced inhibition of bone resorption. However, ERT also may directly increase the TRCa maximum in response to PTH.

Adult↗
PubMed1995

Interleukin-1 and tumor necrosis factor-alpha increase insulin-like growth factor-binding protein-3 (IGFBP-3) production and IGFBP-3 protease activity in human articular chondrocytes.

IGF-I is the major anabolic factor for cartilage matrix production. Chondrocytes and cartilage treated with interleukin-1 alpha (IL-1 alpha), and chondrocytes from several models of inflammatory joint disease, exhibit reduced responsiveness to IGF-I. Since the IGF-binding proteins (IGFBPs) modulate the effects of IGF-I, we examined the effect of IL-1 alpha and tumor necrosis factor-alpha (TNF-alpha) on IGFBP production by normal human articular chondrocytes in primary culture. Western ligand blots and immunoprecipitation of conditioned medium samples showed that articular chondrocytes produced IGFBPs-2, -3 and -4 and glycosylated IGFBP-4. Both IL-1 alpha and TNF-alpha increased chondrocyte production of IGFBP-3, but did not alter IGFBP-4 production. The activity of a neutral metalloprotease with the ability to cleave IGFBP-3 was also increased by IL-1 alpha. These data suggest that the cytokines IL-1 alpha and TNF-alpha may act to reduce IGF-I access to chondrocytes by increasing production of IGFBP-3. This may be a factor in the decreased matrix production in the inflammatory arthritides.

Blotting, Western↗
PubMed1995

Endocrinology of growth and growth factors.

This review discusses normal growth patterns and the appropriate use of preprinted growth curves. The important roles of thyroid and growth hormone in the modulation of growth are delineated. I present an approach to the evaluation and proper management of children and adolescents with short stature and poor growth.

Adolescent↗
PubMed1995

Oxandrolone therapy in constitutionally delayed growth and puberty. Bio-Technology General Corporation Cooperative Study Group.

BACKGROUND: Male adolescents with constitutional delay of growth and puberty may have significant psychosocial difficulties related to their sexual immaturity and short stature. The purpose of this study was to test the hypothesis that 1 year of oxandrolone therapy would increase growth velocity and thereby improve psychosocial functioning in boys with constitutional delay of growth and pubertal development. METHODS: Forty boys (ages 11 to 14.7 years) with delayed pubertal development and short stature were recruited from the pediatric endocrine clinics of 14 medical centers. The boys were randomized using a block design stratified for age to receive either oxandrolone (0.1 mg/kg daily for 1 year) or an identical-appearing placebo tablet, using a double-masked design. RESULTS: Growth velocity in the oxandrolone-treated boys was significantly greater than in the control boys (9.5 vs 6.8 cm/y). Likewise, the mean height SD score increased 0.41 in the oxandrolone group, whereas it decreased 0.03 in the control group. Those in the oxandrolone group gained 2.4 kg more than those in the placebo group. Mean predicted adult heights did not change in either group. The mean rates of pubertal progression were equivalent in both groups. Self-image (Piers-Harris Self Concept Scale) and social competence (Child Behavior Profile) were normal at baseline in both groups and did not change significantly over the course of the study in either group. No complications of oxandrolone therapy were identified. CONCLUSIONS: This randomized, placebo-controlled trial demonstrates that low-dose oxandrolone can increase both height and weight velocity in boys with delayed puberty safely. Under the conditions of this study, however, the increased growth velocity in the oxandrolone-treated boys was not associated with a greater improvement in psychosocial status compared with the control boys.

Adolescent↗
PubMed1995

CALIPER: individualized-growth curves for the monitoring of children's growth.

Monitoring children's growth is a fundamental part of pediatric care. Deviation from the expected growth pattern can be an important sign of disease and often results in parental anxiety. Most preprinted growth curves are based on cross-sectional data derived from population-based studies of normal children. Since the age of the pubertal growth spurt varies substantially among the normal curves, these curves don't adequately reflect the expected growth pattern of an individual child. In addition, any preprinted growth curve based on the general population becomes less useful when the maturation of a child and the heights of it's parents differ substantially from the average. Established methods exist to adjust the general reference-growth curves for parental height. However, these methods generally are too time consuming to be used in clinic. Only heuristic methods are known to us to adjust the general-reference curves for maturation. We have developed the decision-support system CALIPER, that enables and standardizes the generation of individualized reference-growth curves. CALIPER consists of a graphical interface for data entry, a progress-report generator, and a module for the interactive, dynamic display of general-reference curves and individualized-reference curves. Preference settings such as ethnic background and gender determine the required population curves and individualization method. Individualization can be based on parental height and/or maturation. Maturation is based on an assessment of a child's bone age and/or pubertal stage. The bone age can be assessed by different methods. We have performed an evaluation of CALIPER's methodology by assessing the effect of individualization on the reference growth curves for 466 normally growing children. The individualized-reference curves reflect the growth pattern of children significantly better than the general-reference curves. CALIPER can be used on a case by case base as an aid in clinic (assessment of children's growth and communication with patient and parents) or as a tool to investigate current clinical questions concerning the relation of bone age, pubertal stage, and growth pattern for any part of the population. Besides providing for decision support by the interactive graphical representation of individualized-reference curves and growth data, CALIPER will be linked to a module that can provide automatic interpretation of the data (Kuilboer et al, SCAMC-93). CALIPER runs on a Macintosh, and requires 600K of memory. A color monitor is preferable, but not required. We will demonstrate several cases that will illustrate the clinical problem and CALIPER's potential.

Body Height↗
PubMed1994

Results of long-term treatment with orthophosphate and pyridoxine in patients with primary hyperoxaluria.

BACKGROUND: The prognosis for patients with primary hyperoxaluria has been ominous, with the expectation of renal failure, poor results with transplantation, and early death. METHODS: We studied the long-term effects of orthophosphate and pyridoxine therapy in 25 patients with primary hyperoxaluria who were treated for an average of 10 years (range, 0.3 to 26). Their mean age at the start of treatment was 12 years (median, 6; range, 0.5 to 32). We also studied the effect of orthophosphate and pyridoxine on urinary supersaturation with calcium oxalate, crystal inhibition using a seeded growth system, and crystal formation using scanning electron microscopy in 12 patients during three-day stays in the clinical research center. RESULTS: The mean (+/- SD) glomerular filtration rate at the start of treatment was 91 +/- 26 ml per minute per 1.73 m2. The median decline in glomerular filtration rates was 1.4 ml per minute per 1.73 m2 of body-surface area per year. The actuarial survival free of end-stage renal disease was 96, 89, 74, and 74 percent of 5, 10, 15, and 20 years, respectively. Treatment with orthophosphate and pyridoxine reduced urinary supersaturation with calcium oxalate from 8.3 +/- 3.0 to 2.1 +/- 1.7 kJ per mole at 38 degrees C (P < 0.001), increased the inhibition of calcium oxalate formation from 63 +/- 11 to 108 +/- 10 inhibitor units per 24 hours (P < 0.001), and improved the crystalluria score from 2.6 +/- 0.3 to 0.6 +/- 0.1 (P < 0.001). CONCLUSIONS: Treatment of patients with primary hyperoxaluria with orthophosphate and pyridoxine decreases urinary calcium oxalate crystallization and appears to preserve renal function.

Actuarial Analysis↗