The Effects of Zero Magnesium Dialysate and Magnesium Supplements on Ionised Calcium Concentration in Patients on Regular Dialysis Treatment

The effect of oral magnesium carbonate aluminium hydroxide onserum ionised calcium, total calcium, aluminium and magnesium,was assessed in 31 patients with chronic renal failure, duringand after one haemodialysis. The behaviour of ionised calcium and total calcium was the samein both groups. Each showed a slight fall during dialysis, whichwas not significant. Serum total calcium was 0.2–0.3 mmol/l(0.8–1.2 mg/dl) greater throughout the period of dialysisin the group taking aluminium hydroxide. Serum magnesium andaluminium were both lower in the group treated with magnesiumcarbonate. In the group taking magnesium carbonate, serum magnesium concentrationsfell markedly during dialysis, but otherwise were maintainedwithin the reference range by the use of a magnesium-free dialysate.These results show the effectiveness of magnesium carbonateoral phosphate-binding agents and zero magnesium dialysate inreducing serum aluminium without affecting the behaviour ofserum calcium fractions during dialysis.     

Calcium homeostasis in second trimester fetuses.

The concentrations of ionised calcium ions (Ca++), total calcium, parathyroid hormone, pH, total protein, albumin, sodium, and potassium were measured in paired fetal and maternal blood from pregnancies at 15 to 24 weeks' gestation. Pure fetal blood samples were obtained fetoscopically. The concentrations of fetal ionised calcium ions (n = 26); mean (SD) 1.33 (0.12) mmol/l (5.32 (0.48) mg/100 ml) and those of parathyroid hormone (n = 9); 68 (19) pmol/l (58 (16) micrograms/100 ml) were significantly higher than those of the mothers: 1.18 (0.09) mmol/l (4.7 (0.4) mg/100 ml), and 40 pmol/l (less than 34 micrograms/100 ml), respectively. There was no difference between measured fetal and maternal total calcium, pH, and electrolytes. The fetal total protein and albumin concentrations increased with gestation but were always lower than the equivalent maternal values. The calculated total calcium was 0.23-0.45 mmol/l (0.9-1.8 mg/100 ml) higher in the fetal than in maternal blood from the same pregnancy. There were no fetal arteriovenous differences in ionised calcium ions despite higher venous pH.     

Factors affecting the surgical management of infective endocarditis

Congestive heart failure and septic embolism complicate the clinical course of patients with infective endocarditis (IE). This study reviews the clinical records of patients with systemic disease secondary to IE and stratifies their disease severity according to individual risk factors and medical, and surgical interventions. The hospital records of all patients presenting to our institution from 1992 through 1997 with heart valve destruction secondary to IE were reviewed. Ten patients with hemodynamically significant valve lesions were included in this study: seven with aortic valve disease and two with mitral valve disease, and one with combined aortic and mitral valve lesions. All were diagnosed by echocardiogram. All ten patients experienced systemic septic arterial emboli: four intracranial lesions, four visceral lesions, and three extremity arterial occlusive events. Two patients required peripheral arterial repair. Cultures revealed infection secondary to Staphylococcus aureus in five, Streptococcus species in three, Coxiella species in one, and an unidentified organism in one patient. Seven patients underwent valve replacement. Three patients died from their disease processes. Statistical significance was established by Wilcoxon rank analysis with a two-tailed P < 0.05. Patients with IE secondary to staphylococcal infections suffered a more acute and virulent disease process (P = 0.04), with a 40 per cent mortality rate in the first 48 hours. There was no increased incidence of embolization associated with longer duration of symptoms (P = 0.32). Surgical repair conferred improved clinical outcome as compared with no surgical intervention (P = 0.03). Improved patient outcome was associated with nonstaphylococcal infection (P = 0.02), and a successful initial antibiotic regimen (P = 0.03). Peripheral arterial repair was successful in both cases.     

Clonal origin of non-medullary thyroid tumours assessed by non-random X-chromosome inactivation.

OBJECTIVE: X-chromosome inactivation analysis was performed in order to assess the clonal origin of non-medullary thyroid tumours and to distinguish between multicentricity and multifocality in multiple papillary thyroid carcinoma (PTC). METHODS: One hundred and thirteen tumour samples from 31 patients with isolated PTC, 16 patients with multinodular PTC, 14 patients with follicular thyroid adenoma (FTA) and 15 patients with follicular thyroid carcinoma (FTC) were collected. The corresponding normal thyroid tissues were analysed, and in 14 cases, tumour-surrounding tissue was also studied. Genomic DNA was digested with HpaII and HhaI previous to PCR amplification of the polymorphic CAG repeat, on exon 1 of the human androgen receptor gene (HUMARA). PCR products were analysed by denaturing gel electrophoresis, silver staining and densitometric analysis. PCR products were also used to determine the number of CAG repeats of patients with isolated PTC, FTA, FTC and of 41 healthy volunteers. RESULTS: Heterozygosity for the HUMARA polymorphism was found in 64/76 (84%) cases. Lyonization of the thyroid was observed in 15/76 (20%) cases, which were excluded from clonal analysis. Except for two cases of isolated PTC, all tumour samples studied presented monoclonal X-inactivation patterns, while normal thyroid tissue was polyclonal. Monoclonal patterns were also found in 4/14 tumour-surrounding tissues. No difference was found in the length of CAG alleles between patients and controls. Of eight informative cases of multinodular PTC, three showed evidence of multicentricity and five revealed patterns consistent with multifocality. CONCLUSIONS: Both isolated and multinodular PTC as well as FTA and FTC are of monoclonal origin. Our results also suggest that approximately one-third of multiple PTC have an independent origin for the different nodules (multicentricity). Monoclonality was also found in tissues surrounding some PTC nodules. No association was found between the length of CAG alleles and thyroid malignancies.     

Skeletal growth and long-term bone turnover after enterocystoplasty in a chronic rat model

OBJECTIVE: To investigate skeletal growth and bone metabolism in a chronic animal model of urinary diversion. MATERIALS AND METHODS: Young male Wistar rats (120) were allocated randomly to four groups undergoing: ileocystoplasty, ileocystoplasty and resection of the ileocaecal segment, colocystoplasty, and controls. All animals received antibiotics for 1 week after surgery; half of each group remained on oral antibiotics. Bone-related biochemistry was measured in serum and urine. Dual-energy X-ray absorptiometry and peripheral quantitative computed tomography (pQCT) were used to determine bone mass ex vivo. RESULTS: Most (90%) of the rats survived the study period (8 months); six rats died from bowel obstruction at the level of the entero-anastomosis and four had to be killed because of persistent severe diarrhoea. Vital intestinal mucosa was found in all augmented bladders. There were no differences in bone length and volume. Loss of bone mass was almost exclusively in rats with ileocystoplasty and resection of the ileocaecal segment (-37.5%, pQCT, P < 0.01). There was no hyperchloraemic metabolic acidosis or gross impairment of renal function. Hypomagnesaemia, hypocalcaemia and decreased insulin-like growth factor-binding protein 3 were the only significant findings on blood analysis. Deoxypyridinoline crosslinks in urine were higher in rats with an enterocystoplasty than in controls. CONCLUSIONS: Enterocystoplasty in rats neither impairs skeletal growth nor bone quantity, but leads to significant loss of bone mass when combined with resection of the ileocaecal segment. Rarefaction of the trabecular network is confined to the metabolically highly active cancellous compartment, most likely as a consequence of intestinal malabsorption.     

Exocrine pancreatic insufficiency in syndromic paucity of interlobular bile ducts

Severe failure to thrive is an important feature in children with both syndromic and nonsyndromic paucity of interlobular bile ducts (PILBD). Thirteen children age 7 months-11 years with PILBD had pancreatic secretions in duodenal aspirate measured for 40 min after secretin-pancreozymin stimulation, six of these children had chronic diarrhoea. Studies were also performed in seven children age 2-12 years who presented with failure to thrive or nonspecific diarrhoea that subsequently resolved. The results of the control and the PILBD children were similar except in the six with chronic diarrhoea. These children had significant reductions in total volume of duodenal aspirate (p less than 0.05), bicarbonate concentration (p less than 0.02) and output (p less than 0.05), and in lipase concentrations (p less than 0.005). Five of these children have had a reduction in stool frequency and more rapid weight gain since receiving pancreatic supplementation. In children with PILBD and diarrhoea, pancreatic insufficiency may be a contributory factor to poor weight gain. These children may benefit from pancreatic extract supplementation.