A survey of hepatitis C virus infection in haemodialysis patients over a 7-year follow-up.
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Biomedical subjects
Publications and source records attributed to F Poggio.
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We studied the significance of free erythrocyte protoporphyrin (FEP) in relation to iron status, aluminum levels and anemia in uremic patients on chronic dialysis. All but 1 patient showed high FEP values closely related to the degree of anemia. Increased FEP levels are due to a defective heme synthesis, not related to iron deficiency or aluminum overload. Treatment of anemia with recombinant human erythropoietin reduced FEP values. We therefore hypothesize that recombinant human erythropoietin ameliorates an enzymatic defect in heme synthesis.
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The efficacy and safety of calcium carbonate as a phosphate binder was evaluated in 20 patients on chronic hemodialysis who had previously received aluminum hydroxide. During the control period the patients were on aluminum hydroxide and calcitriol therapy and had plasma phosphorus levels less than 6 mg/dL (4.95 +/- 0.8 mg/dL). Aluminum hydroxide was then discontinued and no phosphate binder was prescribed for 1 month. Every patient developed hyperphosphatemia so that calcium carbonate treatment was begun and calcitriol dose was adjusted in relation to plasma calcium changes. After 24 months of calcium carbonate therapy, plasma phosphorus was 4.85 +/- 0.7 mg/dL, using a daily dose of calcium carbonate of 2.57 +/- 1.3 g (range, 1 to 6 g). The daily dose per patient of calcitriol was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia. At the end of the study plasma calcium, magnesium, bicarbonate, alkaline phosphatase, and parathyroid hormone values were unchanged in comparison with the control period, whereas a significant reduction in plasma aluminum and plasma aluminum increase induced by deferoxamine infusion was observed. The frequency of hypercalcemic and hyperphosphatemic episodes during the last 12 months of calcium carbonate therapy (6.2% and 16.6%, respectively) was not different from that observed during the 12 months on aluminum hydroxide therapy preceding the control period (4.5% and 14.7%, respectively). It was concluded that calcium carbonate is effective in the control of hyperphosphatemia and secondary hyperparathyroidism in patients on chronic hemodialysis and that the incidence of hypercalcemia is low when the daily dosage is less than 6 g.
Health Micro Data Systems (HMDS), headed by Frank Poggio, president, is headquartered in Madison WI, with more than 40 employees in the home office in Madison and the sales and support office in San Francisco. The firm generates approximately $2.6 million a year strictly with microcomputer based systems for healthcare facilities. Recently, HC&C Editor/Publisher Bill W. Childs had the opportunity to speak with Poggio about HMDS, the firm's role in the industry and some challenges for the present and the future.
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To further elucidate the mechanisms responsible for the hypoxemia we studied ventilation, pulmonary gas exchanges, blood gas pressures and exchanges of CO2-T, CO2-D and HCO-3 in six patients during AD and BD on 1 m2 cuprophan filter and during BF on 1.2 m2 polyacrylonitrile filter. Blood passing through the dialyzer lost 172.8 mM/h of CO2-T in AD, 149.2 mM/h in BF and gained 25.6 mM/h in BD. In AD VE, VA and PaO2 decreased significantly after 30 and 60 min., in BF for the whole duration of dialysis. PoO2 showed a significant decrease both in AD and BF after 60 min. In AD PaCO2 was significantly reduced after 120 and 180 min. All the above parameters remained unchanged in BD. VCO2 remained unchanged in all. VCO2 and R decreased both in AD and BF. However, when VCO2 was corrected for CO2 loss across the dialyzer, overall CO2 loss (ventilated plus filtered) and R returned to basal values. In AD, HCO-3 and pH fell in the first 120 min., while in BD and BF they increased from the beginning of dialysis. In AD hypoventilation, hypoxemia and inadequate correction of acid-base balance were due to the loss of HCO-3 across the filter. In BF also hypoventilation and hypoxemia were due to the loss of HCO-3 across the filter but the acid-base balance was adequately corrected by HCO-3 reinfusion. In BD, there was HCO-3 gain across the filter which induced a gradual correction of acid-base balance without impairment of ventilation.
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In order to elucidate the mechanisms responsible for the hypoxemia observed during acetate dialysis, but not found during bicarbonate dialysis, the authors studied ventilation, blood gases and their exchanges in the lungs and across the dialyzer on 9 patients. Oxygen consumption was similar both in acetate and bicarbonate dialysis. At the beginning of acetate dialysis, hypocapnia, due to CO2 losses through the dialyzer, causes hypoventilation and hypoxemia; afterwards, the worsening of acidosis (due to bicarbonate losses) stimulates ventilation, thus correcting the initial imbalance. Authors also hypothesize a pulmonary mechanism for CO2 "sparing" contributing to compensate CO2 losses through the dialyzer. The absence of hypoxemia during bicarbonate dialysis would be due to the absence of CO2 losses through the dialyzer.
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