Biomedical subjects
Publications and source records attributed to F Husserl.
Physicians can employ communication techniques to improve patient diagnoses, outcomes, and satisfaction and ultimately to decrease their risk of malpractice suit. The skills outlined in this article form the basis of the Miles Program for Physician-Patient Communication of which the author is a participant.
The improvement in the anemia in patients with end-stage renal disease (ESRD) on continuous ambulatory peritoneal dialysis (CAPD) suggests that dialyzable substances present in the sera of uremic patients either inhibit erythropoiesis directly or inactivate erythropoietin (EPO). In the present study predialysis sera from patients with ESRD inhibited erythroid colony (CFU-E) (N = 10) formation to a significantly (P less than 0.01) greater degree than granulocyte-macrophage (CFU-GM) (N = 7) colony formation in mouse bone marrow (MBM) cultures. The polyamines spermine (SP) (18 to 560 nm/ml) and spermidine (SD) (4 to 648 nm/ml) exerted a more significant (P less than 0.05) inhibition of CFU-E (N greater than or equal to 5) than that of CFU-GM (N greater than or equal to 5) growth. Concentrations of 0.80, 1.0, and 1.5 nm/ml of putrescine (PU) were 92%, 85%, and 77% of erythroid colony (CFU-E) controls (N = 4) and 104%, 130%, and 127% of CFU-GM controls (N = 4). Putrescine (PU) at 1.5 nm/ml also produced a significant (P less than 0.05) inhibition of CFU-E, whereas CFU-GM were stimulated by PU. These data suggest that predialysis sera from uremic patients, as well as SP, SD, and PU, are selectively more inhibitory to CFU-E than CFU-GM growth. The immunoreactivity of EPO was not significantly changed when it was coincubated with SP, SD and PU and measured by radioimmunoassay. PU was found to inhibit noncompetitively the bioactivity of EPO in a CFU-E assay. These data support the hypothesis that polyamines may be important uremic toxins in the anemia of ESRD.
Parameters of erythropoiesis were studied in patients with endstage renal disease established on continuous ambulatory peritoneal dialysis (CAPD) and regular hemodialysis treatment (RDT). Serum erythropoietin was measured by radioimmunoassay, and erythroid progenitor cell (CFU-E) formation was assayed in fetal mouse liver cultures. Serum erythropoietin concentrations in both CAPD (35.3 +/- 4.0 mU/ml) and RDT (31.9 +/- 1.9 mU/ml) patients were significantly higher (P less than 0.01) than normal values (23.1 +/- 1.0 mU/ml). The serum erythropoietin concentration did not correlate with either hematocrit or inhibition of CFU-E formation in either group of dialysis patients. In both CAPD and RDT patients the hematocrit correlated significantly (P less than 0.001) with the degree of serum inhibition of CFU-E formation. CFU-E formation decreased from 74.5 +/- 2.5 to 62.5 +/- 3.5% of control with increasing concentrations of uremic serum in cell cultures from 5 to 20%. In RDT patients a single hemodialysis produced a decrease in the mean serum erythropoietin concentration from 31.8 +/- 2.1 to 27.4 +/- 1.8 mU/ml (P less than 0.01) but no significant change in CFU-E formation. In conclusion, although serum immunoreactive erythropoietin levels are elevated above the normal range in dialysis patients, the response remains inadequate for the severity of the anemia, and it is the degree of serum inhibition of erythropoiesis in both CAPD and RDT patients which correlates with and possibly determines the degree of anemia.
Patients with varying degrees of renal insufficiency and patients with end-stage renal disease receiving continuous ambulatory peritoneal dialysis or regular hemodialysis therapy were studied to assess the independent relationship between serum parathyroid hormone concentration, and both severity of anemia and degree of serum inhibition of erythropoiesis. In patients with renal insufficiency not receiving dialysis, a significant curvilinear relationship between serum parathyroid hormone and creatinine concentrations was present (r = 65, p less than 0.001). Serum parathyroid hormone (by radioimmunoassay) also correlated with hematocrit level (r = -0.54, p less than 0.001) and degree of serum inhibition of in vitro erythroid progenitor cell growth in fetal mouse liver cultures (r = -0.45, p less than 0.001). However, multiple linear regression analysis revealed that after controlling for the effect of creatinine, m-parathyroid hormone is no longer a significant predictor of hematocrit level or erythroid progenitor cell growth. On the other hand, when a restricted population of patients with creatinine values between 1 and 4 mg/dl was analyzed separately, controlling for the effect of creatinine, there was still a significant correlation between hematocrit level and m-parathyroid hormone, but no such relationship was seen when participants with parathyroid hormone levels of less than or equal to 1000 pg/ml were analyzed. No significant correlation was seen between hematocrit level or inhibition of erythroid colony growth and serum parathyroid hormone concentrations in patients receiving either regular hemodialysis or continuous ambulatory peritoneal dialysis. In 13 patients given regular hemodialysis studied before and after parathyroidectomy, there was no significant change in serum erythropoietin (by radioimmunoassay) or serum inhibition of erythropoiesis, although hematocrit levels increased in six of the 13 patients. The 1-34 human parathyroid hormone, 1-84 bovine parathyroid hormone, and 1,25-dihydroxycholecalciferol had no effect on in vitro erythroid burst-forming unit growth. Parathyroid hormone (8 mu/ml) inhibited and 1,25-dihydroxycholecalciferol (4.0 ng/ml) stimulated erythroid colony-forming unit growth only in the absence of exogenous erythropoietin in culture. In summary, it was not possible to demonstrate a significant relationship between serum parathyroid hormone levels and anemia or inhibition of erythropoiesis in patients with uremia either before starting dialysis or after receiving long-term dialysis treatment.(ABSTRACT TRUNCATED AT 400 WORDS)