Phosphorus balance and mineral metabolism with 3 h daily hemodialysis.

Poor control of mineral metabolism is independently associated with mortality in patients receiving hemodialysis. We analyzed data from a 12-month, prospective, non-randomized, controlled study of daily hemodialysis (DHD) (six sessions/week 3 h each) (n=26) vs conventional hemodialysis (CHD) (three sessions/week 4 h each) (n=51) for achievement of mineral metabolism goals and we performed a substudy of weekly dialytic phosphorus removal in DHD vs CHD. Phosphorus control was superior in the DHD group (% change from baseline to end-of-study -27+/-30% vs +7%+/-35% in the CHD group, P=0.0001). Percentage of patients using phosphate binders decreased from 77 to 40% among subjects on DHD, whereas these parameters did not change (76 vs 77%) in the CHD group (P=0.03 by Breslow-Day test for homogeneity of the odds ratios). Weekly mean phosphorus removal was higher in the DHD group (2452+/-720 mg/week vs 1572+/-366 mg/week, P=0.04). Mean normalized protein catabolic rate increased (0.90+/-0.43-1.22+/-0.26 g/kg/day, P=0.0013). DHD was also associated with an increase in the percent of subjects achieving three or more mineral metabolism goals (for phosphorus, calcium x phosphorus and parathyroid hormone) (15 vs 46%, P=0.046). In conclusion, DHD improves phosphorus control by increasing dialytic phosphorus removal while maintaining nutritional status and reducing the use of phosphate binders. The net effect allows for improved achievement of mineral metabolism goals.

The use of Alu-PCR to distinguish between typical pulmonary carcinoids versus classic midgut carcinoids.

Although histologically 'typical' pulmonary and 'classic' midgut carcinoids are similar, the small intestine tumors are more aggressive than their pulmonary counterpart. We believe that in contrast to pulmonary carcinoids arising from Kulchitsky cells, 'classical' midgut carcinoids develop from crypt stem cells that differentiate into endocrine ('classical') or exocrine-endocrine ('non-classical' adenocarcinoid) tumors. The different progenitor cells may determine different malignant potentials between these types of carcinoids. To identify genetic differences between 'classical' midgut and typical pulmonary carcinoids using an Alu-PCR genomic profiling method, we reviewed 54 cases of carcinoid tumors that were surgically removed at Hartford Hospital from 1996 through 2001. Histologically these cases were selected into three groups: i) foregut or pulmonary carcinoids, ii) 'classic' midgut carcinoids of small intestine and iii) multiple typical pulmonary carcinoids. Genomic-profiling of DNA from these cases was performed using an Alu-PCR method. Metastases were observed in 18/20 'classical' intestinal carcinoid tumors, 3/30 pulmonary carcinoids, and 0/4 multiple pulmonary carcinoids. These results confirm that pulmonary carcinoids behave in a more benign fashion than intestinal carcinoid tumors. Using Alu-PCR to profile tumor cell genomic DNA, we showed that 68% of small intestine carcinoids and 58% of pulmonary carcinoids had allelic banding patterns suggestive of either amplification or deletion of gene sequences. Alu-PCR demonstrated loss or gain of genetic sequences that were unique for each examined group. These findings strongly suggest that pulmonary carcinoids differ from their intestinal counterparts.

Plasma beta-thromboglobulin in acute myocardial infarction with ventricular arrhythmias.

Patients with myocardial infarction, complicated by ventricular arrhythmias (Lown grade greater than or equal to 2), had higher (p less than 0.05) plasma beta-thromboglobulin level than that found in patients with uncomplicated infarction. This indicates higher platelet activation in the former group than in the latter. Such data provide rationale for clinical trial of antiplatelet drugs in cases of myocardial infarction complicated by severe arrhythmias.

Formation of prostacyclin-sensitive platelet aggregates in human whole blood in vitro. Part II. The occurrence of the phenomenon in males suffering from acute myocardial infarction.

The de-aggregatory effect of prostacyclin (PGI2) and the rate of spontaneous platelet aggregation (SPA) were studied in vitro in whole blood of 24 males with acute myocardial infarction (MI) and 18 males, patient controls (PC). The de-aggregatory effect of PGI2 and the rate of SPA (measured as a percentage of changes in free platelet number in whole blood) were higher (p less than 0.01) in MI than PC. The de-aggregatory effect of PGI2 in whole blood was higher (p less than 0.05) on the first day of MI than on day 14 following MI. The highest de-aggregatory effect of PGI2 was found in whole blood of patients with MI complicated by ventricular fibrillation. In neither of the groups did the de-aggregatory effect of PGI2 correlate with patients' age, haematocrit, erythrocyte and leucocyte counts, triglycerides, HDL, LDL or total cholesterol levels. In the MI group, de-aggregatory effect of PGI2 was correlated with free platelet concentration (r = -0.59, p less than 0.05), elevation of glutamic oxalacetic transaminase (r = 0.53, p less than 0.05) and creatinine phosphokinase (r = 0.69, p less than 0.001). The de-aggregatory effect of PGI2 in blood of patients with evolving MI did not differ from that in PC. It is concluded that the increased rate of SPA and formation of PGI2-sensitive platelet aggregates in vitro in whole blood of MI patients are secondary to myocardial necrosis.

Formation of prostacyclin-sensitive platelet aggregates in human whole blood in vitro. Part I. The occurrence of the phenomenon in healthy male volunteers.

When unstirred citrated blood of young males was left to stand at 21 degrees C, the number of free platelets decreased as measured with a whole blood platelet counter. This decrease indicated spontaneous platelet aggregation (SPA) since it was accompanied by the time-dependent increase in platelet micro-aggregates and plasma beta-thromboglobulin while lactate dehydrogenase level did not change significantly. Addition of PGI2 to whole blood increased free platelet count and decreased the number of platelet micro-aggregates. The de-aggregatory effect of PGI2 (measured as a percentage increase in free platelet number) was correlated with the initial amount of platelet micro-aggregates. Blood storage enhanced SPA and de-aggregatory effect of prostacyclin. Immediately after blood collection de-aggregatory effect of prostacyclin was absent. Our results favour an assumption that prostacyclin-sensitive platelet aggregates in blood of young volunteers are formed in vitro rather than in vivo.