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Progressive disease is the major cause of treatment failure after autologous hematopoietic stem cell transplantation for relapsed or refractory non-Hodgkin's lymphoma. An augmented high-dose regimen of cyclophosphamide 7,200 mg/m2, carmustine 300 - 400 mg/m2, and etoposide 2,400 mg/m2 (CBV) was developed in an attempt to improve disease control post-transplant. Sixty-seven adult patients received augmented CBV followed by infusion of unpurged autologous peripheral blood stem cells. Thirty seven patients had relapsed after standard chemotherapy, 28 patients had primary refractory disease, and 2 patients had transformed lymphoma in first partial response. Treatment-related mortality was 4%. Actuarial four year overall survival and progression-free survival were 46+/-8% and 36+/-6%, respectively. Risk factors for disease progression were histologic involvement of marrow by lymphoma and infusion of increased numbers of CD34 + cells per kg in the stem cell autograft. The outcome for patients with relatively chemorefractory disease (defined as 25 - 49% reduction in tumor volume after salvage chemotherapy) was no different than that for patients with chemosensitive disease. Compared to standard high-dose CBV regimens, augmented CBV does not appear to have substantially improved disease control. Prospective study of the association between inferior progression-free survival and infusion of higher CD34 + cell doses in stem cell autografts is warranted.

In 1975, Lee and Gurland proposed a solution to the Behrens-Fisher problem. It had excellent control of size and power and was relatively simple to use. However it requires extensive special tables. This article proposes a modification of this approach. It replaces the tables with easily computed functions of the sample sizes and a standard t table. Control of size and power are equivalent to that obtained by Lee and Gurland. Furthermore, the test is also compared with the Welch's approximate t test and shows better control of size, with similar power curves when sample sizes are at least four from each of the two normal populations.

Utilization of several genetic models (twins, families of monozygotic twins, characterized hypertensives and normotensive first-degree-relatives of essential hypertensives) has permitted us to probe for evidence of genetic mediation of several components of the blood pressure control system in humans. These studies have identified evidence for genetic mediation of systolic blood pressure in a cross-sectional study of normotensive subjects covering a wide age span. Further, this effect was independent of body size. The twin model, studied under conditions of sodium loading and sodium and volume depletion, demonstrated a genetic component in the response of plasma renin activity, aldosterone, norepinephrine and renal sodium excretion to these maneuvers. Among hypertensive subjects and unexpected abnormality in the distribution of a specific MNS blood group pattern was seen in renal vascular hypertensives. This may provide a new genetic marker for identifying individuals at increased risk to develop this abnormality.

To investigate the role of potassium on blood pressure we measured serum potassium, urinary excretion of potassium and sodium, fractional excretion of potassium, urinary sodium:potassium ratio, plasma renin activity, aldosterone, and norepinephrine during dynamic maneuvers in normotensive and hypertensive subjects. After baseline measurements, we expanded intravascular volume with infusion of intravenous saline and then induced sodium and volume depletion by diuretic administration during a low sodium salt diet. These studies were performed in 431 normotensive and 478 hypertensive subjects enabling evaluation of the effects of age, race, and sex, as well as blood pressure, on the results. Among normotensives, we found that white subjects had significantly P less than 0.05) higher levels of serum and urine potassium, fractional potassium excretion and lower urinary sodium:potassium ratios than black subjects and that males had the same patterns of differences compared to females. Similar, but less consistent racial differences were seen among the hypertensive subjects. We also observed significant (P less than .05) correlations between urinary potassium excretion and body weight in both normal and hypertensive groups. In normal subjects, a significant correlation was observed between the urinary sodium:potassium ratio and blood pressure that was not seen in the hypertensives. The latter, however, displayed a significant (P less than .05) inverse relationship between serum potassium and blood pressure. Multiple regression analysis revealed that urinary potassium excretion was influenced by age, race, sex, body weight, blood pressure, creatinine clearance, renin, and aldosterone. These observations reveal important relationships between potassium homeostasis and blood pressure control that deserve further study.

To examine the effect of chloride-containing potassium supplements on chloride titrator estimates of dietary sodium intake, we gave normal subjects diet containing 10, 100, or 200 mEq/d sodium in random order either as such, or supplemented with one of two potassium supplements. One regimen consisted of potassium 45 mEq/d with 12 mEq/d chloride and 33 mEq/d of citrate and gluconate; the other contained 48 mEq/d potassium and 48mEq/d chloride. Increased potassium intake with either supplemented regimen resulted in increased 24-hour potassium excretion, which was manifested in only the diurnal collections. Increased chloride intake resulted in increased urinary chloride excretion both during the day and at night. At all chloride intakes, urinary sodium and chloride excretion were highly correlated. The 48 mEq/d chloride intake generated a relationship with the same slope but with a different intercept from the other two regimens. The highest chloride intake resulted in a greater chloride titrator reading; however, the relationship was sufficiently predictable that adjustments in interpretation could be easily made. We conclude that if daily potassium chloride intake is known, chloride titrators continue to be reliable tools for estimating dietary sodium intake.