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OBJECTIVE: To compare the neonatal outcome of infants delivered before 39 weeks' gestation following documentation of fetal lung maturity before and after the lamellar body count (LBC) threshold was increased from 30,000 to 50,000 LB/ul. We discuss the algorithm employed for testing fetal lung maturity, the cost of testing and potential savings. MATERIAL AND METHODS: We studied the outcome of infants delivered electively before 39 weeks' gestation after fetal lung maturity was documented by amniotic fluid analysis. We compared the outcome of neonates born before and after the LBC threshold was increased. RESULTS: Our cohort included 527 neonates who were divided into two groups: 264 who underwent fetal lung maturity studies before the change in LBC threshold and 263 who underwent testing after the change. In the first group, 158 neonates met the criteria of LBC >30,000 LB/ul and were delivered without further testing. The second group included 154 neonates who were mature by LBC >50,000 LB/ul and were delivered. Seven of the neonates born in the first group required admission to the neonatal intensive care unit (NICU), whereas in the second group only two neonates required admission (P = 0.02). Additionally, 16 neonates in the first group required respiratory assistance compared with six in the second group (P = 0.04). The overall neonatal complication rate was significantly higher in the first group (P = 0.001). CONCLUSION: Changing the LBC threshold resulted in a significant decrease in neonatal morbidity. Employing the algorithm, we described for testing fetal lung maturity is cost effective, and more importantly, represents sound evidence-based medical management.

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The brief administration of G-CSF to previously treated solid tumor patients has a positive impact on the overall cellularity and progenitor cell content of harvested bone marrow. Fifty-seven patients, fully recovered from therapy and growth factor support, had approximately 500 mL of steady-state marrow harvested as outpatients under local anesthesia. Each patient then received 5 micrograms/kg of G-CSF every 12 hours subcutaneously for either 24 hours (21 patients), 36 hours (20 patients), or 48 hours (16 patients) just before harvesting 500 mL of activated bone marrow. Bone marrow cellularity (x 10(6)/mL) increased from a steady-state mean of 10.7 (+/- 0.9) to 25.7 (+/- 2.8) after 24 hours, 9.3 (+/- 0.7) to 29 (+/- 2.5) after 36 hours, and 9.6 (+/- 0.7) to 28.4 (+/- 2.5) after 48 hours. Although the percentage of CD34+ cells did not significantly change in stimulated marrow, the total number of CD34+ cells (x 10(6)) collected increased from 34 (+/- 6.3) to 52 (+/- 6.6) after two injections, 28 (+/- 3.6) to 65 (+/- 8.5) after three injections, and 28 (+/- 5.4) to 75 (+/- 18) after four injections of G-CSF. Further phenotyping demonstrated significant increases in CD34+HLA-DR+ cells with all three schedules relative to steady-state marrow. There were no changes in the total number of CD34+HLA-DR- cells after two and four shots; however, this population increased from 10 x 10(6) in steady-state marrow to 23 x 10(6) (p = 0.012) after three injections. Analysis of peripheral blood indicated a statistically significant increase in the circulating white count, but more interestingly, there were significant increases in the number of CD34+ cells x 10(4)/mL, suggesting the onset of mobilization. Steady-state blood contained a mean of 0.86 x 10(4)/mL CD34+ cells, which increased to 4.37 x 10(4)/mL, 7.43 x 10(4)/mL, and 8.62 x 10(4)/mL after two, three, and four injections, respectively-levels of CD34+ cells that are comparable to steady-state marrow. Reinfusion of a median of 1.6 x 10(6) activated CD34+ cells/kg resulted in the recovery of > 100/mm3 neutrophils and > 20,000 platelets by days 9 and 19, respectively, which was faster than our previous patients who received steady-state marrow, and comparable to our patients who received mobilized peripheral stem cells.

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This report details a bone marrow harvest procedure performed outside the hospital setting under local anesthesia, thereby avoiding many of the risks associated with the traditional surgical procedure. In approximately 30 minutes, 450 milliliters of marrow can be collected from eight bone punctures, containing a median of 4.18 x 10(9) cells and 33 x 10(6) progenitor cells as defined by CD34 expression. Reinfusion of a median 1.2 x 10(6) CD34+ cells/kg in 10 breast cancer and lung cancer patients after dose-intensive chemotherapy resulted in the recovery of granulocytes > 100/mm3 by day 14 and platelets > 20,000 by day 21. Without progenitor cell support, such recoveries could take 30 and 40 days, respectively. Collection of marrow using this protocol does not compromise the engraftment capability of the progenitor cells, seldom necessitates blood product support, is safer for the patient, and reduces the cost of harvesting by 75% compared to inpatient or day surgery procedures.

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Several retrospective studies suggest that abnormal deoxyribonucleic acid (DNA) content in colorectal carcinoma correlates with adverse clinical outcome. Many of these studies have used naked nuclei retrieved from formalin-fixed, paraffin-embedded tissues for flow cytometry. The purpose of this study was to prospectively analyze 137 colorectal carcinomas using fresh whole-cell suspensions for flow cytometry and to determine whether abnormal DNA content (DNA aneuploidy or tumors with high proliferative activity) correlates with Dukes' stage, histologic grade, lymphocytic infiltration of the tumor, tumor fibrosis, extramural venous spread, or tumor size. Cell suspensions for flow cytometry were prepared by enzyme disaggregation with collagenase XI, DNase, and trypsin. Satisfactory DNA histograms were obtained from 132 of the 137 samples. The mean coefficients of variance for the G1/G0 of the external 2C control, internal 2C populations, and aneuploid populations were 2.5, 3.5, and 3.5, respectively. The mean percentage of viable cells was 97%. Of 132 cases, 102 (77%) demonstrated abnormal DNA histograms, of which 77 (58%) showed DNA aneuploidy. Abnormal DNA histograms of DNA aneuploidy did not correlate with Dukes' stage. Tumors of higher histologic grade were more likely to demonstrate DNA aneuploidy, however, these differences did not reach statistical significance. The authors conclude that (1) satisfactory DNA histograms can be obtained with the use of a fresh, whole-cell technique; (2) abnormal DNA histograms did not statistically correlate with standard clinical, grading, or staging parameters; and (3) carcinomas of high histologic grade showed an increased proportion of aneuploid DNA histograms, but this trend did not reach statistical significance.

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Hepatocellular carcinoma with osteoclast-like giant cells (hepatic giant cell carcinoma [HGCC]) is a rare entity, with only three cases reported. The tumor is histologically similar to giant cell tumor (GCT) of bone, and the origin of the multinucleated giant cells and mononuclear stromal cells has not been determined. The purpose of this report is to present a case of this rare tumor and compare its ultrastructural and immunohistochemical features with those of a conventional GCT of bone. Histologically, the HGCC consists of sheets of osteoclast-like giant cells with a background of mononuclear cells. The giant cells lack the pleomorphism seen in hepatocellular carcinomas with anaplastic giant cells. At the light microscopic level, most of this tumor was nearly identical to a GCT of bone, but several microscopic fields (less than 5% of the tumor) had the histologic appearance of a "usual" hepatocellular carcinoma. The hepatic tumor was negative for HAM 56, epithelial cytokeratins, muramidase, and alpha-1-antitrypsin, with only focal positivity for chymotrypsin in mononuclear and giant cells. The GCT was strongly positive for alpha-1-antitrypsin and chymotrypsin in both the mononuclear and giant cells and showed focal, weak staining for AE1 and AE3 in the mononuclear stromal cells. Ultrastructurally, both mononuclear and giant cells of the HGCC showed features typical of hepatocellular carcinoma. Although the patient presented in this report died, the pattern of growth was different from most hepatocellular carcinomas. The overall histologic features of this tumor are distinctive and appear to justify separating this variant from other types of hepatocellular carcinoma.

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