Outpatient reduction mammaplasty: a review of 338 consecutive cases.

Reduction mammaplasty is usually accomplished under general anesthesia, often with an overnight stay. With cost-containment pressures, the ability to perform this surgery in an outpatient setting would have obvious benefits. We present a series of 338 patients who have undergone bilateral reduction mammaplasty over a 3-year period. Two hundred eighty-six cases (84.6%) were performed on an outpatient basis and 52 (15.4%) were inpatients. Patient age ranged from 13 to 82 years. Significant differences were found between the two groups regarding average age (34.3 and 42.4 years, respectively) and average total resection weights (1,486.1 gm and 1,895.6 gm, respectively). The maximum total resection weight was 6,000 gm in the outpatient group and 7,140 gm in the inpatient group. Surgical techniques included inferior pedicle (N = 273), central mound (N = 54), and free nipple graft (N = 11). There were no substantial differences in the incidence of minor complications, including wound separation, seromas, hypertrophic scars, infection, and hypopigmentation. Autologous transfusion was utilized in 18 patients early in the series. Of the 175 patients (52%) who returned a follow-up questionnaire, all considered their outpatient experience a positive one. In addition, 33% of the inpatients who responded (N = 8/24) felt their hospital stay was unnecessary. Outpatient surgery resulted in a savings of $1,500 to $2,500 when compared to an overnight stay. Reduction mammaplasty can be performed safely in an outpatient setting and is not necessarily limited by age or extent of resection.

Intraoperative ultrasonography of liver: detection of occult liver tumors and treatment by cryosurgery.

A prospective study of 110 patients undergoing liver surgery was undertaken to evaluate the usefulness of intraoperative ultrasonography (IOUS) and cryosurgery in treating primary and metastatic liver tumors. The diagnoses were colorectal cancer (n = 72), hepatocellular carcinoma (n = 15), ovarian cancer (n = 8), cholangiocarcinoma (n = 4), and other tumors (n = 11). IOUS results were compared with preoperative CT scan angioportography. IOUS detected 37 lesions not seen on CT in 21 patients (19%) and 13 lesions not detected by bimanual palpation in 6 patients (5%). IOUS-assisted cryosurgery was carried out to ablate unresectable liver tumors in 21 patients (19%). At median follow-up of 14 months, 5/21 patients (24%) achieved complete response; 24 and 52% of patients recurred in the liver and systematically, respectively. Thus, IOUS is useful in detecting occult liver tumors and in providing assistance in tumor ablative therapies. Cryosurgery is useful in controlling some of the unresectable liver tumors, but the 76% recurrence rate implies the need for an effective regional and systemic chemo/immunotherapy.

Induction of prolyl hydroxylase activity in a nonadherent population of human leukocytes.

A nonadherent population of human monocytes has been shown to express the collagen hydroxylating enzyme prolyl hydroxylase in vitro. Enzyme levels present in freshly isolated nonadherent cells were induced 300% during the first 72 hours of culturing, which could be suppressed by cycloheximide. Maximum induction required both a feeder layer of adherent leukocytes, and 10-15% autologous plasma. Biosynthesis of Clq, a protein which also is hydroxylated by prolyl hydroxylase, by the nonadherent cells was significantly less than the adherent monocytes. Therefore, this collagen biosynthetic marker enzyme was not associated with Clq synthesis, which suggests that the enzyme is present for collagen biosynthesis.

In vitro assays of in vivo exposure to cyclophosphamide: induction of sister-chromatid exchanges in peripheral lymphocytes, bone-marrow cells and in cultured cells exposed to plasma.

The in vivo genotoxic potential of cyclophosphamide (CY) was assessed by sister-chromatid exchange (SCE) induction after removal and in vitro culture of circulating peripheral lymphocytes and bone marrow from CY exposed male, Fischer 344 rats. Plasma was simultaneously obtained and assessed for genotoxic activity by incubation with 4 cultured mammalian cell lines: HepG2, H4-II-E (H4), V79 and IMR-90. These 4 cell types were used to help discriminate the role of metabolism in generating SCE-inducing factors in plasma. HepG2 and H4 have been shown to metabolize certain xenobiotics while V79 and IMR-90 do not. An in vivo dose response to CY at doses of 0, 5, 10, 20, 30 and 50 mg CY/kg assayed 1 h post-i.p. injection was performed. Phytohemagglutinin (PHA)-stimulated lymphocytes showed a dose-related increase in SCE up to 66.7 SCE/cell at 20 mg/kg (30 mg/kg was cytotoxic). Bone marrow also showed an SCE increase to 34.8 SCE/cell at 10 mg/kg (higher doses were cytotoxic). Plasma induced a dose-dependent SCE increase in the 4 cultured cell lines at all tested doses indicating the presence of direct-acting SCE-inducing metabolites of CY. A time course study using 20 mg CY/kg indicated peak plasma levels of CY genotoxic activity at approximately 0.5-1 h post-injection. By 3 h, the level of genotoxic activity in plasma was considerably reduced. Lymphocytes, however, showed a cumulative increase in SCE to 74.7 SCE/cell after 3 h of exposure. These in vivo exposure--in vitro assay techniques may be useful and facile systems with which to develop an integrative testing system for assessing the in vivo genotoxicity of a chemical.

Induction of sister chromatid exchange by diethylstilbestrol in metabolically competent hepatoma cell lines but not in fibroblasts.

The effect of diethylstilbestrol (DES) on sister chromatid exchange (SCE) induction was measured in four cell lines to determine whether metabolic activation of DES is a factor in its genotoxic potential. Two of these, cell lines derived from a human hepatoblastoma (HepG2-GW) and a rat hepatoma (H4-AG), have been shown previously in our laboratory to be capable of metabolizing several procarcinogens to their active forms. DES, in a dose range of 1 X 10(-8) M to 1 X 10(-5) M, increased SCE frequencies by 50 to 60% in both the rat and human hepatoma lines but had no effect on SCE induction in Chinese hamster lung fibroblasts (V79-GW) or human diploid skin fibroblasts (MGH 2C-GW), both of which are nonmetabolizing cell lines. Furthermore, pretreatment of the responsive cell lines (H4-AG and HepG2-GW) with indomethacin, an inhibitor of prostaglandin synthetase-mediated metabolism of DES, effectively prevented the induction of SCE by DES. DES failed to increase the frequency of hypoxanthine-guanine phosphoribosyltransferase locus mutants in H4-AG cells, over a dose range which induced SCE. These observations suggest that DES induces SCE but does not induce gene mutation. These data strongly support growing evidence that metabolic activation of DES may be an important factor in its genotoxic and carcinogenic mechanisms.