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Biomedical subjects

S Anderson

Publications and source records attributed to S Anderson.

At least 397 records · Page 22Linked to original sources
PubMed1990

Lack of late toxicity in patients treated with cisplatin-containing combination chemotherapy for metastatic testicular cancer.

To date, the prevalence and nature of the late toxicity of cisplatin-based combination chemotherapy for advanced testicular cancer has been poorly documented. Thirty men with a median age of 35 years (range, 23 to 63), who had undergone such treatment were assessed with detailed investigation to determine the type and frequency of chronic toxicity. The median follow-up from the time of commencement of chemotherapy was 75 months (range, 48 to 126). The most common late toxic effects were high tone hearing loss in 23 men (77%) and electrophysiological evidence of peripheral nerve damage in 15 (50%). Both the hearing and nerve abnormalities were predominantly asymptomatic. In addition, elevation of serum cholesterol, noted in 20 patients (67%), was significant (P = .014) when compared with a control population. Hyperuricemia was present in nine patients (30%). Only one patient, with other risk factors (smoking, family history), had evidence of ischaemic heart disease while 20% (all with a smoking history) had a diminished single breath diffusing capacity for carbon monoxide (DLCO). Cisplatin-based chemotherapy is relatively free of major long-term side effects and should not be withheld for fear of late toxicity.

Adult↗
PubMed1990

Effects of angiotensin-converting enzyme inhibitors in experimental diabetes.

Clinical and experimental diabetic states are often characterized by an increase in the glomerular filtration rate, and early hyperfiltration may be a risk factor for the later development of diabetic glomerulopathy. Evidence in diabetic animal models suggests that, of the determinants of diabetic hyperfiltration, glomerular capillary hypertension plays a key role in the development of structural injury. In diabetic rats, despite normal systemic blood pressure, the glomerular capillary pressure is elevated because of disproportionate vasodilation of the afferent arteriole. In this normotensive model, a modest reduction in systemic blood pressure with angiotensin I-converting enzyme inhibitor therapy normalizes glomerular capillary pressure and retards the development of injury. However, animal studies suggest that all antihypertensive regimens may not afford equivalent protection. It has been reported that monotherapy with calcium channel blockers, or hydralazine, is less effective in limiting albuminuria than are angiotensin-converting enzyme inhibitors. In a study comparing the effects of angiotensin-converting enzyme inhibitors with those of reserpine, hydrochlorothiazide, and hydralazine, both regimens lowered blood pressure and offered some long-term protection. However, angiotensin-converting enzyme inhibition resulted in significantly greater limitation of injury than did the combination regimen. These results suggest that antihypertensive therapy retards diabetic renal disease; however, some anti-hypertensive regimens may afford superior protection.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Results of emergent versus elective cardiac transplantation procedures.

Twenty-six patients underwent emergent (Group I) and 34 patients elective (Group II) cardiac transplantation (C. Tx.) from June 1985 through June 1989. Age, sex, etiology, presence of diabetes, renal failure and pulmonary artery pressures were comparable for both groups (P greater than 0.5). Twenty-two patients were in New York Heart Association (NYHA) Class IV for Group I and 17 for Group II. Group I included 12 patients on inotropic agents, five on intra-aortic balloon pump (IABP) and one on IABP and cardiopulmonary bypass (CPB). Elective patients were stable at home. Location of the donor heart and mean ischemic times were comparable for both groups. Early mortality (within 30 days) included four patients for Group I and two for Group II. There were four late deaths for Group I patients and six for Group II. Four deaths were due to infection, six to rejection, two to malignancy, two neurological and one each to suicide and multisystem failure. Immunosuppression regimen was similar for both groups. The number and severity of early and late rejection episodes were similar despite blood group crossing in 11 patients for Group I (P less than .01). Incidence of infection was comparable. Favorable lifestyles were comparable, including employment of 12 patients for Group I and 16 for Group II. Cumulative survival for the entire series was 70% at two years. The study indicates that the results of emergent and elective cardiac transplantation procedures are equally gratifying, that mortality is mainly related to rejection and sepsis complications and blood group crossing does not significantly increase the number of rejection episodes.

Bacterial Infections↗
PubMed1990

Front-line hormonal therapy for patients with advanced breast cancer: a community oncology research program.

Megestrol acetate was administered as first-line therapy to 152 patients with advanced breast cancer. Forty-three of 136 evaluable patients (32%) obtained an objective response (95% confidence interval, 24% to 40%). Toxicity was minimal, with only 4 patients requiring dose reduction. Megestrol acetate is an effective, well-tolerated agent in previously untreated patients with advanced breast cancer.

Breast Neoplasms↗
PubMed1990

Irreversible tubulointerstitial damage associated with chronic aminonucleoside nephrosis. Amelioration by angiotensin I converting enzyme inhibition.

Chronic aminonucleoside nephrosis is variably associated with tubulointerstitial damage, depending on the route and frequency of drug administration. Recently, different groups have shown this injurious tubulointerstitial process to be reversible, coinciding with the resolution of heavy proteinuria to normal values. The authors have previously shown that a single jugular intravenous administration of puromycin aminonucleoside (PA) to male Munich-Wistar rats produces a triphasic pattern of glomerular injury and proteinuria, which culminates in focal glomerulosclerosis 70 weeks after drug administration. The authors now report the later progression of the tubulointerstitial morphologic abnormalities associated with acute nephrosis (phase I), despite spontaneous resolution of glomerular injury during the intermediate period (phase II) in this model. Although treatment of rats with the angiotensin I converting enzyme inhibitor enalapril (50 mg/l drinking water) over the 70-week period did not affect the magnitude of proteinuria during the acute nephrotic phase, enalapril prevented the recurrence of proteinuria (phase III), as well as significantly reducing the severity of interstitial fibrosis, extent of tubular dilatation, and number of intratubular casts on semiquantitative scoring at the conclusion of the study. In addition, enalapril-treated rats had less low-molecular-weight protein excretion during the recurrent phase of proteinuria, suggesting a preservation of tubular functional capacity to reabsorb these proteins. In vitro cytotoxicity studies showed only the glomerular visceral epithelial cell to be sensitive to PA, in contrast with rat tubular epithelium and other cellular controls. Although the exact pathogenetic mechanism responsible for the development of the tubulointerstitial damage remains unknown, PA in vitro does not adversely affect rat tubular epithelium; there is however a clear correlation between the magnitude of recurrent proteinuria and the severity of tubulointerstitial morphologic abnormalities, as suggested by the beneficial effect of converting enzyme inhibition on both of these untoward processes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

The Health Club.

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Aged↗
PubMed1989

Angiotensin converting enzyme inhibitors and progressive renal insufficiency. Current experience and future directions.

STUDY OBJECTIVE: To review the rationale for using angiotensin converting enzyme (ACE) inhibitors in progressive renal disease, and to evaluate the experience with these agents in patients with hypertension and renal insufficiency. DATA IDENTIFICATION: Experimental and clinical studies published from January 1977 to November 1988 were identified by searching the literature and by extensive hand searching of bibliographies of identified articles. STUDY SELECTION: Experimental studies of glomerular function during therapy with ACE inhibitors or other antihypertensive regimens were reviewed. Series using ACE inhibitors for treating hypertensive patients with renal disease were evaluated and reports of adverse events were studied. RESULTS OF DATA SYNTHESIS: Experimentally, ACE inhibitors seem to decrease glomerular injury by reducing both systemic and glomerular hypertension. Clinically, ACE inhibitors reduce systemic blood pressure in hypertensive patients with diabetic and nondiabetic renal disease without causing dramatic changes in glomerular filtration rate or renal blood flow. Most studies of nondiabetic renal insufficiency suggest that proteinuria is reduced in most patients. However, no long-term controlled study on the effect of ACE inhibitors on the progression rate of nondiabetic renal disease has been completed. ACE inhibitors have not yet been approved by the Food and Drug Administration (FDA) for treating or preventing progressive renal disease. Such use would therefore be considered "innovative" therapy. CONCLUSIONS: ACE inhibitors are tolerated by azotemic patients, although transient reductions in renal function can occur. Patients with bilateral renal insufficiency or low cardiac output are at increased risk for developing reversible acute renal insufficiency. Hyperkalemia may occur, particularly in patients with diabetes or severe renal insufficiency. In many patients with renal disease, ACE inhibitors dramatically reduce proteinuria, but whether they also reduce the rate of progression of renal disease remains unproved.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. Ticlopidine Aspirin Stroke Study Group.

We report the results of the Ticlopidine Aspirin Stroke Study, a blinded trial at 56 North American centers that compared the effects of ticlopidine hydrochloride (500 mg daily) with those of aspirin (1300 mg daily) on the risk of stroke or death. The medications were randomly assigned to 3069 patients with recent transient or mild persistent focal cerebral or retinal ischemia. Follow-up lasted for two to six years. The three-year event rate for nonfatal stroke or death from any cause was 17 percent for ticlopidine and 19 percent for aspirin--a 12 percent risk reduction (95 percent confidence interval, -2 to 26 percent) with ticlopidine (P = 0.048 for cumulative Kaplan-Meier estimates). The rates of fatal and nonfatal stroke at three years were 10 percent for ticlopidine and 13 percent for aspirin--a 21 percent risk reduction (95 percent confidence interval, 4 to 38 percent) with ticlopidine (P = 0.024 for cumulative Kaplan-Meier estimates). Ticlopidine was more effective than aspirin in both sexes. The adverse effects of aspirin included diarrhea (10 percent), rash (5.5 percent), peptic ulceration (3 percent), gastritis (2 percent), and gastrointestinal bleeding (1 percent). With ticlopidine, diarrhea (20 percent), skin rash (14 percent), and severe but reversible neutropenia (less than 1 percent) were noted. The mean increase in total cholesterol level was 9 percent with ticlopidine and 2 percent with aspirin (P less than 0.01). The ratios of high-density lipoprotein and low-density lipoprotein to total cholesterol were similar in both treatment groups. We conclude that ticlopidine was somewhat more effective than aspirin in preventing strokes in this population, although the risks of side effects were greater.

Aspirin↗
PubMed1989

Induction of murine hemopoietic growth factors by toxic shock syndrome toxin-1.

Toxic shock syndrome toxin-1 (TSST-1), an extra-cellular 22 kDa single chain protein produced by most Staphylococcus aureus strains isolated from patients with toxic shock syndrome (TSS), induces modifications of blood cell values similar to those observed during TSS. We therefore analyzed the effects of TSST-1 on the proliferation and differentiation of murine granulocyte-macrophage progenitor cells (CFU-culture) and the eventual role of endotoxin in this response. TSST-1 had no direct effect on the proliferation of CFU-culture and was unable to influence the CSF-induced proliferation and differentiation of these progenitors. In contrast, TSST-1 was a potent inducer in spleen cell cultures of a factor with an ability to induce both colony formation by bone marrow cells and proliferation of an IL-3-dependent cell line. Nanogram amounts of TSST-1 were able to induce the release of CSF activity in spleen cell cultures from both normal and LPS-hyporesponsive mice. Cells from C3H/HeJ mice were as responsive as cells from C3H/He Pas mice. Furthermore, in spleen cell cultures from normal mice, TSST-1 and LPS did not act synergistically to induce CSF activity. Nanogram amounts of TSST-1 were also able to induce CSF activity in vivo but failed to induce IL-3 activity in the serum and organ-conditioned media from TSST-1-treated mice.

Animals↗
PubMed1989

Slowing of cell cycle traverse for cells in exponential monolayer cultures placed into plateau-fed and starved medium.

MCa-11 tumor cells in exponential monolayer cultures were pulse/chase-labeled with [3H]thymidine and then regrown in fresh, plateau-fed, or starved medium. We measured the DNA content and autoradiographic labeling of these cells by absorption cytophotometry at intervals of 0, 2, 4, 8, 12, and 24 h to follow the progress through the cell cycle of those cells which had incorporated isotope. We found that for the cells grown in plateau-fed and starved medium the G0/G1, S, and G2 phases of the cell cycle were prolonged when compared to those for cells grown in fresh medium. These results show that, under adverse microenvironmental conditions, the growth of tumor cells can be regulated in all phases of the cell cycle, and that this regulation can include lengthening and even cessation of replicative DNA synthesis.

Cell Cycle↗
PubMed1989

Bone marrow involvement in small cell lung cancer. Clinical significance and correlation with routine laboratory variables.

Of 129 patients with small cell lung cancer (SCLC) who underwent bone marrow examination for staging, 39 (30%) had bone marrow involvement. Only three of 129 patients (2.3%) had bone marrow involvement as the only site of metastatic disease. When patients with bone marrow metastasis were compared with patients whose bone marrow was normal, there were significant differences in serum levels of lactate dehydrogenase (LDH), glutamic oxalacetic transaminase (SGOT), glutamic pyruvic transaminase (SGPT), alkaline phosphatase (AP), albumin, and sodium (Na). We found no clinically significant difference in survival between patients with extensive disease with or without bone marrow involvement. Serum Na, albumin, SGOT, and uric acid were important prognostic determinants of survival. Based on the results of this study, we do not recommend routine bone marrow examinations in the staging of SCLC.

Adult↗
PubMed1989

Emergency angioplasty in acute anterior myocardial infarction.

Ninety-three patients with acute anterior myocardial infarction were treated with emergency percutaneous transluminal coronary angioplasty (PTCA). All were found to have a high-grade obstruction in the left anterior descending (LAD) vessel or the bypass graft to this vessel; 64 patients had a total occlusion. A completely successful PTCA, defined as a residual lesion of less than or equal to 50%, was achieved in 73 (78%) patients. A partially successful PTCA, with a residual lesion of 51% to 99%, was achieved in 12 (13%) patients. PTCA was unsuccessful in eight (9%) patients. Hospital mortality was 14%. Three parameters viewed separately each predicted hospital mortality: presence of shock, a proximal location of the LAD vessel occlusion, and the residual stenosis after PTCA. Reocclusion was found in only 11% of patients but 34% had evidence of restenosis on restudy.

Aged↗