"Crack" cocaine-associated stroke

We present three cases of "crack" cocaine-associated stroke, together with a review of cocaine-associated cerebrovascular complications. Unlike previously reported cases tentatively associating ischemic stroke with cocaine, our patients had no other potential causes for their strokes. Although the exact mechanism of cocaine-related stroke remains uncertain, both disordered neurogenic control of the cerebral circulation as well as systemic factors (ie, acute hypertension) may play a role.     

Prohibition of preventive health care: an analysis of Medicaid non-reimbursement for indigent women

This paper presents a policy analysis of the impact of prohibiting Medicaid reimbursement funding for tubal ligations by indigent women, under 21 years of age. Because this population is dependent upon Medicaid funds, the freedom of self determination is limited. The current policy does not provide any alternative to the age rule, even if the patient is infected with a life-threatening disease, such as human immunodeficiency virus (HIV). The policy, therefore, creates serious problems for those individuals who choose to prevent a pregnancy under certain life-threatening circumstances. As the incidence of AIDS continues to increase, the absence of an age alternative for tubal ligations will become a problem of increasing practical and statistical significance. The conceptual framework for the analysis of Medicaid nonreimbursement for tubal ligations, with respect to age demands was adopted from the work of Gilbert and Specht, 1986. Four dimensions of choice are addressed: (1) the bases of social allocation, (2) the nature/type of social provisions, (3) the delivery system and (4) finances. Although all areas will be addressed, the major emphasis will be placed on social allocation.     

Interventions to reduce cardiovascular risk factors in children and adolescents

Certain modifiable risk factors for cardiovascular disease have their beginnings in childhood. Cigarette smoking, hypertension, physical inactivity, obesity, hypercholesterolemia, hyperinsulinemia, homocysteinemia and poor nutrition in childhood and adolescence may all contribute to the development of cardiovascular disease in adulthood. Identifying at-risk children and adolescents is the first step in modifying or preventing these risk factors. Intervention is most effectively accomplished with an integrated family-oriented approach. Involving the entire family in counseling about interventions to reduce the risk factors for coronary artery disease is important. The family should complete a questionnaire about the family's history and risk of cardiovascular disease. The child, along with other family members, should be given advice on dietary changes to reduce fat intake. Incorporating a cardiovascular health schedule into routine office visits is useful for monitoring the risk of cardiovascular disease and for reinforcing the need to maintain healthy habits.     

Pelvic inflammatory disease. Key treatment issues and options.

OBJECTIVE.--To examine available data regarding optimal antimicrobial therapy for pelvic inflammatory disease (PID) and to address selected treatment issues confronting clinicians caring for women with PID. DATA SOURCES.--Studies evaluated to help establish the Centers for Disease Control's 1989 Sexually Transmitted Diseases Treatment Guidelines and other reports published since 1985. A MEDLINE search of English-language literature was conducted using the indexing terms "pelvic inflammatory disease" or "pelvic infections" or "salpingitis" and "treatment". In addition, abstracts and bibliographies of articles and books were reviewed. STUDY SELECTION.--Studies were selected for detailed review if they evaluated the effectiveness of an antimicrobial regimen for treatment of PID. DATA EXTRACTION.--All studies were evaluated to determine the numbers of women treated and the percentage with clinical or microbiologic evidence of cure. DATA SYNTHESIS.--A variety of combination antimicrobial regimens are highly effective in providing clinical and microbiologic evidence of cure; few data are available to assess optimal therapy for prevention of late sequelae. Because PID is polymicrobial in cause, recommended antimicrobial regimens are broad-spectrum in coverage. CONCLUSIONS.--No single agent that provides sufficient coverage is currently available. Several combination regimens appear highly effective clinically even among women with tubo-ovarian abscess formation. Uncertainties regarding the effectiveness of antimicrobial therapy for prevention of late sequelae complicate decisions regarding the choice among regimens and the appropriateness of ambulatory treatment of women with PID. Pending better data, hospitalization should be strongly considered, where feasible, particularly for those women with PID desiring further childbearing. Sex partners of all women with PID should be treated.     

Effects of intermittent exposure to aflatoxin B1 on DNA and RNA adduct formation in rat liver: dose-response and temporal patterns.

We studied the effects of intermittent exposure to aflatoxin B1 (AFB1) on hepatic DNA and RNA adduct formation. Fisher-344 male rats were fed 0.01, 0.04, 0.4, or 1.6 ppm of AFB1 intermittently for 8, 12, 16, and 20 weeks, alternating with 4 weeks of dosing and 4 weeks of rest. Other groups of rats were fed 1.6 ppm of AFB1 continuously for 4, 8, 12, and 16 weeks. Control rats received AFB1-free NIH-31 meal diet. AFB1-DNA and -RNA adducts were measured by HPLC with fluorescence detection. The data are presented as total DNA or RNA adducts. The DNA and RNA adduct levels increased or decreased depending on the cycles of dosing and rest. Rats removed from treatment 1 month after 1 or 2 dosing cycles (8 and 16 weeks of intermittent exposure) showed approximately a twofold decrease in DNA adduct levels and a two- to elevenfold decrease in RNA adduct levels compared with rats euthanized immediately after the last dosing cycle (12 and 20 weeks of intermittent exposure). Our data indicate that DNA and RNA adducts increased linearly, from 0.01 ppm to 1.6 ppm of AFB1 after 12 and 20 weeks of intermittent treatment. A linear dose response was also apparent for DNA but not for RNA adducts after 8 and 16 weeks of treatment. As biomarkers of exposure, AFB1-RNA adducts were three to nine times more sensitive than AFB1-DNA adducts but showed greater variability. These results suggest that binding of AFB1 to hepatic DNA is a linear function of the dose, regardless of the way this is administered. The dose-response relationship for RNA adducts depends on the length of the no-dosing cycles and on the turnover rate of RNA.     

Toxic cardiogenic shock in a patient receiving weekly 24-h infusion of high-dose 5-fluorouracil and leucovorin

A 54-year-old man was treated with weekly 24-h infusion of high-dose 5-fluorouracil (2600 mg/m2) and leucovorin (100 mg/m2) for metastatic colon cancer. At first, he tolerated the treatment well and no significant toxicity was identified. After a total of eight courses of treatment, a stable disease was observed, but mild shortness of breath was found on occasion. The patient had no previous history of cardiac disease and the heart performance assessed by left ventricular ejection fraction before treatment was normal. Unfortunately, acute pulmonary edema with lethal cardiogenic shock occurred during the ninth course of treatment, in spite of intensive medical treatment. The chest X-ray showed extreme cardiomegaly. Repeated assessment of his heart function by echocardiogram and ventricular ejection fraction revealed a very poor cardiac performance. Toxic cardiogenic shock during weekly 24-h infusion of high-dose 5-fluorouracil and leucovorin is extremely rare. To the best of our knowledge, no case has been reported in the English literature. We report a case and the relevant literature about the incidence, clinical picture and possible pathophysiology on 5-fluorouracil-related cardioxicity is reviewed.      

Mortality: What Are the Roles of Risk Factor Prevalence,Screening, and Use of Recommended Treatment?

CONTEXT: Despite advances in early detection and prevention of cervical cancer, women living in rural areas, and particularly in Appalachia, the rural South, the Texas/Mexico border, and the central valley of California, have had consistently higher rates of cervical cancer mortality than their counterparts in other areas during the past several decades. METHODS: This paper reviews the published literature from 1966 to July 2002 to assess three potential pathways underlying this excess mortality--high human papilloma virus (HPV) prevalence, lack of or infrequent screening and advanced disease at diagnosis, and under-use of recommended treatment and shorter survival. FINDINGS: Living in rural areas may impose barriers to cervical cancer control, including lack of transportation and medical care infrastructures. Population characteristics that place women at greater risk for developing and dying from cervical cancer, such as low income, lack of health insurance, and physician availability, are concentrated in rural areas. Published data, however, are insufficient to identify the key reasons for the observed mortality patterns. CONCLUSIONS: At this time, given the lack of definitive evidence in the published literature, decisions about priorities in areas with high rates of cervical cancer mortality will depend on knowledge of current levels of screening, incidence, and stage distribution; and service delivery infrastructures, resources, and acceptability of interventions to the target population.