FAM chemotherapy +/- aminoglutethimide in the treatment of pancreatic carcinoma.

Human pancreas contains receptors for estrogens and androgens as well as aromatase activity. FAM chemotherapy was administered to 14 patients with pancreatic cancer (seven at Stage IV). The median survival of these patients was 24.4 +/- 4.8 weeks. FAM chemotherapy plus aminoglutethimide/hydrocortisone (AG/HC) (250 mg bid AG + 20 mg bid HC) was administered to 14 patients (seven at stage IV). The median survival of this group was 17.3 +/- 2.9 weeks (P = 0.74 vs FAM alone). We conclude that addition of AG/HC does not add to the survival of patients with carcinoma of the pancreas treated with chemotherapy.

Guidelines for cleaning to protect patients from AIDS.

As the AIDS virus spreads into the general population, protecting the public, health workers and patients from possible infection becomes increasingly important. The Surgeon General recommends testing all surgery patients for the presence of AIDS prior to surgery; however, it is often impossible to complete these tests on emergency surgery, labor and delivery and emergency department patients because of the emergent nature of the admission. As the author notes, these patients require special precautions. In this article, the author summarizes the effective disinfection procedures for AIDS recommended by CDC and offers a detailed procedure to be used for cleaning the surgical/delivery suites and emergency room. This procedure upgrades the standards already in existence.

A randomized trial of aminoglutethimide +/- estrogen before chemotherapy in advanced breast cancer.

Recent reports have suggested that the sensitivity to chemotherapy of endocrine-dependent breast cancer may be enhanced by transient exposure to hormonal stimulation. To test this concept, 39 postmenopausal women with proven metastatic breast carcinoma and measurable disease were entered into this prospective, double-blind trial; 35 are currently evaluable. All patients were continuously treated with aminoglutethimide and hydrocortisone to lower estrogen production, plus cyclic chemotherapy. Patients in the "stimulation" arm received in addition, Estrace 2 mg b.i.d. sublingually for 3 days before and on the day of chemotherapy. Estrace administration appeared to accelerate tumor growth as demonstrated by increased bone pain, hypercalcemia, and growth of skin lesions. Response rates, response duration, and survival were similar in the stimulation and control groups.

Addition of etoposide to cyclophosphamide, doxorubicin, and vincristine for remission induction and survival in patients with small cell lung cancer.

A total of 116 patients with small cell lung cancer were randomized to receive either: cyclophosphamide, 750 mg/m2, doxorubicin, 50 mg/m2, and vincristine, 2 mg iv (Regimen A), or the same drugs plus etoposide, 100 mg/m2 iv daily for 2 days (Regimen B) every 3 weeks. Complete responders received whole-brain radiation therapy. The overall response rates were 50% for Regimen A and 65% for Regimen B (P less than 0.05). The complete response rates were 18% for Regimen A and 44% for Regimen B (P less than 0.01). For patients with limited disease, the complete responders were 35% on Regimen A and 52% on Regimen B (P = 0.26); for those with extensive disease, the complete responders were 0% on Regimen A and 35% on Regimen B (P = 0.002). The median survival for complete responders was 17 months on Regimen A and 20 months on Regimen B. The difference is not statistically significant. Toxicity was tolerable for both groups; however, it was greater for the etoposide arm. We conclude that although etoposide improves the overall response rates in patients with small cell lung cancer, especially those with extensive disease, the addition of this drug does not lead to improved survival.

Nonmedical costs to patients and their families associated with outpatient chemotherapy.

One hundred thirty-nine patients receiving outpatient chemotherapy kept diaries of nonmedical expenses resulting from their disease and its treatment. Diaries were kept for both treatment and nontreatment weeks. Results showed that the mean cost to patients and their families for treatment weeks was $72.81, and for nontreatment weeks it was $45.88. Approximately 45% of these costs were out-of-pocket expenses, and 55% were wages lost. Transportation and food were the largest out-of-pocket expenses. Patients living at greater distance from treatment had higher out-of-pocket costs, and younger patients reported more wages lost. Fourteen percent of the patients were estimated to be spending more than 50% of their weekly incomes on nonmedical expenses, and these patients were found largely in the lower-income categories. A method is proposed for using these data to estimate total nonmedical expenses for different treatment regimens, and also for estimating cancer patients' total nonmedical costs nationally.

Extended plasma source for short-wavelength amplifiers.

An elongated plasma of length approximately 8 mm with an aspect ratio of ~6:1 has been formed by channeling a laser-produced plasma created in a point focus on a carbon surface. Densities of C(6+) ions near 10(16) cm(-3) were observed in a contracted region beyond the guiding channel, suggesting a use for short-wavelength amplification.

Heparin induced thrombocytopenia: eight cases with thrombotic-hemorrhagic complications.

Increased heparin tolerance and recurrent thromboembolism which included myocardial infarction (3 patients), pulmonary embolism (2 patients) and complete aorto-iliac occlusion (2 patients), heralded the development of thrombocytopenia between the eighth and twelfth day of heparin therapy in six women and two men. The thrombocytopenia persisted until heparin was discontinued. Bleeding (cerebral hemorrhage) was the initial complication in one patients and occurred in conjunction with thrombotic complications in four other patients. Agglutination absorption testing in one and complement fixation testing in five patients suggested the presence of heparin dependent antiplatelet antibodies. After platelet recovery, four of the eight patients responded to parenteral heparin rechallenge with rapid decreases in their platelet counts. The early recognition of the syndrome with cessation of heparin therapy is imperative for the successful management of afflicted patients.

Mechanism of complement-mediated activation of human blood platelets in vitro: comparison of normal and paroxysmal nocturnal hemoglobinuria platelets.

The paroxysmal nocturnal hemoglobinuria (PNH) platelet differs from the normal human platelet in its interaction with activated complement components: (a) when complement is activated by the alternative pathway, greater amounts of C3 are fixed to the PNH platelet than to the normal platelet; (b) the platelet-release reaction, as measured by serotonin release, occurs after C3 fixation to the PNH platelet. This reaction does not occur with normal platelets; (c) although serotonin release mediated by antibody alone was the same for normal and PNH platelets, antibody-initiated complement activation resulted in the fixation of greater amounts of C3 to PNH platelets and greater consequent serotonin release; and (d) nearly maximal serotonin release; and (d) nearly maximal serotonin release from PNH platelets occurs after the fixation of C3 (or perhaps C5) to the membrane without completion of the terminal sequence. In contrast, completion of the terminal complement sequence beyond C5 is required for maximal serotonin release from normal platelets. These abnormalities of interaction of complement components and PNH platelets may explain the occurrence of thromboses in this disease.