Cervical cancer: a call for political will.

Cervical cancer kills over a quarter of a million women worldwide on an annual basis, with 80% of these deaths occurring in developing countries. Cytology-based screening programs, widely used in industrialized countries, are difficult to implement in low-resource settings. Non-cytological methods for screening and treatment have been developed and studied over the last decade. Given the barriers to widespread, good quality screening and early treatment, the most promising new prevention strategy will be the introduction of a vaccine to prevent human papillomavirus infection, the cause of cervical cancer. Understanding women's health-seeking behaviors is critical to successful dissemination and uptake of both screening and vaccine prevention strategies.

Propylthiouracil (PTU)-induced agranulocytosis treated with recombinant human granulocyte colony-stimulating factor (G-CSF).

Two premenopausal female patients with Graves' hyperthyroidism and propylthiouracil (PTU)-induced agranulocytosis are presented. The first patient, age 47, received 300 mg of PTU per day and developed agranulocytosis within 6 weeks of the commencement of therapy. There were no granulocytes in the peripheral smear and a bone marrow biopsy demonstrated an absence of the entire myeloid cell line as well as the presence of many granulomas. The second patient, age 39, received PTU 1600 mg per day for two and half weeks and then 2 days of methimazole, 200 mg per day. She developed complete agranulocytosis on peripheral smear within 3 weeks of the initiation of therapy. Her bone marrow biopsy demonstrated maturation arrest of the granulocytic cell line at the myelocyte stage. In addition to discontinuing their antithyroid drugs, both patients were treated with G-CSF subcutaneously. The first patient received 300 micrograms of G-CSF on days 2 and 4 after discontinuing PTU with the appearance of 4.7 x 10(9)/L granulocytes and granulocyte precursors on day 4. The second patient received 575 micrograms of G-CSF for 2 days and 300 micrograms for 1 additional day beginning on the third day after discontinuing antithyroid drugs. On the second treatment day there were 5.8 x 10(9)/L granulocytes and granulocyte precursors on the peripheral smear. A comparison to previously published cases on antithyroid drug induced agranulocytosis suggests that the use of G-CSF decreased the amount of time required for marrow recovery after the cessation of the offending drug.

Late-onset 21-hydroxylase deficiency and polycystic ovary disease. A case report.

In a case of late-onset 21-hydroxylase deficiency (21HD), the clinical presentation was that of polycystic ovary disease (PCOD). Wedge resection of the ovaries yielded tissue that, on histology, was consistent with PCOD. Most likely the PCOD was secondary to the late-onset 21HD.

Hormone-induced homologous and heterologous desensitization in the rat adipocyte.

We examined the process of desensitization in the isolated rat adipocyte. When adipocytes were exposed to isoproterenol (10(-7) or 10(-5) M) or ACTH (250 mU/ml) for 2 h, there was a marked decline of as much as 77% in response upon restimulation by hormone, as measured by glycerol release or cAMP levels. This desensitization was both heterologous as well as homologous. Thus, for example, exposure of adipocytes to isoproterenol desensitized them to further stimulation by both isoproterenol and ACTH. The process was time dependent, since augmentation rather than desensitization was seen if cells were initially exposed to hormone for 30 min rather than 2 h. No desensitization was seen when the cells were restimulated with the nonhormonal lipolytic agent dibutyryl cAP. Similarly, no desensitization was seen when cells were first exposed to dibutyryl cAMP and then restimulated with hormone. We draw the following conclusions. First, desensitization in the adipocyte is a time- and dose-dependent process that is specific for adenylate cyclase-activating hormones. Secondly, the process is heterologous as well as homologous. Initial exposure of the adipocyte to one adenylate cyclase-activating hormone reduces its adenylate cyclase or lipolytic response upon reexposure to either the same or a different adenylate cyclase-activating hormone. Finally, the reduction in the end result of hormone activation, lipolysis, is due in part to a decrease in inducible levels of cAMP.