Exophthalmos and blindness disclosing an ethmoidal-maxillary malignant non-Hodgkin's T-cell lymphoma. Apropos of a case]

BACKGROUND: We report a case of non-Hodgkin's malignant lymphoma of the cervicofacial region revealed by unilateral exophthalmos and blindness, an unusual mode of expression. CASE REPORT: A 40-year-old man with a 4-month history of diabetes mellitus had suffered from exophthalmos and blindness of the right eye for 20 years. Physical examination showed a homolateral hemifacial tumefaction and ophthalmoplegia. The right ocular fundus showed papillar edema and non-proliferative diabetic retinopathy. The left eye was normal. The otolaryngology explorations revealed a voluminous tumor in the anterior nasal cavity and in the cavum. Two biopsies were performed. Histology reported non-Hodgkin's T-cell lymphoma. Orbitocerebral and cervicofacial computed tomography visualized the aggressive ethmoidomaxillary extension with intraorbital and intracranial involvement. Chemotherapy (CHOP) combined with radiotherapy led to tumor regression and involution of the exophthalmos. Diagnostic difficulties, management and prognosis are discussed.     

Insulin-like growth factor-I regulates proliferation and osteoblastic differentiation of calcifying vascular cells via extracellular signal-regulated protein kinase and phosphatidylinositol 3-kinase pathways

Vascular calcification develops within atherosclerotic lesions and results from a process similar to osteogenesis. One of the paracrine regulators of bone-derived osteoblasts, insulin-like growth factor-I (IGF-I), is also present in atherosclerotic lesions. To evaluate its possible role in vascular calcification, we assessed its in vitro effects on proliferation and differentiation in calcifying vascular cells (CVCs), a subpopulation of bovine aortic medial cells. Results showed that IGF-I inhibited spontaneous CVC differentiation and mineralization as evidenced by decreased alkaline phosphatase (AP) activity and decreased matrix calcium incorporation, respectively. Furthermore, IGF-I inhibited the AP activity induced by bacterial lipopolysaccharide, TNF-alpha, or H2O2. It also induced CVC proliferation based on 3H-thymidine incorporation. Results from Northern analysis and tests using IGF-I analogs suggest that IGF-I effects are mediated through the IGF-I receptor. IGF-I also activated both the extracellular signal-regulated protein kinase (ERK) and phosphatidylinositol 3-kinase (PI3K) pathways. Inhibition of either the ERK or PI3K pathway reversed IGF-I effects on CVC proliferation and AP activity, suggesting a common downstream target. Overexpression of ERK activator also mimicked IGF-I inhibition of lipopolysaccharide-induced AP activity. These results suggest that IGF-I promotes proliferation and inhibits osteoblastic differentiation and mineralization of vascular cells via both ERK and PI3K pathways.     

Paucity of antigen-specific IgA responses in sera and external secretions of HIV-type 1-infected individuals

This study was undertaken to resolve existing controversies with respect to the detection of IgA HIV-1-specific mucosal antibodies in infected individuals. External secretions, including tears, nasal, rectal, and vaginal washes, saliva, semen, urine, and sera were obtained from 50 HIV-1-infected individuals and 20 controls using collection procedures that minimize the irritation of mucosal surfaces. Levels of total and antigen (gp120 and gp160)-specific antibodies of the IgG and IgA isotypes were measured by assays that proved reliable in a large multicenter study: quantitative ELISA and chemiluminescence-enhanced Western blot analyses. Although the levels of total IgG and IgA were increased or remained unchanged in body fluids of HIV-1-infected individuals as compared to the controls, HIV-1-specific IgA antibodies were either absent or present at low levels even in secretions with characteristically high relative contents of total IgA vs. IgG (saliva, tears, and rectal and nasal washes). In these secretions, HIV-1-specific IgG antibodies dominated. In assessing levels and frequency of detection of IgG antibodies, both female and male genital tract secretions, urine, and nasal wash were preferable to parotid saliva and especially to rectal wash. External secretions contained IgG antibodies to gp160> gp120> gp41 and p24; when present, IgA antibodies were predominantly directed at gp160. Analyses of peripheral blood antibody-secreting cells (ASC) isolated from the same individuals paralleled these serological findings: gp160-specific IgG-secreting ASC were dominant. Therefore, in striking contrast to other mucosally encountered microbial infections, HIV-1 does not induce vigorous specific IgA responses in any body fluid examined or in ASC in peripheral blood.