For HIV-infected adults in Côte d'Ivoire, co-trimoxazole prophylaxis is reasonably cost-effective and most effective if initiated when WHO stage > or = 2. Early co-trimoxazole prophylaxis will prevent complications prior to antiretroviral therapy initiation and should be considered an essential component of care for early HIV in sub-Saharan Africa.

Circulating opsonin levels and reticuloendothelial (RE) phagocytic activity were investigated in anesthetized rats subjected to Noble-Collip drum (NCD) trauma. Reticuloendothelial function was assessed by colloid clearance kinetics and circulating opsonin levels by in vitro tissue slice bioassay. After sublethal shock, both hepatic RE phagocytosis and plasma opsonic activity were significantly (P less than 0.001) depressed in the 0.5- to 6-h posttrauma period. Pulmonary and bone marrow localization of the blood-borne test microparticles significantly (P less than 0.05) increased during hepatic RES depression. Hepatic RE cells from animals during the interval of posttraumatic in vivo phagocytic depression exhibited normal phagocytosis when incubated in normal pretrauma plasma and decreased phagocytic activity when incubated in posttrauma plasma. After sublethal shock, restoration or opsonin levels by 24 h after shock resulted in hepatic RE recovery. Plasma opsonin levels declined in direct relationship to the degree of trauma. Progressive hepatic RE failure was correlated with the progressive decline in circulating plasma opsonic activity. The findings indicate that opsonic depletion may be involved in the etiology of hepatic reticuloendothelial depression after traumatic shock.

To determine adherence by health care providers to guidelines for antiretroviral therapy and for prevention of opportunistic infections (OIs) in adults with HIV infection in federally funded facilities in the United States, we reviewed records of HIV-infected adults (>13 years) in 11 Ryan White Title III facilities in four states for information on eight standard-of-care recommendations during November 1996 through September 1997. Eligibility required a visit to the facility within 6 months before record abstraction and a lowest CD4+ lymphocyte count <500 cells/microl. Reviews were completed for 148 patients in Maryland, 355 in New York, 370 in Georgia, and 538 in Illinois. Adherence to prevention measures by health care providers was >85% for HIV plasma RNA testing, prescription of antiretroviral therapy, Pneumocystis carinii pneumonia (PCP) prophylaxis, anti-Toxoplasma antibody testing, and obtaining Papanicolaou (Pap) smears but lower (69%-80%) for Mycobacterium avium complex (MAC) prophylaxis, tuberculin skin testing (TST), and pneumococcal vaccination. Adherence was similar by patient age, gender, racial/ethnic group, urban versus rural, and hospital versus clinic setting but was generally lower for injecting drug users (IDUs) than for patients with other HIV exposures (p < .05 by multivariate analysis for TST, anti-Toxoplasma antibody testing, Pap smear, and measurement of HIV plasma RNA). Adherence by health care providers to guidelines for preventing OIs in these federally funded facilities is generally high but could be improved for some prevention measures, for instance, MAC prophylaxis, TST, and pneumococcal vaccination, especially for IDUs.

No abstract

SummaryThe effect of platelets on polymorphonuclear leukocytes (PMN) O− 2 production was examined using autologous sheep and human cell systems. Coincubation of sheep platelets with sheep PMNs in the absence of thrombin resulted in a significant inhibition in basal PMN O− 2 production. The platelet-derived inhibitory activity was released into the medium and could be destroyed by adenosine deaminase suggesting that the inhibitor was adenosine. Addition of alpha-thrombin or platelet activating factor (PAF) enhanced PMN O− 2 production but only when platelets were present. The enhancement of O− 2 production in response to thrombin was dependent upon the thrombin concentration and the platelet-PMN ratio. With a platelet:PMN ratio of 30:1, addition of 10 nM thrombin to sheep cells resulted in a 5-fold increase in O− 2 production, whereas addition of 10 nM PAF caused a 2-fold increase in O− 2. Addition of thrombin or PAF to either PMNs or platelets by themselves did not initiate an increase in O− 2 generation. The response of human cells was similar except that both thrombin and PAF triggered a 2-fold increase in PMN O− 2 production in the presence of platelets. The platelet-derived enhancement activity was not released into the medium and was not blocked by WEB 2086, NDGA, ETYA, aspirin or adenosine deaminase. The enhancement effect appeared to be localized to the platelet membrane and we believe requires platelet-PMN contact.