The introduction of highly active antiretroviral therapy (HAART) has drastically changed the scope and spectrum of diseases associated with HIV, shifting from AIDS-related to non-AIDS-related diseases. Studies linking HIV/AIDS databases to cancer registries have shown a dramatic decrease in AIDS-related malignancies and a steady increase in non-AIDS-defining malignancies (NADM). We review the causes underlying the rise in incidence of NADM and the clinical presentation, pathology, and treatment outcomes of the four most commonly encountered NADM in the HAART era. Meta-analysis of published studies show an increase in NADM over the general population, mostly among infection-related cancers such as anal cancer, Hodgkin lymphoma, and liver cancer. Among the non-infection-related cancers, lung and skin cancers predominate. The overall effect of HAART on NADM is unsettled. As HIV-infected individuals survive longer, better screening strategies are needed to detect cancer earlier, and prospective data are needed to assess the impact of HAART on cancer outcomes.

A 20-day-old male infant presented with fever, decreased alertness and quadriparesis as a result of Pasteurella multocida meningitis and C1-2 vertebral osteomyelitis. Although his household contained 2 pet cats, there was no history of bites, scratches or licks. We speculate that colonization of the nasopharynx was followed by contiguous spread to the retropharyngeal soft tissue, cervical vertebrae and meninges.

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The relationships of O2 tension in mesenteric lymph (PmlO2) and mesenteric venous blood (PmvO2) to intestinal O2 delivery/O2 consumption (DO2/VO2) were examined after graded hemorrhage (10 dogs), stepwise increments in FIO2 (4 dogs), and regional infusion of papaverine (2 mg/min or IV glucagon (25 microgram/kg) (4 dogs). Measurements included superior mesenteric arterial flow (SMA-Q), PaO2, PmlO2, and arterial and mesenteric venous blood O2 content (CaO2, CmvO2). Intestinal DO2 was calculated as the product of SMA-Q and CaO2, and VO2 was calculated from the Fick equation [SMA-Q X (CaO2 - CmvO2)]. Graded hemorrhage lowered SMA-Q, DO2 and DO2/VO2 and increased splanchnic O2 extraction (CaO2 - CmvO2). Elevation of FIO2 increased PaO2, PmvO2, and PmlO2. Both PmlO2 and PmvO2 varied directly with DO2/VO2 and PaO2, but PmlO2 showed greater sensitivity to PaO2. Papaverine and glucagon both increased SMA-Q, DO2, CmvO2, and PmvO2, BUT PmlO2 rose after papaverine, indicating greater capillary perfusion, and fell after glucagon, suggesting diversion of mesenteric blood flow through arteriovenous shunts. Thus, either PmvO2 or PmlO2 is ordinarily an accurate measure of intestinal tissue oxygenation, but the disparate response after glucagon suggests that PmlO2 is a more reliable indicator.

The formation of deoxyhemoglobin S (deoxy-Hb S) polymers is the key triggering event for the complex pathophysiologic manifestations of sickle cell anemia (SCA). This polymer formation is associated with a marked right-shifted oxyhemoglobin dissociation curve (decreased affinity, increased P50), which results in a decrease in arterial oxygen saturation (SaO2). There is a delay period (“delay time”) from the formation of deoxy-Hb S to polymerization that is markedly sensitive (to the power of 30–40) to the concentration and solubility changes of deoxy-Hb S. Deoxy-Hb S polymer formation leads to sickle cell vaso-occlusion, a unique characteristic of SCA. This theoretical study, which views SCA as a disease of oxygen transport, provides a novel framework to suggest that a small to modest increase in cardiac index (by decreasing the P50 and thus increasing the SaO2) could change the distribution of the delay times (sec) such that the balance between occlusion and opening of microcirculatory vessels is shifted favoring the opening of these vessels, therefore disfavoring vaso-occlusion. Our approach integrates a mathematical model of oxygen transport in SCA with: (1) the expression relating the solubility of deoxy-Hb S to SaO2, and (2) the kinetic expression relating the delay time to the solubility of deoxy-Hb S.