Hydrophilic polymers are commonly applied as surface coatings on vascular devices and have been shown to dissociate during endovascular use, causing hydrophilic polymer embolism (HPE). Adverse effects related to this phenomenon have been recognized and reported. The prevalence of this complication is unknown. We conducted a retrospective study to determine the prevalence of HPE among hospital autopsies over a 29-month period. Postmortem tissue was histologically evaluated for the presence, location(s) and extent of HPE. HPE findings were correlated with documented clinical and laboratory data and patient outcome. Of 136 hospital autopsies examined, 18 (13%) showed evidence of HPE involving the lungs (n = 18), heart (n = 1) or central nervous system (n = 1). Localized pulmonary HPE was seen in 12 patients (9%). Multifocal pulmonary HPE was found in 6 patients (4%) and was associated with clinical vasculitis (33%; P < .0001), suspected pulmonary ischemia (50%; P = .008), coagulopathy (67%; P = .002), and constitutional disease (83%; P = .01). Within affected lung, associated histopathologic changes included occlusive intravascular or perivascular inflammation (89%), intravascular fibrous response (56%), microthrombus formation (44%), vasculitis (28%), and/or pulmonary microinfarction (28%). Statistically significant differences in hospital days (P = .008) and number of vascular interventions (P = .01) were noted between affected and unaffected patients. We conclude that HPE is an underdiagnosed phenomenon with primary involvement of the lungs, where secondary vascular changes are common. Additional studies may be needed to clarify risks and to identify preventative strategies for this iatrogenic complication of catheterizations and “minimally invasive” endovascular techniques.

The results from this study demonstrate that systemic and peripheral fat mitochondria improve in patients switched to tenofovir following long-term exposure to stavudine, while continuing protease inhibitor therapy.

Transplacental nucleoside analogue exposure can affect infant mitochondrial DNA (mtDNA). We evaluated mitochondria in peripheral blood mononuclear cells of children with and without clinical signs of mitochondrial dysfunction (MD) and antiretroviral (ARV) exposure. We previously identified 20 children with signs of MD (cases) among 1037 HIV-uninfected children born to HIV-infected women. We measured mtDNA copies/cell and oxidative phosphorylation (OXPHOS) NADH dehydrogenase (complex I) and cytochrome c oxidase (complex IV) protein levels and enzyme activities, determined mtDNA haplogroups and deletions in 18 of 20 cases with stored samples and in sex-and age-matched HIV-uninfected children, both ARV exposed and unexposed, (1) within 18 months of birth and (2) at the time of presentation of signs of MD. In specimens drawn within 18 months of birth, mtDNA levels were higher and OXPHOS protein levels and enzyme activities lower in cases than controls. In contrast, at the time of MD presentation, cases and ARV-exposed controls had lower mtDNA levels, 214 and 215 copies/cell, respectively, than ARV-unexposed controls, 254 copies/cell. OXPHOS protein levels and enzyme activities were lower in cases than exposed controls, and higher in cases than unexposed controls, except for complex IV activity, which was higher in cases. Haplotype H was less frequent among cases (6%) than controls (31%). No deletions were found. The long-term significance of these small but potentially important alterations should continue to be studied as these children enter adolescence and adulthood.

Purpose HIV infection has been implicated in dysregulation of the autonomic nervous system. Method Cross-sectional study examining the relationship between the presence of persistent detectable HIV viral load with autonomic function, measured by heart rate variability (HRV). Non-virologic suppression (NVS) was defined as having a detectable viral load for at least 3 months prior to autonomic function testing. HRV was measured during the following 4 maneuvers: resting and paced respirations and sustained handgrip and tilt. Inferences on parasympathetic and sympathetic modulations were determined by analyzing time and frequency domains of HRV. Results 57 participants were enrolled in 3 groups: 22 were HIV-infected participants with HIV virologic suppression (VS; undetectable HIV viral load), 9 were HIV-infected participants who had NVS, and 26 were HIV seronegative controls. There were lower time domain parameters in the HIV-infected group as a whole compared to controls. There were no significant differences in time domain parameters among HIV-infected participants. There were no differences in frequency domain parameters during any of the maneuvers between controls and all HIV-infected participants, nor between the NVS and VS groups. Conclusion There were differences in autonomic function between HIV-infected individuals and HIV seronegative controls, but not between the NVS and VS groups.

An HIV-infected male patient who had sex with men and with a penicillin allergy presented with liver dysfunction due to secondary syphilis and was successfully treated with doxycycline. This case highlights that syphilitic hepatitis may be overlooked in this particular population, and health care providers should be attuned to this diagnosis. Doxycycline may be an acceptable alternative to penicillin for treatment of this clinical syndrome.