Provider-initiated HIV testing for paediatric inpatients and their caretakers is feasible and acceptable

Objectives  Early diagnosis of HIV-infected children remains a major challenge in Africa. Children who are hospitalised represent an opportunity for HIV diagnosis and appropriate treatment. We introduced HIV Counselling and Testing (HCT) for hospitalised children and their caretakers in Mulago teaching hospital in Uganda to assess its feasibility.
Methods  We analysed routine program data for children and caretakers who were tested between February 2005 and February 2008 to assess the proportion of children and caretakers who were HIV-infected. We also assessed the level of immune suppression (CD4 percentage) in a subset of HIV infected children tested between January 2007 and December 2007.
Results  Caretakers agreed to HIV testing for 8990 (92.8%) of the 9687 children who were offered HIV testing. Among the caretakers, 89.8% agreed to be tested. At the time of hospitalization, 41.3% of the caretakers had previously tested for HIV. Although 313 parents (mothers and fathers) reported that they had previously tested HIV positive, only 113 (36.3%) of these had tested their children prior to hospitalization. Overall HIV prevalence among caretakers was 16.7%. HIV prevalence among children was 12.4%, highest on the nutrition ward (30.8%). Of those children who underwent CD4 counts, 56.4% had a CD4 percentage of <20%.
Conclusion  HCT for hospitalized children and their caretakers identified a significant number of HIV infected children and caretakers. More than half of the children had advanced HIV disease. More intensive efforts are needed to ensure earlier diagnosis and linkage to care for HIV infected children.     

Vascular disorders in athletes

Athletes rarely present with symptoms or clinical findings suggestive of vascular disease. However, vascular etiologies should be considered when an athlete complains of persistent symptoms which are refractory to conservative therapies commonly used for presumed musculoskeletal injuries. A comprehensive history should be performed, with special consideration to the postures the athlete assumes repeatedly during their chosen sport. Musculoskeletal anatomy surrounding the vascular bed of interest should be thoroughly reviewed. Physical examination should include provocative maneuvers specific to the suspected vascular disorder. The proper use of noninvasive diagnostic studies, including duplex ultrasonography, computerized tomography (CT), and magnetic resonance imaging (MRI), along with catheter-based angiography, when indicated, can ensure prompt diagnosis. Appropriate, multifaceted treatment of an athlete affected by a vascular disorder can facilitate an expeditious return to previous levels of activity.     

CRIM-negative infantile Pompe disease: 42-month treatment outcome

Pompe disease is a rare lysosomal glycogen storage disorder characterized by deficiency of acid α-glucosidase enzyme (GAA) and caused by mutations in the GAA gene. Infantile-type Pompe disease is a multiorgan disorder presenting with cardiomyopathy, hypotonia, and muscular weakness, which is usually fatal. Enzyme replacement therapy (ERT) with recombinant human GAA (rhGAA) has recently been shown to be effective and subsequently yielded promising results in cross-reactive immunologic material (CRIM)-positive patients. CRIM-negative patients showed a limited response to ERT and died or were ventilator dependant. Over a period of 44 months, we monitored cognitive and motor development, behavior, auditory function, and brain imaging of a CRIM-negative infantile Pompe disease patient on rhGAA and monoclonal anti-immunoglobulin E (anti-IgE) antibody (omalizumab) treatment due to severe allergic reaction. Cardiorespiratory and skeletal muscle response was significant, with almost normal motor development. Cognitive development—in particular, speech and language—deviated increasingly from normal age-appropriate development and was markedly delayed at 44 months, unexplained by moderate sensorineural hearing impairment. Brain magnetic resonance imaging (MRI) at 18, 30, and 44 months of age revealed symmetrical signal alteration of the deep white matter. Titer values of IgG antibodies to rhGAA always remained <1:800. The potential role of omalizumab in immune modulation remains to be elucidated; however, this is the first report presenting a ventilator-free survival of a CRIM-negative patient beyond the age of 36 months. The central nervous system (CNS) findings are hypothesized to be part of a yet not fully described CNS phenotype in treated patients with longer survival.     

Incidence of Contrast-Induced Nephropathy after Contrast-Enhanced Computed Tomography in the Outpatient Setting

Background and objectives: No prospective study has reported the incidence of contrast-induced nephropathy (CIN) or the associated morbidity and mortality after contrast-enhanced computed tomography (CECT) in the outpatient setting.Design, setting, participants, & measurements: We enrolled and followed a prospective, consecutive cohort (June 2007 through January 2009) of patients who received intravenous contrast for CECT in the emergency department of a large, academic, tertiary care center. Outcomes measured were as follows (1) CIN: An increase in serum creatinine ≥0.5 mg/dl or ≥25% 2 to 7 d after contrast administration; (2) severe renal failure: An increase in serum creatinine to ≥3.0 mg/dl or the need for dialysis at 45 d; and (3) renal failure as a contributing cause of death (consensus of three independent physicians) at 45 d.Results: The incidence of CIN was 11% (70 of 633) among the 633 patients enrolled. Fifteen (2%) patients died within 45 d, including six deaths after study-defined CIN. Seven (1%) patients developed severe renal failure, six of whom had study-defined CIN. Of the six patients with CIN and severe renal failure, four died, and adjudicators determined that renal failure significantly contributed to all four deaths. Thus, CIN was associated with an increased risk for severe renal failure and death from renal failure.Conclusions: CIN occurs in >10% of patients who undergo CECT in the outpatient setting and is associated with a significant risk for severe renal failure and death.Contrast-induced nephropathy (CIN) is a known complication of intravenous, iodinated contrast; is a common cause of renal failure in the inpatient setting (1–5); and is associated with both short- and long-term adverse outcomes (6,7). Previous reports indicated that CIN occurs in 4 to 20% of patients after intra-arterial administration after coronary angiography (5–9). In the outpatient setting, the use of intravenous contrast to enhance (contrast-enhanced computed tomography [CECT]) imaging has increased sharply in recent years. Despite that >6% of all emergency department (ED) patients undergo CECT in the United States (10), no prospective data allow clinicians to estimate the rate of CIN or the associated morbidity and mortality after CECT in the outpatient setting in a heterogeneous population. Previous, retrospective work in outpatients who underwent CECT found the prevalence of CIN to be 5 to 13% (11–14) and indicates that patients without baseline renal insufficiency or chronic kidney disease may still be at risk for CIN in this population (11); however, these studies were limited by retrospective design and selection bias related to inclusion of inpatients with existing kidney disease (11–14). Thus, the absence of predicate literature required to estimate both the incidence and the clinical significance of CIN after CECT provided rationale for this work.In this study, we sought to define prospectively the incidence of CIN in an unselected, consecutive, heterogeneous population of ED patients who received low-osmolar, nonionic contrast for a CECT study of any body region. We tested the hypothesis that the incidence of CIN in the ED population exceeds 4% and that CIN is associated with a high rate of severe renal failure and death (5–9,11).     

Triclosan: environmental exposure, toxicity and mechanisms of action

Triclosan [5-chloro-2-(2,4-dichlorophenoxy)phenol; TCS] is a broad spectrum antibacterial agent used in personal care, veterinary, industrial and household products. TCS is commonly detected in aquatic ecosystems, as it is only partially removed during the wastewater treatment process. Sorption, biodegradation and photolytic degradation mitigate the availability of TCS to aquatic biota; however the by-products such as methyltriclosan and other chlorinated phenols may be more resistant to degradation and have higher toxicity than the parent compound. The continuous exposure of aquatic organisms to TCS, coupled with its bioaccumulation potential, have led to detectable levels of the antimicrobial in a number of aquatic species. TCS has been also detected in breast milk, urine and plasma, with levels of TCS in the blood correlating with consumer use patterns of the antimicrobial. Mammalian systemic toxicity studies indicate that TCS is neither acutely toxic, mutagenic, carcinogenic, nor a developmental toxicant. Recently, however, concern has been raised over TCS's potential for endocrine disruption, as the antimicrobial has been shown to disrupt thyroid hormone homeostasis and possibly the reproductive axis. Moreover, there is strong evidence that aquatic species such as algae, invertebrates and certain types of fish are much more sensitive to TCS than mammals. TCS is highly toxic to algae and exerts reproductive and developmental effects in some fish. The potential for endocrine disruption and antibiotic cross-resistance highlights the importance of the judicious use of TCS, whereby the use of TCS should be limited to applications where it has been shown to be effective.