Food insecurity, which affects >1 billion people worldwide, is inextricably linked to the HIV epidemic. We present a conceptual framework of the multiple pathways through which food insecurity and HIV/AIDS may be linked at the community, household, and individual levels. Whereas the mechanisms through which HIV/AIDS can cause food insecurity have been fairly well elucidated, the ways in which food insecurity can lead to HIV are less well understood. We argue that there are nutritional, mental health, and behavioral pathways through which food insecurity leads to HIV acquisition and disease progression. Specifically, food insecurity can lead to macronutrient and micronutrient deficiencies, which can affect both vertical and horizontal transmission of HIV, and can also contribute to immunologic decline and increased morbidity and mortality among those already infected. Food insecurity can have mental health consequences, such as depression and increased drug abuse, which, in turn, contribute to HIV transmission risk and incomplete HIV viral load suppression, increased probability of AIDS-defining illness, and AIDS-related mortality among HIV-infected individuals. As a result of the inability to procure food in socially or personally acceptable ways, food insecurity also contributes to risky sexual practices and enhanced HIV transmission, as well as to antiretroviral therapy nonadherence, treatment interruptions, and missed clinic visits, which are strong determinants of worse HIV health outcomes. More research on the relative importance of each of these pathways is warranted because effective interventions to reduce food insecurity and HIV depend on a rigorous understanding of these multifaceted relationships.

The Model for End-Stage Liver Disease (MELD) score incorporates serum creatinine and was introduced to facilitate allocation of orthotopic liver transplantation (LT). The objective is to determine the impact of MELD and kidney function on all-cause mortality. Among LTs performed in a tertiary referral hospital between 1995 and 2009, 419 cases were studied. Cox proportional hazards models were constructed to estimate the hazard ratios (HR) and 95% confidence intervals (CI) for death. Over mean follow-ups of 8.4 and 3.1 years during the pre-MELD and MELD era, 57 and 63 deaths were observed, respectively. Those transplanted during the MELD era had a higher likelihood of hepatorenal syndrome (8% vs 2%, P < 0.01), lower kidney function (median estimated glomerular filtration rate [eGFR] 77.8 vs 92.6 mL/ min/1.73 m(2), P < 0.01), and more pretransplantation renal replacement therapy (RRT) (5% vs 1%; P < 0.01). All-cause mortality risk was similar in the MELD vs the pre-MELD era (HR: 0.98, 95% CI: 0.58-1.65). The risk of death, however, was nearly 3-fold greater (95% CI: 1.14-6.60) among those requiring pre- transplant RRT. Similarly, eGFR < 60 mL/min/1.73 m(2) post-transplant was associated with a 2.5-fold higher mortality (95% CI: 1.48-4.11). The study suggests that MELD implementation had no impact on all-cause mortality post-LT. However, the need for pre-transplant RRT and post-transplant kidney dysfunction was associated with a more than 2-fold greater risk of subsequent death.

BACKGROUND & AIMS

Diverticular bleeding is the most common cause of acute severe lower gastrointestinal bleeding (LGIB) in Western countries. Diagnostic and therapeutic approaches, including endoscopy, radiology, or surgery, have not been standardized. We investigated colonoscopy as a first-line modality to diagnose and manage patients with LGIB.

METHODS

We performed a retrospective study of data collected from 2 tertiary Veterans hospitals of 64 patients (61 men, 76 ± 11 years) with acute severe diverticular bleeding, based on colonoscopy examination. We assessed primary hemostasis using endoscopic clipping for diverticular bleeding and described the bleeding stigmata. We measured early (<30 days) and late rebleeding, blood transfusion requirements, hospital stay and complications.

RESULTS

Patients received 3.1 ± 3.0 and 0.9 ± 2.2 U of blood before and after colonoscopy, respectively. Twenty-four of the 64 patients (38%) had diverticular stigmata of recent hemorrhage; and 21 of these patients (88%) were treated successfully using endoscopic clips, without complication or early rebleeding. Hospital stays averaged 6.4 ± 5.6 days. Endoscopic clipping provided primary hemostasis in 9/12 patients (75%) with active diverticular bleeding. During 35 ± 18 months of follow-up, late recurrent diverticular bleeding occurred in 22% of the patients (14/64) after a mean time period of 22 months; 5 of the patients (21%) with stigmata of recent hemorrhage who received clip treatment had rebleeding at 43 months. Rebleeding was self-limited in 8 patients (57%), was clipped in 4 (29%), or was embolized in 2 (14%).

CONCLUSIONS

Colonoscopy can be a safe first-line diagnostic and therapeutic approach for patients with severe LGIB. Endoscopic clipping provides hemostasis of active diverticular bleeding. Recurrent bleeding occurs in about 21% of patients who were treated with clips, at approximately 4 years; most bleeding is self-limited or can be retreated by endoscopic clipping.

BACKGROUND

Whether HIV viremia, particularly at low levels is associated with inflammation, increased coagulation, and all-cause mortality is unclear.

METHODS

The associations of HIV RNA level with C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and mortality were evaluated in 1116 HIV-infected participants from the Study of Fat Redistribution and Metabolic Change in HIV infection. HIV RNA level was categorized as undetectable (i.e., "target not detected"), 1-19, 20-399, 400-9999, and ≥ 10,000 copies/ml. Covariates included demographics, lifestyle, adipose tissue, and HIV-related factors.

RESULTS

HIV RNA level had little association with CRP. Categories of HIV RNA below 10,000 copies/ml had similar levels of IL-6 compared with an undetectable HIV RNA level, while HIV RNA ≥ 10,000 copies/ml was associated with 89% higher IL-6 (p<0.001). This association was attenuated by ~50% after adjustment for CD4+ cell count. Higher HIV RNA was associated with higher fibrinogen. Compared to an undetectable HIV RNA level, fibrinogen was 0.6%, 1.9%, 4.5%, 4.6%, and 9.4% higher across HIV RNA categories, respectively, and statistically significant at the highest level (p = 0.0002 for HIV RNA ≥ 10,000 copies/ml). Higher HIV RNA was associated with mortality during follow-up in unadjusted analysis, but showed little association after adjustment for CD4+ cell count and inflammation.

CONCLUSION

HIV RNA ≥ 10,000 copies/ml was associated with higher IL-6 and fibrinogen, but lower levels of viremia appeared similar, and there was little association with CRP. The relationship of HIV RNA with IL-6 was strongly affected by CD4 cell depletion. After adjustment for CD4+ cell count and inflammation, viremia did not appear to be substantially associated with mortality risk over 5 years.