Despite major advances in the treatment and survival of patients infected with human immunodeficiency virus (HIV), weight loss and wasting remain common problems. In the HIV-infected population, weight loss is associated with lower CD4+ cell counts and is an independent predictor of mortality. The etiology of weight loss and wasting is complex and multifactorial. We discuss, on the basis of a large longitudinal cohort that examined nutritional status in HIV infection, data on weight loss and wasting from the present clinical era. The definition, prevalence, and significance of HIV-associated weight loss and wasting are summarized. The etiology of weight loss is discussed for 2 main categories: inadequate nutrient intake and altered metabolism. Finally, studies of interventions to treat HIV-associated weight loss and wasting are discussed. This information is intended to raise awareness among health care providers of HIV-infected patients that weight loss and wasting remain important acquired immunodeficiency syndrome-defining conditions, despite the advent of HAART.

The prevalence of urinary stone disease (USD) is rapidly rising. However, the factors driving this increase are unknown. Recent microbiome studies suggest that dysbiosis may in part contribute to the increasing prevalence. The objective of the current study was to determine the nature and location of dysbiosis associated with USD. We conducted microbiome analysis from the gastrointestinal and urinary tracts, along with a metabolomic analysis of the urinary metabolome, from subjects with an active episode of USD or no history of the disease. Higher rates of antibiotic use among USD patients along with integrated microbiome and metabolomic results support the hypothesis that USD is associated with an antibiotic-driven shift in the microbiome from one that protects against USD to one that promotes the disease. Specifically, our study implicates urinary tract Lactobacillus and Enterobacteriaceae in protective and pathogenic roles for USD, respectively, which conventional, culture-based methods of bacterial analysis from urine and kidney stones would not necessarily detect. Results suggest that antibiotics produce a long-term shift in the microbiome that may increase the risk for USD, with the urinary tract microbiome holding more relevance for USD than the gut microbiome.

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Patients with localized prostate cancer who are on active surveillance demonstrated a low rate of active surveillance failure, prostate cancer specific mortality and metastases regardless of baseline risk.

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4 weeks post-transplant there was a 58% decrease in urinary calcium (p<0.001), an 18% decrease in urinary oxalate (p<0.01), a 0.7 unit pH increase (p<0.001), and 29% increase in GI alkali absorption (p<0.04) (Figure 1). There was also a 56% and 44% decrease in Slc26a3 protein expression in the cecum and ileum of the transplanted mice (p<0.01), respectively. Slc26a6 protein expression increased 162% in the cecum and decreased by 46% in the ileum of the transplanted compared to germ-free mice (p<0.01). Age matched control germ free mice showed none of these changes.CONCLUSIONS: Introduction of a GMB via fecal transplant to a germ free mouse leads to dramatic changes in urinary calcium and oxalate. Moreover, changes in urinary chemistry seen after fecal transplant were accompanied by significantly altered expression of intestinal transporters responsible for calcium and oxalate homeostasis. These results demonstrate for the first time that the GMB can modulate urinary parameters that are important determinants for USD.