Does true Gleason pattern 3 merit its cancer descriptor?

Nearly five decades following its conception, the Gleason grading system remains a cornerstone in the prognostication and management of patients with prostate cancer. In the past few years, a debate has been growing whether Gleason score 3 + 3 = 6 prostate cancer is a clinically significant disease. Clinical, molecular and genetic research is addressing the question whether well characterized Gleason score 3 + 3 = 6 disease has the ability to affect the morbidity and quality of life of an individual in whom it is diagnosed. The consequences of treatment of Gleason score 3 + 3 = 6 disease are considerable; few men get through their treatments without sustaining some harm. Further modification of the classification of prostate cancer and dropping the label cancer for Gleason score 3 + 3 = 6 disease might be warranted

Re: Variation in kidney stone composition within the United States

© Copyright 2018, Mary Ann Liebert, Inc., publishers 2018. Introduction and Objectives: Kidney stone incidence has been known to vary with temperature and climate. However, little is known about any variation in the composition of kidney stones across different regions of the United States. We attempted to evaluate whether stone composition changes depending on region. Methods: We were given access to de-identified data from LABCORPs database of kidney stone composition from August 1, 2016, to October 24, 2016, for states in seven representative areas of the country: Virginia, Minnesota, Florida, Arizona, Colorado, California, and Texas. We analyzed each component of kidney stones with optical microscopy supplemented with Fourier-Transform infrared spectroscopy (FT-IR) spectrometry using both the percentage of the stone that was composed of that component as well as a binary variable coded none vs any. Univariate associations between component and state were examined using chi-square or Fisher\u27s exact test for the binary indicator, and analysis of variance for the continuous percentage. The same set of analyses was used for decade of age vs each component. The association between age and state was examined using analysis of variance. Results: Data were available for 4335 kidney stones, from patients in the 7 states mentioned. The most common components across all stones were calcium oxalate monohydrate and calcium phosphate (both present in 93% of stones), calcium oxalate dihydrate (in 57% of stones), and uric acid (in 12% of stones). Stone composition did not vary widely across regions, except for uric acid stones, which were more prevalent in Florida compared to other states, with an odds ratio of 1.43 (95% confidence interval 1.12, 1.83). Conclusion: Kidney stone composition does not vary widely by region within the United States. Although temperature and humidity play a role in stone incidence, there does not appear to be a large variation between different climates, with the exception of uric acid stone formation in Florida

The effects of oxazyme on oxalate degradation: Results and implications of in vitro experiments

Background and Purpose: Urinary oxalate excretion influences the development of calcium oxalate kidney stones. Urinary oxalate is derived from dietary sources and endogenous synthesis. Oxalate decarboxylase metabolizes oxalate and, if consumed, could theoretically accomplish this in the gastrointestinal tract. This study aimed to determine whether a commercially produced form of oxalate decarboxylase (Oxazyme®) could degrade oxalate in simulated gastric and intestinal environments. Materials and Methods: One buffer (pH 3.6) simulated the gastric environment, while another (pH 6.5), approximated the proximal intestine. Potassium oxalate (soluble form of oxalate) and whole and homogenized spinach (a high oxalate containing food) were incubated in the different buffered solutions, with or without Oxazyme. Oxalate content, after incubation, was measured using established ion chromatographic techniques. Results: Oxazyme resulted in complete degradation of oxalate derived from potassium oxalate in the intestinal buffer; meanwhile, oxalate derived from potassium oxalate in the gastric buffer was profoundly digested by Oxazyme. Adding Oxazyme also substantially reduced the oxalate content of both whole and homogenized spinach preparations, in either buffer. Conclusions: These in vitro findings demonstrate that Oxazyme can metabolize oxalate in both simulated gastric and small intestinal environments. © Copyright 2013, Mary Ann Liebert, Inc. 2013

The effects of oxazyme on oxalate degradation: Results and implications of in vitro experiments

Background and Purpose: Urinary oxalate excretion influences the development of calcium oxalate kidney stones. Urinary oxalate is derived from dietary sources and endogenous synthesis. Oxalate decarboxylase metabolizes oxalate and, if consumed, could theoretically accomplish this in the gastrointestinal tract. This study aimed to determine whether a commercially produced form of oxalate decarboxylase (Oxazyme®) could degrade oxalate in simulated gastric and intestinal environments. Materials and Methods: One buffer (pH 3.6) simulated the gastric environment, while another (pH 6.5), approximated the proximal intestine. Potassium oxalate (soluble form of oxalate) and whole and homogenized spinach (a high oxalate containing food) were incubated in the different buffered solutions, with or without Oxazyme. Oxalate content, after incubation, was measured using established ion chromatographic techniques. Results: Oxazyme resulted in complete degradation of oxalate derived from potassium oxalate in the intestinal buffer; meanwhile, oxalate derived from potassium oxalate in the gastric buffer was profoundly digested by Oxazyme. Adding Oxazyme also substantially reduced the oxalate content of both whole and homogenized spinach preparations, in either buffer. Conclusions: These in vitro findings demonstrate that Oxazyme can metabolize oxalate in both simulated gastric and small intestinal environments. © Copyright 2013, Mary Ann Liebert, Inc. 2013

The association of cardiovascular disease and metabolic syndrome with nephrolithiasis

Purpose of Review: This review describes the relationship between nephrolithiasis, vascular disease and metabolic syndrome. Recent Findings: There is increasing evidence that kidney stone formation is associated with a number of systemic problems including cardiovascular disease, metabolic syndrome and its components. Some of these associations are bidirectional. The reasons for these associations are not totally clear, but potential factors include metabolic responses associated with these disorders that promote a stone forming milieu in urine, environmental factors such as diet, oxidative stress and inflammation and molecular changes impacting the transport of certain analytes in urine. Summary: Urologists need to be cognizant of these associations as they may be able to contribute to an early diagnosis of a significant medical problem, or provide counseling to patients to prevent their occurrence. © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins

Fish oil supplementation and urinary oxalate excretion in normal subjects on a low-oxalate diet

© 2014 Elsevier Inc. All rights reserved. Objective To determine if fish oil supplementation reduces endogenous oxalate synthesis in healthy subjects. Materials and Methods Fifteen healthy non-stone-forming adults participated in this study. Subjects first abstained from using vitamins, medications, or foods enriched in omega-3 fatty acids for 30 days. Next, they collected two 24-hour urine specimens while consuming a self-selected diet. Subjects consumed an extremely low-oxalate and normal-calcium diet for 5 days and collected 24-hour urine specimens on the last 3 days of this diet. Next, the subjects took 2 fish oil capsules containing 650-mg eicosapentaenoic acid and 450-mg docosahexaenoic acid twice daily for 30 days. They consumed a self-selected diet on days 1-25 and the controlled diet on days 26-30. Twenty-four-hour urine samples were collected on days 28-30. Excretion levels of urinary analytes including oxalate and glycolate were analyzed. Results Although there was a significant reduction in urinary oxalate, magnesium, and potassium excretions and an increase in uric acid excretion during the controlled dietary phases compared with the self-selected diet, there were no significant differences in their excretion during controlled diet phases with and without fish oil supplementation. Conclusion These results suggest that fish oil supplementation does not reduce endogenous oxalate synthesis or urinary oxalate excretion in normal adults during periods of extremely low oxalate intake. However, these results do not challenge the previously described reduction in urinary oxalate excretion demonstrated in normal subjects consuming a moderate amount of oxalate in conjunction with fish oil

Fish oil supplementation and urinary oxalate excretion in normal subjects on a low-oxalate diet.

© 2014 Elsevier Inc. All rights reserved. Objective To determine if fish oil supplementation reduces endogenous oxalate synthesis in healthy subjects. Materials and Methods Fifteen healthy non-stone-forming adults participated in this study. Subjects first abstained from using vitamins, medications, or foods enriched in omega-3 fatty acids for 30 days. Next, they collected two 24-hour urine specimens while consuming a self-selected diet. Subjects consumed an extremely low-oxalate and normal-calcium diet for 5 days and collected 24-hour urine specimens on the last 3 days of this diet. Next, the subjects took 2 fish oil capsules containing 650-mg eicosapentaenoic acid and 450-mg docosahexaenoic acid twice daily for 30 days. They consumed a self-selected diet on days 1-25 and the controlled diet on days 26-30. Twenty-four-hour urine samples were collected on days 28-30. Excretion levels of urinary analytes including oxalate and glycolate were analyzed. Results Although there was a significant reduction in urinary oxalate, magnesium, and potassium excretions and an increase in uric acid excretion during the controlled dietary phases compared with the self-selected diet, there were no significant differences in their excretion during controlled diet phases with and without fish oil supplementation. Conclusion These results suggest that fish oil supplementation does not reduce endogenous oxalate synthesis or urinary oxalate excretion in normal adults during periods of extremely low oxalate intake. However, these results do not challenge the previously described reduction in urinary oxalate excretion demonstrated in normal subjects consuming a moderate amount of oxalate in conjunction with fish oil