HGPIN & Statins.

[pjoshea13]

New study below.

In a recent thread on 5alpha-reductase inhibitors (e.g. Avodart/Dutasteride), which can dramatically reduce the incidence of indolent low-grade PCa, I posted a study that showed no benefit for men with high-grade PIN [HGPIN].

HGPIN is generally considered to advance to PCa within 12 months following diagnosis. However, the new study found that statin users had a 61% reduction in risk at follow-up.

Statins reduce inflammation, but the authors claim that this did not explain the benefit.

-Patrick

ncbi.nlm.nih.gov/pubmed/296...

Carcinogenesis. 2018 Apr 3. doi: 10.1093/carcin/bgy050. [Epub ahead of print]

Statin Use Linked with a Decrease in the Conversion from High-Grade Prostatic Intraepithelial Neoplasia (HGPIN) to Prostate Cancer.

Fowke JH1,2, Motley SS1.

Author information

1

Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN.

2

Division of Epidemiology, Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN.

Abstract

The roles of obesity, metabolic dysregulation, and systemic inflammation to advance prostate carcinogenesis are unclear. This study investigates metabolic and inflammatory factors in the transition from high-grade prostatic intraepithelial neoplasia (HGPIN) to prostate cancer (PC). We prospectively followed 160 men diagnosed with HGPIN at biopsy, and therefore at high-risk and clinically monitored for PC. Analyses investigated body mass index (BMI), waist circumference, waist-hip ratio, height, fat mass, lean mass % body fat, NSAIDs, statins, metformin, diabetes, hypertension, hypercholesterolemia representing metabolic dysregulation on the risk of a PC diagnosis during follow-up. Systemic inflammation was estimated through measurement of 13 plasma cytokine levels. Statin use was significantly linked with overall PC at follow-up (OR=0.45, (0.23, 0.91), p=0.03), with a somewhat stronger link with high-grade (OR=0.39, (0.15, 1.04), p=0.06) PC compared to low-grade PC (OR=0.50, (0.23, 1.12), p=0.09). Non-statin cholesterol lowering medications, BMI, waist-hip ratio, diabetes, hypertension, and percent body fat were not significantly associated with PC. Although blood IL-12p70, IL-2, and IL-1β levels were significantly lower among statin users, inflammatory markers were not significantly linked with PC and did not explain the observed relationship between statins and lower PC risk. In summary, this prospective study of HGPIN patients at high-risk for PC finds that statin use was significantly associated with reduced risk of PC detection at follow-up. Systemic markers of inflammation did not mediate this association, suggesting that statins affect prostate cancer progression through alternative pathways.

PMID: 29617729 DOI: 10.1093/carcin/bgy050

[Hidden]

If HGPIN converts to PC, what grade Gleason does it convert to?

Trying to fit it into the overall existing progression map.

[pjoshea13 in reply to Hidden]

Most of us are not diagnosed at the HGPIN stage or even Gleason score 3+3.

My GS 4+3 (2nd biopsy) came as a shock. Perhaps the progression is rapid?

I can't see progression skipping a step.

-Patrick

[Hidden in reply to pjoshea13]

I ask because I have a person describe his condition as "Pre-cancer", and people at the group meeting acted like that was a perfectly clear state and reason enough for a robotic prostatectomy. It has to be someplace on the "Gleason" metric, even if it is Gleason 0.