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Possible reduction in nocturia, nighttime urination, or BPH after taking vitamin D

This is just a set of clippings from the internet May 7 2010 after a retired doctor friend mentioned that he had much less nighttime urination after taking 5,000 IU of vitamin D daily and raising his blood levels above 40 ng/ml.

Many sites, like the Cleveland Clinic http://my.clevelandclinic.org/disorders/nocturia/hic_nocturia.aspx, states that excessive nocturia is caused by “Certain drugs, including diuretics (water pills), cardiac glycosides, demeclocycline, lithium, methoxyflurane, phenytoin, propoxyphene, and excessive vitamin D”
I found “Excessive vitamin D” scores of times on the internet, but not a single time was “excessive” quantified. Also, unclear if it was just excessive D2 and not excessive D3. Found various reference that 50,000 IU of D2 could cause nocturia.
No confirmation from 2 hours of surfing, in fact, found hints that vitamin D could increase nocturia.
Tried searching for: "vitamin D" Benign Prostatic Hyperplasia – much better results

AUA: New Therapies Show Promise for BPH

From: http://www.medpagetoday.com/MeetingCoverage/AUA/9616
By Charles Bankhead, Staff Writer, MedPage Today Published: May 27, 2008
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine. Earn CME/CE credit for reading medical news

ORLANDO, May 27 2010-- Two new therapeutic strategies for benign prostatic hyperplasia (BPH) — one oral, one injectable — showed promise in clinical trials, investigators said here.
The vitamin D agonist elocalcitol significantly slowed prostate growth and improved urinary flow in a placebo-controlled dose-finding study reported at the American Urological Association meeting.
A second study found that a single intraprostatic injection of a PSA-activated protoxin significantly reduced prostate symptoms and volume in a small phase 1 clinical evaluation.
Elocalcitol is a nonhypercalcemic vitamin D agonist that demonstrated anti-inflammatory and antiproliferative activity in preclinical studies, said Francesco Montorsi, M.D., of the Universita Vita Salute San Raffaele in Milan, Italy. Preliminary clinical studies showed that elocalcitol arrests prostate growth and improves bladder function.
Clinical investigation continued in a dose-finding study involving 540 men with symptomatic BPH.
The patients were randomized to placebo or to one of three active therapies: elocalcitol 75 or 150 mcg or elocalcitol 150 mcg plus the alpha blocker tamsulosin (Flomax) at a dose of 0.4 mg.
Treatment continued for six months, and the primary endpoint was the percentage change in total prostate volume from baseline.
All three active-therapy groups did significantly better compared with placebo, which had a mean increase in prostate volume of 3.52%.
Prostate volume increased by 1.52% with the 75 mcg dose of elocalcitol (P<0.0135), 0.54% with 150 mcg of elocalcitol (PP=0.0059).
"The rate of prostate growth in the placebo group was in line with published literature," Dr. Montorsi said. "The reduced rate of growth with elocalcitol shows that the drug can arrest prostate growth."
Prostate symptoms improved by five to six points on the International Prostate Symptom Scale and did not differ between groups. Similarly, maximum urinary flow (Qmax) improved by about 1 to 2 mL/sec in all four groups.

"The results seem to be comparable to those historically obtained with the 'gold standard' alpha-blockers," said Dr. Montorsi.
In a subgroup analysis of men with IPSS scores ?12 and at least three urgency episodes daily at baseline, the 150 mcg dose of elocalcitol led to significant improvement (P<0.01) compared with placebo, as did combination therapy (P<0.04).
Adverse events occurred less frequently with elocalcitol monotherapy compared with placebo and slightly more often with the combination, but the differences were not significant.
In particular, elocalcitol did not adversely affect sexual function compared with placebo.
Explaining the second strategy, investigators in Canada and at Johns Hopkins presented data from 15 patients treated with PRX302, a modified bacterial protoxin injected into the prostate.
The modified protoxin (proaerolysin) is activated by PSA, resulting in the release of C-terminal inhibitory peptide and generation of active toxin, said Peter J. Pommerville, M.D., of Can-Med Clinical Research in Victoria, British Columbia.
"We believe the activated toxin bores small holes into cell membranes, allowing the cell contents to leak out and promoting apoptosis," Dr. Pommerville said in an interview. "The end result is a reduction in prostate volume."
In the phase I study, three patients each received one of five doses of PRX302. Using transrectal ultrasound guidance, investigators injected the protoxin transperineally into both prostatic lobes. Additionally, three or four deposits per injection were made in the transition zone along the urethra.
The baseline prostate volume averaged 45.3 cm3 and decreased to 37.7 cm3 at 90 days (P<0.01).
IPSS score decreased from a baseline mean of 19.1 to 9.4 at 90 days (P=0.015).
Quality-of-life score improved from a mean of 4.3 at baseline to 1.8 at 90 days (P<0.01).
"We hypothesize that the reduction in prostate mass reduces the pressure on the urethra, leading to a reduction in prostate symptoms," said Dr. Pommerville.
The protoxin was well tolerated; no grade 3-4 adverse events occurred during the study, he added. The most common adverse event was urinary frequency.
Dr. Montorsi disclosed relationships with GlaxoSmithKline, Pfizer, Bayer, Eli Lilly, Pierre Fabre, and AMS. Dr. Pommerville disclosed that he is an investigator for Protox Therapeutics.
Primary source: Journal of Urology Source reference:
Montorsi F, et al "Elocalcitol in the treatment of BPH: a multicenter, randomized, placebo-controlled phase IIb clinical trial" J Urol 2008; 179(suppl): 700; Abstract 2035.
Additional source: Journal of Urology Source reference:
Pommerville PJ, et al "A PSA-activated protoxin (PRX302) administered transperineally to men with symptomatic benign prostatic hyperplasia is well tolerated and exhibits signs of activity" J Urol 2008; 179(suppl): 673; Abstract 1961.

Vitamin D better than Flomax? by Garyk_3960, Aug 01, 2008

From http://www.medhelp.org/posts/Urology/Vitamin-D-better-than-Flomax/show/586210
I can't use Flomax or other Beta Blockers due to side effects — disturbed sleep. Uroxatral even cause me to sleepwalk, waking when I fell flat on my faceFace pain! Separately, due to a Vitamin D deficiency, my doc put me on 50,000 units per week for 8 weeks, followed by biweekly doses. And guess what...the Vitamin D almost instantly "cured" the BPHBph

  • Pubmed had 20 hits for BPH "vitamin D", including the following

   (BPH = benign prostatic hyperplasia )
Vitamin D receptor agonists target static, dynamic, and inflammatory components of benign prostatic hyperplasia.
Ann N Y Acad Sci. 2010 Apr;1193(1):146-52.
Adorini L, Penna G, Fibbi B, Maggi M.
Intercept Pharmaceuticals, Corciano (Perugia), Italy.

The bioactive form of vitamin D, 1,25-dihydroxyvitamin D(3), is a secosteroid hormone that binds to the vitamin D receptor (VDR), a member of the nuclear receptor superfamily, and modulates a variety of biological functions. The VDR is expressed by most cell types, including cells of the urogenital system, such as prostate and bladder cells. In particular, the prostate is a target organ of VDR agonists and represents an extrarenal synthesis site of 1,25-dihydroxyvitamin D(3). We have analyzed the capacity of VDR agonists to treat benign prostatic hyperplasia (BPH), a complex syndrome characterized by a static component related to prostate overgrowth, a dynamic component responsible for urinary irritative symptoms, and an inflammatory component. Data reviewed here demonstrate that VDR agonists, and notably elocalcitol, reduce the static component of BPH by inhibiting the activity of intraprostatic growth factors downstream of the androgen receptor, the dynamic component by targeting the RhoA/ROCK pathway in prostate and bladder cells, and the inflammatory component by targeting the NF-kappaB pathway. PMID: 20398021

Human prostatic urethra expresses Vitamin D receptor and responds to Vitamin D receptor ligation.

J Endocrinol Invest. 2010 Apr 12. [Epub ahead of print]
Comeglio P, Chavalmane AK, Fibbi B, Filippi S, Marchetta M, Marini M, Morelli A, Penna G, Vignozzi L, Vannelli GB, Adorini L, Maggi M.
Andrology Unit, Department of Clinical Physiopathology, University of Florence, Florence, Italy.

Background. Chronic inflammation is now considered a determinant of benign prostatic hyperplasia (BPH), promoting, together with the hormonal milieu, prostate overgrowth and lower urinary tract symptoms (LUTS). Prostatic urethra actively participates in determining progression of LUTS associated with BPH.

Aim. To investigate expression of the vitamin D receptor (VDR) and the ability of the VDR agonist elocalcitol to reduce inflammatory responses in human prostatic urethra (hPU) cells.
Materials and Methods. Human prostatic urethra, prostate and bladder neck were obtained from patients affected by BPH. Immunohistochemical studies for VDR expression were performed in tissue samples, from which primary cell cultures were also derived. In hPU cells, proliferation and chemiotaxis were studied, along with ROCK activity (MYPT-1 phosphorylation) by western blot. Quantitative RT-PCR was performed for VDR, cyclooxygenase (COX-2) and interleukin-8 (IL-8) expression.

Results. Urethra displays higher VDR expression compared to prostate and bladder neck tissues. The VDR agonist elocalcitol partially reverts COX-2 and IL-8 mRNA upregulation induced by a pro-inflammatory cytokine mixture (IL-17, IFN-gamma TNF-alpha and inhibits cell migration in urethral cells. Elocalcitol prevents activation of ROCK, as previously demonstrated in bladder and prostate cell cultures.

Conclusions. Our results suggest that prostatic urethra is, within the lower urinary tract, a novel target for VDR agonists, as shown by the capacity of elocalcitol to inhibit ROCK activity and to limit inflammatory responses in human primary urethra cells. PMID: 20386089

Vitamin D Council has: Vitamin D Research Benign Prostatic Hyperplasia; which includes:

Chronic inflammation in the pathogenesis of benign prostatic hyperplasia. Int J Androl. 2009 Jun 8.

Elocalcitol, a vitamin D3 analog for the potential treatment of benign prostatic hyperplasia, overactive bladder and male infertility.

IDrugs. 2009 Jun;12(6):381–93.

The vitamin D receptor agonist elocalcitol inhibits IL-8-dependent benign prostatic hyperplasia

stromal cell proliferation and inflammatory response by targeting the RhoA/Rho kinase and NF-kappaB pathways. Prostate. 2009 Apr 1;69(5):480–93.

Prostate disease prevalence with epidemiological and hormonal analysis in randomly selected male population in Croatia.

Coll Antropol. 2008 Dec;32(4):1195–202.

Dietary patterns, supplement use, and the risk of symptomatic benign prostatic hyperplasia:

results from the prostate cancer prevention trial. Am J Epidemiol. 2008 Apr 15;167(8):925–34.

Pathophysiology and therapy of benign prostatic hyperplasia.

Wien Klin Wochenschr. 2008;120(13–14):390–401. Review.

Inhibition of prostate growth and inflammation by the vitamin D receptor agonist BXL-628 (elocalcitol).

J Steroid Biochem Mol Biol. 2007 Mar;103(3–5):689–93.

Intake of selected micronutrients and the risk of surgically treated benign prostatic hyperplasia:

a case-control study from Italy. Eur Urol. 2006 Sep;50(3):549–54.

Pre-clinical evidence and clinical translation of benign prostatic hyperplasia treatment by the vitamin D receptor agonist BXL-628 (Elocalcitol).

J Endocrinol Invest. 2006 Jul–Aug;29(7):665–74. Review.

Growth factor, cytokine, and vitamin D receptor polymorphisms and risk of benign prostatic hyperplasia in a community-based cohort of men.

Urology. 2006 Feb;67(2):300–5.

Chemoprevention of prostate cancer by diet-derived antioxidant agents and hormonal manipulation

(Review). Int J Oncol. 2003 Jan;22(1):5–13. Review.

See also VitaminDWiki

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