Sexual Dysfunction

[not_James_Bond]

Hey guys have a read of this and let me know if any of you benefited from the discussion;

Penis - burning sensation mainly after ejaculation | Sexual Transmitted Diseases (STD) discussions | Family Health center | SteadyHealth.com

I know I have to drink water (a lot) before sex, otherwise the first pee afterwards is a bit like peeing fire! I think its something to do with semen being alkaline, and urine being acidic fwiw.

 

[Jing]

Hey guys have a read of this and let me know if any of you benefited from the discussion;

Penis - burning sensation mainly after ejaculation | Sexual Transmitted Diseases (STD) discussions | Family Health center | SteadyHealth.com

I know I have to drink water (a lot) before sex, otherwise the first pee afterwards is a bit like peeing fire! I think its something to do with semen being alkaline, and urine being acidic fwiw.

I don't have STDs I've been tested . And it's not a burning pain when peeing it's just general burning pain in my penis .

 

[Tristan Loscha]

Doesn't tell me the cause of mine lol

Maybe it can give you or others clues by showing similarity in syndromes. What Antibiotics did you take?

Spoiler: infodump

Cytokine polymorphisms in men with chronic prostatitis/chronic pelvic pain syndrome: association with diagnosis and treatment response
Daniel A Shoskes, Qussay Albakri, Kim Thomas, Daniel Cook
The Journal of urology 168 (1), 331-335, 2002
Purpose:
The chronic pelvic pain syndrome is a common disorder of unknown etiology. Elevated cytokines in prostate fluid and semen are frequent findings. We studied genetic polymorphisms that can alter cytokine gene expression in men with the chronic pelvic pain syndrome.
Materials and Methods:
Genomic DNA was extracted from blood from 36 men with the chronic pelvic pain syndrome. Reversed sequence specific oligonucleotide probing was used to genotype the polymorphisms for cytokine promoter sites, namely tumor necrosis factor (TNF)-α 308, transforming growth factor (TGF)-β 25, TGF-β 10, interleukin (IL)-10 1082 and IL-6 174. Genotype frequencies were compared with 252 controls as well as among groups of patients with the chronic pelvic pain syndrome according to diagnostic category and treatment response.
Results:
There were no differences in men with the chronic pelvic pain syndrome and control patients in the frequency of TNF-α, TGF-β or IL-6 alleles, although those with the chronic pelvic pain syndrome were more likely to express the genotype associated with low IL-10 production (30.6% versus 12.1%, p = 0.007). When comparing National Institutes of Health diagnoses, category IIIa patients were more likely to have the low TNF-α genotype (categories II, IIIa and IIIb 33%, 100% and 18%, respectively, p = 0.04). All 11 of the 28 patients treated with the anti-inflammatory quercetin in whom treatment failed had the low TNF-α genotype versus 29.4% of those in whom treatment succeeded (p = 0.0003). Similarly men with quercetin treatment failure were much less likely to have the low IL-10 genotype than those with treatment success (9.1% versus 47.1%, p = 0.04).
Conclusions:
Patients with the chronic pelvic pain syndrome are more likely to have a low IL-10 producing genotype, suggesting autoimmunity as a potential etiology. Anti-inflammatory phytotherapy failure was associated with low TNF-α and high IL-10 phenotypes, which may help define a subset of patients with the chronic pelvic pain syndrome without an inflammatory etiology.





Detection of nanobacteria in patients with chronic prostatitis and vaginitis by reverse transcriptase polymerase chain reaction
Tae-Hyoung Kim, Hye Ryoun Kim, Soon-Chul Myung
Korean journal of urology 52 (3), 194-199, 2011
Purpose
We aimed to investigate the detection of nanobacteria (NB) from expressed prostatic secretions (EPS) in patients with category III chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and from vaginal swabs in patients with vaginitis by reverse transcriptase polymerase chain reaction (RT-PCR) and to evaluate the association between NB and Neisseria gonorrhea, Chlamydia trachomatis, Ureaplasma urealyticum (U. urealyticum), Mycoplasma hominis, Trichomonas vaginalis, and Mycoplasma genitalium.
Materials and Methods
A group of 11 men attending a specialized CP/CPPS clinic and a group of 157 women who reported symptoms of lower genital tract infection were enrolled in this study. NB were detected by RT-PCR. A Seeplex Sexually Transmitted Disease Detection assay (Seegene Inc., Seoul, Korea) was used that could detect DNA for 6 types of sexually transmitted pathogens.
Results
In EPS samples, the detection rate of NB in patients with CP/CPPS was 9.1%, and 9 (5.7%) of 157 vaginitis patients showed positive results in RT-PCR for NB in vaginal swabs. Associations observed among the 7 microorganisms included 6 (54.5%) patients who tested positive on EPS and 75 (47.8%) patients who tested positive on vaginal swabs. Five patients with vaginitis were found to have monoinfection of NB (6.7%).
Conclusions
We found that conventional RT-PCR for NB was rapid, simple, low in cost, and easily available for the detection of NB, and that NB may be a possible etiological factor for vaginitis and CP/CPPS. The prevalence of U. urealyticum among the four patients with NB coinfection was 75%; the presence of U. urealyticum might therefore raise suspicion for nanobacterial infection.






Characterization of circulating CD4+ CD25high regulatory T cells in men with chronic prostatitis/chronic pelvic pain syndrome.
J Bai, S Wang, J Liu, Z Ye, X Yu, Q Xi, D Hu, S Su
Urology 75 (4), 938, 2010
OBJECTIVES:
To identify the characteristics of circulating CD4 (+) CD25 (high) regulatory T cells in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). We sought to discover the possible mechanism underlying induction of CP/CPPS by autoimmune factors.
METHODS:
A total of 69 men with CP/CPPS and 25 age-matched, asymptomatic controls underwent quantification of peripheral blood CD4 (+) CD25 (high) regulatory T cells, using flow cytometry, followed by measurement of interleukin (IL)-6, IL-10, tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta1 (TGFbeta1) in serum, and forkhead box P3 (FOXP3) mRNA level in peripheral blood mononuclear cells, using enzyme-linked immunosorbent assay and real-time quantitative reverse transcriptase-polymerase chain reaction, respectively.
RESULTS:
The FOXP3 gene mRNA level in CP/CPPS patients was significantly lower than that in controls. Serum TNF-alpha level increased but the TGFbeta1 level decreased in CP/CPPS patients. No change was observed in the levels of IL-6 and IL-10. However, there was normal frequency of CD4 (+) CD25 (high) T cells in CP/CPPS patients. No differences were observed in expression of FOXP3 and serum cytokines and population of CD4 (+) CD25 (high) T cells between CP/CPPS IIIA and IIIB patients. In addition, statistically significant correlation was only found between serum IL-6 production and national institutes of health-chronic prostatitis symptom index total score of CP/CPPS patients. The frequency of CD4 (+) CD25 (high) T cells and FOXP3 expression level did not correlate with age, duration, and total national institutes of health-chronic prostatitis symptom index score of CP/CPPS patients.
CONCLUSIONS:
FOXP3 and serum cytokines, such as TNF-alpha and TGFbeta1, might be important for the pathogenesis of CP/CPPS and possibly affect the suppressive function of CD4 (+) CD25 (high) regulatory T cells. This influence may result in the onset of CP/CPPS, but its assessment requires further study. Copyright 2010 Elsevier Inc. All rights reserved.



Nociceptive and inflammatory mediator upregulation in a mouse model of chronic prostatitis
Erica S Schwartz, Amy Xie, GF Jun-Ho La
Pain 156 (8), 1537, 2015
Chronic nonbacterial prostatitis, characterized by genitourinary pain in the pelvic region in the absence of an identifiable cause, is common in adult males. Surprisingly, the sensory innervation of the prostate and mediators that sensitize its innervation have received little attention. We thus characterized a mouse model of chronic prostatitis, focusing on the prostate innervation and how organ inflammation affects gene expression of putative nociceptive markers in prostate afferent somata in dorsal root ganglia (DRG) and mediators in the prostate. Retrograde tracing (fast blue, FB) from the prostate revealed that thoracolumbar (TL) and lumbosacral (LS) DRG are the principal sources of somata of prostate afferents. Nociceptive markers (eg, TRP, TREK and P2X channels) were upregulated in FB-labeled TL and LS somata for up to four weeks after inflaming the prostate (intra-prostate injection of zymosan). Prostatic inflammation was evident histologically, by monocyte infiltration and a significant increase in mast cell tryptase activity 14, 21 and 28 days after zymosan injection. Interleukin-10 and NGF were also significantly upregulated in the prostate throughout the four weeks of inflammation. Open field pain-related behaviors (eg, rearing) were unchanged in prostate-inflamed mice, suggesting the absence of ongoing nociception, but withdrawal thresholds to lower abdominal pressure were significantly reduced. The increases in IL-10, mast cell tryptase and NGF in the inflamed prostate were cotemporaneous with reduced thresholds to probing of the abdomen and upregulation of nociceptive markers in DRG somata innervating the prostate. The results provide insight and direction for study of mechanisms underlying pain in chronic prostatitis.




Trimethoprim/sulfamethoxazole therapy of chronic bacterial prostatitis

 

[Jing]

Maybe it can give you or others clues by showing similarity in syndromes. What Antibiotics did you take?

Spoiler: infodump

Cytokine polymorphisms in men with chronic prostatitis/chronic pelvic pain syndrome: association with diagnosis and treatment response
Daniel A Shoskes, Qussay Albakri, Kim Thomas, Daniel Cook
The Journal of urology 168 (1), 331-335, 2002
Purpose:
The chronic pelvic pain syndrome is a common disorder of unknown etiology. Elevated cytokines in prostate fluid and semen are frequent findings. We studied genetic polymorphisms that can alter cytokine gene expression in men with the chronic pelvic pain syndrome.
Materials and Methods:
Genomic DNA was extracted from blood from 36 men with the chronic pelvic pain syndrome. Reversed sequence specific oligonucleotide probing was used to genotype the polymorphisms for cytokine promoter sites, namely tumor necrosis factor (TNF)-α 308, transforming growth factor (TGF)-β 25, TGF-β 10, interleukin (IL)-10 1082 and IL-6 174. Genotype frequencies were compared with 252 controls as well as among groups of patients with the chronic pelvic pain syndrome according to diagnostic category and treatment response.
Results:
There were no differences in men with the chronic pelvic pain syndrome and control patients in the frequency of TNF-α, TGF-β or IL-6 alleles, although those with the chronic pelvic pain syndrome were more likely to express the genotype associated with low IL-10 production (30.6% versus 12.1%, p = 0.007). When comparing National Institutes of Health diagnoses, category IIIa patients were more likely to have the low TNF-α genotype (categories II, IIIa and IIIb 33%, 100% and 18%, respectively, p = 0.04). All 11 of the 28 patients treated with the anti-inflammatory quercetin in whom treatment failed had the low TNF-α genotype versus 29.4% of those in whom treatment succeeded (p = 0.0003). Similarly men with quercetin treatment failure were much less likely to have the low IL-10 genotype than those with treatment success (9.1% versus 47.1%, p = 0.04).
Conclusions:
Patients with the chronic pelvic pain syndrome are more likely to have a low IL-10 producing genotype, suggesting autoimmunity as a potential etiology. Anti-inflammatory phytotherapy failure was associated with low TNF-α and high IL-10 phenotypes, which may help define a subset of patients with the chronic pelvic pain syndrome without an inflammatory etiology.





Detection of nanobacteria in patients with chronic prostatitis and vaginitis by reverse transcriptase polymerase chain reaction
Tae-Hyoung Kim, Hye Ryoun Kim, Soon-Chul Myung
Korean journal of urology 52 (3), 194-199, 2011
Purpose
We aimed to investigate the detection of nanobacteria (NB) from expressed prostatic secretions (EPS) in patients with category III chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and from vaginal swabs in patients with vaginitis by reverse transcriptase polymerase chain reaction (RT-PCR) and to evaluate the association between NB and Neisseria gonorrhea, Chlamydia trachomatis, Ureaplasma urealyticum (U. urealyticum), Mycoplasma hominis, Trichomonas vaginalis, and Mycoplasma genitalium.
Materials and Methods
A group of 11 men attending a specialized CP/CPPS clinic and a group of 157 women who reported symptoms of lower genital tract infection were enrolled in this study. NB were detected by RT-PCR. A Seeplex Sexually Transmitted Disease Detection assay (Seegene Inc., Seoul, Korea) was used that could detect DNA for 6 types of sexually transmitted pathogens.
Results
In EPS samples, the detection rate of NB in patients with CP/CPPS was 9.1%, and 9 (5.7%) of 157 vaginitis patients showed positive results in RT-PCR for NB in vaginal swabs. Associations observed among the 7 microorganisms included 6 (54.5%) patients who tested positive on EPS and 75 (47.8%) patients who tested positive on vaginal swabs. Five patients with vaginitis were found to have monoinfection of NB (6.7%).
Conclusions
We found that conventional RT-PCR for NB was rapid, simple, low in cost, and easily available for the detection of NB, and that NB may be a possible etiological factor for vaginitis and CP/CPPS. The prevalence of U. urealyticum among the four patients with NB coinfection was 75%; the presence of U. urealyticum might therefore raise suspicion for nanobacterial infection.






Characterization of circulating CD4+ CD25high regulatory T cells in men with chronic prostatitis/chronic pelvic pain syndrome.
J Bai, S Wang, J Liu, Z Ye, X Yu, Q Xi, D Hu, S Su
Urology 75 (4), 938, 2010
OBJECTIVES:
To identify the characteristics of circulating CD4 (+) CD25 (high) regulatory T cells in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). We sought to discover the possible mechanism underlying induction of CP/CPPS by autoimmune factors.
METHODS:
A total of 69 men with CP/CPPS and 25 age-matched, asymptomatic controls underwent quantification of peripheral blood CD4 (+) CD25 (high) regulatory T cells, using flow cytometry, followed by measurement of interleukin (IL)-6, IL-10, tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta1 (TGFbeta1) in serum, and forkhead box P3 (FOXP3) mRNA level in peripheral blood mononuclear cells, using enzyme-linked immunosorbent assay and real-time quantitative reverse transcriptase-polymerase chain reaction, respectively.
RESULTS:
The FOXP3 gene mRNA level in CP/CPPS patients was significantly lower than that in controls. Serum TNF-alpha level increased but the TGFbeta1 level decreased in CP/CPPS patients. No change was observed in the levels of IL-6 and IL-10. However, there was normal frequency of CD4 (+) CD25 (high) T cells in CP/CPPS patients. No differences were observed in expression of FOXP3 and serum cytokines and population of CD4 (+) CD25 (high) T cells between CP/CPPS IIIA and IIIB patients. In addition, statistically significant correlation was only found between serum IL-6 production and national institutes of health-chronic prostatitis symptom index total score of CP/CPPS patients. The frequency of CD4 (+) CD25 (high) T cells and FOXP3 expression level did not correlate with age, duration, and total national institutes of health-chronic prostatitis symptom index score of CP/CPPS patients.
CONCLUSIONS:
FOXP3 and serum cytokines, such as TNF-alpha and TGFbeta1, might be important for the pathogenesis of CP/CPPS and possibly affect the suppressive function of CD4 (+) CD25 (high) regulatory T cells. This influence may result in the onset of CP/CPPS, but its assessment requires further study. Copyright 2010 Elsevier Inc. All rights reserved.



Nociceptive and inflammatory mediator upregulation in a mouse model of chronic prostatitis
Erica S Schwartz, Amy Xie, GF Jun-Ho La
Pain 156 (8), 1537, 2015
Chronic nonbacterial prostatitis, characterized by genitourinary pain in the pelvic region in the absence of an identifiable cause, is common in adult males. Surprisingly, the sensory innervation of the prostate and mediators that sensitize its innervation have received little attention. We thus characterized a mouse model of chronic prostatitis, focusing on the prostate innervation and how organ inflammation affects gene expression of putative nociceptive markers in prostate afferent somata in dorsal root ganglia (DRG) and mediators in the prostate. Retrograde tracing (fast blue, FB) from the prostate revealed that thoracolumbar (TL) and lumbosacral (LS) DRG are the principal sources of somata of prostate afferents. Nociceptive markers (eg, TRP, TREK and P2X channels) were upregulated in FB-labeled TL and LS somata for up to four weeks after inflaming the prostate (intra-prostate injection of zymosan). Prostatic inflammation was evident histologically, by monocyte infiltration and a significant increase in mast cell tryptase activity 14, 21 and 28 days after zymosan injection. Interleukin-10 and NGF were also significantly upregulated in the prostate throughout the four weeks of inflammation. Open field pain-related behaviors (eg, rearing) were unchanged in prostate-inflamed mice, suggesting the absence of ongoing nociception, but withdrawal thresholds to lower abdominal pressure were significantly reduced. The increases in IL-10, mast cell tryptase and NGF in the inflamed prostate were cotemporaneous with reduced thresholds to probing of the abdomen and upregulation of nociceptive markers in DRG somata innervating the prostate. The results provide insight and direction for study of mechanisms underlying pain in chronic prostatitis.




Trimethoprim/sulfamethoxazole therapy of chronic bacterial prostatitis

I can't remember the name of the antibiotic I was prescribed used it when I first got symptoms about 6 years ago . Tbh it's probably something to do with pelvic floor in my case because even constipation can trigger pain

 

[not_James_Bond]

I don't have STDs I've been tested . And it's not a burning pain when peeing it's just general burning pain in my penis .

There was never any intention to imply you have an STD, chill. The article was to start a discussion and to be aware that 'thousands' of guys have this/your issue.

 

[Jing]

There was never any intention to imply you have an STD, chill. The article was to start a discussion and to be aware that 'thousands' of guys have this/your issue.

I am chill lol was just saying I don't have STDs.