Seminal Ventrical Calcification

Repeater

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Joined
Nov 1, 2016
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3
Hey guys, this is my first post but I’ve been a long-time lurker.

About a year ago, I noticed vein engorgement along the left side of my member that was accompanied by a dull testicular ache. I went to the gen physician, thinking I possibly had epididymitis and was put on a cycle of ciprofloxacin to no avail. In a later exam, it was noted as “left seminal ventricle calcification.” I’m thinking prostatitis? I’m going in for another exam soon to see if I can gain further clarification as to what's going on.

Also a while ago, it was noted I had kidney stones and have been having hip pain which seem related to me.

I’ve been eating a pretty peatish diet for the past 6 or so years (eggs, cheese, milk, coffee, gelatin, oj, fruit, oysters, carrot salad, haagen daz, coconut oil, etc.) but have definitely missed out on Vit A, as I haven’t been regularly eating liver nor supplementing it. In addition to that, I’d been chronically taking 5000 IU of now brand D3 along with various kinds of k2, the past year or so it’s been 600 mcg of Full Spectrum K2 (MK-4 and MK-7 blend, which I stopped recently due to heart palpitations that I believe were caused by MK-7.)

I halted D3 supplementation for a couple months to see if I could begin reversing the calcification then recently started taking 2 drops of Kuinone, 40 drops of Energin, magnesium bicarbonate w/ oj in the morning and 8 drops of Estroban, 500 mg aspirin and magnesium bicarbonate w/ oj at night.

Here are some recent labs I had done:

Screenshot 2016-11-24 03.00.19.png


I'm not really sure what else would be relevant.

I’m wondering what direction(s) might be worth exploring.
Would a cycle of famotidine and cyproheptadine possibly help?


Thanks
 
Joined
Nov 21, 2015
Messages
10,501
how do you know it's calcification?

Fibrotic tissue is this way too.

Serrapeptase, nattokinase and proteolytic enzymes are a great help.

Aspirin is also. And large amounts of K2, MK4 type, like 15mg - 45mg per day.

It could be calcification as you say. There is some evidence of nanobacteria involvement and these respond to some antibiotics just fine.

EDTA anal suppositories and antibiotics (oral) are a therapy for those.

Forgetting the gobbledygook in this study, EDTA rectal suppositories and tetracycline helped. Minocycline might be better.

http://www.sciencedirect.com/science/article/pii/S0928468004000793

Pathogen-triggered calcification could play a role in CAD. Recent reports suggest that infectious blood nanobacteria (NB) emerge to be such a trigger. So far, minimal or no reversal of atherosclerosis has been claimed by therapies with iv ethylenediaminetetraacetic acid disodium salt (EDTA), antibiotics, or other regimens, and therapies for atherosclerosis remain non-curative. We have now combined EDTA with antibiotic tetracycline (comET), an in vitro proven nanobacteriocidal treatment, and tested comET therapy in patients with documented CAD. Three hypotheses were probed: (1) Are NB present in patients with CAD?; (2) Does treatment with comET affect blood NB antigen and serology?; (3) Does a comET decrease CAC scores?

One hundred patients with stable CAD and positive CAC scores were enrolled into a 4 month study of comET therapy. ComET therapy is composed of (1) Nutraceutical Powder (Vitamin C, Vitamin B6, Niacin, Folic Acid, Selenium, EDTA, l-Arginine, l-Lysine, l-Ornithine, Bromelain, Trypsin, CoQ10, Grapeseed Extract, Hawthorn Berry, Papain) 5 cm3 taken orally every evening; (2) Tetracycline HCl 500 mg taken orally every evening; (3) EDTA 1500 mg taken in a rectal suppository base every evening. CAC scoring was repeated at 4 months and serum samples were analyzed for NB antigen and serology at baseline, 2 and 4 months. Complete blood count, metabolic panel, liver function, C-reactive protein (hs-CRP) and lipids were analyzed at baseline and 4 months.

Seventy-seven patients completed the study and all patients were positive for NB serology, antigen or both. Responders (n = 44; 57%) had significant decreases in total CAC scores (P = 0.001), the average decrease being 14%. Non-responders (n = 33; 44%) had no change or had increases in CAC scores. Angina was decreased or ablated in 16 of 19 patients (84%). Lipid profiles improved to non-atherogenic direction significantly (P = 0.001), a remarkable finding in a patient group where 86% were on continuous statin medication already before the trial. No adverse physiologic effects were seen in renal, hepatic, or hematopoetic systems.

In conclusion, CAC scores decreased during ComET therapy trial in most CAD patients inferring regression of calcified coronary artery plaque volume. The patients tolerated the therapy well and their angina and lipid profiles improved. Further treatment trials for long term therapy with matched controls are warranted.
 
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Repeater

Repeater

New Member
Joined
Nov 1, 2016
Messages
3
how do you know it's calcification?

I’m just going off what information I have. Here’s what I’ve collected from my charts:

Pelvic/hip x-ray notes:

Calcified left seminal vesicle of uncertain significance.
Considerations include remote prior infection or inflammation,
however this is an unusual finding and clinical correlation is
recommended.

Urologist Examination:

Young male in NAD
Abd flat, soft, NT
no inguinal adenopathy
nl circ phallus, nl urethral meatus, no drainage, prominent dorsal vein
along L shaft
bilat descended testes, L slightly tender to palpation
equal in size, no atrophy
small L epididymal cyst palpable, no testicular mass or nodules
no sign of acute epididymitis, no firmness of equisite tenderness
A/P: h/o epididymitis with continued orchalgia
ua/std w/u negative
bilateral varicoceles/hydroceles/spermatoceles

Impression:
small bilateral varicoceles, more prominent on the left
small bilateral hydroceles
small bilateral epididymal cysts, larger on the left measuring 0.7cm
no focal testicular abnormality bilaterally

Serrapeptase, nattokinase and proteolytic enzymes are a great help.

Aspirin is also. And large amounts of K2, MK4 type, like 15mg - 45mg per day.

It could be calcification as you say. There is some evidence of nanobacteria involvement and these respond to some antibiotics just fine.

EDTA anal suppositories and antibiotics (oral) are a therapy for those.

Forgetting the gobbledygook in this study, EDTA rectal suppositories and tetracycline helped. Minocycline might be better.

http://www.sciencedirect.com/science/article/pii/S0928468004000793

Pathogen-triggered calcification could play a role in CAD. Recent reports suggest that infectious blood nanobacteria (NB) emerge to be such a trigger. So far, minimal or no reversal of atherosclerosis has been claimed by therapies with iv ethylenediaminetetraacetic acid disodium salt (EDTA), antibiotics, or other regimens, and therapies for atherosclerosis remain non-curative. We have now combined EDTA with antibiotic tetracycline (comET), an in vitro proven nanobacteriocidal treatment, and tested comET therapy in patients with documented CAD. Three hypotheses were probed: (1) Are NB present in patients with CAD?; (2) Does treatment with comET affect blood NB antigen and serology?; (3) Does a comET decrease CAC scores?

One hundred patients with stable CAD and positive CAC scores were enrolled into a 4 month study of comET therapy. ComET therapy is composed of (1) Nutraceutical Powder (Vitamin C, Vitamin B6, Niacin, Folic Acid, Selenium, EDTA, l-Arginine, l-Lysine, l-Ornithine, Bromelain, Trypsin, CoQ10, Grapeseed Extract, Hawthorn Berry, Papain) 5 cm3 taken orally every evening; (2) Tetracycline HCl 500 mg taken orally every evening; (3) EDTA 1500 mg taken in a rectal suppository base every evening. CAC scoring was repeated at 4 months and serum samples were analyzed for NB antigen and serology at baseline, 2 and 4 months. Complete blood count, metabolic panel, liver function, C-reactive protein (hs-CRP) and lipids were analyzed at baseline and 4 months.

Seventy-seven patients completed the study and all patients were positive for NB serology, antigen or both. Responders (n = 44; 57%) had significant decreases in total CAC scores (P = 0.001), the average decrease being 14%. Non-responders (n = 33; 44%) had no change or had increases in CAC scores. Angina was decreased or ablated in 16 of 19 patients (84%). Lipid profiles improved to non-atherogenic direction significantly (P = 0.001), a remarkable finding in a patient group where 86% were on continuous statin medication already before the trial. No adverse physiologic effects were seen in renal, hepatic, or hematopoetic systems.

In conclusion, CAC scores decreased during ComET therapy trial in most CAD patients inferring regression of calcified coronary artery plaque volume. The patients tolerated the therapy well and their angina and lipid profiles improved. Further treatment trials for long term therapy with matched controls are warranted.

Thanks so much, I’ll look more into those enzymes, up my K2 dose and talk with my doc about the EDTA and minocycline. That study is interesting. The 44% of patients that had no change or had increases in CAC scores is somewhat underwhelming/ concerning, however. No less, I'd be down to give it a go.
 
Joined
Nov 21, 2015
Messages
10,501
I’m just going off what information I have. Here’s what I’ve collected from my charts:

Pelvic/hip x-ray notes:

Calcified left seminal vesicle of uncertain significance.
Considerations include remote prior infection or inflammation,
however this is an unusual finding and clinical correlation is
recommended.



Thanks so much, I’ll look more into those enzymes, up my K2 dose and talk with my doc about the EDTA and minocycline. That study is interesting. The 44% of patients that had no change or had increases in CAC scores is somewhat underwhelming/ concerning, however. No less, I'd be down to give it a go.

I suspect that many stones and calcifications are due to nanobacteria but some are not. Some nanobacteria may not be susceptible to minocycline. EDTA seems to have to be rectal suppository (or enema) or IV. There are lots of variables here.
 

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