Health Matters

Sustained Spinal Cord Compression: Part II: Effect of ...Part II: Effect of Methylprednisolone on Regional Blood Flow and Recovery of ... Department of Orthopedic Surgery and Reeve-Irvine Research Center, ...
www.ejbjs.org/cgi/content/abstract/85/1/95 - Similar pages

methylprednisolone realy seemed to help me.. feel good yesterday and today even better!
stoppped swests, definitely must lift or stabilise estrogens/progesterone.. stops the burning a bit in toes and helps skin heal on toes.
this is what my dad took to recover his dreadful peeling and red raw underneath with white/light yellowish tiny pinheads on the raw red skin.. all went away as did the itch that accompanied it with methylprednisolone and hasnt come back

BAD things about methylprednisolone..
1. reduces your immune system..
Christopher Reeve (superman) died from an infection
2. bone thinning

so shouldnt stay on more than a week then taper over 2 - 3 weeks if not on a tiny only amount?

using advantan cream

I rubbed some methylprednisolone cream (brand name Advantan) between my toes for tinea/sore rash treatment yesterday and found my sweating related to estrogen changes relieved..so I went looking for why. Mind you, one can't take prednisolone long term (usually not longer than a week..and one should taper like for cortisol as well)
A good dose for me seems to be between each toe rubbed in.
I needed adrenal support , especially when taking thyroid hormones.. and I found this cream seems to be "gentler" and more "balanced", probably as "broader in effect" than cortisol or hyrodcortisone cream(ie it changes down the line to sex homrones as well as the cortisone and ? I don't know, perhaps other adrenal type support?). I like the creams as it gives the time release effec, as does hydrocortisone cream rubbed into inner wrist and just above.(hydrocortisone cream effect within 20-30 mins).. will have to redo methylprednisolone and see how long before effect and how long again, I've forgotten

Gynecol Obstet Invest. 1990;29(3):188-91
Prednisolone promotes the secretion of progesterone and oestradiol by luteinised granulosa cells independent of human chorionic gonadotropin
Wurfel W, Steck T, von Hertwig I, Albert P.
Universitatsfrauenklinik und Hebammenschule Wurzburg, FRG.

An in vitro model based on luteinised granulosa cells gained during an in vitro fertilisation programme examines the question of whether prednisolone, and thus glucocorticoids in general, are capable of exerting an influence on the secretion of oestradiol and progesterone. It can be demonstrated that prednisolone leads to dosage-dependent increases in the concentration of both steroids, even independently of concurrent stimulation by human chorionic gonadotropin. A similar mechanism for aromatase activity of human adipose cells is suggested.

PMID: 2358193 [PubMed - indexed for MEDLINE]

http://www.power-surge.com/transcripts/warga.htm

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Help save the lungfish (world's oldest living fossil), the ONLy place it lives is to be flooded with an unnecessary and unwanted by everyone I have spoken to dam.. damn (its politics gone crazy again IMO)

last desperate plea.. please sign the online petition and read about it at
http://jantea.blog.co.uk/2007/01/12/need_your_help_lungfish_very_likely_to_b~1544473

http://www.thepetitionsite.com/takeaction/610807318

Please read about it though and decide for yourself.

If you agree the lungfish worth saving, please sign the online petition and even forward to your friends on the net.

The "caution" in Australia
http://www.menopause.org.au/public/media_detail.asp?ID=72
http://www.menopause.org.au/public/media_detail.asp?ID=38

http://www.menopause.org.au/public/media_detail.asp?ID=39 componding pharmacies and docs
Note the strongly made unsubstantiated statement

These expensive formulations are no more bio-identical than oestrogen therapy available as TGA approved oral and non oral hormone therapies (patches, implants, gels). Some might argue that they contain a unique mix of oestradiol, oestrone and oestriol, but this is really a sales pitch as in the body these oestrogens are naturally inter-converted whether administered as oestradiol or oestrone as the primary form

ahh, if only just once I had a ref with this conversion from oestriol to oestradiol and vice versa!.. or even a rough estimate of the range of amounts of oestriol in a premenopausal non pregnant female..,measured over a few independant labs, and preferably not midcycle!

I've had sore knees , intense pain after use and then knee gives way on me. The pain increases with use and eases with non activity and rest. Physiotherapy did not help, if anything the taping made it worse.
I am not saying its an injury to my the anterior cruciate ligament , it could be some form of arthritis but it doesn't repond to exercise by improving..or it could be some lack of collagen padding in joint?
Its not like the arthritis I had in my 30's with red swollen joints which went away.

The pain started when I reduced the estradiol and used more estriol with the progesterone(may be coincidence).. so I'm looking to see if there is anything in this,as well as adding back the estradiol.
(also wondering about collagen in the knee joints, but so far all I can find is oestriol and oestradiol depleting collagen- I need to read more on this one)

The correlations between estradiol, estrone, estriol, progesterone, and sex hormone-binding globulin and anterior cruciate ligament stiffness in healthy, active females.Romani W, Patrie J, Curl LA, Flaws JA.
Department of Physical Therapy, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. wromani@som.umaryland.edu

BACKGROUND: Injury to the anterior cruciate ligament (ACL) often requires surgery and extensive rehabilitation. Women who participate in collegiate sports and military drills are more likely to injure their ACL than are men participating in similar activities.
The influence of the normal fluctuation of sex hormones on the physical properties of the ACL is one potential cause for this disparity. The purpose of this study was to report the correlation between estradiol, estrone, estriol, progesterone, and sex hormone binding globulin (SHBG) and ACL stiffness during three phases of the menstrual cycle in normally cycling, healthy females.
METHODS: We tested ACL stiffness and collected blood from 20 female subjects who were not using oral contraception during three phases of their menstrual cycle. Ligament stiffness was tested with the KT-2000 trade mark knee arthrometer (MEDmetric, San Diego, CA). Concentrations of estradiol and SHBG were assessed via radioimmunoassay (RIA). Progesterone, estriol, and estrone concentrations were determined via enzyme-linked immunoassay.

RESULTS: Spearman rank correlation analysis indicated a significant correlation between estradiol concentration and ACL stiffness and estrone concentration and ACL stiffness near ovulation. With the effects of the other variables controlled, there was a significant partial correlation between estradiol , estriol, and progesterone and ACL stiffness near ovulation.

CONCLUSIONS: Our results indicate that there is a significant correlation between estradiol, estriol, and progesterone and ACL stiffness suggesting that fluctuating levels of sex hormones may influence the stiffness of the ACL near ovulation.
Future studies that examine the relationship between sex hormones and the physical properties of the ACL should be focused near the ovulation phase of the menstrual cycle.

PMID: 12804359 [PubMed - indexed for MEDLINE]
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Levels of hormones in plasma and in synovial fluid of knee joint of patients with rheumatoid arthritis
Ustav experimentalnej endokrinologie SAV Bratislava. ueenlaco@savba.cz
BACKGROUND: Dysfunction of endocrine system is very likely one of the important risk factors involved in the pathogenesis of rheumatoid arthritis. The aim of the present study was to investigate the levels of selected hormones in plasma and in synovial fluid of knee joint of patients with rheumatoid arthritis or with osteoarthritis, which could affect the inflammatory processes. METHODS AND RESULTS: Thirty nine patients with rheumatoid arthritis (22 females and 17 males) and 12 patients with osteoarthritis (6 females and 6 males) were investigated. Concentrations of the following hormones were determined in plasma and synovial fluids: cortisol, 17-beta-estradiol, progesterone, dehydroepiandrosterone, aldosterone, testosterone, prolactin, insulin and C-peptide by using radioimmunoassay kits. Increased levels of 17-beta-estradiol and insulin were found in patients with rheumatoid arthritis as compared to those with osteoarthritis. The plasma concentrations of other hormones under study were not significantly different in these groups of patients. Higher levels of 17-beta estradiol, progesterone and aldosterone were noted in inflammatory knee exudate of patients with rheumatoid arthritis. The levels of other hormones in exudates of patients with rheumatoid arthritis and those with osteoarthritis were not significantly different. The ratio of 17-beta estradiol / cortisol, 17-beta estradiol / testosterone and 17-beta estradiol / dehydroepiandrosterone showed increased proportions of estrogens over androgens or glucocorticoids in exudate from patients with rheumatoid arthritis. CONCLUSIONS: These results demonstrated that steroid and peptide hormones are transferred to synovial fluid of knee. The presence of insulin, C-peptide and aldosterone was described for the first time in synovial fluid. In patients with rheumatoid arthritis a predomination of the levels of proinflammatory estrogens over androgens was found in knee exudate. Also the levels of aldosterone and progesterone were elevated in inflammation knee exudate. This suggests that these hormones present in synovial fluid may affect the local rheumatoid inflammatory processes.
Cas Lek Cesk. 2007;146(3):292-6
PMID: 17419316 [PubMed - in process]

Comment by Bob:
this looks highly relevant it may not be that you've got RA or OA but the work is showing what hormones turn up in the knee ....and their relationship to disease processes .....

or does the estrogen, itself, have this effect on polymerised hyaluronic acid (mucoploysaccharide?)........
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Increased estrogen formation and estrogen to androgen ratio in the synovial fluid of patients with rheumatoid arthritis
I had a LOT of knee and finger joint inflammation in my late 30's which would probably have been when I had a too high estrogen/progesterone ratio. I was not taking any hormones exogenously at all.
I suspect, at present, perhpas a lower than optimal iodine .. which may convert the estrogens to estriol?.. probably lowering all these female hormones to more "normal optimal" levels?.. just a suspicion.
I wasn't at that stage on exogenous thyroid hormones, and I was getting fatigued easily.
I was not on any iodized salt at that time, and my kelp supplements were no longer available as they had been 10 years previously, and I could not find any good seafood to eat either..so it's a possibility?
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Ovarian follicular fluid contains immunoreactive estriol: lack of correlation with estradiol concentrations
"no studies on the possible presence and/or changes of estriol are available"

"follicular fluid contains a high concentration of estriol and that its changes are independent of the ovulatory cycle and estradiol concentrations, supporting an independent origin and suggesting a different function for estriol"

..now just to find out what they were??
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 Better estriol/estradiol papers (but alternate medicine reviews)

http://www.thorne.com/media/estriol_estradiol_estrogen.pdf
Comparative Measurements of Serum Estriol, Estradiol, and Estrone in Non-pregnant, Premenopausal Women: A Preliminary Investigation (PDF)
Jonathan V. Wright, MD, Brian Schliesman, MS, and Lynn Robinson, MLT
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http://www.thorne.com/media/estriol.pdf
Estriol: Safety and Efficacy (PDF)
Kathleen A. Head, N.D.
"While it is commonly believed most estriol results from conversion of estradiol and estrone, in his study there was evidence of no more than 0.4 percent peripheral conversion of either estrone or estradiol.

The researchers concluded either there is a small secretion of estriol directly from the adrenals or ovaries of reproductive- age women, or that other precursors exist.1

Other researchers have found similar ratios of radio-labeled estrone and urinary estriol, indicating most of the estriol had come from estrone.2

Longcope noted others have reported direct conversion of androstenedione to estriol without passing through the blood pool of estrone.1"

1.

Studies on estriol metabolism and production were carried out in normal reproductive-aged and post-menopausal women using pulse injections and constant infusions of radiolabeled estriol, estrone and estradiol. The circulating levels were measured by radioimmunoassay. Following an intravenous pulse of [3H]estriol, the disappearance of radioactivity as estriol could be described as a function which was sum of two exponentials with t 1/2's of 3.6 and 64 min. The initial volume of distribution was 201. Using the constant infusion technique the metabolic clearance rate (MCR) of estriol was 2100 1/day in the follicular phase of the cycle and similar in the luteal phase. In postmenopausal women the MCR was 1890 1/day. The circulating levels of estriol were 7 and 11 pg/ml in the follicular and luteal phases respectively and 6 pg/ml in post-menopausal women. The production rates of estriol were 14 and 23 micrograms/day in the follicular and luteal phases of the cycle and 11 micrograms/day in post-menopausal women. In many of the women infused with radiolabeled estrone or estradiol, no radioactivity could be identified in the blood as estriol. The maximal conversion of estrone and estradiol was less than 0.4%. Estriol circulates at low but relatively steady levels in the blood. In some women estriol appears to be secreted by the ovary, especially in the luteal phase.

Immune Modulation in Multiple Sclerosis Patients Treated with the Pregnancy Hormone Estriol 1
Samantha S. Soldan, Ana Isabel Alvarez Retuerto, Nancy L. Sicotte and Rhonda R. Voskuhl2
Department of Neurology, Reed Neurological Research Center, University of California School of Medicine, Los Angeles, CA 90095

The protective effect of pregnancy on putative Th1-mediated autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis, is associated with a Th1 to Th2 immune shift during pregnancy. The hormone estriol increases during pregnancy and has been shown to ameliorate experimental autoimmune encephalomyelitis and collagen-induced arthritis. In addition, estrogens induce cytokine changes consistent with a Th1 to Th2 shift when administered in vitro to human immune cells and in vivo to mice. In a pilot trial, oral estriol treatment of relapsing remitting multiple sclerosis patients caused significant decreases in enhancing lesions on brain magnetic resonance imaging. Here, the immunomodulatory effects of oral estriol therapy were assessed. PBMCs collected longitudinally during the trial were stimulated with mitogens, recall Ags, and glatiramer acetate. Cytokine profiles of stimulated PBMCs were determined by intracellular cytokine staining (IL-5, IL-10, IL-12 p40, TNF-, and IFN-) and cytometric bead array (IL-2, IL-4, IL-5, IL-10, TNF-, and IFN-). Significantly increased levels of IL-5 and IL-10 and decreased TNF- were observed in stimulated PBMC isolated during estriol treatment. These changes in cytokines correlated with reductions of enhancing lesions on magnetic resonance imaging in relapsing remitting multiple sclerosis. The increase in IL-5 was primarily due to an increase in CD4+ and CD8+ T cells, the increase in IL-10 was primarily due to an increase in CD64+ monocytes/macrophages with some effect in T cells, while the decrease in TNF- was primarily due to a decrease in CD8+ T cells. Further study of oral estriol therapy is warranted in Th1-mediated autoimmune diseases with known improvement during pregnancy.

Beneficial Effects of Estrogens on Indices of Renal Damage in Uninephrectomized SHRsp Rats.
(pls read on above link if available)

Renal diseases tend to be less severe among premenopausal female patients, compared with male patients.

Experimental data on the effects of estrogens on renal damage are controversial, and potential underlying mechanisms have not been fully clarified.

Three-month-old, female, uninephrectomized (UNX), sham-operated or ovariectomized (OVX) SHRsp rats were left untreated or received either 17beta-estradiol 3-benzoate (25 micro g/d) or estriol (0.02 mg/d) daily.

After 3 mo, indices of renal damage (glomerulosclerosis index and tubulointerstitial damage index) and glomerular geometric parameters were investigated.

The expression of desmin, TGF-beta, endothelin-1, collagen IV, endothelial nitric oxide synthase, and estrogen receptors alpha and beta in the glomeruli and tubulointerstitium was immunohistochemically evaluated.

Estradiol and estriol did not significantly affect kidney weights or BP.

 Estradiol and estriol caused significant reductions in albuminuria
(vehicle-treated   UNX/OVX animals, 25.4 +/- 8.52 mg/24 h;
estradiol-treated UNX/OVX animals, 15.37 +/- 6.12 mg/24 h;
estriol-treated    UNX/OVX animals,     6.54 +/- 2.24 mg/24 h).
The glomerulosclerosis index was significantly lower in estriol- and estradiol-treated animals
(estradiol-treated UNX/OVX animals, 0.69 +/- 0.16;
 estriol-treated UNX/OVX animals, 0.21 +/- 0.12; P < 0.05),
compared with vehicle-treated animals (1.46 +/- 0.09);
 the tubulointerstitial damage index exhibited a similar pattern.

The mean glomerular volume was significantly less in estrogen-treated animals. UNX/OVX animals demonstrated significantly greater expression of TGF-beta and endothelin-1 in immunohistochemical, in situ hybridization, and reverse transcription-PCR assays.

This increase was abrogated by estriol but not estradiol. Similarly, significantly higher glomerular and tubulointerstitial expression of proliferating cell nuclear antigen and collagen IV was observed in UNX/OVX animals, and expression was decreased by estriol but not estradiol.
It was concluded that, in the UNX model of spontaneous renal damage, glomerular lesions and glomerular hypertrophy were reduced by estriol but less consistently by estradiol.
 In parallel, loss of podocytes, evidence of podocyte injury (i.e., desmin expression), and expression of mediator systems of glomerular damage were decreased, pointing to a major renoprotective action of estriol.

J. Am. Soc. Nephrol. (2004)