Hepatitis Researcher: question on Pituitary function, GH Deficiency and Osteoporosis.

[DoubleDose]

In light of several recent threads regarding Pituitary issues, leading to Growth Hormone Deficiency, and also the thread concerning a research study correlating HCV to Osteoporosis, I would like to ask your opinion or understanding regarding these potential problems.  Specifically, are you aware of research that points to either HCV, or combination treatment having a significant effect on Pituitary function, the production of growth hormone, or the development of osteoporosis?

Studies linked below, along with a  forum member's experiences with GH therapy provoke my questions, along with the fact that my own functional and lab profile seems to fit the profile for GH deficient adults, on just about every count.  I now wonder if either the long periods of treatment, or just having been HCV+ for several decades have had a major impact on my Pituitary function, thus creating a host of symptoms post-tx that seem to have no particular etiology, other than calling it 'post-treatment syndrome'.  Maybe there is a physical/functional specific cause for these problems that might be addressed with the proper hormonal therapies.

If you have any light to shed on this subject, please feel free to elaborate.  Thanks for your input.

Also, any information or research that our forum members are aware of would be of interest to this thread.  Please feel free to provide input.

DoubleDose

[merryBe]

bump

[merryBe]

I for one will look forward to the middle of march then!!  Have a good trip HR!!!!!!!!

[Hepatitis Researcher]

Hi, just about to leave, your topic deserves, and i think i have available, a broad conceptual approach, that needs to take into account the body-wide responses of all arms of the defense system in case of a chronic infection with a proliferating multiantigen, like HCV, that also is distributed passively - consider the Trillion a day of peripherally " decaying" or swallowed HCV virions, their nucleic acids and how they might interfere with finding genuine "infection' defined as intracellular propagation, of such a virus.( False positives because of blood contamination of samples investigated with high sensitivity PCR??)

The body-wide disseminated response to such numbers of stimulating antigens must be formidable, and the resulting attack of the Tcells on the liver as the major organ of de novo production of such virions intracellularly is only the major manifestation of such body-wide antigen recognition. Thus chronic inflammatory responses in many organs aside from the liver are likely to expect and the inherent susceptibility particularly of endocrine organs to autoimmune attack due to their esoteric, not truly tolerant set of expressed proteins will make such endocrine autoimmunity (exemplified as thyreoditis, but not limited to such or islet cell pancreatitis, leading to diabetes) appear in a higher percentage than in the population background not chronically stimulated by viral antigens and not exposed to the exacerbating effect of IFN to all such processes. This will al be superimkposed on the "normal' frequency of age related autoimmune phenomena, that are just a reflection of the inherent fundamental difficulty to fight off and kill structures that are quite similar in design to our own makeup - thus immune reactions hurt and make us "ill". and are often not complete - and we are fighting a system like HCV that has a trillion times higher power of adaption by selection and invention.

We can continue in more detail perhaps in the middle of march.

[DoubleDose]

Just wanted to make sure that anyone out there who has related information on this subject, please feel free to comment, or cite any studies, anecdotal info. etc.

Thanks      DD