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HGH for Low T Cells
Oct 11, 2003

Hi Nelson!

I just got my labs and they are a little confusing.

After being diagnosed in May, I had some labs done for three months to see what was going on:

June CD4 389 Viral Load 1,700

July CD4 310 Viral Load 1,300

AUgust CD4 280 Viral Load 1,100

Based on the CD4s dropping, I decided to start treatment on Viramune/Emtriva/Viread.

One month into it, my viral load is undectectable BUT my T-Cells continue to drop this time to 230. My t cell percentage dropped too.

I read a study that tested hiv poz men and found there t cells improved after taking it.

My doc is not a fan of Serostim but i wanted your take on whether or not you feel it is a therapy that one can benefit with short term (due to cost) or long term. And, other than the help with weight maintenance, do you feel it can help regenerate t-cells?

Big Thanks

Jim

Response from Mr. Vergel

Jim:

There are some studies going on right now looking at the potential benefit of growth hormone on the thymus gland. It would not hurt to try it if you can get a prescription. If you do try it, please let us know what happens. Keep a close eye on your blood sugar since growth hormone can induce diabetes in some patients. Also, no one knows what the effective dose is (one study looked at 4 mg/day). You may have to adjust the dose to minimize joint aches and water retention.

Here are two studies:

Increased thymic mass and circulating naive CD4 T cells in HIV-1-infected adults treated with growth hormone.

Napolitano LA, Lo JC, Gotway MB, Mulligan K, Barbour JD, Schmidt D, Grant RM, Halvorsen RA, Schambelan M, McCune JM.

AIDS. 2002 May 24;16(8):1103-11.

Gladstone Institute of Virology and Immunology, University of California at San Francisco, San Francisco, CA 94141, USA.

OBJECTIVE: To determine whether treatment with growth hormone (GH) enhances thymopoiesis in individuals infected with HIV-1. METHODS: Five HIV-1-infected adults were treated with GH for 6-12 months in a prospective open-label study. Immunological analyses were performed before GH treatment and repeated at 3 month intervals after GH initiation. Thymic mass was analysed using computed tomography with quantitative density and volume analysis. Analysis of circulating lymphocytes, including naive and memory T cell subsets, was performed using multiparameter flow cytometry. RESULTS: GH treatment was associated with a marked increase in thymic mass in all GH recipients. Circulating naive CD4 T cells also increased significantly in all patients during GH therapy, suggesting an enhancement of thymopoiesis. CONCLUSION: GH has significant effects on the human immune system, including the reversal of thymic atrophy in HIV-1-infected adults. De-novo T cell production may thus be inducible in immunodeficient adults.

Administration of recombinant human growth hormone (rhGH) with HAART may partially reverse the defects exerted on the immune system by HIV-1.

Pires A, Pido-Lopez J, Moyle G, Gazzard B, Gotch F, Imami N.

Int Conf AIDS. 2002 Jul 7-12;14:abstract no. ThPeA7089.

Imperial College of Science Technology and Medicine, London, United Kingdom

Administration of hrGH with HAART in HIV-1 infection may increase thymic activity, resulting in the production of naive T cells, and drive differentiation into functional memory/effector cells. Twelve chronic HIV-1 infected individuals mean age 43.4 +/- 7.4 years on HAART received rhGH. Viral load was undetectable in 10 patients and mean CD4+ T cell counts were 478.4 +/- 192.7 cells/l blood. We carried out four colour flow cytometry at baseline, 12 weeks post receiving 4mg/day of rhGH and 24 weeks after randomisation into 3 groups (receiving placebo or, alternate day or, twice weekly dosing of rhGH). Parameters assessed were: naive, memory and effector subsets based on CD45RA/CD27, CD45RO and CCR7 expression, and activation marker CD38. T cell receptor rearrangement excision circles (TREC) analysis was performed for all time points. At baseline, 4 patients showed a second, activated subset of lymphocytes. Twelve weeks post administration of rhGH this was seen in 11 patients. This subset comprised mainly of CD8+ memory/effector T cells as assessed by CD45RA and CCR7 expression. There was an increase in the naive compartment in the smaller subset, from 24.9% to 37% (p<0.01) and from 23.6% to 32% (p<0.01) in CD4+ and CD8+ T cells respectively. Changes in TREC levels correlated with phenotype in 5 patients. By week 24 all patients had undetectable TREC levels, which may be due to dilution by proliferative effector cells. The larger lymphocyte subset was sustained in 11 patients, the majority of these cells comprising of CD8+ T cells. A significant increase was seen in expression of CD38 on both CD4+ and CD8+ T cells to 68.9% and 71% respectively, from baseline to week 12 (p<0.01 for both). The use of rhGH appears to have a direct effect on thymic function, promotes thymocyte development resulting in an increase in naive T cells, and induces differentiation into functional memory effector T cells.



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