i've seen the labs myself... low GH and normal IGF-1. I spent the better part of the night researching and came across this in case anyone needs to see it in the future:
MAJOR RECOMMENDATIONS
Definitions for the levels (grades) of evidence (very low, low, moderate, high) and for the difference between a "recommendation" and a "suggestion" are provided at the end of the Major Recommendations field.
Recommendations
* Patients with childhood-onset growth hormone deficiency (GHD) who are appropriate candidates for growth hormone (GH) therapy should be retested for GHD as adults unless they have known mutations, embryopathic lesions, or irreversible structural lesions/damage (level of evidence, high).
* Adult patients with evidence of structural hypothalamic/pituitary disease, surgery or irradiation to these areas, or other pituitary hormone deficiencies should be considered for evaluation for acquired GHD (level of evidence, high).
* The insulin tolerance test (ITT) or the growth hormone releasing hormone (GHRH)-arginine test is the preferred test for establishing the diagnosis of GHD. However, in those with clearly established recent hypothalamic causes of suspected GHD (e.g. irradiation) testing with GHRH-arginine may be misleading (level of evidence, high).
* Because of the irreversible nature of the cause of the GHD in children with structural lesions with multiple hormone deficiencies and those with proven genetic causes, a low insulin-like growth factor I (IGF-I) level at least 1 month off GH therapy is sufficient documentation of persistent GHD without additional provocative testing (level of evidence, moderate).
* GH therapy of GH-deficient adults offers significant clinical benefits in body composition, exercise capacity, skeletal integrity, and quality of life measures (level of evidence, moderate).
* GH treatment is most likely to benefit those patients who have more severe clinical and biochemical abnormalities and should be encouraged in such patients (level of evidence, moderate).
* GH treatment is contraindicated in the presence of an active malignancy (level of evidence, low).
* GH dosing regimens should be individualized rather than weight-based (level of evidence, high).
* GH treatment should start with low doses and be titrated according to clinical response, side effects, and IGF-I levels (level of evidence, high).
* GH dosing should take age, sex, and estrogen status into consideration (level of evidence, high).
* During GH treatment, patients should be monitored at 1- to 2-month intervals during dose titration and semiannually thereafter with a clinical assessment and an evaluation for adverse effects, IGF-I levels, and other parameters of GH response (level of evidence, moderate).
Suggestions
* A normal IGF-I level does not exclude the diagnosis of GHD and, in the context of other pituitary disease, makes provocative testing mandatory to make the diagnosis of GHD (level of evidence, high).
* A low IGF-I level, in the absence of catabolic conditions and liver disease, indicates severe GHD and may be useful in identifying patients who will benefit from treatment (level of evidence, moderate).
* The presence of deficiencies in three or more pituitary axes strongly suggests the presence of GHD, and in this context provocative testing is optional (level of evidence, moderate).
* GH treatment in patients with diabetes mellitus may require adjustments in antidiabetic medications (level of evidence, moderate).
Still can't find anything clearly outlining the biochemical differences between the two compounds though. Also could it be that although my IGF-1 levels are normal, they are still below where they should be given the low GH levels?
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