Metabolic complications are common in treated HIV patients. Their etiology is multifactorial and the development of increased abdominal fat contributes to cardiovascular risk and impaired quality of life. Treated patients with fat mass distribution changes have relative growth hormone deficiency. Both pharmacologic and physiologic doses of growth hormone reduce the increased visceral adipose tissue and improve the associated abnormal lipid profiles in short-term studies. However, impaired glucose homeostasis changes and significant musculoskeletal toxicity occurs. A novel growth hormone-releasing factor analogue, tesamorelin, provides a physiologic means of restoring a normal growth hormone secretion profile and reduces increased visceral adipose tissue, improving both abnormal lipid profiles and patients' quality of life. Glucose homeostasis is generally well maintained. Cessation of treatment with either growth hormone or tesamorelin results in a prompt return of truncal obesity. Management strategies for the long-term maintenance of the reduced visceral adipose tissue have not yet been clarified and long-term effects on decreasing cardiovascular risks and improving clinical outcomes are uncertain.
In a study done on Testosterone Enanthate , a dose as high as 600 mg’s produced better results in subjects compared to those who received lower doses. The most fat was lost and lean body mass, strength and size was gained by the group who used the highest dose (600 mg/week), when compared to any of the lower doses studied (2). In the same study, HDL cholesterol was lowered and some acne was experienced by the subjects. There was roughly a 15% gain in Lean Body Mass from 20 weeks of 600mgs/week of testosterone enanthate . HDL cholesterol was also lowered and the subjects experienced acne.
Abstract In steroid responders, topical or systemic application of steroids leads to extracellular deposits in the trabecular meshwork which increase trabecular meshwork outflow resistance. 30–40 % of the normal population are steroid responders. About 5 % develop an intraocular pressure (IOP) rise of > 15 mmHg. These patients are termed “high responders”. In patients with primary open angle glaucoma (POAG), the proportion of steroid responders sums up to 90 %. The extent of steroid response depends on the kind of steroid used and on the duration of its administration. Dexamethasone has the highest IOP increasing potency. Differential diagnoses are POAG, ocular hypertension, normal tension glaucoma, pseudoexfoliation glaucoma and secondary glaucoma due to different reasons. To make the diagnosis, a detailed anamnesis is crucial. A recompensated IOP after the end of steroid use proves the diagnosis. The treatment of steroid glaucoma includes topical antiglaucoma medications, glaucoma filtration surgery, trabeculotomy, and laser surgery. So far, only few comparative studies on different treatment options have been published on steroid glaucoma. In some cases of therapy-resistant IOP increases following intravitreal or subconjunctival steroid administration, operative removal of the steroids can be considered. A gene therapy treatment of steroid glaucoma is still a topic of research.