Nicolaus
Member
Hello,
Has anyone taken accutane long term/ or even short term and have experienced permanent ED, and low testosterone (bloodwork) even after cessation of the medication?
If so, were you ever able to find out the cause? Any MRI conducted? Could accutane possibly affect the pituitary?
Not quite sure what this means shown below,
Isotretinoin (13-cis RA) is the most potent agent in the treatment of acne. Insights into its mechanism of action can lead to drug discovery of alternative compounds with comparable efficacy but improved safety. The goal of this study is to compare the temporal changes in gene expression in the skin of acne patients after 1 week and 8 weeks of treatment with isotretinoin. Microarray analysis was performed on skin biopsies taken from eight acne patients prior to and at 8 weeks of treatment with isotretinoin. Results were compared with data obtained from seven acne patients biopsied at one week of treatment in a prior study. Distinctly different patterns of gene expression were noted. At 8 weeks, genes encoding extracellular matrix proteins were upregulated and numerous genes encoding lipid metabolizing enzymes were downregulated. At 1 week, genes encoding differentiation markers, tumor suppressors and serine proteases were upregulated. Only three genes were commonly downregulated. The temporal changes in gene expression in patient skin noted with isotretinoin substantiate many previously reported effects of isotretinoin and other retinoids, suggesting a model wherein isotretinoin induces apoptosis leading to reduced sebaceous gland size, decreased expression of lipid metabolizing enzymes and increased matrix remodeling during acne resolution.
And a simple search from Wikipedia which I know is not reliable but worth a shot,
Isotretinoin's exact mechanism of action is unknown, but several studies have shown that isotretinoin induces apoptosis (programmatic cell death) in various cells in the body. Cell death may be instigated in the meibomian glands,[43][55] hypothalamic cells,[56]hippocampus cells[57][58] and—important for treatment of acne—in sebaceous glandcells.[59][60] Isotretinoin has a low affinity for retinoic acid receptors (RAR) and retinoid X receptors (RXR), but may be converted intracellularly to metabolites that act as agonists of RAR and RXR nuclear receptors.[5]
One study suggests the drug amplifies production of neutrophil gelatinase-associated lipocalin (NGAL) in the skin, which has been shown to reduce sebum production by inducing apoptosis in sebaceous gland cells, while exhibiting an antimicrobial effect on Propionibacterium acnes.[61][62][63] The drug decreases the size and sebum output of the sebaceous glands.[64] Isotretinoin is the only available acne drug that affects all four major pathogenic processes in acne, which distinguishes it from alternative treatments (such as antibiotics) and accounts for its efficacy in severe, nodulocystic cases.[65] The effect of Isotretinoin on sebum production can be temporary,[66] or remission of the disease can be "complete and prolonged."[64][67][68]
Isotretinoin has been speculated to down-regulate the telomerase enzyme and hTERT, inhibiting "cellular immortalization and tumorigenesis."[69] In a 2007 study, Isotretinoin was proven to inhibit the action of the metalloprotease MMP-9 (gelatinase) in sebumwithout any influence in the action of TIMP1and TIMP2 (the tissue inhibitors of metalloproteases).[70] It is already known that metalloproteases play an important role in the pathogenesis of acne.[71]
Could any of this possibly permanently affect testosterone and the HPTA?
Has anyone taken accutane long term/ or even short term and have experienced permanent ED, and low testosterone (bloodwork) even after cessation of the medication?
If so, were you ever able to find out the cause? Any MRI conducted? Could accutane possibly affect the pituitary?
Not quite sure what this means shown below,
Isotretinoin (13-cis RA) is the most potent agent in the treatment of acne. Insights into its mechanism of action can lead to drug discovery of alternative compounds with comparable efficacy but improved safety. The goal of this study is to compare the temporal changes in gene expression in the skin of acne patients after 1 week and 8 weeks of treatment with isotretinoin. Microarray analysis was performed on skin biopsies taken from eight acne patients prior to and at 8 weeks of treatment with isotretinoin. Results were compared with data obtained from seven acne patients biopsied at one week of treatment in a prior study. Distinctly different patterns of gene expression were noted. At 8 weeks, genes encoding extracellular matrix proteins were upregulated and numerous genes encoding lipid metabolizing enzymes were downregulated. At 1 week, genes encoding differentiation markers, tumor suppressors and serine proteases were upregulated. Only three genes were commonly downregulated. The temporal changes in gene expression in patient skin noted with isotretinoin substantiate many previously reported effects of isotretinoin and other retinoids, suggesting a model wherein isotretinoin induces apoptosis leading to reduced sebaceous gland size, decreased expression of lipid metabolizing enzymes and increased matrix remodeling during acne resolution.
And a simple search from Wikipedia which I know is not reliable but worth a shot,
Isotretinoin's exact mechanism of action is unknown, but several studies have shown that isotretinoin induces apoptosis (programmatic cell death) in various cells in the body. Cell death may be instigated in the meibomian glands,[43][55] hypothalamic cells,[56]hippocampus cells[57][58] and—important for treatment of acne—in sebaceous glandcells.[59][60] Isotretinoin has a low affinity for retinoic acid receptors (RAR) and retinoid X receptors (RXR), but may be converted intracellularly to metabolites that act as agonists of RAR and RXR nuclear receptors.[5]
One study suggests the drug amplifies production of neutrophil gelatinase-associated lipocalin (NGAL) in the skin, which has been shown to reduce sebum production by inducing apoptosis in sebaceous gland cells, while exhibiting an antimicrobial effect on Propionibacterium acnes.[61][62][63] The drug decreases the size and sebum output of the sebaceous glands.[64] Isotretinoin is the only available acne drug that affects all four major pathogenic processes in acne, which distinguishes it from alternative treatments (such as antibiotics) and accounts for its efficacy in severe, nodulocystic cases.[65] The effect of Isotretinoin on sebum production can be temporary,[66] or remission of the disease can be "complete and prolonged."[64][67][68]
Isotretinoin has been speculated to down-regulate the telomerase enzyme and hTERT, inhibiting "cellular immortalization and tumorigenesis."[69] In a 2007 study, Isotretinoin was proven to inhibit the action of the metalloprotease MMP-9 (gelatinase) in sebumwithout any influence in the action of TIMP1and TIMP2 (the tissue inhibitors of metalloproteases).[70] It is already known that metalloproteases play an important role in the pathogenesis of acne.[71]
Could any of this possibly permanently affect testosterone and the HPTA?
