Academy Exchange

I have multiple long-term survivors with lipodystrophy/lipohypertrophy as well as hepatic steatosis and in some cases fibrosis. I am trying to come up with a parsimonious way to approach these folks. For instance, Egrifta might help with fat redistribution, but it can also raise blood sugar; Pioglitazone may be less effective for lipodystrophy, but at least it is also [slightly] helpful for hepatic steatosis. The new MASH drug Resmetirom seems to be quite liver-specific and I doubt it will turn out to have any effect on overall fat redistribution. I think the GLP1s seem like the most promising option for both problems, if one can manage to get them covered. Am I missing another approach?

(PS - is anyone enrolling patients for a study of GLP1s for HIV + MASLD? Or want to do one?)

Hi Julia,

I think that the key question is whether your patients have truly more visceral adipose tissue (VAT) or subcutaneous adipose tissue (SAT).  It has been my general practice to do a "pinch test" to determine how much SAT a patient has and if there is not much SAT, then the majority of their fat is likely VAT, and therefore, I put them more likely in the category of lipohypertrophy/excess visceral adipose tissue, which often is associated with hepatic steatosis (another marker of excess visceral fat deposition).  For these patients, I tend to favor using tesamorelin (Egrifta SV) because it is more specific for reducing VAT > SAT.  In my experience, tesamorelin can slightly raise blood sugar initially and temporarily, but with reduction of the VAT, the blood sugar and a1c will come back to normal or drop (if significant VAT loss).  There is data on tesamorelin and reduction of hepatic steatosis (see Fourman, et al.).

If there is a lot more SAT on exam (suggestive of obesity), then I favor using the GLP-1s or GLP/GIP combination as these are more specific for treatment of obesity.  The GLP-1s appear to reduce both SAT and VAT (but is not necessarily specific for VAT, in my opinion), and can also reduce liver fat as well.  Of note, it is not uncommon that I have had patients on both agents (tesamorelin + GLP1s) as well.

I cannot comment on Resmetirom, but I think you may be correct in that it is liver specific, and unclear what it's effect, if any, on SAT or VAT...

Hope this helps!

I have multiple long-term survivors with lipodystrophy/lipohypertrophy as well as hepatic steatosis and in some cases fibrosis. I am trying to come up with a parsimonious way to approach these folks. For instance, Egrifta might help with fat redistribution, but it can also raise blood sugar; Pioglitazone may be less effective for lipodystrophy, but at least it is also [slightly] helpful for hepatic steatosis. The new MASH drug Resmetirom seems to be quite liver-specific and I doubt it will turn out to have any effect on overall fat redistribution. I think the GLP1s seem like the most promising option for both problems, if one can manage to get them covered. Am I missing another approach?

(PS - is anyone enrolling patients for a study of GLP1s for HIV + MASLD? Or want to do one?)

By the way, if anyone is interested, check out the AAHIVM webinar on Impact of HIV and Its Treatment on Weight and Body Habitus: https://education.aahivm.org/webinars/69752.  I'll be talking about these issues at the webinar...

Hi Julia,

I think that the key question is whether your patients have truly more visceral adipose tissue (VAT) or subcutaneous adipose tissue (SAT).  It has been my general practice to do a "pinch test" to determine how much SAT a patient has and if there is not much SAT, then the majority of their fat is likely VAT, and therefore, I put them more likely in the category of lipohypertrophy/excess visceral adipose tissue, which often is associated with hepatic steatosis (another marker of excess visceral fat deposition).  For these patients, I tend to favor using tesamorelin (Egrifta SV) because it is more specific for reducing VAT > SAT.  In my experience, tesamorelin can slightly raise blood sugar initially and temporarily, but with reduction of the VAT, the blood sugar and a1c will come back to normal or drop (if significant VAT loss).  There is data on tesamorelin and reduction of hepatic steatosis (see Fourman, et al.).

If there is a lot more SAT on exam (suggestive of obesity), then I favor using the GLP-1s or GLP/GIP combination as these are more specific for treatment of obesity.  The GLP-1s appear to reduce both SAT and VAT (but is not necessarily specific for VAT, in my opinion), and can also reduce liver fat as well.  Of note, it is not uncommon that I have had patients on both agents (tesamorelin + GLP1s) as well.

I cannot comment on Resmetirom, but I think you may be correct in that it is liver specific, and unclear what it's effect, if any, on SAT or VAT...

Hope this helps!

I have multiple long-term survivors with lipodystrophy/lipohypertrophy as well as hepatic steatosis and in some cases fibrosis. I am trying to come up with a parsimonious way to approach these folks. For instance, Egrifta might help with fat redistribution, but it can also raise blood sugar; Pioglitazone may be less effective for lipodystrophy, but at least it is also [slightly] helpful for hepatic steatosis. The new MASH drug Resmetirom seems to be quite liver-specific and I doubt it will turn out to have any effect on overall fat redistribution. I think the GLP1s seem like the most promising option for both problems, if one can manage to get them covered. Am I missing another approach?

(PS - is anyone enrolling patients for a study of GLP1s for HIV + MASLD? Or want to do one?)

I have multiple long-term survivors with lipodystrophy/lipohypertrophy as well as hepatic steatosis and in some cases fibrosis. I am trying to come up with a parsimonious way to approach these folks. For instance, Egrifta might help with fat redistribution, but it can also raise blood sugar; Pioglitazone may be less effective for lipodystrophy, but at least it is also [slightly] helpful for hepatic steatosis. The new MASH drug Resmetirom seems to be quite liver-specific and I doubt it will turn out to have any effect on overall fat redistribution. I think the GLP1s seem like the most promising option for both problems, if one can manage to get them covered. Am I missing another approach?

(PS - is anyone enrolling patients for a study of GLP1s for HIV + MASLD? Or want to do one?)