When they say “FDA approved”, does that mean it’s already on the market? If so, how come no one’s noticed this “side effect” before? (There must be other bald arthritis patients…)
Seems like inflammation is more involved with baldness than first discovered. Obviously this is only one case and the patient has a unique condition.
[left]GENERIC NAME: Tofacitinib citrate
DRUG CLASS AND MECHANISM: Tofacitinib is an oral drug used for treating
rheumatoid arthritis. It belongs to a class of drugs called Janus kinase
(JAK) inhibitors. JAKs are enzymes (proteins) that regulate chemical signaling
pathways that control biologic processes such as blood formation and the
immune response response that causes the pain, tenderness and swelling of
inflammation. JAKs are found in many cells, especially stem cells in bones
and joints. Inhibition of JAKs by tofacitinib prevents inflammation and tissue
destruction that is associated with the inflammation of rheumatoid arthritis.
Tofacitinib was approved in November 2012.
DRUG INTERACTIONS: Ketoconazole (Nizoral, Extina, Xolegel, Kuric) and fluconazole
Diflucan) slow down the metabolism (elimination) of tofacitinib, increasing tofacitinib
levels in the body.[/left]
I don’t doubt that it worked in this particular patient, but I was just wondering whether this is a product that is already on the market or whether it has just passed FDA approval and is just about to hit the market. If it is already on the maket, then we can safely assume that it won’t restore a full head of hair in all patients, as it would have done so in patients using the drug to treat their arthritis. (And I’m sure we would have read about that.)
First, I know that there have been other instances of drugs used to treat rheumatoid arthritis – many of this family of drugs have names ending in “-nib” – causing hair growth on some patients. Sometimes it’s significant hair growth.
But I think these drugs mainly grow hair on patients with auto-immune hairloss disorders, like alopecia totalis or alopecia universalis.
The medical causes for those kinds of hair loss actually are much different from what causes Male Pattern Baldness. MPB is not mainly an inflammatory disease, although what makes it really confusing is that some extreme cases of MPB have a big inflammatory component.
I think that this inflammatory component seen in skin biopsies of some patients with MPB leads many people to mistakenly assume that ALL MPB sufferers have inflammation, or that inflammation is a necessary result of the genetic condition of MPB, and that it’s always present.
The reality is that inflammation is really present only in a relatively small MINORITY of MPB cases, and that is what confuses the hell out of a lot of people, because they think the inflammation and MPB always go hand-in-hand, when that’s not the case at all.
This family of anti-arthritis drugs appears to be suppressing an auto-immune inflammation in these patients, and secondarily causing their hair to grow back, but just because it does that in these patients with autoimmune disorders, doesn’t mean it will cure all people with MPB. I can almost guarantee it won’t. In fact, this class of drugs is also potentially dangerous and has a lot of side effects, so I doubt they’ll ever become a standard or commonly used MPB treatment.
hey don’t nobody take the hairloss community serious that’s why its always s.c.a.m.s and studies
that don’t mean nothing I don’t think there will never be no cure from what I was reading last night
WOW
The previous cases of regrowth from this class of drugs were not enough to spark any study on the matter from the MPB resarch community. (Heads too far up their asses.)
The cases included regrowth on a balded area, and growth on the end of a person’s nose where there shouldn’t have been any balded follicles to heal up. IMO it’s a potential source of MPB treatment regardless of whether it acts directly on the MPB mechanism or not.
But the fact that other patients on similar drugs aren’t walking around w/o massive regrowth suggests that it won’t be as easy as popping a pill.
[quote][postedby]Originally Posted by cal[/postedby]
The previous cases of regrowth from this class of drugs were not enough to spark any study on the matter from the MPB resarch community. (Heads too far up their asses.)
The cases included regrowth on a balded area, and growth on the end of a person’s nose where there shouldn’t have been any balded follicles to heal up. IMO it’s a potential source of MPB treatment regardless of whether it acts directly on the MPB mechanism or not.
But the fact that other patients on similar drugs aren’t walking around w/o massive regrowth suggests that it won’t be as easy as popping a pill.[/quote]
True but it is hard to ignore when the regrowth for this guy is so dramatic, I have never seen a bald guy growing back that much hair! I think he has just as much hair as he used to when he was 18.
Yeah but this is one case, and it’s not MPB-caused loss. Too many variables to call it.
There are other drugs in this class on the market and they have been linked to funny hair growth too. I’m sure it isn’t as simple as just taking this med and getting our hair back. We would have discovered it long before now.
But the fact remains that there is definitely SOMETHING to learn from this phenomenon. Maybe it can’t act against MPB but it can still treat it. It seems capable of putting hair onto heads, at least occasionally, regardless of why the old hair was lost. Dismissing it on the basis that it’s probably not treating MPB is flawed logic. Minox doesn’t fight the MPB process either but we still value its ability to thicken existing hair.
Like I have said before - how many more cases of regrowth from this class of drugs will it take? How many is enough to make the MPB researchers start pulling their heads out of their asses and getting curious about it? This is at least the 3rd dramatic case that I know of.
[quote][postedby]Originally Posted by roger_that[/postedby]
First, I know that there have been other instances of drugs used to treat rheumatoid arthritis – many of this family of drugs have names ending in “-nib” – causing hair growth on some patients. Sometimes it’s significant hair growth.
But I think these drugs mainly grow hair on patients with auto-immune hairloss disorders, like alopecia totalis or alopecia universalis.
The medical causes for those kinds of hair loss actually are much different from what causes Male Pattern Baldness. MPB is not mainly an inflammatory disease, although what makes it really confusing is that some extreme cases of MPB have a big inflammatory component.
I think that this inflammatory component seen in skin biopsies of some patients with MPB leads many people to mistakenly assume that ALL MPB sufferers have inflammation, or that inflammation is a necessary result of the genetic condition of MPB, and that it’s always present.
The reality is that inflammation is really present only in a relatively small MINORITY of MPB cases, and that is what confuses the hell out of a lot of people, because they think the inflammation and MPB always go hand-in-hand, when that’s not the case at all.
This family of anti-arthritis drugs appears to be suppressing an auto-immune inflammation in these patients, and secondarily causing their hair to grow back, but just because it does that in these patients with autoimmune disorders, doesn’t mean it will cure all people with MPB. I can almost guarantee it won’t. In fact, this class of drugs is also potentially dangerous and has a lot of side effects, so I doubt they’ll ever become a standard or commonly used MPB treatment.[/quote]
While MPB may not be considered an autoimmune condition in the classical sense, its pathogenesis is still intimately tied to the immune system.
How?
I would actually dispute what you say. Immune-like response (only cell-mediated) is seen in only some cases of MPB – a minority of cases, not all. For MPB to be “intimately tied” to the immune system, it would have to have an immune component categorically, in all cases. I don’t think that’s the case, and I don’t think you can point to research that shows that is so in all cases of MPB. Maybe you’ve heard of some research that I haven’t, but I don’t think I’ve seen this proven anywhere.
[quote][postedby]Originally Posted by cal[/postedby]
Yeah but this is one case, and it’s not MPB-caused loss. Too many variables to call it.
There are other drugs in this class on the market and they have been linked to funny hair growth too. I’m sure it isn’t as simple as just taking this med and getting our hair back. We would have discovered it long before now.
But the fact remains that there is definitely SOMETHING to learn from this phenomenon. Maybe it can’t act against MPB but it can still treat it. It seems capable of putting hair onto heads, at least occasionally, regardless of why the old hair was lost. Dismissing it on the basis that it’s probably not treating MPB is flawed logic. Minox doesn’t fight the MPB process either but we still value its ability to thicken existing hair. [/quote]
I totally agree with everything you’ve said above. Some very good points there.
whatever
Dr. Cots in an interview with CNN bashed it as a potential hairloss treatment. Specifically stated it would not work for AA cases. What a jerk! Lol
This drug was given to patients with arthritis, they later developed psoriasis, which this drug suppose to treat as well. Such a delicate balance when it comes to our immune system.
[quote]While MPB may not be considered an autoimmune condition in the classical sense, its pathogenesis is still intimately tied to the immune system.
[postedby]Originally Posted by roger_that[/postedby]
How?
I would actually dispute what you say. Immune-like response (only cell-mediated) is seen in only some cases of MPB – a minority of cases, not all. For MPB to be “intimately tied” to the immune system, it would have to have an immune component categorically, in all cases. I don’t think that’s the case, and I don’t think you can point to research that shows that is so in all cases of MPB. Maybe you’ve heard of some research that I haven’t, but I don’t think I’ve seen this proven anywhere.[/quote]
I am not referring specifically to antibody-type responses. There is evidence to suggest that AGA patterning results from the distribution of particular mast (immune) cell components (prostaglandin d-synthase). So yes, I would maintain that it is intimately tied to the immune system in that we know the patterning (or PGD2 mediated hair loss) depends on immune cells.
I know you have read this before (at least the abstract):
Larson, Allison R., et al. “A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning.” Journal of cutaneous pathology 41.4 (2014): 364-369.
Some other papers:
Mast cells actively de-granulate in AGA areas of scalp:
JAWORSKY, CHRISTINE, A. M. Kligman, and G. F. Murphy. “Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis.” British Journal of Dermatology 127.3 (1992): 239-246.
- Which (de-granulation) may:
Mayo, Juan C., et al. “Androgen-dependent mast cell degranulation in the Harderian gland of female Syrian hamsters: in vivo and organ culture evidence.” Anatomy and embryology 196.2 (1997): 133-140.
- or may not be (depending on where you look):
Chen, WenChieh, et al. “Human mast cells express androgen receptors but treatment with testosterone exerts no influence on IgE-independent mast cell degranulation elicited by neuromuscular blocking agents.” Experimental dermatology 19.3 (2010): 302-304.
- regulated by mast cell androgen receptors.
-Significantly greater numbers of mast cells were present in subjects with AGA (contrary to the lack of a statistically significant difference in the above Larson et al., 2014 paper):
Won, Chong Hyun, et al. “Dermal fibrosis in male pattern hair loss: a suggestive implication of mast cells.” Archives of dermatological research 300.3 (2008): 147-152.
The function of mast cells in a range of autoimmune disorders is an area of active research.
[quote]While MPB may not be considered an autoimmune condition in the classical sense, its pathogenesis is still intimately tied to the immune system.
[postedby]Originally Posted by roger_that[/postedby]
How?
I would actually dispute what you say. Immune-like response (only cell-mediated) is seen in only some cases of MPB – a minority of cases, not all. For MPB to be “intimately tied” to the immune system, it would have to have an immune component categorically, in all cases. I don’t think that’s the case, and I don’t think you can point to research that shows that is so in all cases of MPB. Maybe you’ve heard of some research that I haven’t, but I don’t think I’ve seen this proven anywhere.
[postedby]Originally Posted by walrus[/postedby]
I am not referring specifically to antibody-type responses. There is evidence to suggest that AGA patterning results from the distribution of particular mast (immune) cell components (prostaglandin d-synthase). So yes, I would maintain that it is intimately tied to the immune system in that we know the patterning (or PGD2 mediated hair loss) depends on immune cells.
I know you have read this before (at least the abstract):
Larson, Allison R., et al. “A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning.” Journal of cutaneous pathology 41.4 (2014): 364-369.
Some other papers:
Mast cells actively de-granulate in AGA areas of scalp:
JAWORSKY, CHRISTINE, A. M. Kligman, and G. F. Murphy. “Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis.” British Journal of Dermatology 127.3 (1992): 239-246.
- Which (de-granulation) may:
Mayo, Juan C., et al. “Androgen-dependent mast cell degranulation in the Harderian gland of female Syrian hamsters: in vivo and organ culture evidence.” Anatomy and embryology 196.2 (1997): 133-140.
- or may not be (depending on where you look):
Chen, WenChieh, et al. “Human mast cells express androgen receptors but treatment with testosterone exerts no influence on IgE-independent mast cell degranulation elicited by neuromuscular blocking agents.” Experimental dermatology 19.3 (2010): 302-304.
- regulated by mast cell androgen receptors.
-Significantly greater numbers of mast cells were present in subjects with AGA (contrary to the lack of a statistically significant difference in the above Larson et al., 2014 paper):
Won, Chong Hyun, et al. “Dermal fibrosis in male pattern hair loss: a suggestive implication of mast cells.” Archives of dermatological research 300.3 (2008): 147-152.
The function of mast cells in a range of autoimmune disorders is an area of active research.[/quote]
OK, fair enough. The connection to prostaglandins in particular PDG2 is very clear. I wasn’t counting that as necessarily part if the immune system, since I don’t believe PDG2 or prostaglandins in general are synthesized ONLY in the Mast cells, but I see your point.
Incidentally, I wondered why, in Drs Cotsarelis and Garza’s PDG2 study, they didn’t make much of a point about Mast cells at all – they completely ignored the issue and just focused on PGD2.
I should just add and clarify that those who envision, or like to describe, AGA as a primarily immune or auto-immune disorder, or those who like to broadly characterize it in that way, are wrong. That idea is a misconception, but it’s popular among a lot of people who deal in pseudo-science. It’s kind of like the people who claim that childhood measles, mumps and rubella vaccines cause autism.
I think, when trying to answer this question, we have to be very careful. We do see inflammation, seborrheic dermatitis, and micro-fibrosis in people with MPB, but it’s not in all MPB patients and in fact it’s actually a minority, a relatively small subset of MPB patients. The majority of people with MPB never show these phenomena.
I am well aware of some research to the contrary, that suggests that most or all MPB patients have micro-fibrosis or “scarring” type alopecia, but that is not mainstream research and not accepted by the majority of scientists and doctors who are familiar with MPB pathophysiology.
Well, I definitely have sebhorrea dermatitis so the drug might work for
someone like me.
Haven’t been here in a while and wonder if anyone’s tried a concoction of baking
soda and lemon juice (making a weak sodium salicylate) sprayed on the scalp to
inhibit mast cell degranulation which in turn should help inhibit pgd2.
[quote][postedby]Originally Posted by roger_that[/postedby]… It’s kind of like the people who claim that childhood measles, mumps and rubella vaccines cause autism. [/quote] Have you read about the correlation between number of vaccines per child in a country and the number of cases of autism?
The key is the mercury (2nd most powerful neurotoxin) in vaccines. That mercury is included in vaccines is a well-known fact not open to debate.