Hair Breakage and Hair Growth in Central Centrifugal Cicatricial Alopecia (CCCA)

CCCA: How do I overcome my hair breakage?

I’ve selected this question below for this week’s question of the week. It allows us to the review some key concepts in the management of central centrifugal cicatricial alopecia (CCCA) and the importance of hair breakage in patients.

QUESTION

I recently was officially diagnosed with CCCA. I am a 35 year old black woman. I started having hair breakage on the vertex of my scalp since around June of last year. I stumbled across your papers, watched your seminars on youtube etc etc. and I had a strong suspicion that I had a diagnosis of central centrifugal cicatricial alopecia (CCCA).

I went to see the physician but by that time, my hair was growing back in that area (I had to wait several months to see a specialist) so the specialist did not think it was CCCA and diagnosed me with another hair condition called Trichorrhexis Nodosa as there were nodules on my hair shaft and I had a positive pull test.

Long story short, my hair seemed to be doing relatively well for awhile but around the end of March of this year, what seemed like overnight, I had hair breakage in my vertex again with the hair shaft super short. Basically I had a peach fuzz in that area. So I immediately called my dermatologist again and pushed for a biopsy. Three weeks later I was diagnosed with an inflammatory scarring alopecia, with the differential being CCCA.

This is what my biopsy said:

Microscopic Examination: There is concentric perifollicular fibrosis and the level of the isthmus, with associated patchy perifollicular lymphocytic inflammation. There are decreased sebaceous glands and focal interface dermatitis involving follicular epithelium. The features are of a lymphocytic inflammatory scarring alopecia, with the differential including lichen planopilaris and CCCA. Clinical correlation is recommended.
- Final Diagnosis SKIN BIOPSY SCALP: INFLAMMATORY SCARRING ALOPECIA"

So, now to my question.

I do not have any external scarring....as in I am not bald on any area of my scalp. I just have a small island maybe the size of a golf ball of short hair while the surrounding hair is significantly longer. At the end of March when I noticed the breakage, it was a peach fuzz. Since getting the biopsy and waiting on the results it has grown a little. It is now measured at a little less than 1.5 inches. So the hair in that area seems to be growing. However, will it grow continuously OR will it grow to a certain point and break off? I have internal follicular scarring at the level of the isthmus and my dermatologist told me that that is irreversible (though I want to explore the 10% metformin in Lidoderm that is hypothesized to reverse scarring).

So, assuming I had CCCA since last year, I am afraid that I will go through a cycle of hair growth to a couple inches and then breakage even if I am able to get the inflammation under control with the oral doxycycline and topical clobetasol that I was prescribed. I assume that the follicular fibrosis at the level of the isthmus has probably affected the formation or structure of the hair shaft and that's why some patients experience hair breakage early on in the disease? So, in your experience, have you seen continuous hair growth when CCCA is caught at the hair breakage stage or did it go through a cycle of grow and break?

Also, should I be taking clobetasol breaks? My dermatologist prescribed it once a day, every day indefinitely. Well, I suppose we will reassess when I see him again in 4 months but I remember reading on your site that you suggest steroid holidays every couple weeks. I use very little in that area daily as I am aware of, and afraid of any side effects.

ANSWER

This is a great question.

Hair breakage is very common in CCCA. In fact, hair breakage can be one of the very first clues that a patient has to the disease process. Hair breakage can happen prior to hair loss and prior to the appearance of ‘patches.’ You may wish to review a previous article I wrote:

Hair Breakage in Black Women: Not to Be OverLooked!

It’s true that “trichorrhexis nodosa” is associated with the hair breakage as you write - but the reason the hair is breaking in these situations is partly due to the underlying scarring alopecia. Heat and chemicals and hair styling might still have a role in some so that needs to be investigated in your case too. You and your dermatologists can review that.

The pattern that you describe of these short hairs that don’t seem to grow very long is very typical of CCCA. Usually these areas on the scalp are about the size of a tennis ball, although sometimes the area is bigger and sometimes smaller.

Hair breakage is common in CCCA and may appear as small patches about 2- 6 cm in diameter that simply fail to grow longer. Proper treatment of the CCCA reduces the inflammation under the scalp and sometimes helps the hairs to elongate and areas to fill in more normally.

This hair breakage issue is so important to recognize because it can be a sign of very early CCCA (or what I term subclinical CCCA).

Will my hair grow longer?

These areas of short hair might grow longer - yes! It’s possible that’s for sure. However, the overall chances this area will regrow is higher if you choose to aggressively treat your scarring alopecia than if you choose to less aggressively treat your scarring alopecia. By “aggressive treatment”, I mean the use of a plan that really works to chase away inflammation. This plan might include periodic topical steroids with steroid injections and oral doxycycline. You and your doctors can decide what is right for you and if you have any specific contraindications to these medications (ie reasons why you should not use). Topical 10 % metformin is an option too but no it’s not a “first line” treatment. It is a newer treatment and it’s not clear how many it helps. Maybe someday it will be first line treatment, but it’s not right now. Topical metformin does not reverse scarring, that would not be correct. Nothing reverses scarring - that’s permanent. However, topical metformin most certainly can help with stopping inflammation and getting hairs to sprout back up. There is a big difference between helping with hair growth and reversing scarring. Many treatments for early staged scarring alopecia can get hairs growing and help the patient achieve improved density. But that’s not because it reverses scarring.

To review the treatments for CCCA, you might wish to review the prior article but I’ll go into it a bit more here to review.

CCCA: Diagnosis and Treatment

It could be that topical steroids like clobetasol alone (as the sole treatment) might be sufficient to treat CCCA but for many women with CCCA, clobetasol alone is not enough to stop the disease. An aggressive approach might involve use of topical clobetasol with periodic steroid injections and a 3-6 month course of oral doxycycline. I am also a big fan of topical tacrolimus ointment as well in treating CCCA and it can be used with the clobetasol. How exactly these are used depends on the patient and her story and how much inflammation seems to be present. Treatment might initially involve daily clobetasol in the morning and tacroliumus in the evening or clobetasol three times weekly (Monday, Wednesday and Friday) and then Tacrolimus the other days. This is always re-evaluated every 3-5 months. No treatment is forever, except perhaps minoxidil if the patient also has a diagnosis of androgenetic alopecia.

I’m all very much a big fan of reducing heat and chemical as much as possible for at least 6 months. I know it’s not always possible but it does seem to help a great deal during this period where the hair is really weak. Your hair will be better able to tolerate heat and chemicals in the near future if we can get rid of the inflammation.

The ‘gold medal’ or first line treatments for CCCA are shown below together with second line (silver medalist) and third line treatments (bronze medalist):

You can see from the list above that 10 % metformin is certainly an option, but jumping on board with this as the first step would not be considered “first line”. There are only a small number of patient around the world treated with topical metformin so if that’s the route you want to take that’s fine. But know ahead of time that you are going at this without the backup of thousands upon thousands who have used the other first line treatments. It still could be a good option.

It may take 3-5 months to see changes but the patient often sees less breakage, less itching, less tenderness and this is followed by some degree of improvement. Early stages of CCCA are more likely to have some degree of improvement in terms of a bit of hair regrowth. Late stages usually do not.

I do feel that periodic breaks in using steroids are needed. I like my own patients to initially treat as aggressively as they are comfortable with. This means topical steroids daily for 4-6 weeks and then a 2-3 week holiday whereby no topical steroid are applied. This ‘holiday period’ is a great time for applying tacrolimus ointment as tacrolimus does not thin the skin and has very little in the way of absorption. After the two week clobetasol drug holiday is over, I might advise the patient to do another 4-6 weeks. However, if things are going well, we’ll often drop down to using clobetasol 3-4 days per week (and possibly use the Tacrolimus on some of the other days). So, to answer your question, use of clobetasol is not lifelong for patients with CCCA. Clobetasol is used until the point in time that we feel we don’t need daily treatment any more because of how good the scalp looks or feels or how well things are growing. But for those who need it, I have no issues with using clobetasol longer term provided we have some “steroid holiday” periods mixed in there.

It’s okay to be afraid of side effects, but periodic topical clobetasol, steroid injections, tacrolimus, and topical metformin are very well tolerated for the vast majority. Even doxycycline is well tolerated for most, although you’ll want to be comfortable with all the side effects of doxycycline if you go down that route.

All patients with CCCA need blood tests for CBC, TSH (thyroid studies), ferritin (iron), and 25 hyroxyvitamin D, glucose and hemoglobin A1c. If any of these are abnormal, they need to be addressed.

I hope this helps. If you treat the inflammation and limit injury to hairs for the next 6 months, you can break this hair breakage cycle.

Thank you again for the question.

Reference

Callender V et al Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012 Sep;148(9):1047-52.

Excessive Shedding in the 30's: Why is my hair still shedding?

Excessive hair shedding in the early 30s: What are the reasons?

I’ve selected this question below for this week’s question of the week. It allows us to discuss diagnosis of hair loss in women 30-40 years of age with chronic shedding. Here is the question….

QUESTION

Can oral vitamin + iron supplementation increase shedding the way minoxidil does?

I am a 35 years old female. I have always been under a lot of stress, especially in 2016-2017. In spring 2018 I noticed my hair got thinner (I always had rather fine hair); my scalp could be seen under direct light. I used castor oil and took spiruline tablets hoping it would improve; got the impression it did so I stopped. I was vegetarian then, too. I got preoccupied with the fear of getting bald, did a lot of research on the Internet that frightenend me even more and finally I got the courage to get an appointment with a dermatologist this summer (2020). She didn't notice hair loss (pull test); said my density was normal and scalp looked ok. She said it didn't look like AGA at all. She prescribed my iron supplementation (low ferritin (24)) and advised me to change my diet. I lack vitamin B12 too. From the end of July onwards I've been taking iron, spiruline, biotin and B12 supplementation. Since I didn't agree with the diagnosis ("no visible hair loss") I began counting the hair I'm shedding each day. The amount is horrible: it's more than 200 hair/day! The supplementation I'm taking and the changes I made to my diet don't seem to decrease the shedding at all. I've booked a appointment with anonther dermatologist for a second opinion (I'm truly terrified: my scalp feels strange; a bit of itching and burning + "crawling" sensations; my hair keeps falling out and for my dermatologist there's no problem...!) I'm surprised I still have hair left on my scalp when I see the amount that's falling every day... 
I have read that those who use Minoxidil experience shedding in the first months which is a sign that new hair is on the way (I do see regrowth but it doesn't make my hair volume look any better). So I am wondering: can oral supplementation cause a similar shedding, which proves that the treatment is working? If not, what should I do? I got no "real" dagnosis; from what I read on the internet it seems to look like TE but how can I be sure?

I would like to add that from time to time I have small pimples on my scalp that come and go. Not a lot of them though, but they can be itchy. My skin (on face) is oily, I have the same sort of sores on my face from time to time too. I don't know if this information is important.

Thank you for reading and I hope you'll be able to answer my question since my own dermatologist doesn't seem to take my problem seriously...I think the thinning is all over, but mostly noticable on the top of my scalp and at the temples. My hair become very flat, no volume at all. I wash it daily because it greases very fast (eversince I was in my early teens).

ANSWER

Thanks for the question. There’s really two very good ways to determine the cause of your hair loss - and that is to share your story with a hair specialist and have him or her

1) Evaluate your scalp up close with “trichsocopy” (magnified imaging)

or

2) Perform a 4 mm scalp biopsy

So there is a way for you to get your answer.

I’d like to discuss several important things in the question you ask and the information you have submitted. Let’s get to it.

Before we do go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s story

2) the findings uncovered during the process of the scalp examination including trichoscopy

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis.

AGA must be the Default Diagnosis in Women 30-40 with Increased Hair Shedding

I would need to examine your scalp to determine if you have androgenetic alopecia or telogen effluvium or both …. or some other diagnosis.

However, I strongly believe that the first diagnosis that must be ruled in or ruled out in any female patient with hair loss in the 30s is androgenetic alopecia. One must not move on until this issue has been fully settled. Once that it settled one can determine if the patient has or does not have telogen effluvium (with AGA or by itself ) and whether or not the patient has some other hair loss condition.

How does AGA present or ‘announce itself in women’? With shedding ! .. and with thinning in the top or often also diffusely!

How does telogen effluvium TE present itself or announce itself? With shedding ! …and with thinning diffusely !

It’s important to be aware that TE and AGA can look identical - at least at first glance.

What’s the most likely cause of hair loss in a 30-35 year old female with hair loss for 3 years and shedding and thinning? Androgenetic alopecia by far.

Of course, I can’t say what you have as I have not examined your scalp. But these are the principles that guide the entire discussion.

Therefore, the key question that must be asked in your story is “Does this patient have androgenetic alopecia (AGA)?” That’s the key question. That’s the number one question. The key question should not be what supplement can this patient take? ….. or what shampoo should this patient use? The key question is “does this patient have androgenetic alopecia?”

What is needed now is proof that you do have AGA or proof that you don’t have AGA. One should not rest until this question has been solved. Once we solve that question, we can move on to figuring out if any other diagnosis is present.

For now, we need to determine if AGA is present. That is what is needed now. Your doctors might be able to solve this with trichoscopy or they might need to solve it with a biopsy.

We can not always solve it with simply looking at the scalp from afar.

Only you know what your hair looked like before and your doctors do not. If you hair looks thinner to you but just fine to another person - then guess what? You still have hair loss.

The Three Stages of Hair Loss

There are 3 stages of hair loss that I describe for patient’s with androgenetic alopecia. What is so important in your case is to determine once and for all as to whether you are in stage 2 AGA or whether you don’t even have AGA at all. Here are the stages.

Stage 1 of Androgenetic Alopecia

In stage 1, hair density is slowly reducing but the patient is unaware. There may be a slight increase in hair being shed in the shower or coming out daily in the brush. However, this generally goes by unnoticed by the patient. A biopsy can sometimes (but not always) capture a T:V ratio below 4:1 and some degree of miniaturization (and anisotrichosis) may be present. Much of the time it's challenging to confidently diagnose AGA in this stage. Some stay in stage 1 for a very long time; others just a matter of months.

Stage 2 of Androgenetic Alopecia

In stage 2, the patient first becomes aware that something is not quite right. They may see a bit more scalp showing when they look in the mirror. They may feel the hair does not feels as thick when they run their fingers through the hair. Under bright lights they may feel a bit more aware of these changes. When the hair is wet, the thinning is evident.

Nevertheless, in this second stage everyone else tells the patient they look fine. Some patients are told they are "crazy". Even some physicians will tell the patient they "look fine" and need not worry. Patients often feel isolated in this stage because nobody believes them when they say they are losing hair! A biopsy definitely shows a T:V ratio less than 4:1 and miniaturization is clearly seen in more than 20 % of hairs. Many never progress to stage 3 especially those with onset of AGA later in life.

Stage 3 of Androgenetic Alopecia

In stage 3, the hair loss has progressed to a stage where hair loss may become evident not only to the patient but also to others. Of course with use of various hairstyles, products, camouflaging agents it may still be possible to hide one's hair loss from others. As stage 3 progresses it becomes more and more difficult to hide hair loss.

Understanding the Patterns of Hair Loss

Both AGA and TE can cause hair to look thinner. With AGA is typically affects the middle of the scalp whereas with TE is affects all of the scalp fairly equally. We call this a ‘diffuse’ pattern. AGA can sometimes have a diffuse pattern too but very often than not it affects the middle more than other areas. In addition, AGA often affects some areas of the middle a bit more than others.

Your photos show the hair parted in the middle. These types of photos are great for evaluating the scalp. If your part width at the back of the scalp seems smaller than the front of the scalp, the chances start to increase that you might have AGA. By part width, we simply mean the amount of scalp showing when you part your hair in the middle.

In your photos, it’s difficult to get a sense of the exact patterns because I only have photos of the middle. But when I look at these photos I do wonder whether the density towards the crown is a bit less than the density up front. In other words, it seems that even in the mid scalp the density is not reduced equally.

Summary: Putting it All Together

Thanks again for the question. Let’s review everything again.

1. You first asked if oral vitamins can increase shedding like minoxidil does. That answer is not usually. The mechanism is different.

2. You have high shedding rates so something is probably different with your hair cycles than it was 20 years ago.. One can shed 200 hairs daily in AGA and 200 hairs daily in TE so this information is not helpful to actually get to the diagnosis. You could have one, You could have both. You might have neither. Statistically speaking, a 30-35 year old female with shedding has either AGA or TE and with your history AGA is far more likely to be a diagnosis. Of course, we are not statistics and each person requires a proper examination.

3. You mention increased oiliness of the face so one needs to also consider whether you have a component of “seborrheic dermatitis”. This can increase these scalp sensations like you describe - and so can telogen effluvium. Your doctors can determine if you have SD by carefully examining your scalp.

4. Overall, it may be that you’ve had TE at some point in time - and perhaps you also have it now too. It may be that stress was a trigger before for a TE and perhaps maybe now you have different triggers that are causing a TE (such as lower iron). I suspect there was some component of TE back in 2016-2017 when your hair shedding stopped. Your doctors can evaluate these ‘triggers’ for shedding in greater detail. You may or may not need more blood tests but your doctors can review that in detail.

A full work up is needed at this point. You may need more blood tests. However, what you do need next is a thorough scalp examination with trichoscopy. If there is significant “anisotichosis” on trichoscopy then you may have AGA. I can’t tell these with your photos - it needs an up close examination. If it’s still difficult for your doctors to determine with trichsosopy, then a scalp biopsy (with use of horizontal sections) is going to be helpful. The pathologist can determine the number of large terminal hairs and tiny vellus hairs and the number of telogen hairs. A terminal to vellus hair ratio of less than 4:1 usually signals a diagnosis of AGA in women. You can review more about scalp biopsies here Scalp Biopsy Interpretation

I hope this helps and thank you again for the question.

What is causing my beard, body and scalp hair loss?

What’s causing my beard hair loss?

I’ve selected this question below for this week’s question of the week. It allows us to discuss the importance of the speed of hair loss in the diagnosis of hair loss.

Here is the question….

QUESTION

I have diffuse thinning across my entire body. I am male, under 30. The hair loss initially started as rapid thinning on the entire scalp, soon spread across facial hair and body hair. Some distinguishable features of my hair loss are that my beard and body hair only have one hair per follicle, a lot of hairs remain as very short stubble and do not grow, eyebrows experience pain during periods of shedding. I've been to 4 dermatologists and had one scalp biopsy which was inconclusive. Hair loss has been very rapid, from initial onset I lost well over 50% of my hair density within 4 months. My beard presented with patches of hair loss which have grown in.

Beard photos, before (left) and right (after) hair loss

Scalp does not itch and I do not feel any burning. However I feel tenderness and itching in my eyebrows which are constantly shedding. I've been on finasteride ( discontinued ), oral minoxidil for 9 weeks, and steroid injections in the eyebrows which have helped with regrowth. Hair loss started 3 months after I experienced a very traumatic event and has continued well over 1 year now.. After the traumatic event I broke out with very severe cystic acne across my back, scalp neck and face and hair loss soon followed. The way I look today is completely indistinguishable from what I looked like 1 year ago.

What is the likely cause ?

ANSWER

Thanks for submitting your question. There are several possible hair loss conditions that could be causing this, but the most likely cause, by far, is alopecia areata. But it’s certainly not 100%.

To help definitively figure out what’s going on, I would need to (1) ideally see photos of the scalp and eyebrows, (2) know the answers to a lot more questions I have, (3) review your biopsy and (4) review all your blood tests. I’d like to know if you’ve had patches of alopecia areata in the past, whether you have a family history of alopecia areata, how thin the eyebrows were, whether their was redness in the eyebrows too, whether the eyelashes were lost, whether you’ve had changes in your nails, weight loss, or abnormalities in your blood tests. I’d want to know if you’ve started or stopped any prescription medications and supplements in the last 12-16 months, started or stopped any anabolic steroids, and whether you’ve had any skin rashes of any sort in the last 2 years. Fevers, night sweats are important to know about as well. Of course, your entire medical history will be important.

The full list of possibilities for the hair loss includes:

1. Alopecia areata alone

2. Alopecia areata with a telogen effluvium

3. Alopecia areata with seborrheic dermatitis

4. Alopecia area with a telogen effluvium with seborrheic dermatitis

5. Alopecia Areata with a telogen effluvium with seborrheic dermatitis with male balding of the scalp.

6. Telogen effluvium with seborrheic dermatitis

7. Frontal fibrosing alopecia/lichen planopilaris

8. Rare mimickers - syphilis, cutaneous T cell lymphoma

There are many features of the story here which fit well with alopecia areata. First, the speed of hair loss is fast. The loss of 50 % density in 4 months is seen in alopecia areata and sometimes telogen effluvium but this kind of rapid hair loss is more typical of alopecia areata. it’s far too fast for androgenetic alopecia but of course this may be a part of the hair loss that is happening as well (more chronically). It’s too fast for most scarring alopecias too (and I would not expect regrowth to occur in the manner you described if this were the case). It’s not impossible for FFA, but it is an uncommon story for FFA.

I’ve written about the importance of the speed of hair loss in the past. Alopecia areata is classically quite fast and has the potential to cause more rapid hair loss than telogen effluvium if the alopecia areata is active.

It’s possible of course, that a person has a telogen effluvium and alopecia areata too. A person can have two diagnoses or three or even four or five. The intense stress you had from the traumatic event can cause a telogen effluvium and if you are genetically predisposed, it could precipitate alopecia areata too.

The regrowth of your eyebrows with steroid injections is best in keeping with alopecia areata. I would need more information to know it it’s a little or a lot of regrowth. It would be helpful to know what the brows actually looked like before. If the regrowth has been really significant with the steroid injections, alopecia areata remains at the top of the list. That said, any inflammatory condition of the eyebrows can cause hair loss and steroid injections can help with regrowth. Seborrheic dermatitis of the eyebrow can cause a little bit of loss but it’s usually mild and steroid injections can settle down the redness and help get brows regrowing. Even frontal fibrosing alopecia can show some regrowth so the simple fact there was regrowth does not prove it is AA. Eyebrows can improve with steroid injections in quite a few conditions so this feature alone does not prove it’s alopecia areata.

The beard photos you’ve submitted are most in keeping with a diagnosis of alopecia areata. Are there mimicking conditions that can look 100% the same ? Yes, there certainly are. Rarely, a seborrheic dermatitis can cause beard loss but that’s quite unusual to be patchy in this manner. Rarely, an immune based issue can cause beard loss too (lichen planopilaris/frontal fibrosing alopecia) but regrowth is less likely in these types of situations. Frontal fibrosing alopecia really is one of the key conditions that you and your doctors need to rule out confidently. Beard hair loss or beard thinning happens in about 30-40 % of patients with FFA. Telogen effluvium affecting the beard in a patchy manner like shown in the photos is not typical so telogen effluvium would not explain the beard loss but could, of course, still be involved. Syphilis is not common cause of the hair loss pattern you are describing but this diagnosis needs to be considered by your doctors in a presentation like this. It is a great mimicker of alopecia areata. A rare condition of the blood cells (mycosis fungoides/cutaneous T cell lymphoma) needs to be considered if things don’t improve. I would not expect these latter two conditions to have spontaneous improvement you have described without treatment so they probably don’t fit well in your particular case. Alopecia areata is still at the top of the list of causes but your dermatologists can review these entities and perform a full skin examination.

The acne eruption you describe may or may not be related to the hair loss. I suspect it is related in some manner. Acne eruptions of this kind can be seen in alopecia areata. (See previous article alopecia areata and acne). In order to understand how hair could have a role in acne development, it is important to understand the function of hair. During the process of normal skin turnover, the shed skin cells from the hair follicle epithelium are carried upward in the follicular canal towards the skin surface. It is thought that the sebum that is secreted by the sebaceous glands helps in this process but helping the shed cells efficiency move out of the hair follicle canal.

Ringrose and colleagues first reported the relationship between acne and alopecia areata back in 1952. They described a male patient who developed acne, milia and cystic type eruptions only in the areas of alopecia. The authors proposed that the hair helps keep the follicular orfice open to allow sebaceous contents to be properly removed. They described the hair follicle as a “natural drain” to the removal of sebum.

These same authors performed some interesting histological studies by examining biopsies of these acne lesions. They found that acne lesions were not seen in areas that contained hair and were not seen in areas where the pilosebaceous unit was completely degenerated. The proposal here was the acne lesions of alopecia areata represented a transition period - between normal growth patterns and complete loss.

in 2007, Sergeant and colleagues proposed that the hair follicle acts as a type of ‘wick’ and acts to draw sebum up towards the skin surface. They stated that the hairs on the scalp may do this more efficiently that hairs on the face and therefore the hairs on the face may be predisposed to the formation of “micocomedones” and the typical lesions of acne. Microcomedones are a prerequisite for the ultimate acne lesion.

So in your case, there is a high likelihood a diagnosis of alopecia areata is present. It is certainly not 100 % but the likelihood is quite high. It will be really helpful to follow all hair bearing areas - as definitive signs of alopecia areata (or scarring alopecia or another condition) may show up over time. In my opinion, frontal fibrosing alopecia is the mimicker that really needs to be ruled out.

FINAL COMMENTS

At this point, the evidence would suggest alopecia areata but I would need more information to confirm or refute that. I would recommend that you speak to your doctors about these issues as they will know your case best. I would suggest you considering asking them about blood tests for CBC, TSH, ferritin, testosterone, B12, ESR, ANA, zinc, vitamin D, RPR, creatinine, AST, ALT, urinalysis if you have not already. if any of these are missing you might get them done. If the diagnosis is not clear, a repeat scalp biopsy can be considered. It may be that with trichoscopy a dermatologist can evaluate whether alopecia areata is present although I certainly do appreciate that your story is complex and you’ve probably had many evaluations (with trichoscopy too). Biopsies of the arm hair, leg hair and eyebrows are trickier and often given less information. If a repeat biopsy is needed, it should come from the scalp. The main thing we are trying to distuish in the biopsy is alopecia areata vs scarring alopecia (ie frontal fibrosing alopecia) .

If it is alopecia areata that you have, I suspect that over time, a patch of typical alopecia areata hair loss will occur that will allow your doctor to definitively tell you if that’s what it is. There are ways to explore the diagnostic possibilities further. Certainly, the blood tests above are important. You’ll want to make sure there are no systemic issues that increase the chances for cystic acne and hair loss. We’ve spoken about the possibility of having a repeat biopsy. This should be done on the scalp and be 4 mm and be done with horizontal sections and read by an expert dermatopathologist. Alopecia areata can be tricky to diagnose in some cases. However, an increased proportion of catagen and telogen hairs and eosinophils in the tracts and peribulbar inflammation can all point to the diagnosis. A biopsy will pick up immune based issues, lymphomas, and if the percent of telogen hairs is high the biopsies will give an idea of how high it really is.

Sometimes in a situation like this, we consider a "therapeutic challenge.” A therapeutic challenge means we give certain medications to observe what happens when those medications are given. If the response to the medications is exactly what we predicted, it suggests we are probably correct with our diagnosis. I would need to know more about your story to describe exactly what might be appropriate but you and your doctor could consider therapeutic challenges like steroid injections to the entire scalp, or a 4-6 week course of oral steroids is an approach therapeutic challenge if alopecia areata is considered. If you get significant regrowth during these types of therapies, it’s a pretty good indication that there is an inflammatory issue that was blocking the growth of hair. Alopecia areata would be the most likely diagnosis in such as case.

If alopecia areata is the final diagnosis, then continued beard injections together with other systemic options would be possible including dexamethasone, methotrexate, cyclosporine, tofacitinib. A return to oral minoxidil could be reconsidered depending on exactly what your story was when you stopped it

Thanks again for submitting your case. I hope this was helpful.

What's the reason for my hair loss? What does my trichoscopy show?

Why am I experiencing hair loss?

I’ve selected this question below for this week’s question of the week. It allows us to discuss some of the finer aspects of interpreting trichoscopy and how the clinical history must be interpreted together with all trichoscopic analyses.

Here is the question….

QUESTION

I really hope you can help me with the diagnosis of my hair loss that I've been experiencing for a year now without being able to get a real diagnosis, doctors can't seem to find anything else than '' light dermatitis'', yet I can' t help but notice everyday that this isn't normal and I have no clue so far. 
About a year ago I suddenly noticed that I had way less hair and I could see my scalp, which never happened before. A few weeks later I've started to notice redness in my scalp and itching that never left ever since. The itching seems to come and go without any logical pattern, and the more red and itching my scalp gets, the more hair I seem to lose. I did a trichoscopy 2 weeks ago, where you can see the results.

I'm quite desperate to get a real diagnosis because I don't think something innocuous would last that long and cause hair loss without stopping. Overall I am in good health. Blood tests were all okay 

ANSWER

This is a great question because it allows us to talk about so many things.

Before we go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s Story

2) the findings uncovered during the process of the scalp examination and

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis.

I’d like to know a lot more about this story ideally but of course the magic of the “question of the week” is that I tackle questions with limited information.

I can’t be sure of what’s going on entirely without seeing your scalp up close myself and knowing your entire story. Your age, and details about your scalp symptoms all matter.

In my opinion there are 4 possibilities for what you have:

1. Androgenetic alopecia with seborrheic dermatitis (AGA + SD)

2. Androgenetic alopecia with mild telogen effluvium with seborrheic dermatitis (AGA + TE+ SD)

3. Mild telogen effluvium with seborrheic dermatitis (TE + SD)

4. Seborrheic dermatitis alone (SD alone)

I’d like to make a few comments about the type of thinking that is needed in case like this.

A few comments

1. It’s true that you have very nice trichoscopy pictures - but what’s also important is just getting a sense if the frontal density is truly the same as the back. There certainly is a suggestion that your frontal density may be less than the back (occipital area) despite all the numbers that you see in your measurements. If there truly is a significant difference in the density in the frontal and back then we need to think about a patterned hair loss (ie androgenetic alopecia).

2. A physician can get a better sense of density by parting the hair down the middle from front to back and comparing the part width in the front to the back. If the part width is wider in the front than the back that means there may be more hair loss in the front compared to the back - and this might be a suggestion that there is some degree of androgenetic alopecia.

3. It does seem that your blood tests have been normal so we’ll assume that. This does not mean that a person can not have telogen effluvium or androgenetic alopecia with normal blood tests. In fact, most people with hair loss have normal blood tests. I have not seen your blood tests of course, but I would hope that you have had CBC, TSH, ferritin, 25 hydroxyvitamin D. If your periods are irregular you should have a hormonal panel. If you have other symptoms, you might need other testing too.

4. There appears to be clear differences with the photos in the frontal areas compared to the occipital (back) areas including more single hairs and less density. While this could be simply suggesting diffuse loss as in a telogen effluvium, we need to consider the possibility that this could represent a pattern to the loss (and female pattern alopecia also called androgenetic alopecia).

5. Your average hair caliber seems to be lower than expected at 60 um. This depends on your background and your type of hair but it certainly does make me wonder if there is some change happening that affect caliber especially a diffuse process like a diffuse AGA. Of course, androgenetic alopecia is one of the more common hair loss conditions that affect caliber. Your data from the trichoscopy is not definite so I can’t completely rule in or rule out this particular diagnosis.

6. If you do not have much in the way of increased shedding, I would favour a diagnosis of AGA. If there is a lot of shedding that you have, it still could be AGA but a mild effluvium (TE) certainly does not need to be considered. Your story of suddenly “noticing” that you have less hair is more typical of AGA than TE. The degree that you are shedding today and the degree that you have been shedding in the past 6-9 months would sway me someone as far as how likely a diagnosis of TE really is.

7. I do favour options 1 and 2 but it’s by no means definite based on the information you have given. It will be helpful to follow the trichsocopy measurements over time. If you have a TE like in option 3, the measurements and numbers will likely get better over time. If it’s an AGA (option 1 and 2), the numbers will not likely improve and may get slightly worse in 6-12 months. Photos will also be very helpful. If it does become clear that the density in the frontal areas is slightly less than the back of the scalp, one needs to consider androgenetic alopecia.

8. If you are concerned a scalp biopsy or a 5 day modified hair wash test might help. Sometimes in the very early stages a a biopsy only slightly helpful so I am not of the opinion that you must have a biopsy. However, if the terminal to vellus ratio of your biopsy is shown to be less than 4:1 it indicates androgenetic alopecia is likely to be present. If the terminal to vellus ratio is above 4:1 is suggests that TE alone (option 3 or 4) is more likely. A biopsy can also capture any rare mimickers of redness such as lichen planopilaris, although I do not suspect that is what is going on (the density and changes are far too similar in the 3 areas to really support early LPP - and the story I have so far and the trichoscopy does not really support that diagnosis). A modified hair wash test can give a sense of how many hairs are being shed and whether any of these are small. What’s interesting in your photos is that it does appear that there are more vellus hairs in the photos from the frontal area than the measurements state in the information you were given. I am personally a big believer not only in looking at the measurements these computers give but also in looking at the images myself and looking at the scalp myself and getting sense if the measurements the computer gives makes sense or not. The presence of thinner and thinner hairs (miniaturized hairs) and the presence of thinner and shorter hairs (vellus hairs) is what androgenetic alopecia is all about.

9. I do think that there is likely a component of seborrheic dermatitis complicating the picture here. Your dermatologist can review with you at your next appointment. The trichoscopy would suggest this as well. SD is not typically a major cause of hair loss but can give a bit of shedding if severe enough. If you do have SD, it is mild and may contribute to symptoms like itching and tingling from time to time and then there will be periods where the scalp feels good again. The involvement of the temples is quite typical of SD and your photos are noticeably most red in the temples. There are no signs of scarring alopecia in the trichoscopy images provided but again a biopsy can help further clarify.

FINAL SUMMARY

Thanks for the great question. With the information provided, I can’t say one way or another exactly what is the diagnosis. However, a scalp biopsy or 5 day modified hair wash test could take you that much closer to understanding the diagnosis if there is really debate. I am suspicious about their being androgenetic alopecia here but I can’t tell for sure and ideally would want to see the scalp in a situation like this. Once you have the proper diagnosis, you can plan treatment. In addition, it is going to become much clearer over time what the diagnosis is especially if you do repeat trichoscopy measurements in 6 and 12 months. The frontal density and caliber of the hair in the frontal area will decrease and the number of single hairs is going to increase in the frontal if AGA is truly what is present. For now, treating the seborrheic dermatitis is quite reasonable. I would normally recommend that efforts be put into confirming the diagnosis with certainty. Some of the treatments for TE overlap with AGA treatments including laser and topical minoxidil and oral minoxidil so one can certainly get started with a plan once the diagnosis is made. Certain other treatments however, like anti androgens, are only effective in AGA and will not be effective if TE is the true diagnosis.

Thank you for your question.