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AMVC
AMCV or atrophia maculosa varioliformis cutis presents as depressed idiopathic scarring primarily affecting the face in young adults. The cause is unknown, & treatments are often unsuccessful. This is one of life’s true mysteries. Over the next few years, we will know more about this condition. It is much more common than what the literature reports.
FactsFacts On AMVC
- This condition is more common than what is reported in the literature
- Regardless, AMVC is a diagnosis of exclusion
- Atrophic scars can be post inflammatory, post infectious & immune related
- A medical dermatologist can exclude others causes mimicking AMCV
- A biopsy can be useful in the diagnosis
- AMVC should ideally be managed in a departmental setting in a university
- There are no universally accepted treatments for this form of macular atrophy
What is AMCV?
This poorly understood entity was first described over a century ago. It has many forms & shapes, typically presenting as non-inflammatory shallow depressions (atrophy), typically involving the face of young adults. Fortunately, most cases are mild, hence the term macular or flat.
This entity is much more common than in the literature, however most people do not know they have it (referring to milder cases).
What causes atrophic scars from AMVC?
As with everything else that has no concrete aetiology, the probable cause is genetics, coupled with environmental changes or stimuli; epigenetics. This means your skin has a predetermined genetic mutation that is activated by a trigger. Both trigger & mutation are yet unknown.
What clinical variants are there?
Based upon the clinical reports & my experience, the following variants are reported
- Feline variant: reported in India, linear whisker like atrophic areas around the mouth
- Crescentic variant: common, sides of face, temples, suggestive of traumatic origin but absent history.
- Cribriform variant: forehead. Super rare variant, hard to treat.
- Circular variant: looks like chickenpox but no history of inflammation. Biopsy shows atrophy with no fibrosis.
I do believe that atrophoderma of Moulin is a separate entity & more towards the morphea spectrum. PIH is seen in Moulin due to dermal pigment secondary to lichenoid changes, I disagree with a paper lumping Moulin with AMVC.
Will more scars develop?
Highly unlikely. Though spontaneous in nature, the majority of AMVC cases do not get worse in time. The flipside is that established scars rarely spontaneously resolve.
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What topical treatments are possible?
There are many reports of tretinoin & retinol based topicals trailed in patients with atrophic scarring. The results to date have been disappointing. Having said that, it is worth a try. Retinoids are cost effective, with little if any side effects, providing you exert common sense in the application.
Do lasers treat AMVC?
In theory, based upon the histological findings of epidermal atrophy, a thin & atrophic papillary dermis & a lack of inflammatory cells, lasers may be a sensible option to stimulate collagen production.
With so many unknown variables, my usual practice is to deliver multiple, low energy settings of fractional lasers over a timeline of 18 months. Conservative CO2 is best, using logic & science. In some cases, a test spot is required, meaning a small area is treated, then followed up in 6 months to ascertain whether treatment is successful or not. Test spots are best conducted in a department or university setting.
What are experimental treatment options?
I do believe over the next two decades we will have a better understanding of this mysterious condition. Working backwards from the histology, treatment options for AMVC may include-
Dermal grafting & stems: Either manual grafting or the dermis or novel treatments such as Rigenera / Regenera. True results, as per studies, are not seen until the 24-month mark.
Modified epidermal micrografting: I am currently working on this as of 2022. It may work, it may not. Higher risk procedure than novel techniques & fractional CO2. Ideally this should be conducted in a university or hospital setting, see below.
Off label dermal fillers: I am currently trialling PLLA & Ca OH fillers, delivered via the epidermis. The atrophy is too shallow for traditional HA dermal fillers. I have not got a set protocol yet, as of 2022.
What other conditions need to be excluded?
There are conditions that can look like AMVC both clinically & histopathological. Therefore patients require a review by a team of medical dermatologists before a label of AMCV is given. Ideally this should be done at a hospital or university setting. Conditions include-
- Atrophic pathology secondary to inflammatory dermatoses including morphea, atrophoderma of Moulin, subclinical DLE, keratosis pilaris atrophicans & acne
- Missed post infection pathology: Zoster, HSV atrophy, elastolysis secondary to infection including folliculitis & resultant elastolysis
- Missed accidental traumatic scars: from childhood
- Psychological issues including dermatitis artefact
Disclaimer: The above conditions need to be excluded by a medical dermatologist. AMCV is a diagnosis of exclusion. My job now is an operator, & not a diagnostic dermatologist.
What tests are done to confirm or exclude AMVC?
Ideally a biopsy is conducted on the lesion to confirm or exclude this condition (exclusion is less likely, as if you have true atrophy, it will be confirmed on pathology. The question is – if atrophy is due to some other pathology).
True AMVC has the following histological features, epidermal & papillary atrophy with the absence of cellular inflammation, namely a quiescent immune system without lichenoid changes. I also believe that true cases of atrophia maculosa will have an absence of dermal melanin (points towards a lichenoid cause).
Blood work up will show a normal ESR, CRP, negative ANA, ENA & other antibodies. A clinical examination may show associated incidental acne, &/or atrophic lesions elsewhere.
Note: If you are really concerned about your AMCV, you should see a department of dermatology near you. Ideally the test above will be useful. Collection of biopsy specimens will aid further research. I do not take biopsies; however I will be more than happy to confirm or exclude the diagnosis if contacted by your consultant specialist. I do not get involved in patient management, just a second opinion arranged by your dermatologist.
What does research say about AMVC?
Lots of theories, nothing proven. To date papers have suggested that this can be related to hepatic problems, genetic conditions & acne. Other papers have postulated that this is a form of burnt out subclinical / sub-inflammatory morphea, classifying this as atrophoderma of Moulin. The bottom line is that we really do not understand this condition well.
If we do not understand a problem, then there is no universal solution. Hence why I feel this entity should be treated in a university or departmental setting.
What is the current thought regarding AMVC & morphea?
The debate arises whether AMVC is burnt out morphea or atrophoderma of Moulin. This is based on histological & clinical findings. I have seen cases of Moulin, & these look very different from true AMVC of the face. Moulin cases are Blaschkoid on the trunk. They are hyperpigmented (at least the ones I have seen).
AMVC is polymorphic, I acknowledge that some patterns are linear following modified Blaschko lines, however many cases do not follow this pattern. I have seen punctate, circular, linear, crescentic & geographical patterns of AMVC.
What is my experience with AMVC?
Lots, but like others I do not have a reliable solution, nor do I have a true understanding of the aetiology. Unlike acne scars whereby in many cases there is a clear & defined treatment pathway, AMCV has a dearth of unknown factors.
I do believe in this entity, though I do think that in some of the published cases scars resemble chicken pox, trauma (crescent shape, possibly nails), dermatitis artefacta (for real!) or unusual geographic forms of acne scars (box car like linear scars).
Where should patients ideally go to for help?
Ideally Atrophia Maculosa Varioliformis Cutis should be managed in a hospital or university setting. My reasons for this include-
Collection of Data: much easier in a department of dermatology, as enrolment of patients is easier. Additionally ancillary help from registrars are provided. This saves time & resources.
Access to a group of dermatologists is a big advantage. Many sets of eyes are useful to confirm/exclude the diagnosis. Any input from colleagues are useful.
Costs: this is important for patients. IMO all experimental options should be subsidised. This can not be done in a private practice setting. It places pressure on patients & treating dermatologists, not ideal. Treatments should be conservative.
Follow ups: Again resources & costs can be better allocated in a university or hospital setting. This way data can be shared to other departments worldwide.
Do I treat AMCV?
It depends on the situation. If this condition falls under the objective classification of severe (as defined by the Goodman Baron classification), I do treat it. If objective & subjective viewpoints are not met, I do not treat it. This means if AMCV cannot be readily seen at conversational distances in normal lighting, I do not take the case on. You are best seen at a tertiary level.
In many cases, autoimmune conditions need to be excluded. A general dermatologist can assist.
What is BDD & where is the line in the sand in the context of AMCV?
There are many patients who have AMCV & subsequent BDD or body dysmorphic syndrome. Unlike most cases of inflammatory dermatosis, the majority of AMCV is subtle, hence the name macular (flat or relatively flat), the exception to this rule are cribriform & feline variants of atrophia maculosa. These two variants warrant treatment due to the extent & depth.
If you have AMCV & the average person at conversational distances cannot see the problem, then objective scar assessment falls under the minor category. This does not mean that you can’t have your condition treated, it means that I am not the right dermatologist for you. My work is primarily focused on severe objective grades of scarring. See my comments below.
What is dermatitis artefacta & how is it related to AMVC?
This entity spoils it for everyone involved in research. As the name suggests, it is an artifact, or caused by the patient. Yes, this really slows down R & D & takes up much needed human resources that can be devoted into real clinical outcomes. This subgroup of patients exist (believe it or not), they create trauma & scar patterns to gain attention for others; either online or in real life.
This condition is best treated in a public hospital by a senior dermatologist.
Dermatitis Artefacta patients frequently troll websites & support groups including acne.org, realself & FB Groups.
Who should you see if you have AMVC?
In Australia, if you have objectively severe AMVC I will be more than happy to take up your case. Additionally, if you have associated Grade 4B acne scars & minor AMCV, again I would be super happy to treat you.
If you reside overseas, you should see a dermatologist near you. Ideally your cases should be viewed by a team of dermatologists to confirm or exclude other causes of atrophy including inflammatory & post inflammatory conditions. You are best served in a university or hospital setting.
Disclaimer: I do not treat body dysmorphic patients. If objective photography cannot capture your scars in normal lighting, you may have BDD. It is not that you cannot have treatments, it just means that I do not perform high risk procedures in this patient group.
What home DIY treatments are there?
Keyboard professors will have their own viewpoint on forums. Some may be sensible, others somewhat silly. My job is to provide safe advice, not the most aggressive. Any advice given must account for the lowest common denominator, or the blunt tool in the shed. If you want to ‘have a go’, try some dermastamping.
- Clean area.
- Use a dermastamper, it is far safer than a roller or pen. Stamp 0.25 to 0.3 mm.
- Apply a retinoid after.
- Do this every 3-4 weeks, for 12 months.
- Do not try acupuncture needles or acids, your skin is atrophic to begin with.
What is the future of AMVC research?
In the future we will know more about this condition. AMCV was first reported in 1918, fast forward a century later & we still don’t know about this condition. I do believe that newer technologies to deliver stems/fibroblasts/keratinocytes to the affected area should yield better results in the next few decades.
An efficient method of data collection is to have these patients filtered in a University or department setting in a hospital. This way data can be readily shared worldwide, further aiding research. This includes a collection of biopsies, as this acts as a library for future lesional genetic coding & mutation testing.
Davin’s Viewpoint on Atrophia Maculosa Varioliformis Cutis
AMVC is much more common than what you believe it to be. I see at least half a dozen cases a year in private practice. Even though I can pick this up, it does not mean I have an answer. Much like other dermatologists worldwide, I do not understand this condition, & I do not have a reliable way of treating it.
The majority of AMVC I see are incidental findings as I treat these patients with severe acne scars. I often do not point out macular scarring if they do not see it. In some cases, I treat these incidental findings with low fluence fractional lasers. In some patients they respond, in others they do not.
There is an overlap between AMVC & body dysmorphic disorder. Firstly, AMVC does exist, as macular atrophic scarring can be demonstrated with examination, photography & in many cases pathology. The question of whether we treat this in private practice is debatable. My view is that only objectively severe pathology is treated. This favours the benefit: risk ratio, as compared to objectively mild, but subjectively severe pathology where the risk bit of the ratio is much higher. These patients are best managed by a team of dermatologist, psychologist & psychiatrist.
My viewpoint is not that patients with mild forms (objective mild) of atrophia maculosa should not be treated, that is not the point of the argument. This statement means that I am not the dermatologist to treat this. My work focuses on objectively severe disease. There are many other dermatologists that will take this job on. In this case, possibly the use of gentle treatments like microneedling, dermal delivery of collagen stimulating filler, conservative erbium & CO2 lasers or other fractional lasers may be a sensible option.
IMO all patients should have a biopsy (this is arranged by your dermatologist). This means specimens are collected in your country and state, providing a database for future DNA studies / genetic testing. This cannot be done in private practice as records are fragmented. One hospital, one department, all records. This aids in R & D.
The relationship between mild AMVC, BDD & dermatitis artefacta needs to be explored in more detail. Some but not all cases are DA, which projects as body dysmorphic syndrome in turn mimicking AMVC. That really sucks as these people really hamper research into this condition. I do not have an answer for this problem as it requires a multidisciplinary approach including a medical dermatologist, psychologist & psychiatrist.