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KA v's SCC Spot Diagnosis Discussion 6th July


Dr. Richard Carr

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Thank you for the additional discussion of this case (I think it was 6th July which was a regressing KA). I could spend a very long time discussing KA v's SCC.Firstly a serious caveat - I am not sure the diagnosis is safe in the hands of experts let alone non-experts to be honest!That said we in Warwick are (currently) firmly in the camp that KA is a distinct Clinical-Pathological diagnosis.Provided a lesion is typical clinically and histologically we can make a confident diagnosis (in the knowledge that there is a risk of true malignant transformation and exceedingly rarely metastasis - in otherwise typical - but usually to local lymph nodes). Early KA (in our view) does often include quite striking cellular pleorphism and typically the early lesions have highly proliferative infiltrative (not pushing circumscript borders like well differentiated SCC) borders with prominent elastic incorporation in the proliferative phase. Despite the frighteningly worrying peripheral component in all areas of the tumor there is central (often abprupt) transition to highly differentiated and distincitive pilar keratinisation. In excision biopsies the symmetrical exoendophytic nature and rounded silhouette are obviously helpful. In a small biopsy one can easily diagnose an early KA as a poorly (not well) differentiated SCC if one does not spot the central differentiation in all islands (suggest multiple levels are examined on small biopsies to demonstrate this feature of KA). Incorporation of elastic can be a feature of poorly differentiated SCC but not, in my experience, a well differentiated SCC (that usually have much more pushing mitotically inactive borders)and in my view is rarely a true diagnostic consideration in the histological differential diagnosis of an early KA. Obviously clinical information is essential as well differented SCC does not grow rapidly in a few weeks like a KA. Otherwise typical clinicopathological KA with frank (bowenoid) atypia (probably about 30% of our cases of early KA!) in my opinion is of uncertain biological significance but would lead us to recommend complete excision (in partial biopsies i.e. malignant transformation must be a serious consideration)and probably follow-up as for SCC (when seen in isolation in an excision specimen). We tend to opt for complete excision with clear margins on most cases (of even classicaly clinicopathological early KA) in any case. Often patients prefer not to have an unsightly smelly rapidly growing lesion on their face and conservative excision is cosmetically acceptable in good hands. However for some typical (biopsy confirmed) cases watchful waiting (i.e. active close follow-up with a low threshold for excision of persistent or actively growing lesions) may be an option for some individual lesions for some patients. Obviously patient's and clinicians will vary on how brave they are prepared to be watching a lesion that may or may not undergo true malginant transformation. Because of the complexity of the above and the many caveats you will hopefully understand why I am saying I am not sure the diagnosis of KA is entirely safe! I have not even discussed the many lesions we are now referring to as follicularSCC that may closely, at first glance, resemble KA (often they have acantholysis and central follicular mucin - features we do not see in KA - but most are well differentiate with lobular circumscribed pushing bordres). We also often sit on the fence or admit defeat in a significant proportion of cases (even with good clinico-pathological corration). We certainly discuss each and every case in a multi-disciplinary setting and I hope an awareness of the difficulties and a shared team approach is the safest way of managing these patient's
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Dr. Phillip McKee

Posted

Thank you Richard for an excellent blog. I like your comment that the diagnosis of KA is not even safe in the hands of so-called experts. The only useful statement that I can add is that in a life-tme of dermatopathology, I have never encountered a dermatologist prepared to adopt a wait and see approach. They all get removed. I don't suppose we will ever solve this thorny issue unless the molecular folk can find the answer!
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Dr. Richard Carr

Posted

I hope Phillip's comments are not going to go unchallenged -
there must be an awful lot of experienced dermatologists out there who regularly
curette (I know this is remove) or even observe (?) classical KA -
please do add some fuel to the fire!!

I have read in a small book of dermatology for trainees recently (by a very
experienced UK dermatologist) that KA is benign and can be left or treated
with curettage if preferred. It was quite funny as I know the pathologists
in that same authors region never report early KA without the caveat that SCC cannot be
excluded. This obviously puts the clinical colleague in a difficult situation!
I really do wonder if a proper study is warrented that included curettage and
watchful waiting - but of course would this be ethical? Contributions please...
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Dr. Phillip McKee

Posted

My comments are straight out of the mouths of all the dermatologists that I have ever discussed this thorny topic with. Mind you, there may be a transatlantic divide on the issue!
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On rotating from a teaching hospital to a general district hospital, I've found that my general pathologist consultants rarely diagnose KAs (as opposed to dermatopathologists). Their philosophy is that KAs are falling out of fashion (that KAs are SCCs). I've changed my approach accordingly. This seems to be the case in the US. Klaus Busam, in his textbook, states that: "Many pathologists nowadays imply, when they use the term KA, the presence of a crateriform variant of SCC."
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Mark A. Hurt MD

Posted

My experience of over 30 years in dealing with the problem is that the concept has evolved considerably. KA's used to be diagnosed at the drop of a hat. Ackerman himself staunchly defended the concept until 1993; Weedon still defends it today.

I am curious to know the opinion of others on this blog thread. Here is how I have dealt with the problem. I regard SCC as neoplastic, but I don't think that KA is a neoplasm. I regard it, rather, as a form of hyperplasia. One would expect hyperplasia to involute, it being stimulus [u][i]dependent[/i][/u]. Yet, one would not expect neoplasia to involute, it being stimulus [u][i]independent[/i][/u].

Practically, I separate SCC and KA as follows. Whenever I identify lobules that lose there lobular pattern (become more like strands and cords), and when their keratocytes become pleomorphic at the edges of the lobules, in almost every case, they are carcinomas. In lesions that I regard as KA's, their lobules are well formed, and the keratocytes become smaller at the edges of the lobules.

When using these criteria, I find that the number of KA's I diagnose is a small number. Most are carcinomas.

I have to admit that this is not a scientific, but is, rather, an empirical consideration. I think, however, it probably has merit.

Any comments are welcome.
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Dr. Richard Carr

Posted

Thanks Mark.
I am guessing you would call most of our cases that we diagnose as
"in keeping with KA" as SCC. I have done a little pole of UK dermatopathologists
and we in Warwick have the highest ratio (25 to 30%) of coding for KA v's SCC in the UK!
This ratio is similar to Weedon's (I have read this but cannot give the reference
off the top of my head). I emphasise coding as I am sure many of the reports will not
be entirely didactic! We still call the early KA's with pleomorphism (as an isolated
aberrent feature"in keeping with KA" but with the caveats I discussed above.
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Mark A. Hurt MD

Posted

It's hard to say. Perhaps it might be of some value for us to show each other some of these cases to get a better sense of what we think are KA's vs KA-like SCC's.
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I am a Sydney dermatopathologist.

For better or foir worse, I reserve the term KA for very well-differentiated craters with little squamous proliferation and rarely make the diagnosis.

I use the term SCC of KA type for craters with more proliferation.

I note that, in my experience, the metastatic rate of SCC is extraordinarily lower than the literature suggests. This could mean that we are overdiagnosing KA as SCC - dunno


I have seen case reports of SCC developing in a KA come from Dr Weedon's lab - not sure what this means
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