I can't join the workshop; the link keeps redirecting. I don't understand what the problem isI can't join the workshop; the link keeps redirecting. I don't understand what the problem isHello everyone 👋
Is it possible to share challenging cases from our practice here?
Here is the reference from our prior live Group case discussion defining how collarettes are formed:
Jacoby RA, Ackerman AB. Is the so-called epidermal collarette formed by epidermal or adnexal epithelium? Am J Dermatopathol. 1982; 4(2):117-24. PMID: 7103013
Key Finding: The study demonstrates that these tissue infoldings are actually formed by epithelial adnexa (adnexal epithelium) rather than the epidermis itself.
Hi everyone!
I'm so glad to be a part of this community🙏
Just a question,
Do you recommend re-excising severly dysplastic nevi with 5 mm margin? (they are completely excised in the planes of examined sections(1-2 mm), young patients, no solar elastosis of course)
Follow up Discussion with Claude about Dermpedia Case 3 from 6.16.26 (Dr Zembowicz asked me to share this with the group)
What is the relationship of Atrophy Blanche and Livedoid Vasculopathy?
Atrophie Blanche (AB) and Livedoid Vasculopathy (LV) are closely related dermatological conditions — in fact, Atrophie Blanche is considered the end-stage scar of Livedoid Vasculopathy, not a separate disease.
Their Relationship
Livedoid Vasculopathy (LV) is the active disease process characterized by:
• Recurrent thrombosis of small dermal blood vessels (primarily in the lower legs and ankles) • Painful purpuric papules and ulcerations • A chronic, relapsing course • Underlying hypercoagulable states in many patients
Atrophie Blanche (AB) is the resulting scar that forms after LV ulcerations heal, characterized by:
• Porcelain-white, stellate (star-shaped) atrophic scars • Surrounded by hyperpigmentation and telangiectasias • Located on the lower legs and dorsal feet • Representing healed infarcts from prior thrombotic episodes
Key Points
• AB is a clinical sign, not a diagnosis — it is the morphological endpoint/sequela of LV. • Historically, AB was thought to be a primary condition, but it is now understood to be a non-specific scar that can result from LV or other conditions causing dermal vascular occlusion (e.g., antiphospholipid syndrome, sickle cell disease, chronic venous insufficiency). • The terms were once used interchangeably in older literature, which caused some confusion. • A patient with LV will eventually develop AB scars if the thrombotic episodes recur and heal repeatedly.
In Summary
|Feature |Livedoid Vasculopathy |Atrophie Blanche ||----------------|--------------------
That is how I think of it.
Great minds think alike! It’s a conceptually clean way to understand them — one is the storm, the other is the damage left behind. The historical confusion from older literature using the terms interchangeably didn’t help, but the modern framework of LV as the active thrombotic process and AB as its scar makes the pathophysiology much more intuitive.
Is there a particular aspect of LV/AB you’re exploring — management, workup for hypercoagulable states, or something else?
It was a case for diagnosis and discussion on Dermpedia today.
That’s a great teaching case topic — LV is one of those conditions that can be genuinely tricky to diagnose, especially early on when it just looks like painful purpura or ulcers that aren’t healing well. It’s easy to misattribute it to venous insufficiency or vasculitis initially.
Did the Dermpedia case highlight anything particular — like an interesting workup finding, an unusual presentation, or a specific treatment approach they featured?
The person who contributed the case for consultation noted that there has been clinical suspicion of pyoderma gangrenosum and bx was done with a question of Atrophie Blanche by the clinician. Histologically, there was a hyalinizing and fibrinoid dermal vasculopathy.
That’s a classic and clinically important diagnostic dilemma! PG vs LV is a well-known pitfall, and the case illustrates exactly why histopathology is so critical here.
Why PG Gets Suspected
• Both present with painful ulcers on the lower legs that seem recalcitrant
• PG is often in the differential when ulcers don’t heal as expected
• The “pathergy” phenomenon in PG can even be mistakenly triggered by biopsy attempts
Why Histology Resolves It
The findings you described are telling:
• Hyalinizing/fibrinoid dermal vasculopathy — thickened, eosinophilic vessel walls with intraluminal fibrin thrombi — is the hallmark of LV
• PG histology shows a neutrophilic infiltrate with dermal necrosis, without the vascular occlusive/fibrinoid changes
• The absence of a true vasculitis (no leukocytoclasia, no vessel wall destruction by inflammation) further supports LV over an inflammatory process
The Clinical Lesson
This case underscores a key teaching point: PG is a diagnosis of exclusion, and before committing to it (and potentially immunosuppressing a patient), ruling out LV with biopsy is essential — since the treatments are essentially opposite in direction (immunosuppression vs. anticoagulation/antiplatelet therapy).
The clinician’s instinct to also raise atrophie blanche was astute — recognizing the scarring component pointed toward the thrombotic etiology. Was there any discussion of the patient’s hypercoagulable workup?
No
That would have been an interesting addition to the discussion — since identifying an underlying hypercoagulable state (antiphospholipid antibodies, factor V Leiden, MTHFR mutations, protein C/S deficiency, etc.) can directly guide long-term management, particularly around anticoagulation decisions.
But even without it, the case as presented is a great teaching example just on the clinicopathological correlation alone — the journey from clinical suspicion of PG, to the biopsy, to landing on LV based on the fibrinoid vasculopathy is a very instructive diagnostic narrative.
Dermpedia cases like that are valuable precisely because they reflect real-world diagnostic uncertainty rather than a textbook-perfect presentation.
I believe Dermpedia is an excellent resource for academics but also a great companion for dermpaths in their daily challenges. I look forward to ISDP and its members being able to benefit from Dermpedia.
I cannot watch "the Dysplastic and non dusplastic oral keratoses" session by Dr Sook-Bin Woo either, Am I doing something wrong ?
Thank you for your help !
Hi everyone,
Does someone have access to "session XI lecture : vulvar pathology of squamous lesion preview of upcoming updated WHO classifocation" course by Carlos Parra-Herran?
Thank you in advance for your answers
Hi everyone,
I am currently subscribed to the highest membership tier available on Dermpedia. However, when trying to watch certain videos, I still encounter an error message stating: "Content not accessible with your current subscription."
Has anyone else experienced this? Is there a specific way to fix this issue or unlock these restricted videos?
Thank you in advance for your help!
Dear Artur, Great concepts that deserve to be widely supported in both the Dermatology and Dermatopathology communities. But you are placing a great weight on your shoulders! I see you are coming to Australia this year in October to present at our Dermpath Society Meeting in Brisbane . It will be good to catch up with you and discuss these concepts further. My field is primarily Dermatology. Overall Dermpath is not being taught to Dermatology Trainees here as fully as it used to be. I dont know if that is the situation in the States as well. When the late Bernie Ackerman came out here he really stimulated interest in Dermpath. I am sure your visit will have the same effect!
Best wishes
Ian McColl FACD