Dermatitis: Difference between revisions

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===Non vesicullobullous, non-pustular lesions without epidermal changes, lymphocytic infiltrate===
===Non vesicullobullous, non-pustular lesions without epidermal changes===
====Lymphocytic infiltrate====
{|class="wikitable"
{|class="wikitable"
! Main conditions<ref name="Alsaad2005"/> !! Characteristics !! Image
! Main conditions<ref name="Alsaad2005"/> !! Characteristics !! Image
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| A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.<ref name="Alsaad2005"/>
| A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.<ref name="Alsaad2005"/>
|}
|}
====Lymphoeosinophilic infiltrate====
{|class="wikitable"
! Main conditions<ref name="Alsaad2005"/> !! Characteristics !! Image
|-
! Urticaria, lymphocyte predominant
| Perivascular location. Mast cells are relatively sparse, potentially demonstrated with special stains, preferably tryptase stain. Extravasated erythrocytes are present in about 50% of the cases. No vasculitis.<ref name="BarzilaiSagi2017"/>
| [[File:Micrograph of urticaria.jpg|190px]] Dermal edema (solid arrows) and a sparse superficial predominantly perivascular and interstitial infiltrate of lymphocytes and eosinophils (dashed arrow)
|-
! Prevesicular stage of bullous pemphigoid
| Image at right shows influx of inflammatory cells including eosinophils and neutrophils in the dermis (solid arrow) and blister cavity (dashed arrows), and deposition of fibrin (asterisks).<ref>{{cite journal|last1=Giang|first1=Jenny|last2=Seelen|first2=Marc A. J.|last3=van Doorn|first3=Martijn B. A.|last4=Rissmann|first4=Robert|last5=Prens|first5=Errol P.|last6=Damman|first6=Jeffrey|title=Complement Activation in Inflammatory Skin Diseases|journal=Frontiers in Immunology|volume=9|year=2018|issn=1664-3224|doi=10.3389/fimmu.2018.00639}}</ref> However, the diagnosis of bullous pemphigoid consist of at least 2 positive results out of 3 criteria:<ref>{{cite journal | vauthors = Meijer JM, Diercks GF, de Lang EW, Pas HH, Jonkman MF | title = Assessment of diagnostic strategy for early recognition of bullous and nonbullous variants of pemphigoid. | journal = JAMA Dermatol | volume = 155 | issue = 2 | pages = 158–165 | doi = 10.1001/jamadermatol.2018.4390 | pmid = 30624575 | pmc = 6439538 | date = December 2018 }}</ref>
*Pruritus and/or predominant cutaneous blisters
*Linear IgG and/or C3c deposits (in an n- serrated pattern) by direct [[immunofluorescence]] microscopy (DIF)
*Positive epidermal side staining by [[indirect immunofluorescence]] microscopy on human salt-split skin (IIF SSS) on a serum sample.
| [[File:Micrograph of infiltrate in bullous pemphigoid.jpg|thumb|
|-
! Not otherwise specified
| A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.<ref name="Alsaad2005"/>
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Revision as of 08:46, 5 November 2019

Author: Mikael Häggström [note 1]

Sampling

  • For punch biopsies, a size of 4 mm is preferred for most inflammatory dermatoses.[1]
  • Panniculitis or cutaneous lymphoproliferative disorders: 6 mm punch biopsy or skin excision.[1]

A superficial or shave biopsy is regarded as insufficient.[1]

Fixation

Staining

3 H&E sections and one section with periodic acid Schiff (PAS)[notes 1][1]

  • If suspected bacterial and fungal microorganisms, consider Gram stain and Gomori methenamine silver stain.[1]

Microscopic evaluation

One approach is to classify into mainly either of the following, primarily based on depth of involvement:[1]

  • Epidermis, papillary dermis, and superficial vascular plexus:
  • Vesiculobullous lesions
  • Pustular dermatosis
  • Non vesicullobullous, non-pustular
  • With epidermal changes
  • Without epidermal changes. These characteristically have a superficial perivascular inflammatory infiltrate, and can be classified by type of cell infiltrate:[1]
  • Lymphocytic (most common)
  • Lymphoeosinophilic
  • Lymphoplasmacytic
  • Mast cell
  • Lymphohistiocytic
  • Neutrophilic

Continue in corresponding section:

Non vesicullobullous, non-pustular lesions with epidermal changes

Main types[1] Characteristics Image
Spongiotic dermatitis
Interface dermatitis
Psoriaform dermatitis

Non vesicullobullous, non-pustular lesions without epidermal changes

Lymphocytic infiltrate

Main conditions[1] Characteristics Image
Urticaria, lymphocyte predominant Perivascular location. Mast cells are relatively sparse, potentially demonstrated with special stains, preferably tryptase stain. Extravasated erythrocytes are present in about 50% of the cases. No vasculitis.[4]
Fungal skin infection Visible fungus. Other signs depend on fungus species.[5]
Pigmented purpuric dermatosis
  • Perivascular infiltrate, but may involve the dermis, further away from blood vessels.[6]
  • Sometimes tendency for lichenoid infiltrate[notes 2][6]
  • Mild vascular damage, mainly endothelial swelling and focal karyorrhectic debris.[6]
  • Red blood cell extravasation.[6]
  • The epidermis may be normal or may exhibit spongiosis, focal parakeratosis, exocytosis and/or vacuolar change.[6]
 File:Histopathology of Schamberg disease.jpg
Erythema annulare centrifugum
  • Superficial types:[7]
  • Mild spongiosis, parakeratosis and microvesiculation.
  • "Coat-sleeve anomaly": tight lymphohistiocytic infiltrate surrounding superficial vessels

Deep lesions: Sharply demarcated perivascular mononuclear cell infiltrate in middle to deep dermis[7]

File:Micrograph of erythema annulare centrifugum.jpg
Not otherwise specified A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.[1]

Lymphoeosinophilic infiltrate

Main conditions[1] Characteristics Image
Urticaria, lymphocyte predominant Perivascular location. Mast cells are relatively sparse, potentially demonstrated with special stains, preferably tryptase stain. Extravasated erythrocytes are present in about 50% of the cases. No vasculitis.[4] File:Micrograph of urticaria.jpg Dermal edema (solid arrows) and a sparse superficial predominantly perivascular and interstitial infiltrate of lymphocytes and eosinophils (dashed arrow)
Prevesicular stage of bullous pemphigoid Image at right shows influx of inflammatory cells including eosinophils and neutrophils in the dermis (solid arrow) and blister cavity (dashed arrows), and deposition of fibrin (asterisks).[8] However, the diagnosis of bullous pemphigoid consist of at least 2 positive results out of 3 criteria:[9]
  • Pruritus and/or predominant cutaneous blisters
  • Linear IgG and/or C3c deposits (in an n- serrated pattern) by direct immunofluorescence microscopy (DIF)
  • Positive epidermal side staining by indirect immunofluorescence microscopy on human salt-split skin (IIF SSS) on a serum sample.
 [[File:Micrograph of infiltrate in bullous pemphigoid.jpg|thumb|
Not otherwise specified A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.[1]

Notes

  1. ↑ PAS is for evaluation of the epidermal basement membrane, blood vessels, and the presence of fungal organisms
  2. ↑ Pigmented purpuric dermatitis of Gougerot and Blum particularly have a tendency for lichenoid infiltrate.
  1. ↑ For a full list of contributors, see article history. Creators of images are attributed at the image description pages, seen by clicking on the images. See Patholines:Authorship for details.

Main page

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 Alsaad, K O (2005). "My approach to superficial inflammatory dermatoses ". Journal of Clinical Pathology 58 (12): 1233–1241. doi:10.1136/jcp.2005.027151. ISSN 0021-9746. 
  2. ↑ 2.0 2.1 Katarzyna Lundmark, Krynitz, Ismini Vassilaki, Lena Mölne, Annika Ternesten Bratel. Handläggning av hudprover – provtagningsanvisningar, utskärningsprinciper och snittning (Handling of skin samples - Instructions for sampling, cutting and incision. KVAST (Swedish Society of Pathology). Retrieved on 2019-09-09.
  3. ↑ Page 678 in: Chhabra, Seema; Minz, RanjanaWalker; Saikia, Biman (2012). "Immunofluorescence in dermatology ". Indian Journal of Dermatology, Venereology, and Leprology 78 (6): 677. doi:10.4103/0378-6323.102355. ISSN 0378-6323. Archived from the original. . 
  4. ↑ 4.0 4.1 Barzilai, Aviv; Sagi, Lior; Baum, Sharon; Trau, Henri; Schvimer, Michael; Barshack, Iris; Solomon, Michal (2017). "The Histopathology of Urticaria Revisited—Clinical Pathological Study ". The American Journal of Dermatopathology 39 (10): 753–759. doi:10.1097/DAD.0000000000000786. ISSN 0193-1091. 
  5. ↑ Guarner, J.; Brandt, M. E. (2011). "Histopathologic Diagnosis of Fungal Infections in the 21st Century ". Clinical Microbiology Reviews 24 (2): 247–280. doi:10.1128/CMR.00053-10. ISSN 0893-8512. 
  6. ↑ 6.0 6.1 6.2 6.3 6.4 Stephen Lyle. Pigmented purpuric dermatoses. Dermpedia.org. Retrieved on 2019-11-05.
  7. ↑ 7.0 7.1 . Histology of erythema annulare centrifugum. DermNet NZ. Retrieved on 2019-11-05.
  8. ↑ Giang, Jenny; Seelen, Marc A. J.; van Doorn, Martijn B. A.; Rissmann, Robert; Prens, Errol P.; Damman, Jeffrey (2018). "Complement Activation in Inflammatory Skin Diseases ". Frontiers in Immunology 9. doi:10.3389/fimmu.2018.00639. ISSN 1664-3224. 
  9. ↑ "Assessment of diagnostic strategy for early recognition of bullous and nonbullous variants of pemphigoid. ". JAMA Dermatol 155 (2): 158–165. December 2018. doi:10.1001/jamadermatol.2018.4390. PMID 30624575. 

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