Dermatitis

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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

Spongiotic dermatitis

It is characterized by epithelial intercellular edema.[1]

Characteristics Micrograph Photograph
Acute Subacute Chronic
Generally/Not otherwise specified[notes 2] Typical findings:[1]
  • Variable degree of epidermal spongiosis and vesicle formation, filled with proteinaceous fluid containing lymphocytes and histiocytes.
  • Usually superficial dermal edema with perivascular lymphocytic infiltrate, with exocytosis.
  • No acanthosis or parakeratosis.
 Typical findings:[1]
  • Mild to moderate spongiosis and exocytosis of inflammatory cells
  • Irregular acanthosis and parakeratosis.
  • Superficial dermal perivascular lymphohistiocytic infiltrate
  • Swelling of endothelial cells
  • Papillary dermal edema are present
 Typical findings:[1]
  • The spongiosis is mild to absent
  • Pronounced irregular acanthosis, hyperkeratosis, and parakeratosis
  • Minimal dermal inflammation and exocytosis of inflammatory cells are present.
  • Possibly fibrosis of papillary dermis

PAS stain is essential to exclude fungal infection.[1]

File:Micrograph of subacute spongiotic dermatitis.jpg Subacute
Allergic/contact dermatitis or atopic dermatitis As above. Eosinophils may be present in the dermis and epidermis (eosinophilic spongiosis).[1] File:Spongiotic dermatitis from drug allergy.jpg Allergic dermatitis File:Eczema (14100950936).jpg Atopic dermatitis
Seborrheic dermatitis Typical findings:[4]
  • Focal, usually mild, spongiosis with overlying scale crust, with a few neutrophils
  • The crust is often centered on a follicle
  • The papillary dermis is generally mildly edematous
  • Dilated blood vessels in the superficial vascular plexus
  • Mild superficial perivascular infiltrate of lymphocytes, histiocytes and occasional neutrophils. There is some exocytosis of inflammatory cells but not as prominent as in nummular dermatitis
 Typical findings:[4]
  • Psoriasiform hyperplasia, initially slight, with mild spongiosis
  • Usually numerous yeast-like organisms in the surface keratin
  • Same changes as seen in acute stage.
 Typical findings:[4]
  • More pronounced psoriasiform hyperplasia
  • Only minimal spongiosis
  • Presence of scaling crusts in a folliculocentric distribution, distinguishes from psoriasis.
 File:Seborrhoeic dermatitis example.jpg

In addition to above, an unspecific spongiotic dermatitis can be consistent with nummular dermatitis, dyshidrotic dermatitis, Id reaction, dermatophytosis, miliaria, Gianotti-Crosti syndrome5 and pityriasis rosea.[1][notes 2]

Interface dermatitis

These are sorted into either:[1]

  • Interface dermatitis with vacuolar change
  • Interface dermatitis with lichenoid inflammation
Vacuolar change
Main conditions[1] Characteristics Micrograph Photograph
Generally/Not otherwise specified Typical findings:[1]
  • Mild inflammatory cell infiltrate along the dermoepidermal junction
  • Vacuolar change within the basal keratinocytes
  • Often necrotic, predominantly basal, individual keratinocytes, manifesting as colloid or Civatte bodies
Acute graft-versus-host-disease
  • Vacuolar alteration of various severity, from focal or diffuse vacuolation of the basal keratinocytes (grade I), to separation at the dermoepidermal junction (grade III)
  • Involvement of the hair follicle[1]
  • Rarely eosinophils[1]
 File:Micrographs of grades of skin graft-versus-host-disease.jpg
Allergic drug reaction
  • Rarely involvement of hair follicles.[1]
  • Frequently eosinophils[1]
 File:Spongiotic dermatitis from drug allergy.jpg
Lichen sclerosis et atrophicus Hyperkeratosis, atrophic epidermis, sclerosis of dermis and dermal lymphocytes.[5] The biopsies are also checked for signs of dysplasia.[6] File:Micrograph of lichen sclerosus.jpg

An interface dermatitis with vacuolar alteration, not otherwise specified, may be caused by viral exanthems, phototoxic dermatitis, acute radiation dermatitis, erythema multiforme, erythema dyschromicum perstans and lupus erythematosus, dermatomyositis.[1]

Psoriaform dermatitis

Main conditions[1] Characteristics Micrograph Photograph
Interface dermatitis
Psoriaform dermatitis

Non vesicullobullous, non-pustular lesions without epidermal changes

Lymphocytic infiltrate

Main conditions[1] Characteristics Micrograph Photograph
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.[7] File:Micrograph of urticaria.jpg Dermal edema [solid arrows in (A,B)] and a sparse superficial predominantly perivascular and interstitial infiltrate of lymphocytes and eosinophils without signs of vasculitis (dashed arrow).[8] File:Urticaria near navel.jpg
Fungal skin infection Often visible fungus. Other signs depend on fungus species.[9]
Pigmented purpuric dermatosis
  • Perivascular infiltrate, but may involve the dermis, further away from blood vessels.[10]
  • Sometimes tendency for lichenoid infiltrate[notes 3][10]
  • Mild vascular damage, mainly endothelial swelling and focal karyorrhectic debris.[10]
  • Red blood cell extravasation.[10]
  • The epidermis may be normal or may exhibit spongiosis, focal parakeratosis, exocytosis and/or vacuolar change.[10]
 File:Histopathology of Schamberg disease.jpg File:Schambergdisease-26male.png
Erythema annulare centrifugum
  • Superficial types:[11]
  • 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[11]

File:Micrograph of erythema annulare centrifugum.jpg File:Erythema annulare centrifugum on arms and legs.jpg
Not otherwise specified[notes 2] A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.[1][notes 2]

Lymphoeosinophilic infiltrate

Main conditions[1] Characteristics Micrograph Photograph
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.[7] File:Micrograph of urticaria.jpg Dermal edema (solid arrows) and a sparse superficial predominantly perivascular and interstitial infiltrate of lymphocytes and eosinophils (dashed arrow) File:Urticaria near navel.jpg
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).[12] However, the diagnosis of bullous pemphigoid consist of at least 2 positive results out of 3 criteria:[13]
  • 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
Not otherwise specified[notes 2] A lesion with superficial lymphoeosinophilic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.[1][notes 2]

Lymphoplasmacytic infiltrate

Main conditions[1] Characteristics Micrograph Photograph
Rosacea Typically enlarged, dilated capillaries and venules located in the upper dermis, angulated telangiectasias, perivascular and perifollicular lymphocytic infiltration, and superficial dermal edema.[14] File:Micrograph of rosacea.jpg File:Rosacea.jpg
Secondary syphilis Various, but often one or a combination of:[15]
  • Psoriasiform hyperplasia with superficial neutrophils
  • Lichenoid tissue reaction, epidermal apoptosis and exocytosis of neutrophils
  • Superficial and deep chronic infiltrate in the dermis
  • Often numerous plasma cells in about 1/3 of cases
  • Often endothelial swelling.
 File:Micrograph of secondary syphilis, HE.jpg File:Secondary stage syphilis sores (lesions) on the soles of the feet. Plantar lesions-CDC.jpg
Erythema migrans Typically a superficial and deep perivascular lymphocytic infiltrate.[16] Plasma cells are typically located at the periphery of the lesion, whereas eosinophils are in the center.[16] File:Erythema migrans - erythematous rash in Lyme disease - PHIL 9875.jpg
Kaposi’s sarcoma in patch stage The patch stage typically shows irregular proliferation of jagged vascular channels in the dermis below an integral epidermis. The so-called promontory sign is sometimes found in patch stage lesions and denotes vascular spaces surrounding pre-existing blood (see image).[17]

vessels

File:Micrograph of promontory sign of kaposi's sarcoma.jpg File:Patch stage Kaposi's sarcoma.jpg
Not otherwise specified[notes 2] A lesion with superficial lymphoplasmacytic infiltrate without additional histopathologic characteristics can be due to for example trauma, ulceration, scar and early cutaneous connective tissue diseases.[1][notes 2]

Mastocytosis

Main conditions[1] Characteristics Micrograph Photograph
Urticaria pigmentosa Mastocytosis with a clinical picture of darkish spots. File:Histopathology of urticaria pigmentosa.jpg File:Urticaria pigmentosa lesions on a child.jpg
Not otherwise specified[notes 2] Includes the rare disease of primary mastocytosis.[1][notes 2]

Lymphohistiocytic infiltrate

File:Histopathology of leprosy.jpg
Leprosy

These include bacterial infections including leprosy, and the sample should therefore be stained with Ziel-Neelsen, acid fast stains, Gomori methenamine silver, PAS, and Fite stains.[1] If negative, an unspecific lymphohistocytic dermatosis may be caused by drug reactions and viral infections.[1][notes 2]

Neutrophilic infiltrate

Main conditions[1] Characteristics Micrograph Photograph
Urticaria, neutrophil predominant
  • Interstitial location[7]
  • Relatively dense infiltrate[7]
  • Mast cells are relatively sparse, potentially demonstrated with special stains, preferably tryptase stain.[7]
  • Extravasated erythrocytes are present in about 50% of the cases [7]
  • No vasculitis.[7]
 File:Micrograph of neutrophilic urticarial dermatosis.jpg File:Neutrophilic urticarial dermatosis.jpg
Dermatitis herpetiformis
  • Subepidermal vesicles and blisters associated with accumulation of neutrophils at the papillary tips.[18]
  • Sometimes presence of eosinophils, giving an appearance similar to bullous pemphigoid.[18]
  • The histopathology is unspecific in approximately 35%–40% of the cases,[18] and direct immunofluorescence is needed, showing deposition of IgA in the papillary dermis in a granular or fibrillar pattern.[19]
 File:Micrograph of dermatitis herpetiformis.jpg File:Dermatitis herpetiformis.jpg
Early linear IgA bullous dermatosis Subepidermal blister formation.[20] File:Micrograph of linear IgA bullous dermatosis.jpg File:Linear IgA bullous dermatosis.jpg
Early febrile neutrophilic dermatosis (Sweet's syndrome) Neutrophilic and lymphohistiocytic infiltrate and edema.[21] File:Sweet's syndrome pathology.jpg File:Sweet's syndrome Crohn's disease.gif
Connective tissue disorders
  • Usually associated with epidermal changes.[1] (Systemic lupus erythematosis pictured)
 File:Histopathology of systemic lupus erythematosus.jpg File:Butterfly rash of lupus erythematosus.jpg
Cutaneous small-vessel vasculitis
  • Neutrophils with nuclear dust (dashed arrows in image), with high affinity for postcapillary venules.[22]
  • Features of vascular injury: fibrinoid necrosis (asterisks) and erytrocyt extravasation (solid arrows)
 File:Micrograph of cutaneous small-vessel vasculitis.jpg File:Cutaneous small-vessel vasculitis.jpg

Notes

  1. ↑ PAS is for evaluation of the epidermal basement membrane, blood vessels, and the presence of fungal organisms
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 A description of the findings attained so far is generally enough as a diagnosis in "not otherwise specified" cases, but may mention when it can be consistent with a diagnosis that is clinically suspected according to the referral.
  3. ↑ 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 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 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 4.2 Mowafak Hamodat. Skin inflammatory (nontumor) > Spongiotic, psoriasiform and pustular reaction patterns > Seborrheic dermatitis. PathologyOutlines.com. Topic Completed: 1 August 2011. Revised: 26 March 2019
  5. ↑ Template:EMedicine
  6. ↑ Shelley, W. B.; Shelley, E. D.; Amurao, C. V. (2006). "Treatment of lichen sclerosus with antibiotics ". International Journal of Dermatology 45 (9): 1104–1106. doi:10.1111/j.1365-4632.2006.02978.x. PMID 16961523. 
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 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. 
  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. ↑ 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. 
  10. ↑ 10.0 10.1 10.2 10.3 10.4 Stephen Lyle. Pigmented purpuric dermatoses. Dermpedia.org. Retrieved on 2019-11-05.
  11. ↑ 11.0 11.1 . Histology of erythema annulare centrifugum. DermNet NZ. Retrieved on 2019-11-05.
  12. ↑ 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. 
  13. ↑ "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. 
  14. ↑ Celiker, Hande; Toker, Ebru; Ergun, Tulin; Cinel, Leyla (2017). "An unusual presentation of ocular rosacea ". Arquivos Brasileiros de Oftalmologia 80 (6). doi:10.5935/0004-2749.20170097. ISSN 0004-2749. 
  15. ↑ . Syphilis pathology. Dermnet NZ (2013).
  16. ↑ 16.0 16.1 Wilson, Thomas C.; Legler, Allison; Madison, Kathi C.; Fairley, Janet A.; Swick, Brian L. (2012). "Erythema Migrans ". The American Journal of Dermatopathology 34 (8): 834–837. doi:10.1097/DAD.0b013e31825879be. ISSN 0193-1091. 
  17. ↑ Soyer, H. Peter; Jakob, Lena; Metzler, Gisela; Chen, Ko-Ming; Garbe, Claus (2011). "Non-AIDS Associated Kaposi's Sarcoma: Clinical Features and Treatment Outcome ". PLoS ONE 6 (4): e18397. doi:10.1371/journal.pone.0018397. ISSN 1932-6203. 
  18. ↑ 18.0 18.1 18.2 Antiga, Emiliano; Caproni, Marzia (2015). "The diagnosis and treatment of dermatitis herpetiformis ". Clinical, Cosmetic and Investigational Dermatology: 257. doi:10.2147/CCID.S69127. ISSN 1178-7015. 
  19. ↑ Huma A. Mirza; Amani Gharbi; William Gossman.. Dermatitis Herpetiformis. StatPearls at National Center for Biotechnology Information. Last Update: July 11, 2019.
  20. ↑ Saleem, Maryam; Iftikhar, Hassaan (2019). "Linear IgA Disease: A Rare Complication of Vancomycin ". Cureus. doi:10.7759/cureus.4848. ISSN 2168-8184. 
  21. ↑ Casarin Costa, Jose Ricardo; Virgens, Anangelica Rodrigues; de Oliveira Mestre, Luisa; Dias, Natasha Favoretto; Samorano, Luciana Paula; Valente, Neusa Yuriko Sakai; Festa Neto, Cyro (2017). "Sweet Syndrome: Clinical Features, Histopathology, and Associations of 83 Cases ". Journal of Cutaneous Medicine and Surgery 21 (3): 211–216. doi:10.1177/1203475417690719. ISSN 1203-4754. 
  22. ↑ 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. 
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