Dermatitis: Difference between revisions

Latest revision as of 16:49, 19 June 2022

Author: Mikael Häggström ^{[note 1]}
Scope: This article deals with skin conditions where inflammation is the main finding, excluding suspected malignant skin excisions (where inflammation is often a concurrent finding).

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

Generally 10% neutral buffered formalin.

Suspected immunologic disease:^[2] Fixation for immunofluorescence, with for example Michel's solution.^[3] For details, see immunofluorescense of skin tissues

See also: General notes on fixation

Gross processing

Gross pathology processing of skin lesions with benign appearance, by lesion size:^[4]
<4 mm	4 - 8 mm	9 - 15 mm

In table above, each top image shows recommended lines for cutting out slices to be submitted for further processing. Bottom image shows which side of the slice that should be put to microtomy. Dashed lines here mean that either side could be used. Further information: Gross processing of skin excisions

Staining

3 H&E sections and one section with periodic acid Schiff (PAS)^{[note 2]}^[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

No visible pathology

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	Micrograph	Photograph
Generally/Not otherwise specified^{[note 3]}	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]	Subacute
Allergic/contact dermatitis or atopic dermatitis	As above. Eosinophils may be present in the dermis and epidermis (eosinophilic spongiosis).^[1]			Allergic dermatitis	Atopic dermatitis
Seborrheic dermatitis	Typical findings:^[5] 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:^[5] 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:^[5] More pronounced psoriasiform hyperplasia Only minimal spongiosis Presence of scaling crusts in a folliculocentric distribution, distinguishes from psoriasis.

In addition to above, an unspecific spongiotic dermatitis can be consistent with nummular dermatitis, dyshidrotic dermatitis, Id reaction, dermatophytosis, miliaria, Gianotti-Crosti syndrome and pityriasis rosea.^[1]^{[note 3]}

Interface dermatitis

These are sorted into either:^[1]

Interface dermatitis with vacuolar change
Interface dermatitis with lichenoid inflammation

Interface dermatitis with vacuolar change

Causes of vacuolar interface dermatitis edit
Main conditions^[6]	Characteristics	Micrograph	Photograph
Generally/Not otherwise specified	Typical findings, called "vacuolar interface dermatitis":^[6] Mild inflammatory cell infiltrate along the dermoepidermal junction (black arrow in image) Vacuolization within the basal keratinocytes (white arrow in image) 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^[6] Rarely eosinophils^[6]
Allergic drug reaction	Rarely involvement of hair follicles.^[6] Frequently eosinophils^[6]
Lichen sclerosus	Hyperkeratosis, atrophic epidermis, sclerosis of dermis and dermal lymphocytes.^[7]
Erythema multiforme
Lupus erythematosis	Typical findings in systemic lupus erythematosus:^[8] Fibrinoid necrosis at the dermoepidermal junction Liquefactive degeneration and atrophy of the epidermis Mucin deposition in the reticular dermis Edema, small hemorrhages Mild and mainly lymphocytic infiltrate in the upper dermis Fibrinoid material in the dermis around capillary blood vessels, on collagen and in the interstitium In non-bullous cases, perivascular and interstitial neutrophils are sometimes present in the upper dermis, with damage to blood vessels

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

Further information: Vacuolar interface dermatitis

Interface dermatitis with lichenoid inflammation

Main conditions^[1]	Characteristics	Micrograph
Generally/Not otherwise specified	Typical findings:^[1] In the papillary dermis: a confluent, band-like, dense inflammation of mainly small lymphocytes and a few histiocytes, along or hugging the dermoepidermal junction. Often vacuolar degeneration of basal keratinocytes and apoptotic bodies (colloid or Civatte bodies).
Lichen planus	Irregular epidermal hyperplasia with a jagged “sawtooth” appearance, compact hyperkeratosis or orthokeratosis, foci of wedge-shaped hypergranulosis, basilar vacuolar degeneration, slight spongiosis in the spinous layer, and squamatization. The dermal papillae between the elongated rete ridges are frequently dome shaped. Necrotic keratinocytes can be observed in the basal layer of the epidermis and at the dermal-epidermal junction. Eosinophilic remnants of anucleate apoptotic basal cells may also be found in the dermis and are referred to as “colloid or civatte bodies”. Whickham striae are usually seen in the areas of hypergranulosis. Vacuolar degeneration at the basal layer may be noted leading to focal subepidermal clefts (Max Joseph spaces). Squamatization occurs as a result of maturation and flattening of cells in the basal layer. It happens in areas of marked hypergranulosis with prominence of the sawtooth pattern of rete ridges. Wedge-shaped hypergranulosis can occur in the eccrine ducts (acrosyringia) or hair follicles (acrotrichia). In the hypertrophic subtype, the associated hyperkeratosis, parakeratosis, hypergranulosis, papillomatosis, acanthosis, and hyperplasia markedly increased with thicker collagen bundles forming in the dermis. Moreover, the rete ridges are more elongated and rounded as opposed to the typical sawtooth pattern. In atrophic LP, loss of the rete ridges and dermal fibrosis is prominent. In vesiculobullous LP, the disease progression is quicker. Hence, some of the distinctive features such as hyperkeratosis, hypergranulosis, or dense lymphocytic dermal-epidermal infiltrate may not be present. LP lesion may resolve with residual hyperpigmentation caused by a persistent increase in the number of melanophages in the papillary dermis.^[9]
Lichenoid drug reaction	Can virtually be indistinguishable from cutaneous LP both clinically and histopathologically. Typically, lesions have a photodistribution in the absence of oral mucosal involvement.^[9] Characteristically parakeratosis, a dermal eosinophilic infiltrate, and a perivascular lymphocytic infiltrate affecting the reticular dermis. Epidermal changes are less common in lichenoid drug eruptions when compared to classic lichen planus. However, a higher concentration of necrotic keratinocyte and eosinophils in the infiltrate can be helpful in distinguishing lichenoid drug reaction from cutaneous lichen planus. A lengthy interval between the commencement of drug therapy and the onset of lesions does not exclude a diagnosis of lichenoid drug reaction. Resolution of the lesions often occurs within weeks to months after discontinuation of the offending drug.^[9]
Lichen nitidus	Localized granulomatous lymphohistiocytic infiltrate in an expanded dermal papilla. Thinning of overlying epidermis and downward extension of the rete ridges at the lateral margin of the infiltrate, resulting in a typical "claw clutching a ball" appearance.^[10]
Lichen amyloidosus	Presence of amyloid, possibly with direct immunofluorescence and Congo red staining.^[11]	Congo red.

Interface dermatitis with lichenoid inflammation, not otherwise specified, can be caused by lichen planus-like keratosis, lichenoid actinic keratosis, lichenoid lupus erythematosus, lichenoid GVHD (chronic GVHD), pigmented purpuric dermatosis, pityriasis rosea, and pityriasis lichenoides chronica.^[1] Unusual conditions that can be associated with a lichenoid inflammatory cell infiltrate are HIV dermatitis, syphilis, mycosis fungoides, urticaria pigmentosa, and post-inflammatory hyperpigmentation.^[1] In cases of post-inflammatory hyperpigmentation, it is important to exclude potentially harmful mimics such as a regressed melanocytic lesion or lichenoid pigmented actinic keratosis.^[1]

Psoriaform dermatitis

Examining multiple deeper levels is recommended if initial cuts do not correlate well with the clinical history.^[1]

Psoriaform dermatitis typically displays:^[1]

Regular epidermal hyperplasia, elongation of the rete ridges, hyperkeratosis, and parakeratosis.
Usually:A superficial perivascular inflammatory infiltrate
Often: Thinning of epidermal cells overlying the tips of dermal papillae (suprapapillary plates), and dilated, tortuous blood vessels within these papillae

Further histopathologic diagnosis is performed by the following parameters:

Psoriasiform dermatitis^[1]
Condition	Hyperkeratosis	Parakeratosis	Acanthosis	Suprapapillary plate	Spinous cell layer changes	Other distinctive feature	Micrograph
Psoriasis	Present	Diffuse	Regular	Thin	Increased mitoses; minimal spongiosis Clubbed rete pegs^[12] ^[13]	Microabscesses Thin or absent granular cell layer
Psoriasiform drug reaction	Present	Focal	Regular and irregular	Normal or thick	Spongiosis; eosinophilic infiltrate	Basal cell layer with inflammatory cells; Civatte bodies
Chronic allergic/contact and atopic dermatitis	Present	Focal; crust may be present	Irregular	Normal or thick	Spongiosis; eosinophilic infiltrate
Fungal infection	Compact	Focal; crust may be present	Irregular	Normal or thick	Occasional neutrophiles;
Lichen simplex chronicus	Present	Focal; thick crust	Regular or irregular	Thin or thick	±minimal inflammatory infiltrate	Thickened granular cell layer
Scabies	Present	Focal or diffuse	Irregular	Normal or thick	Inflammatory infiltrate; eosinophilic spongiosis
Seborrheic dermatitis and HIV dermatitis	Present	Focal	Irregular	Normal or thick	Spongiosis; lymphocytic and neutrophilic infiltrate
Pityriasis rubra pilaris	Compact	Shoulder parakeratosis^{[note 4]}; alternating orthokeratosis and parakeratosis	Regular or irregular	Normal or thick	Spongiosis; lymphocytic infiltrate; rare acantholysis
Pityriasis rosea	Present	Focal	Irregular	Normal or thick	Small foci of spongiosis; lymphocytic infiltrate	Occasional necrotic keratinocytes of basal layer
Syphilis	Present	Focal	Regular or irregular	Normal or thick	Lymphocytes and neutrophils	Basal layer interface change
Pityriasis lichenoides chronica	Present	Caps of parakeratosis	Irregular	Normal	Mild spongiosis, lymphocytic infiltrate; necrotic keratinocytes	Necrotic keratinocytes of basal layer
Mycosis fungoides	Present	Focal	Regular or irregular	Normal	Minimal or no spongiosis; ±Pautrier microabscess	Atypical lymphoid cells lining the dermo–epidermal junction	Pautrier microabscesses

Non vesicullobullous, non-pustular lesions without epidermal changes

Lymphocytic infiltrate

Main conditions^[1]	Characteristics	Micrograph
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.^[14]	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).^[15]
Fungal skin infection	Often visible fungus. Other signs depend on fungus species.^[16]
Pigmented purpuric dermatosis	Perivascular infiltrate, but may involve the dermis, further away from blood vessels.^[17] Sometimes tendency for lichenoid infiltrate^{[note 5]}^[17] Mild vascular damage, mainly endothelial swelling and focal karyorrhectic debris.^[17] Red blood cell extravasation.^[17] The epidermis may be normal or may exhibit spongiosis, focal parakeratosis, exocytosis and/or vacuolar change.^[17]
Erythema annulare centrifugum	Superficial types:^[18] 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^[18]
Not otherwise specified^{[note 3]}	A lesion with superficial lymphocytic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.^[1]^{[note 3]}

Lymphoeosinophilic infiltrate

Main conditions^[1]	Characteristics	Micrograph
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.^[14]	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).^[19] However, the diagnosis of bullous pemphigoid consist of at least 2 positive results out of 3 criteria:^[20] 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.
Not otherwise specified^{[note 3]}	A lesion with superficial lymphoeosinophilic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites.^[1]^{[note 3]}

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.^[21]
Secondary syphilis	Various, but often one or a combination of:^[22] 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.
Erythema migrans	Typically a superficial and deep perivascular lymphocytic infiltrate.^[23] Plasma cells are typically located at the periphery of the lesion, whereas eosinophils are in the center.^[23]
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).^[24] vessels
Not otherwise specified^{[note 3]}	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]^{[note 3]}

Mastocytosis

Main conditions^[1]	Characteristics	Micrograph	Photograph
Urticaria pigmentosa	Mastocytosis with a clinical picture of darkish spots.
Not otherwise specified^{[note 3]}	Includes the rare disease of primary mastocytosis.^[1]^{[note 3]}

Lymphohistiocytic infiltrate

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]^{[note 3]}

Granulomatous inflammation

Further information: Granulomatous skin inflammation Granulomatous inflammation is defined by the presence of mononuclear leukocytes, specifically histiocytes, appearing as epithelioid cells with round to oval nuclei, often with irregular contours and abundant granular eosinophilic cytoplasm with indistinct cell borders. They may also coalesce to form multinucleated giant cells.^[25]

Foreign body: Suture granuloma, with multinucleated giant cells surrounding (grey) suture material.

Neutrophilic infiltrate

Main conditions^[1]	Characteristics	Micrograph	Photograph
Urticaria, neutrophil predominant	Interstitial location^[14] Relatively dense infiltrate^[14] Mast cells are relatively sparse, potentially demonstrated with special stains, preferably tryptase stain.^[14] Extravasated erythrocytes are present in about 50% of the cases ^[14] No vasculitis.^[14]
Dermatitis herpetiformis	Subepidermal vesicles and blisters associated with accumulation of neutrophils at the papillary tips.^[26] Sometimes presence of eosinophils, giving an appearance similar to bullous pemphigoid.^[26] The histopathology is unspecific in approximately 35%–40% of the cases,^[26] and direct immunofluorescence is needed, showing deposition of IgA in the papillary dermis in a granular or fibrillar pattern.^[27]
Early linear IgA bullous dermatosis	Subepidermal blister formation.^[28]
Early febrile neutrophilic dermatosis (Sweet's syndrome)	Neutrophilic and lymphohistiocytic infiltrate and edema.^[29]
Connective tissue disorders	Usually associated with epidermal changes.^[1] (Systemic lupus erythematosis pictured)
Cutaneous small-vessel vasculitis	Neutrophils with nuclear dust (dashed arrows in image), with high affinity for postcapillary venules.^[30] 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
Acute inflammation (not otherwise specified)	Neutrophilic infiltrate not conforming to any of the above mentioned conditions.	File:Histopathology of dermal edema.jpg Dermal edema in a case of cellulitis.

No visible pathology

In a referral with a rash or other suspicion of dermatitis, but no visible pathology is seen, generally do a fungal stain, as fungal infections may have no visible pathology on H&E stain.

Notes

↑ 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.
↑ PAS is for evaluation of the epidermal basement membrane, blood vessels, and the presence of fungal organisms
↑ ^3.00 ^3.01 ^3.02 ^3.03 ^3.04 ^3.05 ^3.06 ^3.07 ^3.08 ^3.09 ^3.10 In "not otherwise specified" cases, a description of the findings attained so far is generally enough as a diagnosis, but may mention when it can be consistent with a diagnosis that is clinically suspected according to the referral. A more comprehensive approach is to include a comment such as the following:
"Differential diagnosis for this condition include: ____, ____ and ____. Clinical correlation is recommended.
↑ Parakeratotic mounds at the edge of follicular ostia.
↑ Pigmented purpuric dermatitis of Gougerot and Blum particularly have a tendency for lichenoid infiltrate.

Main page

Main page of Patholines

References

↑ ^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 ^1.35 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.
↑ 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. .
↑ 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.
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- . Handläggning av hudprover – provtagningsanvisningar, utskärningsprinciper och snittning (Handling of skin samples - sampling instructions, cutting principles and incision. Swedish Society of Pathology.
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- "The principles of mohs micrographic surgery for cutaneous neoplasia
". Ochsner J 5 (2): 22–33. 2003. PMID 22826680. PMC: 3399331. Archived from the original. .
- With a "standard histologic examination" that, in addition to the lesion, only includes one section from each side along the longest diameter of the specimen.
- It also shows an example of circular coverage, with equal coverage distance in all four directions.
- The entire specimen may be submitted if the risk of malignancy is high.
↑ ^5.0 ^5.1 ^5.2 Mowafak Hamodat. Skin inflammatory (nontumor) > Spongiotic, psoriasiform and pustular reaction patterns > Seborrheic dermatitis. PathologyOutlines.com. Topic Completed: 1 August 2011. Revised: 26 March 2019
↑ ^6.0 ^6.1 ^6.2 ^6.3 ^6.4 ^6.5 Unless else specified in boxes, reference is: 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.
↑ Lisa K Pappas-Taffer. Lichen Sclerosus. Medscape. Updated: May 17, 2018
↑ Mowafak Hamodat. Skin inflammatory (nontumor) > Lichenoid and interface reaction patterns > Lupus: systemic lupus erythematosus (SLE). PathologyOutlines. Topic Completed: 1 August 2011. Revised: 26 March 2019
↑ ^9.0 ^9.1 ^9.2 Gorouhi, Farzam; Davari, Parastoo; Fazel, Nasim (2014). "Cutaneous and Mucosal Lichen Planus: A Comprehensive Review of Clinical Subtypes, Risk Factors, Diagnosis, and Prognosis ". The Scientific World Journal 2014: 1–22. doi:10.1155/2014/742826. ISSN 2356-6140.
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↑ "Generalized lichen nitidus ". Pediatr Dermatol 22 (2): 158–60. 2005. doi:10.1111/j.1525-1470.2005.22215.x. PMID 15804308.
↑ Shenoi, SD; Balachandran, C; Mehta, VandanaRai; Salim, T (2005). "Lichen amyloidosus: A study of clinical, histopathologic and immunofluorescence findings in 30 cases ". Indian Journal of Dermatology, Venereology and Leprology 71 (3): 166. doi:10.4103/0378-6323.16230. ISSN 0378-6323.
↑ "Cytokines and cytokine profiles in human autoimmune diseases and animal models of autoimmunity ". Mediators of Inflammation 2009: 1–20. 2009. doi:10.1155/2009/979258. PMID 19884985.
↑ "Diagnosis and classification of psoriasis ". Autoimmunity Reviews 13 (4–5): 490–5. January 2014. doi:10.1016/j.autrev.2014.01.008. PMID 24434359.
↑ ^14.0 ^14.1 ^14.2 ^14.3 ^14.4 ^14.5 ^14.6 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.
↑ 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.
↑ 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.
↑ ^17.0 ^17.1 ^17.2 ^17.3 ^17.4 Stephen Lyle. Pigmented purpuric dermatoses. Dermpedia.org. Retrieved on 2019-11-05.
↑ ^18.0 ^18.1 . Histology of erythema annulare centrifugum. DermNet NZ. Retrieved on 2019-11-05.
↑ 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.
↑ "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.
↑ 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.
↑ Assoc Prof Patrick Emanuel (2013). Syphilis pathology. Dermnet NZ.
↑ ^23.0 ^23.1 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.
↑ 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.
↑ Shah, Kabeer K.; Pritt, Bobbi S.; Alexander, Mariam P. (2017). "Histopathologic review of granulomatous inflammation ". Journal of Clinical Tuberculosis and Other Mycobacterial Diseases 7: 1–12. doi:10.1016/j.jctube.2017.02.001. ISSN 24055794.
↑ ^26.0 ^26.1 ^26.2 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.
↑ Huma A. Mirza; Amani Gharbi; William Gossman.. Dermatitis Herpetiformis. StatPearls at National Center for Biotechnology Information. Last Update: July 11, 2019.
↑ Saleem, Maryam; Iftikhar, Hassaan (2019). "Linear IgA Disease: A Rare Complication of Vancomycin ". Cureus. doi:10.7759/cureus.4848. ISSN 2168-8184.
↑ 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.
↑
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.
- "Figures - available via license: CC BY 4.0"

Image sources

[contributors-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.

[6] PAS is for evaluation of the epidermal basement membrane, blood vessels, and the presence of fungal organisms

[not-otherwise-specified-7] 3.00 ^3.01 ^3.02 ^3.03 ^3.04 ^3.05 ^3.06 ^3.07 ^3.08 ^3.09 ^3.10 In "not otherwise specified" cases, a description of the findings attained so far is generally enough as a diagnosis, but may mention when it can be consistent with a diagnosis that is clinically suspected according to the referral. A more comprehensive approach is to include a comment such as the following:
"Differential diagnosis for this condition include: ____, ____ and ____. Clinical correlation is recommended.

[17] Parakeratotic mounds at the edge of follicular ostia.

[22] Pigmented purpuric dermatitis of Gougerot and Blum particularly have a tendency for lichenoid infiltrate.

[Alsaad2005-2] 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 ^1.35 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.

[ChhabraMinz2012-3] 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. .

[kvast-4] 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.

[skin-processing-benign-5] 
. Handläggning av hudprover – provtagningsanvisningar, utskärningsprinciper och snittning (Handling of skin samples - sampling instructions, cutting principles and incision. Swedish Society of Pathology.
- For number of slices and coverage of lesions, as well as including sections from each edge in case of diffuse border.

. Dermatopathology Grossing Guidelines. University of California, Los Angeles. Retrieved on 2019-10-23.
- For microtomy of the most central side at the lesion

"The principles of mohs micrographic surgery for cutaneous neoplasia
". Ochsner J 5 (2): 22–33. 2003. PMID 22826680. PMC: 3399331. Archived from the original. .
- With a "standard histologic examination" that, in addition to the lesion, only includes one section from each side along the longest diameter of the specimen.
- It also shows an example of circular coverage, with equal coverage distance in all four directions.
- The entire specimen may be submitted if the risk of malignancy is high.

[10] . Handläggning av hudprover – provtagningsanvisningar, utskärningsprinciper och snittning (Handling of skin samples - sampling instructions, cutting principles and incision. Swedish Society of Pathology.
- For number of slices and coverage of lesions, as well as including sections from each edge in case of diffuse border.

[11] . Dermatopathology Grossing Guidelines. University of California, Los Angeles. Retrieved on 2019-10-23.
- For microtomy of the most central side at the lesion

[12] "The principles of mohs micrographic surgery for cutaneous neoplasia

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[Alsaad2005unless-9] 6.0 ^6.1 ^6.2 ^6.3 ^6.4 ^6.5 Unless else specified in boxes, reference is: 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.

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[dermpedia-21] 17.0 ^17.1 ^17.2 ^17.3 ^17.4 Stephen Lyle. Pigmented purpuric dermatoses. Dermpedia.org. Retrieved on 2019-11-05.

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"Figures - available via license: CC BY 4.0"

[39] "Figures - available via license: CC BY 4.0"

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[note 2]

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