Since 1987, we have been fortunate to have the expertise at our LML to back up our doctors (our hospital now running the busiest hospital ER in South Carolina) with very rapid emergency diagnoses using frozen section, same-day direct immunofluorescence, routine next-day histology, and next-day IHC stains. The emergency situations tend to revolve around infectious vs. non-infectious and steroid vs. non-steroid therapy institution, and diffuse, "bad" erythema of non-vesiculating type vs. pre-vesiculating (or already vesiculating/bullous) situations. A growing collection of some examples of some of our DIF cases. An online Czech DIF dermatology atlas ...this atlas covers many other things than just DIF. The Electronic Textbook of Dermatology has lots of details on some blistering dermatoses, etc. Dermis.net is another on-line site. Dr. Mihm's is another. Dr. Ackerman's subscription site is packed with info and presents very frequent e-mailed case discussions. For skin conditions of all types (with ability to study as a patient or a physician), check out this New Zealand website (DermNet NZ).

Even if done just minutes prior to biopsy, biopsy preplanning is crucial to the success of emergency diagnosis. A slightly thick shave biopsy about 1.0 cm. in greatest diameter is mandatory, if possible. It is always an advantage to include the advancing edge of a lesion (junction between normal and lesional skin) if skin is less than generally affected...as long as the biopsy is marked or oriented in such a way that the pathologist can correctly embed it to demonstrate this junction. If there are lesions of a spectrum of ages, it can be very helpful to evaluate biopsies from both a fresh and a middle-aged lesion. A punch biopsy within the interior of the lesion is also additionally helpful, especially if the lesional skin seems deeply involved (indurated). A shave of any vesiculating lesion can also be placed in Michelle's type DIF transport fluid, to be held for DIF studies if truly needed; a  companion serum sample may allow demonstration of various anti-skin auto-antibodies, if need be. 

Lab tests: We offer many skin-related lab tests locally (at LML). We can "conduit" samples to other labs. Some specialty dermatology-tests labs for info: U. of Rochester Med. Ctr. dermatology lab; 

NOTE: A decent thumb-nail resource . With the below listings as a starter, one is encouraged to seek up-to-date information on a particular entity through such as the PubMed medical search engine of the USA National Library of Medicine (and/or your local text and other resources). By using the search-for-images feature of the Google search engine, you might find good photos.

Clinical Differential DiagnosisGroups:

• abnormal palm & sole colors (without keratosis):
  1. too pale...white: anemia.
  2. too red: cirrhosis or other hyperproteinemic, hyperviscous situation.
  3. yellow: jaundice/icterus & carotenemia (excess colored vegetables & fruits) will also make sclerae yellow; hypothyroidism; chronic liver disease; chronic renal disease; and situations of excessive end products of glycation (diabetes mellitus).
• Hypo & hyperpigmentation lesions & syndromes HERE.
• stubborn, usually hyperkeratotic, hand/palm & foot/sole dermatitis (DDX here) [S07-3257, foot; L07-2586 wrist].
• opportunistic skin portal of entry infections:
  1. Aspergillus
  2. Fusarium filamentous mold: mostly from environment where is ubiquitous & often starts in crack or ulcer between toes, or maybe central venous catheter site (or sino-pulmonary tree) & dissemination reflected in skin as papulo-pustules. Most often in aggressive chemo cases with prolonged neutropenia.
• biopsy sent to rule out "eczema" or dermatitis: At its broadest, eczema is a synonym for dermatitis. "Eczema" cases are...as of the time of biopsy...a wastebasket of drematidities, almost always red and probably at least histologically "wet" (spongiotic) , which do not show readily recognizable clinical patterns and features that are typical of a particular & specific dermatitis or dermatological differential diagnosis group...usually somewhat chronic.  Eczema is essentially always a spongiotic papular or papulovesicular disease ^{1, 11}.  It mostly includes contact, perioral (face), atopic, prurigo, LSC, dyshydrotic, and exfoliative (erythema, swelling, diffuse and copious scaling).  So, except for the pattern of "dermal contact sensitivity reaction" (maybe slight acanthosis and parakeratosis of epidermis over fairly heavy & tight perivascular cuffing by lymphs & a few plasmas and eos...Pinkus p. 116¹¹), lack of spongiosis rules out "eczema" (& with the exception of atopic dermatitis and lichen simplex chronicus ²²). Dr. Ackerman dispises the term eczema & urges that doctors refine a patient's disorder down to a particular & specific dermatitis ²²:  
1. breast rash or erythema: be always on the alert for "inflammatory breast cancer".
2. problematic (eczematous) dermatitides which are spongiotic:
• allergic contact dermatitis.
• nummular dermatitis.
• "id" reactions.
• dyshidrotic dermatitis.
• erythema annulare centrifugum (EAC).
• pityriasis rosea (PR): [S-07-3347]...tiny foci of spongiosis/spongiotic vesiculation in a clinically "dry²⁹" eruption...early; more spongiosis & hyperplasia & parakeratosis later [S07-11834] & then the findings wane³⁴.
• guttate parapsoriasis.
• acral papular eruption of childhood.
• seborrheic dermatitis.
• lichen striatus.
• miliaria rubra.
• irritant contact dermatitis.
• photoallergic dermatitis.
• vesicular dermatophytosis.
3. problematic (eczematous) dermatitides which are not spongiotic:
• atopic dermatitis.
• lichen simplex chronicus.
• dermal contact sensitivity reaction (see above).
• pruritic lesions: when chronically pruritic lesions are finally biopsied, all that one may see are the histomorphological consequences of chronic, vigorous scratching & rubbing. These are (1) compact, volar-like orthokeratosis with hypergranulosis, (2) vertical streaks of ipapillary dermal collagen, (3) acanthosis, and (4) stellate fibroblast nuclei in dermis. If that reactive lesion is a plaque, it is "lichen simplex chronicus and if a rash of papules, "prurigo nodularis" (or "prurigo papularis" [S07-9672]), and if an isolated papule, it is a "picker's nodule".
1. nipple, breast: be alert for Paget's disease, almost all of which cases have an underlying breast cancer.
2. dermatitis herpetiformis (DH): intensely pruritic & bilaterally symetrical & extemities & buttocks; polys at tips of dermal papillae & DIF may show IgA at papillae tips.
3. papulosquamous dermatoses: 25% of pityriasis rosea (PR) cases can be severely pruritic; lichen planus (LP) can be pruritic.
4. transient acantholytic dermatosis (Grover's disease) = lymphs & eos.; Grovers disease with lots of eosinophiles may be maddeningly pruritic²².
5. "endogenous eczema".
6. scabies (pediculosis); highly infectious when crusted (Norwegian).
7. drug eruption.
8. pruritic papular eruption (PPE) of AIDS.
9. eosinophilic pustular dermatitis of AIDS.
10. atypical bullous pemphigoid.
11. linear IgA dermatosis.
12. pemphigus herpetiformis: acantholytic w/ intra-epi. polys or eos. (see below).
13. lichen planopilaris: papulosquamous (thickening & scaley), folliculocentric, dead keratinocytes.
14. Pityrosporum folliculitis (is caused by Malassezia furfur/P. ovalae).
15. mast cell lesions.
16. papular dermatitis/subacute prurigo/"itchy red bump disease".
17. pruritic dermatoses of pregnancy.
18. pruriginous (purpuric) angiodermatitis.
19. fiberglass dermatitis.
20. dermal hypersensitivity reaction (JAAD Dec 2002 47:898-907)
• papules/nodules/plaques:
  1. foliculitides, including Majocchi granuloma (MG)...granulomatous folliculitis due to fungus, bacteria, maybe anything that causes perifollicular extrusion of follicular contents
  2. urticarial...see pruritic lesions, above.
  3. papulosquamous dermatoses, including LP
  4. neoplasms & nevi
  5. dyskeratoses
  6. granulomata [S07-8662]: GA, rheumatoid, infectious, sarcoid, granuloma multiforme (annular eruption upper body in older adults central Africa).
  7. perforating (epidermal elimination disorders) dermatoses, inherited or acquired: perf. GA, perf. collagenosis, perf. elastosis, perf. folliculitis, Kyrle disease [S-07-594], perforating PXE, etc)
  8. organisms: luetic; viral (MC & VV).
  9. benign vascular lesions: pyogenic granuloma; stasis lesions such as "acral angiodermatitis" [S06-3532].
  10. granuloma annulare
  11. sarcoid
  12. eruptive xanthomas: yellowish & may reflect hyperlipidosis [L07-1462].
  13. pseudoxanthoma elasticum (PXE): usually as symmetrical asymptomatic yellowish papules of neck, antecubital & popliteal fossae; nitrate exposure (fertilizer/farmers) or medication (penicillamine) or genetic (genetic, at least, implies system-wide defective elastic tissue with potential for vascular problems. The skin elastosis oddly favors deeper (reticular) dermis.
• photodermatitide (light) eruptions:
  1. normal sunburn: the expected burn based on light exposure and duration.
  2. solar urticaria
  3. phototoxic:
     • exaggerated "sunburn" due to an ingested or endogenous phototoxic photosensitizer; not immunologically mediated; papules¹ to vesicles; clues are necrotic and balooned keratinocytes which attract polys (irritant contact "burns" and produces same picture).
     • topical (photocontact) phototoxic photosensitizer: PCT (see below).
  4. photoallergic reaction:appears more as rash than sunburn; almost always¹⁴ histology of superficial & deep perivascular (whereas an allergic eruption is just superficial).
  5. polymorphous light eruption (PMLE): itchy papules & plaques in some...not all...sun-exposed skin. Papillary dermal edema and superficial & deep perivascular.
  6. hydroa aestivale (nonscarring) and hydroa vacciniforme (scarring) = chronically recurrent varioliform (smallpox-like) vesiculations that are not associated with any pophyrin abnormality, usually begin in childhood, and begin as intraepidermal spots of balooning keratocytes which undergo reticular degeneration and a vesicle & roof necrosis²³ [S-06-14352].
• morbilliform eruption:
  1. measles-like, symmetrical (trunk and prox. extremities), red, macular (can be faintly papular, too), and usually 2-10 mm lesions, some confluent
  2. entities causing:
     • Kawasaki disease
     • measles
     • 46% of drug reactions are this pattern
     • is one of the 4 viral exanthem pattern
• annular, polycyclic lesions:
  1. subcorneal pustular dermatosis
  2. subacute cutaneous lupus
• Reticulated pattern dermopathy:
  1. erythema ab igne: heat &/or infra-red injury to skin which may be acute to subacute or, more commonly, chronic. The more acute may have striking endothelial atypia concerning for angiosarcoma but without freely anastamosing channels and with some lumenal rims of fibrin and perivascular reactive stromal cells [S08-1660].
  2. livedo reticularis (LR) = violaceus, reticular, blotchy, or mottled vascular color of skin³¹: it is due to increased visibility of the cutaneous venous plexus either due to venodlation, blood deoxygenation, primary spontaneous arteriolar vasospasm, or a physioloical response to cold exposure. If progresses to nodules or ulcers = livedo vasculitis (ischemia ...infarction). Livedo racemosa = reticular pattern thick...maybe more than 10mm.
     • cold exposure = "cutis marmorata".
     • primary LR.
     • secondary LR (causitive entity usually with increasedvenous outflow resistance):
       1. vasculitis
       2. emboli
       3. hypercoagulable state
• red face²⁰:
  1. rosacea: erythema, some scaliness, no comedones, patches of bumps & pustules (afflicts 13,000,000 Americans) (histo: hypervascular, enlarged seb. glands, seborrheic epidermal change, granulomatous); perioral dermatitis is a variant.
  2. acne: red, comedones, follicular bumps
  3. eosinophilic pustular folliculitis: pruritic
  4. seborrheic dermatitis: yellow scales; Malassezia-type yeast lipase results in increased arachidonic acid irritation
  5. actinic keratoses:
  6. atopic dermatitis: pruritic, flexural folds, lichenified scaly areas, maybe also keratosis pilaris and/or icthyosis vulgaris associated; allergy related
  7. tinea facii: scaly annular lesions due to fungi
  8. ulerythema ophrygenes: from shortly after birth...follicular papules with erythematous haloes (keratosis pilaris atrophicans faciei)
  9. dermatomyositis: periorbital, confluent, macular violaceous erythema (heliotrope)
  10. lupus: histology has junctional activity & may have chronic folliculitis; acute (ACLE) has malar rash sparing nasolabial folds; subacute (SCLE) has hyperkeratotic papulosquamous annular and polycyclic interface vacuolar lesions without atrophy; chronic (CCLE) discoid lesions have tightly adherent scale, follicular plugging, & central atrophy; mixed connective tissue (MCTD) disease is like a lupus & scleroderma overlap.
  11. carcinoid syndrome: erythema only that comes and goes
• purpura/ecchymoses without significant inflammatory infiltrate or vasculitis²:
  1. DIC
  2. "early" infectious lesion...(don't forget rickettsial [typhus, spotted fevers, ehrlichiae])...from endothelialitis [LMC-04-9462] to vasculitis with thrombi.
  3. purpura fulminans (extreme skin DIC)
  4. coumarin/coumadin necrosis
  5. lupus anticoagulant associated necrosis
  6. TTP (proceeding from hemolytic uremic syndrome...HUS; >90% cases from E. coli O157:H7):
     • E. coli induced
     • in severe pneumococcal infections (HUS) [Infect. Med. 18(5):251-258,2001]
  7. PNH
  8. pruriginous (purpuric) angiodermatitis.
  9. monoclonal cryglobulinemic necrosis
  10. bite envenomation (snake or insect/spider)
  11. dramatically acute stasis dermatitis [LMC-04-7886]
  12. at least think of necrotizing fasciitis
• petechiae, purpura/ecchymoses with inflammatory infiltrate and/or vasculitis:
  1. an acute phase of stasis dermatitis [S-01-8706]
  2. vasculitides palpable purpura, nodular vasculitis, and allergic vasculitis are used somewhat synonymously as applied to skin)
  3. older (within days/week) lesion may only have the RBCs, some residua of inflammatory cells, and some beginning hemosiderin macrophages [LMC-01-8237]
  4. at least think of necrotizing fasciitis
  5. infectious...(don't forget rickettsial [typhus, spotted fevers, ehrlichiae])...from endothelialitis to vasculitis viral (hepatitis B or C, IRV [interferon resistant viruses like HIV], cytomegalo virus, Epstein Barr Virus [LMC-04-9462], Parvo B19 ) to septic vasculitis with thrombi.
  6. it is our job to search for & "rule out" as much as we can any of the above causes; remember that there are "bland causes": antiplatelet meds (such as Plavix...LMC-05-6867]), thrombocytopenia, & factors decreasing endothelial integrity
• vegetative plaque: sharp-margined hyperplastic, granulomatous, granulation tissue looking, growth-like plaque
  1. pemphigus vegetans [S-04-6880]
  2. pyodermatitis-pyostomatosis vegetans
• pustulosis: (see histological group below)
  1. acute generalized exanthemous pustulosis (AGEP): often a drug eruption.
  2. impetigo or impetigenized vesicobullous process of other primary etiology.
  3. metastatic pustulosis (from Staph., candida, etc.): tend to be dermal [L-06-8613].
  4. p. orb. fungal pustular folliculitis HERE.
  5. see histological DDX groups, below (intraepidermal/peri-epidermal neutrophiles).
  6. pustular psoriasis, here.
  7. SAPHO syndrome (pustulosis, synovitis, acne, hyperostosis, & osteitis).
  8. these can be assoc. with enteropathic (IBD) CRMO.
  9. pustules can be seen with fire ant bites, H-S purpura [S07-11104], ___.
• vesico-bullous conditions & desquamative oral situation (chart below) :
  1. cell-poor subepidermal bullae:
     • EBA (a few scattered epidermal cell necroses)²
     • PCT (actinic elastosis & stiff papillae with d-PAS positive superficial dermal vessels [S-02-9369; S-05-10872])². Can be reflection of hepatitis C (HCV).
     • bullous pemphigoid, cell-poor (dermal edema & some scattered eosinophiles)²
     • suction blister (factitial?), fluid with or without RBCs.
     • vesicular or bullous stasis dermatitis (stasis vessels may be strongly positive for fibrinogen [L07-3526]).
  2. Full-thickness epidermal necrosis:
     • TEN²
     • thermal burn² (heat or cold, accidental or factitious [LMC-01-7581])
     • hypoxia²
     • fixed drug reaction²
     • grade IV GVH²
     • vascular-related necrosis over cellulitis: phlegmasia [swollen & inflammed] cerulea dolens [painful] (PCD) or plegmasia alba [pale...white; "milk leg"] dolens; both related to "venous gangrene" with large or small vein thrombosis...phlebitis-related or not...which is thought to stimulate arterial vasospsm which leads to gangrene [L07-10666].
  3. Subcorneal subgranular cleavage²:(only clue may be absence of cornified...maybe even granular...layer in the biopsy²²)
     • pemphigus foliaceous (eosinophiles & typical DIF pattern; trunk & extremities)
     • SSSS (generalized)
     • sometimes over cellulitis or deep subcutaneous suppuration as in necrotizing fasciitis [L07-5525].
     • subcorneal pustular dermatosis (SPD)
     • pemphigus erythematosus (eosinophiles & typical DIF pattern; affects face and V-area of neck/chest)
     • bullous impetigo (bacteria [strep. or staph.] and polys).
  4. Cleavage, degeneration in a parakeratotic surface: necrolytic migratory erythema (assoc. with functioning neuroendocrine tumor of pancrease).
  5. scalded skin (widespread flaccid bullae):
     • TEN
     • SSSS
     • bullous impetigo
     • thermal burns
  6. basement membrane zone (BMZ) immunodeposits:
     • granular:
       1. lupus
       2. PNP
     • linear or homogeneous:
       1. pemphigoid
       2. PNP
  7. intercellular peri-keratinocytic immunodeposits:
     • pemphigus, all varieties
     • IgA vesicopustular dermatosis (IAVPD)
  8. epidermal nuclear fluorescence:
     • lupus, rarely
     • MCTD, typically
     • Sjogren's syndrome
• scleroderma (woody induration of skin) ²²:
  1. scleroderma, systemic (multisystem disease & poor prognosis).
  2. scleroderma, localized (good prognosis):
     • morphea (localized firm lesions). (early DFSP and a BCC type can be morpheaform)
     • en coup de sabre (large sword-like lesions).
     • lichen sclerosus et atrophicus (foci of papillary dermal sclerosis).
  3. tryptophane myalgia syndrome.
  4. fasciitis with eosinophilia (eosinophilic fasciitis).
  5. nephrogenic systemic fibrosis (nephrogenic fibrosing dermopathy): is assoc. with renal disease & most visible as papules & plaques of skin with mid-dermal increase in interstitial spindle cells (CD34+ cells & CD68+ cells).
  6. plaques of PCT.
  7. late lesions of GVH.
  8. lipodermosclerosis of chronic venous insufficiency (CVI), usually of lower legs...terminology cross-over with SMX, below. Either CVI or SMX can be suddenly destabilized by an acute thrombosis or external trauma within the abnormal area such that there is tissue necrosis and a new ulcer formed [L08-4650]; and PVD comorbidity can complexify a case.
  9. end-stage fibrotic stage of a number of lesions.
  10. scarring/sclerosis due to trauma; and this can be due to factitious or even such as the functional area of Eckbom syndrome (as it applys to skin...Morgellons disease [S-01-11211 & FA-05-151])...delusions of parasitosis.
  11. the skin of fibrosing chronic "woody induration" lymphedema (scleredema...scleromyxoedema [SMX]): from either localized idiopathic scleredema [B07-247], congenital deficiency of lymphatics (if severe enough it shows up at a young age & less severe it appears with weight gain)...weight loss before permanent tissue changes can reverse the swelling...at an older age &, if only one lower leg, can mimmic the swollen leg of thrombosis), or secondary local lymphatic obstuction (as dependant from a lower extremity ulcer [L07-6036]) or regional due to parasites or transcutaneous entry of silica into lymphatics (podoconiosis). When an extremity is deformed enough, it is called elephantiasis...with skin change being "lymphostatic verrucosis".
• erythroderma (ED)[widespread...e.g. 90%...red skin exfoliating]: most cases are exacerbations of a current skin disease & only 1-6% of ED cases turn out to be MF/T-cell neoplasia.
1. medication reaction: ACE inhibitors, dilantin [LMC-05-8525].
2. mycosis fungoides (l'homme rouge refers to ED that is secondary to cutaneous T-cell lymphoma).
3. as a reflection of internal malignancies.
4. idiopathic erythroderma: elevated serum IgE levels, dermatopathic lymphadenopathy, & marked palmar plantar keratoderma.
5. atopic dermatitis.
6. seborrheic dermatitis.
7. staphylococcal scalded skin syndrome.
8. rare instances of pemphigus foliaceus.
9. hereditary ichthyosis.
10. contact dermatitis.
11. psoriasis (usually no islands of spared skin when ED)[L07-1996].
12. pityriasis rubra pilaris (PRP): resembles psoriasis clinically and histologically (see DDX on DERM 101) but when ED, tends to have some islands od skin sparing.
13. GVH may present with widespread macular erythema.
• Koebner's phenomenon: situation of skin trauma inducing a dermatosis lesion (also so-called "isomorphic phenomenon") at the trauma site (seen in 33% of psoriasis; also LS & A, eczema, lichen planus, and vitiligo) usually within 10-14 days (but between 3 days and 2 years after the trauma)²⁷ [S-06-6799].
• Bites or sores: if worried about a spider bite, also think of MRSA.

Histological Differential Diagnosis Groups:

• superficial perivascular dermatidities devoid of epidermal involvement:
1. incipiently early stage of pityriasis lichenoides acuta (eruptive lesions of Mucha-Habermann disease...PLEVA)²²: lymphocytes around at least the venules of superficial plexus & along the interface along with vacuolar alteration plus necroti c keratinocytes plus parakeratosis. Specificity added if affects deeply also & the infiltrate is wedged shaped, & there are some balooned keratinocytes & there are some polys in the parakeratosis.
2. incipient stage of erythema multiforme²²: lymphocytes around at least the venules of superficial plexus & along the interface along with vacuolar alteration plus necrotic keratinocytes & negative for parakeratosis.
3. incipient stage of psoriasis²²: superficial perivascular mostly lymphocytic infiltrate, dilated tortuous dermal papillary capillaries & mounds of parakeratosis housing polys.
• satellite-cell necrosis (dead, necrotic keratocyte surrounded by mononuclears):
  1. TEN.
  2. acute GVH.
• necrotic keratinocytes: these apoptotic cells will often be associated with pre-necrotic balooned keratinocytes & the necrotic ones tend to attract polys. Seen in EM, PLEVA, fixed drug, irritant, and phototoxic dermatitis¹; and in lichen planopilaris¹⁵, GVH, and in perioral dermatitis [or was the case lupus?...S-04-13280²¹]. PLEVA may cause a sharply discrete small lesion (hardly ever larger than a low power microscopic field) of epidermal necrosis with adjacent epidermis nearly completely lacking in reactive change [S06-15582].
• epidermal reticular or vesicular degeneration of keratocytes:
  1. viral exanthem (cell contents seem lost)
  2. acute eczematous dermatitis (nuclei or partial cell contents noted)
  3. epidermolytic hyperkeratosis
• epidermal spongiotic vesicular degeneration:
1. clue to insect bite is multiloculated vesicle whose locules decrease in size away from lesion center²².
• epidermal acantholytic vesicular degeneration:
  1. acantholysis is a hallmark of pemphigus (but biopsies of very early pemphigus lesions may show only what appears to be spongiosis with polys & eos.).
• intraepidermal/peri-epidermal neutrophiles:
  1. intraepidermal polys:
     • dermatophytosis or superficial bacteriosis
     • intra-epidermal neutrophilic dermatosis (IEN)
     • toxic shock syndrome
     • superficial pyoderma with intra-epidermal polys/pustules
  2. pustules...pustulosis:
     • subcorneal pustular dermatosis (SPD).
     • bites...especially fire ant bites.
     • halogenoderma: (especially bromides) lesions usually of lower extremities and have pseudocarcinomatous downward epidermal growth containing pustules⁵.
     • pustular psoriasis⁵: a key diagnostic finding is polys layered (dried Kogoj's pustule-like perimeter...see DDX) between keratocytes at perimeter of pustule [L07-2586]²³; these 3 are the same with different presentations...
       1. pustular psoriasis of Zumbusch: when outbreak is in a background of clinical psoriasis.
       2. impetigo herpetiformis: hypocalcemia setting...an uncommon pustular dermatosis that typically occurs during pregnancy (or after loss of parathyroids) with sudden onset of severely pruritic erythema and pustules that, within days to weeks, become erythematosquamous plaques bordered by tiny pustules  scattered on  trunk and extremities (pustules may be spongiotic).
       3. acrodermatitis continua of Hallopeau: affecting only hands & feet (dermatitis repens a broader synonym) & like a mix of acral psoriasis and pyoderma.
       4. see pustulosis palmaris et plantaris, just below.
     • acute generalized exanthemous pustulosis (AGEP): often a drug eruption; predilection for distal extremities; may have leukocytoclastic vasculitis.
     • subcorneal pustulosis like drug eruption: [S-02-10387...subsequently found to have drug-induced hepatitis with skin & liver clearing on stopping the drug; L07-2485].
     • pustulosis palmaris et plantaris: may not be a variant of psoriasis though some call it a variant of pustular psoriasis; is a deep epidermal unilocular pustule [S07-3373] & underlying dermis with chronic infiltrate & a few polys⁵.
     • IgG pemphigus herpetiformis, see below.
     • IgA vesicopustular dermatosis (IAVPD) (or "intra-epidermal IgA pustulosis", "IgA pemphigus", "intraepidermal neutrophilic IgA dermatosis", "IgA herpetiform pemphigus", "subcorneal pustular dermatosis with IgA deposition") : 
       1. intra-epidermal neutrophilic (IEN) dermatosis type: polys accumulate in papillae, then into epidermis, then form intra-epidermal pustules [S-01-10098].
       2. subcorneal pustular dermatosis (SPD) type: superficial epidermal pustule formation and pemphigus-like DIF.
  3. spongiform pustules (spongiosis-derived vesiculation):
  • pustular psoriasis (acrodermatitis continua; impetigo herpetiformis...see above, "pustules")...spongiform pustule of Kogoj (superficial keratinocytes get severely edematous and polys get into them and yet the cell walls form a mesh that breaks down as too many polys accumulate)⁵.
  • Reiter's disease: pustules of glands penis, palms, soles & histology psoriatic⁵.
  • rheumatoid neutrophilic dermatitis (RND): severe RA cases, extensor surface papules, plaques, (rarely) vesicles and dermal polys without vasculitis and poly micro-abscesses of papillae.
  • vesicopustular eruption of ulcerative colitis: intraepidermal & subcorneal pustular foci and a linear BMZ IgG.
  • very superficial dermatophytosis.
  • subcorneal pustular dermatosis.
  • eczematous dermatitis with impetiginization.
  • id reaction.
  • dermatitis herpetiformis occasionally has spongiform pustules.
  • secondarily infected pemphigus foliaceous.
• peri-epidermal/papillary dermal polys:
  1. dermatitis herpetiformis (DH): polys at papillary tips and DIF may be positive for IgA at same location (it may take serial stepcut sections to demonstrate...we have found the H&E polys focally & DIF negative).
  2. Sweet's syndrome (SS), see below.
  3. acute lupus.
  4. intra-epidermal neutrophilic dermatosis type of IAVPD.
  5. ? [S-02-8081 8y/o.
• Intraepidermal lymphocytes:
  1. exocytosis: allergic contact, eczema, lichenoid interface, etc.
  2. epidermotropism: mycosis fungoides (MF); Pautrier's non-spongiotic "microabscesses"; lymphs along the basal layer; lymphs with clear perinuclear halo, grooved convoluted nuclei. Lymphs & nuclei bigger than nuclei of dermal lymphs²².
• Interface dermatitis, basal-layer vacuolar dominant²⁴:
  1. lymphocytes nearly monopolize:
     • with ballooning and necrotic keratocytes:
       1. erythema multiforme: cornified layer usually normal.
       2. various lupus types and mixed connective tissue disease (& may have in vivo DIF ANA positivity with IgG...see DIF below).
       3. Mucha-Habermann disease: parakeratosis often.
       4. graft vs. host (GVH) lesion.
       5. paraneoplastic pemphigus.
       6. HSV infection.
       7. as a morphologic effect when nitrogen mustard placed on MF lesion.
     • no ballooning of keratocytes:
       1. discoid lupus.
       2. dermatomyositis.
       3. drug eruption, one type.
       4. LS&A (superficial morphea):look for superficial dermal sclerosis.
       5. postinflammatory pigment alteration (NOS etiology of the inflammation).
  2. mixed lymphocytes plus polys and eosinophiles:
     1. fixed drug eruption.
• Interface dermatitis, dermo-epidermal junction, lichenoid inflammatory cell blurring dominant²⁴:
1. lymphocytes predominate:
   • lichen planus: wedged hypergranuloisis with apoptotic basal keratocytes and Civatte bodies...and can have a sort of pseudoepitheliomatous hypertrophic "look" [S07-3105]; no parakeratosis unless new erruptive lesion [S-06-13280]; beware of LP-like keratoses, both actinic & non-actinic; beware of drug-induced LP-like erruption if see eosinophils & plasma cells...or deeper dermal extension of infiltrate from interface with or without co-expression of the eos and plasma cells ²¹.
   • lichenoid drug eruption: tends to be deeper.
   • ichenoid photodermatitis.
   • DLE.
   • Mucha-Haberman disease.
   • lichen striatus.
   • GVH reaction/eruption of lymphocyte recovery.
   • lichenoid purpura of Gougerot & Blum (lichen aureus), longstanding. lesions may have wiry collagen²² (and so may other longstanding lichenoid lesions²²).
   • LP-like keratosis.
   • disseminated superficial actinic porokeratosis, early.
   • MF, plague: wiry collagen (papillary dermal thickening by wiry collagen... wiry bundles of haphazard collagen within a lichenoid infiltrate²²) in mycosis fungoides usually²²; may have melanophages &, when unilesional [S-06-10521], may be treatable with EBT superficial radiation.
2. lymphocytes & abnormal lymphs plus polys & eos: lymphomatoid papulosis.
3. lymphocytes & histiocytes:
• lichen nitidus.
• lichen striatus.
• sarcoidosis.
4. Langerhan's cells predominate: Letterer-Siwe disease.

1. bite reaction.
2. lymphocytoma cutis of Lyme disease [S-06-12219], and see below.

1. bland fibrin thrombi: in lumens but not venule walls = DIC, TTP; coumarin necrosis [S07-9798].
2. insect bite associated: clearly within a wedge shaped bite reaction.
3. fibrin in venule lumens and venule walls: livedo vasculitis.

1. leukocytoclastic vasculitis: see above & below.
2. lymphocytic vasculitis²⁶:
• venular with ordinary, typical lymphocytic vasculitis:
1. without promininent extrvascular pathology:
1. one type of drug eruption [S07-1562]. It may be hard to seperate this from the tight, coat-sleeve perivascular lymphocytosis of erythema annulare centrifugum (EAC) or from "dermal contact sensitivity".
2. perniosis
3. rickettsial lesion
4. allograft rejection
5. idiopathic
6. livedo vasculopathy
7. Behqet's disease
8. collagen vascular disease
9. resolving leukocytoclastic vasculitis
2. with interface dermatitis:
1. perniosis
2. perniosis-like LE
3. Behqet's disease
4. herpetic dermatitis
5. PL et VA
3. with balooning degeneration: hydroa vacciniforme
4. with psoriasiform epidermal hyperplasia, spongiosis, or focal epidermal necrosis:
1. sting or bite reactions
2. scabietic nodules
5. with extravascular necrosis:
1. papulonecrotic tuberculid
2. rickettsial lesion
6. with panniculitis:
1. lupus panniculitis
2. perniosis
3. pyoderma gangrenosum (uncommonly)
• venular with lymphocytic vasculitis by atypical lymphocytes:
1. lymphomatoid papulosis
2. mycosis fungoides (rarely)

Direct Immunofluorescent (DIF diagnosis) patterns²⁸:
(older lesions can lose immunodeposits and be "false negative"; see biopsy site and immuno-dynamics notes)

This use of cutaneous microscopic histomorppholgical immuno-techniques searches for the presence of auto-antibodies, whether compliment-fixed or not, lodged at various sites in the patient's own skin. Sometimes & in some situations, immune complexes generated elsewhere get caught in the epidermal BMZ. The reagents are antibodies against IgG, IgA, IgM, C3, and fibrinogen.

• epidermal keratocyte speckled nuclear positivity⁶: when seen, especially if the in vivo ANA is IgG specific & with or without BMZ granular positivity for C3, it may indicate MCTD or lupus or some other connective tissue disease [S07-1538].
• pericellular (chickenwire)¹⁸ :
  1. various types of pemphigus.
  2. burn cases.
  3. SLE.
  4. pemphigoid.
  5. rheumatoid arthritis.
  6. some other skin diseases.
• aound intra-epidermal clusters of polys: IgG, IgA, & C3 in this pattern may indicate psoriasis (is a psoriatic pattern) [S-07-302].
• keratinocyte cytoplasm: (tend to see in diseases causing apoptotic or necrotic keratocytes...EM/TEN & maybe fixed drug).
  1. predominately basal cells: TEN-type pattern [S-06-12011, S-07-1189].
  2. other distributions.
• basement membrane zone (BMZ):
  1. linear: implies antibody attacking BMZ component
     • bullous pemphigoid [LMC-04-5899 IFA & DIF neg.].
     • linear IgA dermatosis (atypical DH).
     • some cases of herpes gestationes.
     • EBA.
     • bullous SLE, some cases.
  2. granular: (implies immune-complex deposition in BMZ)
     • lupus.
     • positive lupus band test: deposits of IgG, IgM, IgA or all three in nonlesional, non-facial, sunprotected skin is highly suggestive of SLE.
  3. combinations:
     • pericellular plus BMZ: 
       • paraneoplastic pemphigus (especially in Waldenström's, non-Hodgkin lymphoma, and CLL)¹⁸.
       • herpes gestationes.
     • linear BMZ and sweat gland BMZ:
       • cicatricial pemphigoid, skin Bx [S-04-14973].
       • PCT, see below...can be vascular, too.
     • BMZ plus vascular (except for lupus, the BMZ deposits tend to be weak and focal):
       • PCT (vascular deposits tend much heavier than BMZ & greater in superficial vessels)...mainly IgG, C3, and fibrin.
       • lupus (BMZ staining tends to be much more prominent than vascular).
       • acute & chronic GVH lesions ...mainly IgM, C3, and fibrin.
       • rheumatoid arthritis...mainly IgM, C3, and fibrin.
       • allergic vasculitis...mainly IgM, C3, and fibrin.
       • urticarial vasculitis (leukocytoclastic)...mainly IgM, C3, and fibrin.
       • granuloma annulare...mainly IgM, C3, and fibrin.
       • necrobiosis lipoidica diabeticorum...mainly IgM, C3, and fibrin.
       • fresh lesions of pityriasis lichenoides...mainly IgM, C3, and fibrin.
       • cutaneous sarcoidosis...mainly IgM, C3, and fibrin.
       • erythema multiforme...mainly IgM, C3, and fibrin.
       • arthritis-dermatitis syndrome assoc. with intestinal bypass surgery...mainly IgM, C3, and fibrin.
       • skin trauma (appearing 1-10 days later)...diffuse granular mainly IgM, C3, and fibrin.
       • sun-exposed areas in healthy individuals...mainly IgM, C3, and fibrin.
• dermal vessels, mural positivity:
  • vasculitis...& deposits may "be there" before any good H&E changes; H-S purpura primarily IgA & C3 [S07-11104]; vessels around lesions of Berger's may be IgA & C3 positive²⁸.
  • PCT: IgG, C3, fibrin...and see positivity site combinations, above.
  • nonspecific "inflammatory" positivity.
  • may see DIF deposits in vessels in: pyoderma gangrenosum, angioimmunoblastic lymphadenopathy, angiolymphoid hyperplasia with eosinophilia, Well's syndrome (recurrent granulomatous dermatitis with eosinophilia), diabetes mellitis associated with bullous eruptions, and lepromatous Lucio's phenomenon²⁸.

• anti-epidermal antibodies²⁸:
  • pemphigus-type auto-antibodies to inter-epithelial adhesion components.
  • PV-like & seen in some cases of bullous pemphigoid.
  • PV-like & seen in some cases of cicatricial pemphigoid.
  • PV-like & due to blood group antibody reactions.
  • PV-like & due to thermal burns.
  • PV-like & assoc. w/ TEN.
  • PV-like & assoc. w/ T. rubrum infection.
  • PV-like & assoc. w/ certain bullous drug eruptions.
  • PV-like & assoc. w/ Darier's disease.
  • PV-like & assoc. w/ bullous mycosis fungoides.
  • PV-like & assoc. w/ bullous impetigo.
• anti-nuclear antibodies²⁸: in global fashion, the test may pick up any of a variety of circulating ANAs...a number of which do not show up in commercial-lab style test-tube ANA tests.
• anti-basement-membrane-zone (anti-BMZ) antibodies²⁸:
• bullous pemphigoid-type BMZ antibodies (70% of BP cases & IgG & likely high titer & lamina lucida).
• cicatricial pemphigoid (likely low titer & lamina lucida).
• herpes gestationis (likely low titer & lamina lucida).
• EBA-type BMZ antibodies(likely low titer & lamina densa or just deep to it).
• lupus-type BMZ antibodies as in bullous eruption of SLE (BESLE) (likely low titer & lamina densa or just deep to it).
• DH-type BMZ antibodies (IgA)
• epidermal cytoplasmic antibodies²⁸:
• against all epidermal layers: assoc. w/ nonbullous dermatoses; often in patients w/ neoplasms.
• against upper & middle layers: assoc. w/ bullous dermatoses; often in patients w/ neoplasms.
• against basal-only layer: assoc. w/ medications, pemphigus, pemphigoid.

---

Disease Entities:

• Subcorneal pustular dermatosis (SPD):
  1. strictly subcorneal separation with accumulation of polys
  2. DIF may show IgA intercellular and subcorneal linear deposition⁴ [see IAVPD]
  3. does not have immunoreactant deposits¹⁴

• Pemphigus foliaceous (p. f.):
  1. subcorneal/intraepidermal acantholytic blister (only clue may be absence of cornified...maybe even granular...layer in the biopsy²²)
  2. fluorescent (DIF) positive, pericellular, intragranular IgG
  3. can be pustular and DIF IgA neg.  
  4. serology: patient may carry antibodies (anti-desmoglein 1) to "p. f. antigen"...desmoglein 1^17,18

• Graft vs host disease (GVH)²⁵: (we like biopsy samples for H&E and DIF studies.
1. Acute GVHD²:
   • typical reaction is sparsely cellular interface dermatitis (and some cases subepidermal bullae) and satellite-cell necrosis².
   • epidermal and adnexal duct focal cell necrosis².
   • usually associated with chemotherapy which often induces an epidermal maturation disarray.
   • interface lymphocytic exocytosis, maybe.
   • apoptotic keratocytes may be DIF positive & could have some BMZ DIF positivity.
   • clinically as generalized macular erythematous eruption of trunk, extremities, palms & soles; may hit GI tract & liver².
2. Subacute GVH: some of acute findings and many melanophages & maybe begin hint of LP-like but not yet the more impressive LP-like or scleroderma-like features [L07-1538].
3. Chronic or late GVH: chronic lesions lichenoid like LP (interface lichenoid and hyperkeratosis & hypergranulosis) & late lseions add on scleroderma-like fibrosis.
• Undeclared lupus-suspicious, can't r/o lupus:
  1. interface dermatitis, NOS.
  2. "interface dermatitis with ANA positivity without serological specificity" [S-05-8362].
• SLE (bullous or not):
  1. more dense interface & periadnexal infiltrate.
  2. superficial & deep perivascular dermatitis.
  3. positive ANA serology, especially if anti-DNA is also positive.
  4. granular (can be homogeneous or linear) IgG, IgM and C3 DIF deposits beneath the BM are most common pattern in lesions (also can be in lesions of MCTD, GVH, EED, FDE, vasculitis and other rheumatic); nonlesional skin having positivity (DLE does not) is the "lupus band test" (many other rheumatic-type diseases have a pos. band test)⁹.
  5. bullous SLE can have a leukocytoclastic component, too².
• DLE:
  1. follicular plugging, epidermal atrophy, chronic folliculitis.
  2. ANA serology usually negative.
• SCLE:
  1. first known as ANA-negative lupus
  2. widespread, usually photosensitive annular-polycyclic, sometimes papulosquamous (keratotic) skin lesions
  3. don't get CNS or renal components
  4. >60% have modern (HEp-2) pos. ANAs
  5. most with photosens. component are SS-A (anti-Ro) positive
  6. DIF: only 50% of lesional and 30% nonlesional skin
  7. anti-ds-dna present in low titer in 30%

• Mixed connective tissue disease (MCTD):
• Rheumatoid arthritis:
• Sweet's syndrome: a reactive phenomenon and should be considered to be a cutaneous marker for significant underlying (50% of cases) systemic disease¹²
• PL et VA:
  1. acute lymphocytic vasculitis²
• Fixed drug eruption (FDE):
  1. usually only one (or a few) patches or plaques as lesions, coming back again and again (fixed) at same location
  2. papillary dermal melanophages
  3. vacuolar basal cell interface change and can cleave at this zone
  4. DIF negative
  5. may see full-thickness epidermal necrosis
• Bullous drug eruption³:
  1. cell-poor dermal infiltrate
• EBA (epidermolysis bullosa acquisita) (a type of pemphigoid?):
  1. cell-poor subepidermal blister; almost no dermal infiltrate³
  2. linear IgG (and C3⁶) in BM (on dermal side of NaCl-split [toad¹⁸] skin prep¹⁰) beneath BM/lamina densa⁶
  3. serum IFA: anti-BMZ "EBA antigen" antibodies¹⁶ (anti-collagen IV)¹⁸

• Porphyria:
  1. cell-poor subepidermal blister and essentially no dermal infiltrate
  2. stiffened dermal papillae protrude upward; may reflect HCV.
• Leukocytoclastic vasculitis (LCV) (papular petechial/purpura...old terminology, allergic cutaneous vasculitis³):
  1. most commonly presents as "palpable purpura"...purpuric papules
  2. (1)polys in vessel wall, with poly "clasis" (nuclear dust); (2)perivascular polys
  3. (3)fibrinous degeneration and/or fibrin in vessel walls...must have all 3 & can be very focal and very subtle² (may need lots of step-cuts)
  4. usually superficial plexus @ junct. pap. and retic. dermis
  5. in drug induced LCV [LMC-02-2703], any lumenal fibrin is slight and not much RBC extrav.²
  6. late stages can produce ischemic epidermal necrosis and subepidermal bullae
  7. a few days to a week after petechial showers, the pigmented skin may only show some residual polys, the RBCs, and some early hemosiderin macrophages [LMC-01-8237]
• Septic petechial/purpuric...DIC²:
  1. fairly marked platelet, fibrin ("soft" look whereas "cryo" emboli have a "hard" semi-refractile "look"), and poly thrombi in small superficial capillaries and venules as dominant (DIC) component
  2. polys dermal & perivascular infiltrate
  3. can fairly frequently have a leukocytoclastic component
  4. usually lots of RBC extravasation
  5. usually involves superficial & deep plexus
  6. common acute agents:
     • meningococci: (usually from primary nasopharyngeal infection) may lead to some intraepidermal & subepidermal pustules; lung and kidney hemorrhages; Waterhouse-Freidrichsen syndrome (adrenal hemorrhage); may have some IgG, IgM, or IgA in vessel walls²
     • Staph. aureus (as with SBE) sepsis
     • group A streptococcal sepsis
     • Pseudomonas (as assoc. with ecthyma gangrenosa...looks like skin cigarette burns)
     • toxic shock syndrome has superficial perivascular and interstitial polys and minor component of  eos., sometimes poly  spongiosis; and may have scattered and clumped necrotic  keratinocytes, even to a full-thickness TEN-like picture²
     • Vibrio vulnificus
     • rickettsiae
  7. chronic agents:
     • Lucios erythema necroticans of lepromatous leprosy
     • papulonecrotic tuberculid
     • Lues maligna

• Cryoembolism (cryoprotein, cryoglobulin) lesions:
  1. intravascular fibrin-like plugs or casts which are very eosinophilic by H&E and have a hard "look", almost semi-refractile¹⁹. May reflect HCV infection.
  2. lymphocytes & histiocytes associated
• Rocky Mountain spotted fever (RMSF) (and other rickettsiae):
  1. lymphocytic vasculitis
  2. very acute may show septic-type superficial & deep thrombosis, even with vascular wall necrosis and hemorrhage, BUT, mostly lymphs & histiocytes²
  3. sometimes see intimal/medial intracytoplasmic coccobacillary bodies³
• Coma-associated eccrine gland necrosis²:
  1. epidermal and adnexal focal cell necrosis of anoxic type, see above.
• Drug hypersensitivity reaction:
  1. eosinophiles may be a tip-off.
• Purpura fulminans (extreme cutaneous DIC manifestations)²:
  1. presents with large, suddenly developing extremity ecchymoses
  2. platelet & fibrin thrombi
  3. no significant inflammatory infiltrate or vasculitis
  4. also affects internal organs
• Coumarin or coumadin necrosis²:
  1. begins 2-10 days after institution of coumarin...lightly hemorrhagic at first (until ischemic effect).
  2. predilection for sites with abundant fat (buttocks, flank, breast).
  3. vessels contain homogeneous eosinophilic material².
  4. no significant inflammatory infiltrate or vasculitis.
  5. internal organs not affected.

• Metastatic calcification calciphylaxis: dermal, subcutaneous, vascular involve. of intima with lumenal thrombosis²; precipitators include immunosuppression, steroid therapy, albumin infusion, excess intake of vit. A or D, a chronic infla. process, and trauma
  1. secondary hyperparathyroidism of chronic renal is particularly prone to vascular
  2. secondary hyperparathyroidism of chronic renal on dialysis prone to dermal [LMC-04-5408]
  3. subcut. fat calcification in milk-alkali syndrome, uremia, renal hyperparathyroidism
  4. met. calcif. plus coumarin necrosis picture suggests an additional abnl. protein C activity
• Cholesterol (atheroembolism) embolism²: embolic usually to subdermal or larger vessels; painful distal ulcers; may see  livedo retcularis; distal digital gangrene...early lesions neg. for vasculitis or even dermatitis & very discordant with clinical
  1. spontaneous
  2. post-trauma (including post invasive vascular studies)
  3. post thrombolytic therapy (like streptokinase)
  4. post aortic/arterial grafting
• Pustular psoriasis:
  1. pustules generalized over entire body
  2. 50% of cases in established psoriatics; 50% are the initial psoriatic presentation
  3. spongiotic pustules (which can get secondarily infected)
  4. secondarily infected pemphigus foliaceous (acantholytic) or eczematous (spongiotic) dermatitis can simulate pustular psoriasis clinically
  5. typically lacks classical skin histopathology of psoriasis
  6. in pregnant women, carried the old term "impetigo herpetiformis"
• Mastocytosis syndrome:
  1. diarrhea & abdominal cramps
  2. pruritis and headaches
  3. tachycardia, hypotension, syncope
  4. more than 5 mast cells around a small superficial skin venule is TMEP or a secondary reflection of some chronic urticating disease such as chronic contact dermatitis
  5. presents with numerous small pigmented skin nodules of trunk

• Leukemia cutis:
  1. biopsied because of petechial hemorrhages, thrombocytopenic (possibly even aleukemic...an initial presentation

References:

1. 2nd Ed. Ackerman; Histologic Diagnosis of Inflammatory Skin Disease, 1997.
2. Oct. 1993 ASCP Workshop, Duncan & Mihm, Dermatopathology and Emergency Medicine.
3. March 1978 IAP Workshop, Atlanta, Mark & Mihm, Skin Biopsy in Emergency Diagnosis.
4. Fitzpatrick [dermatology text] 4th Ed, 2 vols [in LMC library]
5. Lever [skin path. text], 794 pages, 1967.
6. Interpretation of Immunofluorescent Patterns in Skin Diseases [text], 1984, Valenzuela, Bergfeld, & Deodhar
7. Murphy, Dermatopathology [text], 1995.
8. 1st  Ed. Ackerman; Histologic Diagnosis of Inflammatory Skin Disease, 1978.
9. Clinics in Lab. Med., 3/1986, chapter on cutaneous immunofluorescence (p85-102), Gene T. Izuno, MD, Scripps Clinic
10. Electronic Textbook of Dermatology, Blistering Diseases web site
11. A Guide to Dermatohistopathology, Pinkus & Mehregan, 2nd Ed., 1976.
12. Habif, TP, Clinical Dermatology, 3rd Ed., 1996 [LMC library]
13. Weedon D, Skin Pathology [text], 1997 (BWD's office)
14. Maize JC, 11/27/01 personal communication &/or case consults [about case of CAP &/or other cases]
15. e-Medicine web site, dermatology
16. ARUP lab's web site differential diagnosis chart
17. Allen CM, Camisa C, Review: Oral Medicine, Paraneoplastic Pemphigus...a review of the literature, Oral Disease 6:208-214,  2000.
18. Bradwell AR, et. al., Atlas of Autoantibody Patterns on Tissues, 1997.
19. Nash JW, et. al., "The Histo....Sites", AJCP 119(1):114-122, Jan. 2003.
20. Barthelette S, et. al., "Common Dermatological Presentations: The Red Face", Journal of Clinical Outcomes Management 11(1):36-50, 2004.
21. comments in expert-consultant case consultations on our cases (Maize).
22. Ackerman AB, A Philosophy of Practice of Surgical Pathology: Dermatopathology as a Model, Ardor Scribendi, Ltd., 1999, 470 pages.
23. Ackerman AB, his Derm 101 website ( http://www.derm101.com/index.asp ).
24. 3rd Ed. Ackerman; Histologic Diagnosis of Inflammatory Skin Disease, 2005.
25. McKee, Calonje, & Granter, 2 vol. text, Pathology of The Skin...
26. Lever text of skin pathology 4th Ed.
27. Maccarelli FJ, et. al., "koebner's Phenomenon...", Postgraduate Medicine 118(6), December 2005.
28. Valenzuela R, Bergfeld WF, and Deodhar SD, Interpretation of Immunofluorescent Patterns in Skin Disease, ASCP Press, 176 pages, 1984 (Dr. Carter's book).
29. Pinkus & Mehregan textbook of about 1975.
30. Jennette JC, Immunohistology In Diagnostic Pathology, CRC Press, 1989.
31. Van Cott EM & Mandal R, CAPToday Q&A, October 2007.
32. Digby S , et. al., "Nephrogenic systemic fibrosis: a histopathological study of eight cases of a recently described entity ", Histopathology 52(4):531-534, March 2008.