{13313} leukocytoclastic vasculitis
{12259} leukocytoclastic vasculitis, palpable purpura

UNDER THE DERMIS

Panniculitis From Chile In Spanish

Fat suffers few diseases. "Panniculitis" is inflammation of the fat under the dermis. These tend to be self-limited and self-healing, but are uncomfortable and unsightly lesions.

Erythema nodosum presents as tender red bumps on the shins. If you biopsy it, you'll see fibrosis of the septa of the fatty panniculus, with a mixed inflammatory infiltration.

The pathophysiology is unknown. Notable causes include any disease the chronic inflammatory cell systems (deep infections, TB, leprosy, rheumatic fever, ulcerative colitis, Crohn's, cancer), or oral contractive pills or sulfa drugs. Most cases follow a strep infection or are "idiopathic". Most cases resolve spontaneously after a few weeks.

{12484} erythema nodosum

* Erythema induratum resembles erythema nodosum, but is less intense, more granulomatous, more vasculitic, and more prone to undergo necrosis and to ulcerate. It is usually idiopathic.

* Weber-Christian disease is a nasty pediatric panniculitis, granuloma annulare features collagen with dead fibroblasts surrounded by a ring ("annulare") of granulomas, and there are a variety of other uncommon inflammatory diseases of subcutaneous fat.

* Chilblains is a poorly-understood process that must involve excessive reactivity of the vessels to cold and/or a cryoglobulin. Feet and ankles exposed to the cold develop painful purple areas (ischemic damage). These resolve spontaneously. Read about it: J. Am. Acad. Derm. 23: 257, 1990; Med. J. Aust. 154: 406, 1991.



Pyoderma gangrenosum is full-thickness necrosis of a patch of skin. The cause and pathophysiology remain elusive. Look for it in ulcerative colitis, diabetes, or by itself.

* Infliximab for pyoderma gangrenosum: Am. J. Gastro. 98: 1821, 2003.

PSORIASIS (Madison Avenue's "heartbreak", etc.; Lancet 361: 1197, 2003; Lancet 370: 263, 2007)

A common, usually banal, exacerbating-and-remitting, mysterious (polygenic and immune) illness generally arising in young adult life, affecting maybe one person in 50.

Nobody knows the cause (* ask whether the patient is taking lithium or quinidine), but one distinctive feature is rapid cell turnover in the epidermis. An epidermal cell ordinarily lives about a month before it's shed; in psoriasis, its life is shortened to three days or so.

The pathogenesis remains obscure. There is no animal model (J. Clin. Inv. 116: 2084, 2006). T-cells in the upper dermis produce cytokines that cause the excessive proliferation of epithelial cells. Clones of activated T-cells from psoriatic lesions induce CDw60 on the keratinocytes; stay tuned: Am. J. Path. 150: 675, 1997.

* Beyond this, you'll go crazy if you try to keep track of the various intercellular adhesion molecules, iommune disturbances, and so forth, in various stages of psoriasis (Arch. Path. Lab. Med. 127: 178, 2003; J. Clin. Inv. 113: 1664, 2004, others) others). Efalizumab for psoriasis: Arch. Derm. 141: 31, 2005. Infliximab for psoriasis: Arch. Derm. 138: 644, 2002; Lancet 366: 1367, 2005. Etanercept is now the most popular with physicians and patients: Arch. Derm. 143: 846, 2007; triumph NEJM 358: 241, 2008). However, in some people treated for other causes, we are now seeing spectacularly severe cases of psoriasis following initiation of anti-tumor necrosis factor therapies (Arth. Rheum. 52: 2513, 2005.)

Most people are familiar with the sharply-demarcated salmon-pink, silver-scaled psoriasis plaques. Look especially on the elbows.

If you pick off the scales, you'll see multiple punctate bleeding points ("Auspitz's sign"). These are, of course, the tips of the dermal papillae.

The histology is distinctive. Look for:

• acanthosis, with elongation of the rete pegs, which tend to be club-shaped;


• extra capillaries in the dermal papillae


• thinning of the stratum granulosum (i.e., little or no granular layer)


• lots of parakeratotic scales on the top of the lesion


• maybe you will also see Kogoj "spongiform pustules"

(clusters of neutrophils in the lower epidermis) and/or "Munro's microabscesses" (clusters of four or more neutrophils in the scale itself)

There are a variety of other common findings in, and variations on, psoriasis.

Nail changes range from pitting and/or discoloration to crumbling.

Koebner's phenomenon is common in psoriasis, with lesions popping up wherever the skin is scratched or otherwise damaged. (* Idea: Activation of genes, production of cytokines that keep one another going, and all that. Note that both psoriasis and morphea are exaggerations of processes that normally occur in healing.)

Psoriatic arthritis is usually mild, but can produce serious deformity. HLA-B27 positive patients are prone to get ankylosing spondylitis, etc., etc.

Total-body confluent plaques of psoriasis is one cause of erythroderma (the other common identifiable cause is Szary's / mycosis fungoides). People consider and even commit suicide over this sort of thing (Br. J. Derm. 139: 846, 1998).

Scaly patches on the scalp can be psoriasis, seborrhea, or something in-between ("seborrhiasis").

* AIDS patients are prone to vicious psoriasis. Like almost everything else about psoriasis, this is mysterious.

{12264} psoriasis
{12574} psoriasis
{12576} psoriasis
{12579} psoriasis
{12580} psoriasis
{12582} psoriasis
{12585} psoriasis
{19367} psoriasis
{19370} psoriasis
{19385} psoriasis
{24875} psoriasis
{12475} psoriasis, Koebner phenomenon
{12513} exfoliative erythroderma, maybe psoriasis, maybe mycosis fungoides, maybe who-knows?

Psoriasis From Chile In Spanish

* Everybody knows about the various older remedies for psoriasis. In the 1990's, the big news was the vitamin D analogue calcipotriene (Mayo Clin. Proc. 68: 835, 1993). The latest exciting news is a monoclonal antibody against IL-12 and IL-23, given as a single dose (NEJM 356: 580, 2007)... is it going to prove to be safe?

LICHEN PLANUS (Am. Fam. Phys. 61: 3319, 2000)

Another mysterious illness. This time, the immune system seems to attack the basal layer.

Usually it is "idiopathic", but certain medications can trigger it, and it is especially common in patients with hepatitis C virus on board.

In contrast to psoriasis, the cell turnover rate is slower than normal.

Physical diagnosticians describe "patches of purple, pruritic, polygonal papules". Good places to look are the glans penis, the flexor surfaces of the wrist and the inner surface of the mouth. In the last location, it will present as a distinctive white filigree of lines.

Microscopically, you'll see hyperkeratosis (probably not parakeratosis), a thick granular layer, a band-like infiltrate of lymphocytes in the upper dermis (hence the purple), conspicuously attacking the basal cells, which usually show hydropic change ("vacuolized"). This also transforms the rete pegs to a sawtooth pattern.

Apoptotic basal cells (* "Civatte bodies" / * "colloid bodies") tend to drop into the dermis.

{12280} lichen planus
{12476} lichen planus
{12591} lichen planus
{12592} lichen planus
{12597} lichen planus
{12600} lichen planus
{12601} lichen planus
{12591} lichen planus
{12604} lichen planus, filigree lesions in mouth

Lichen Planus From Chile In Spanish

LICHEN SCLEROSUS ET ATROPHICUS

A mild, chronic, idiopathic lesion featuring a sharply-circumscribed, hypopigmented plaque on the bottom, typically extending around the genitals (especially on a man's glans) and anus and perhaps up the intergluteal cleft.

Under the microscope, you'll see edema and loss of structure of the normal collagen fibers in the upper dermis.

The lesion can appear at any age. As you would expect, it gets misdiagnosed as "proof of sexual abuse" in children (Am. J. Dis. Child. 145: 1058, 1991).

Management is difficult. Most recently, topical glucocorticoids are reported to work better than topical sex steroids.

{12188} lichen sclerosus et atrophicus
{24988} lichen sclerosus et atrophicus

* There once was a man from Antarctica
Who had balanitis xerotica;
  His wife had kraurosis
  And lichen sclerosus
So neither of them got any erotica!

-- Author fortunately unknown! You'll hear this limerick frequently in the clinic.

* Lichen nitidus features innumerable tiny, same-size flesh-colored papules on the genitals; they'll also appear anywhere that you scratch ("Koebner phenomenon"). The etiology is unknown; I've seen it a couple of times.

DISCOID LUPUS: Very common

You remember that patients with systemic lupus may get a butterfly rash and/or a discoid rash. Or someone may have the discoid rash, and not have systemic lupus. (The situations are about equally common.)

The discoid rash consists of sharply-circumscribed, scaly (hyperkeratotic), shiny (thin epidermis), depigmented (maybe hyperpigmented at the edges), at least semi-bald, red patches that are exacerbated by sunlight.

Histologically, discoid rash is distinctive. You will see:

• a band-like infiltrate of lymphocytes in the upper dermis, especially around adnexal structures;
• hyperkeratosis, especially where the infiltrate is most dense, and especially in hair follicle remnants ("keratin plugs");
• hydropic change ("vacuolization") of the basal layer, especially where the infiltrate is most dense;

The old story is that if you stain for IgG or complement, you'll see granules along the dermal-epidermal junction ("a positive lupus band test"). If the patient has only cutaneous lupus, you'll see this only on sun-exposed skin; if you see this on all skin, it's systemic lupus. It is probably not true: Clin. Exp. Rheum. 17: 427, 1999.

{12273} discoid lupus
{25674} discoid lupus
{25676} discoid lupus
{12324} alopecia secondary to discoid lupus

ACNE VULGARIS

If you never had acne, you probably weren't a teen. Many men keep some until old age. Terms:

Comedone: A solid mass of sebum and keratin from a problem follicle

Open comedone: The familiar blackhead. The black on the surface is oxidized lipid from exposure to the atmosphere.

Closed comedone: The familiar plug buried under the epidermis, out-of-contact with air. Squeeze it before the follicle ruptures, and you'll get the familiar "filament". When the follicle ruptures, inflammation is likely, producing the familiar ripe whitehead; you'll find the plug when you squeeze the pus.

Propionibacterium acnes: A diphtheroid bacillus that enjoys cleaving the triglycerides in sebum into irritating fatty acids.

When you hit puberty, your sebaceous glands undergo hyperplasia in response to androgens, and the dead keratin layer on your epidermis thickens in response to androgens. Young men get both effects more than do young women. Keratin plugs follicles, more keratin accumulates in plugged follicles. Eventually the bacterium becomes involved, and the fatty acids produced by its metabolism generate much of the inflammatory response. The neutrophils enter; in severe cases ("conglobate acne", etc.) they leave the familiar craters (formerly much more common).

Ways to make acne flare include taking extra androgens (i.e., at the gym), taking glucocorticoids, iodine (for your sporotrichosis, perhaps), or bromide (ancient sedative), or getting in agent orange ("chloracne", more and bigger blackheads than you thought possible). Acne mechanica mostly results from sports (less often, physical work) where the clothes rub and the follicles end up occluded. "Controlled studies showing no link between eating chocolate and getting acne" (two from the late sixties, uh, sure) surprised this former teen. Acne isn't the result of not washing.

As long as there's an adult level of androgen on board, acne-types can't expect a cure. Temporary relief comes from killing off the propionibacterium (tetracycline or various other antibiotics work wonders), making the sebaceous glands go away (various vitamin A compounds, systemic or topical), and removing the dead keratin layer from the skin (ineffective enough to be available over-the-counter).

 A quacky laser-therapy for acne fails utterly: JAMA 292: 2834, 2004.

Comedone nevus Prize photograph Institute of Medical Illustrators

{09722} acne
{09725} acne
{12144} acne
{12145} acne
{24919} acne, face; your lecturer age 13
{24981} acne, blackhead city
{12495} acne, closed and open comedones
{12148} acne, open comedone, world's largest blackhead
{12221} acne, open comedone, world's second largest blackhead
{25672} histology of the comedone!
{25673} histology of the comedone!

* Acne fulminans: type III immune injury involving propionobacteria. Nasty. See Br. Med. J. 308: 833, 1994.





Acne rosacea is a poorly-understood acne variant over the malar areas that simulates the butterfly of lupus and dermatomyositis. Topical metronidazole helps for rosacea.

{12149} acne rosacea
{09728} acne rosacea

Rhinophyma ("W.C. Fields' nose", Shakespeare's Bardolph), supposedly a variant of acne rosacea, involves hyperplasia of sebaceous glands, notably on the nose. There can be a conjunctivitis too. Again, the process is mysterious.

PEMPHIGUS VULGARIS (Lancet 354: 667, 1999) and the other blistering disorders

Pemphigus vulgaris is autoimmune destruction of the desmosomes of stratified squamous epithelium. A serious, potentially-lethal blistering disease. We don't know all the steps, but eventually the epidermal cells cease to stick to one another.

The autoantigen is desmoglein 3, a cadherin ("calcium-dependent adhesion molecule"), and the epitope has been found at the sticky spot (J. Clin. Invest. 102: 775, 1998).

Patients are tormented by blistering on the skin and mucosal surfaces. Nikolsky's sign is the appearance of a blister on minor rubbing of the skin. Eventually much of the skin may become lost and/or infected, and death can result.

Histologically, you'll see impressive acantholysis, worst immediately above the basal layer. The top of the blister is where the dead cells are stuck together. Look for the familiar "tombstones", basal cells remaining attached to the basement membrane as all other epidermal cells separate from one another; i.e., the blister is caused by "suprabasal acantholysis".

Immunofluorescence stain, of course, shows IgG between the cells of the epidermis, though not along the basement membrane.

{12123} pemphigus vulgaris
{12124} pemphigus vulgaris
{12651} pemphigus vulgaris
{12657} pemphigus vulgaris
{12658} pemphigus vulgaris

Pemphigus Immunofluorescence "chicken wire" KU Collection

Pemphigus
Great photos
Bill Weems MD / "Dermpath India"

* Pemphigus foliaceous, has a different plakoglobin antigen (desmoglein 1). In the US, it is mostly a sporadic disease of older folks, and may transition to and from pemphigus vulgaris. The granular layer, rather than the spiny layer, takes the worst damage.

"Endemic pemphigus foliaceous" or "fogo selvagem", a endemic disease of young people in rural Latin America, is probably a different disease, though the antibody is the same. Big review: NEJM 343: 23, 2000; update on the molecular biology J. Clin. Inv. 115: 3157, 2005. A variant with antibodies against both desmogleins: Arch. Derm. 143: 895, 2007.

Paraneoplastic pemphigus involves yet a different autoantibody (anti-desmoplakin). triggered by "tumor immunity" (small comfort). Review of autoimmunity against desmosomes and hemidesmosomes: Clin. Exp. Immunol. 107 S-1: 9, 1997. It can also involve the lungs, with lethal effect: Arch. Derm. 137: 193, 2001.

* Hailey-Hailey benign familial pemphigus is an autosomal dominant disease. It is a groin-and-armpit problem. The histopathology is a "dilapidated brick wall". The gene is ATC2C1, an epidermis calcium pump: Nat. Genet. 24: 61, 2000.

* Rituximab for both pemphigus vulgaris and pemphigus foliaceous: Arch. Derm. 143: 1033, 2007.

(BULLOUS) PEMPHIGOID

Another autoimmune, blistering disease, milder than pemphigus, with negative Nikolsky's sign. It may be localized or generalized. In bullous pemphigoid, the attachment of basal cells to the basement membrane is selectively damaged. As you would expect, blisters are "subepidermal" and "non-acantholytic". Immunofluorescence shows a linear (not granular, as in lupus) deposit of immunoglobulin and complement along the basement membrane.

The autoantigen is hemidesmosome collagen (J. Clin. Invest. 87: 734, 1991; J. Imm. 145: 3728, 1990).

* The good news is that the disease responds to nicotinamide plus tetracycline, an innocuous regimen (Arch. Derm. 130: 753, 1994).

* Cicatricial (benign mucosal) pemphigoid involves either of at least two different antigens, and affects mucosal surfaces, most troublesome being eyes and larynx.

* Oral pemphigoid has a different autoantibody set (J. Imm. 176: 1968, 2006).

* Pemphigois gestationis (formerly "herpes gestationis") is a similar, very itchy, thankfully rare disease seen in pregnancy. The placenta triggers production of an antibody that cross-reacts with the basal layer. Of course it has nothing to do with herpes virus. Baby can be affected. Update Arch. Derm. 143: 1168, 2007.

{12125} pemphigoid
{12633} pemphigoid
{12634} pemphigoid
{12636} pemphigoid
{12637} pemphigoid
{12640} pemphigoid
{12643} pemphigoid, histology
{12644} pemphigoid, immunofluorescence (yellow)
{12694} cicatricial pemphigoid

* Misdiagnosis of bullous pemphigoid as "sexual abuse of a little girl": Arch. Derm. 128: 804, 1992. COMMENT: It's terrible to miss true sexual abuse, and it's also terrible when a physician's or nurse's arrogant ignorance traumatizes a family emotionally and economically. For much, much more on this, see Md. Ec. March 8, 1993, p. 79 (chickenpox called cigaret burns, normal anatomic variants illustrated in a child-abuse manual as "proof of sexual abuse", etc., etc.); also Pediatrics 91: 423, 1993. All-too-much of my own pro-bono work results from this kind of stupidity.

Pompholyx ("dyshydrotic eczema") is a common, banal, but annoying disease in which little blisters cover the palms and soles. A minor mystery of medicine, there's a link to nickel allergy (J. Derm. 19: 964, 1994; Cutis 47: 157, 1991), or other metal allergy, in people with sweaty palms.

DERMATITIS HERPETIFORMIS

An autoimmune disease that still presents intriguing riddles. The essential problem seems to be autoantibodies against reticulin (!), which anchors the basement membrane to the dermis proper.

In the clinic, you may order antibodies against endomysium and/or tissue transglutaminase, as for sprue.
We await confirmation of a claim that the sprue patients who get DH are the ones whose antibodies react against the form of transglutaminase found in the skin (J. Exp. Med. 195: 747, 2002), but it makes sense.

Patients come in with symmetric (right-left) patches of little vesicle clusters ("as in real herpes") and/or hives that itch bad. Look especially on elbows, knees, and buttocks.

If you don't recognize the lesion on clinical grounds and decide to biopsy it, you'll see (on H&E) masses of fibrin and groups of polys in the tips of the dermal papillae, and (on immunofluorescence) clumps of IgA at the tips of the dermal papillae. Blistering (if present) occurs underneath the epidermis and its basement membrane.

Almost all of these patients have at least subclinical gluten (gliadin) enteropathy, and if you want the dermatitis herpetiformis to go away, you need to prescribe a gluten-free diet.

* Dapsone, the historic treatment for the skin lesions, does not help the associated intestinal lesions.

* Jean-Paul Marat, amateur scientist and quack doctor turned far-left-wing ideologue, was the French Revolution's first mass-murderer. His skin disease was intensely pruritic, blistering, began in the perianal region, and was associated with weight loss leading to emaciation. He was sick with it for the three years prior to his assassination, and spent most of this time in his bathtub. My choice is dermatitis herpetiformis. Another pathologist agrees: Am. J. Dermpath. 1: 251, 1979. And now you sit in your bathtub, testing the validity of the proposition, "The more you scratch, the more you itch." -- Marat-Sade

{12122} dermatitis herpetiformis
{12663} dermatitis herpetiformis
{12524} dermatitis herpetiformis, eczematized
{12672} dermatitis herpetiformis, immunofluorescence for IgA

* Linear IgA dermatosis features a clinical picture similar to dermatitis herpatiformis and/or bullous pemphigoid, but no link to gluten cnteropathy; sometimes it's a medication side-effect (Medicine 78: 1, 1999). The IgA is deposited along the basement membrane rather than in the dermal papillae.

EPIDERMOLYSIS BULLOSA

Another subepidermal blistering disease, this one caused by autoantibodies against type VII collagen of the basement membrane (Arch. Derm. 128: 58, 1992), and/or inheritance of a defective form of type VII collagen, or a defective basal epidermal keratin (Proc* (Nat. Acad. Derm. 90: 7414, 1993) or integrin (Nat. Genet. 13: 366 & 370, 1996; Am. J. Path. 152: 935, 1998), or overproduction of collagenase, or any of several other defects. There are several variants.

The worst hereditary form makes it impossible to safely handle the child without causing it severe pain.

This disease is a frequent focus for "everybody can have a good quality of life" ethics discussions: J. Med. Ethics 24: 200, 1998.

* Update on the molecular biology of the subepidermal blistering diseases, both autoimmune and hereditary: Virchows Arch. 443: 184, 2003.

Epidermolysis Bullosa

WARTS ("verrucae")

Contagious, auto-inoculable, and sometimes serious. A few terms:

Flat wart ("plana"): Most anyplace. Prone to regress spontaneously; some people claim "suggestion" sometimes works.

Plantar wart: On the sole of the foot, and ground in deep

Condyloma acuminatum ("venereal wart"): At best, a cosmetic problem. At worst, a breeding-ground for cancer.

Bowenoid papulosis: carcinoma in-situ with a tendency to spontaneously regress, caused by HPV 16.

The gross appearance of the wart requires no description. You can appreciate the papillomatosis, especially if you peel off the surface keratin.

You remember that a DNA virus family (HPV) is responsible; common warts are HPV-2. Condyloma acuminatum is often HPV-6. The immunosuppressed may be covered with many, many warts.

Histologically, look for acanthosis, papillomatosis, and hyperkeratosis. Vacuolization (koilocytosis) of some cells produces perinuclear halos. Electron microscopy shows human papillomavirus in the nucleus.

{08203} warts
{12138} wart
{24894} wart
{08983} wart, histology
{08986} wart, histology
{12164} condyloma acuminata

HPV-3 Verruca plana Yutaka Tsutsumi MD

HPV-1 myrmecia Advanced students Yutaka Tsutsumi MD

HPV-60 Plantar wart Yutaka Tsutsumi MD

Any man who knows his trade, does not fear ghosts, has read fifty good books, and practices the common decencies stands out as brilliantly as a wart on a bald head.

-- H.L. Mencken, 1922

MOLLUSCUM CONTAGIOSUM ("dimple warts")

A minor, self-curing, annoying disease caused by a pox-virus spread by touching.

Grossly, you'll see itchy little papules up to 4 mm (bigger in those who are perhaps extra vulnerable). The nodule has a central dimple, and when squeezed or scratched (and the virus knows you will squeeze or scratch it!), a chunk of cheese-like material comes out. This is pox-viruses eager to be spread on your hands to somewhere or someone else.

Microscopically, look for marked acanthosis forming a raised nodule. Infected cells produce an intracytoplasmic molluscum body (pox virus inclusion) as they mature, and as they die, they deposit the virus in the center.

There are a variety of Rx's that seem to work okay. Sodium nitrite with salicylic acid sounds best so far (Br. J. Derm. 141: 1051, 1999).

{08205} molluscum contagiosum
{12174} molluscum contagiosum
{12175} molluscum contagiosum
{24730} molluscum contagiosum
{24731} molluscum contagiosum

Molluscum contagiosum
WebPath Case of the Week

Molluscum Contagiosum
Electron micrographs
VCU Pathology
PITYRIASIS ROSEA (Am. Fam. Phys. 69: 87, 2004)

A relatively common disease, mostly of young adults. The etiology remains obscure; probably it is some virus or other.

The initial lesion is the "herald patch", a pink plaque with its long axis along a dermatome. After a while, this fades, only to be replaced by a widespread eruption of smaller plaques, with their long axes all oriented along the dermatome, too.

Nobody dies of this, but it itches like crazy for a few weeks. A mild sunburn is therapeutic.

* Erythromycin is an empirical remedy (J Am. Acad. Derm 42: 241, 2000); azithromycin fails (Pediatrics 117: 1702, 2006). An attempt to blame Herpes 7 for pityriasis rosea in the late 1990's was a flop.

Pityriasis rosea
Patient photo
Thanks Brian!

{12279} pityriasis rosea
{12487} pityriasis rosea
{12610} pityriasis rosea
{12616} pityriasis rosea

IMPETIGO

Bacterial infection of the epidermis, almost always staphylococci with or without help from β-hemolytic streptococci (the latter can give you glomerulonephritis just like a strep cellulitis can).

Grossly, dermatologists admire the honey-colored crusts (i.e., the usual dried-spongiosis fluid crust seen when epidermis and its basement membrane are damaged, plus honey-color from greenish-yellow dead neutrophils tinged with red cells).

The bacteria produce oozing (and thus access to nutrients) by damaging the desmoglein which holds the cells of the epidermis together.

Eczema and most other diseases involving breaks in the epidermis are prone to impetigenize, i.e., become secondarily infected with bacteria.

Impetigo is somewhat contagious. If you are foolish enough to biopsy impetigo, you'll see neutrophils just under the stratum corneum.

{24970} impetigo
{24971} impetigo
{24972} impetigo
{24973} impetigo
{12128} impetigo, bullous

Staph impetigo Yutaka Tsutsumi MD

Gym types: If you've got ringworm or impetigo, it's basic courtesy to keep it covered with clothing while you are throwing the weights around. Active herpes simplex 1 gets passed from wrestler to wrestler ("herpes gladiatorum") and might survive on mats, gym machines, and so forth, so keep your herpes blisters covered or off the equipment, too. Nobody knows how pityriasis rosea is spread, but it's also worth covering. Molluscum, scabies, and pediculosis are probably also transmissble this way. If you have pseudomas ecthyma, I'm going to assume you are not in the gym. Since the agents of candida, warts, and tinea versicolor are ubiquitous, I would not worry about gym infections. Beyond this, gym transmission of disease seems highly improbable.

* Factitious dermatitis ("dermatitis artefacta") is self-inflicted and usually obvious enough to a skilled physician. English beggars actually had a technology ("cleymes") to cause horrid-appearing sores; they would use a mix of calcium salts, soap, iron rust, and sometimes arsenic under an occlusive dressing.

* "Morgellon's disease", in which patients say they see horrid little worms coming out of their skin lesions, which otherwise look like they result from scratching, remains a mystery (Nat. Med. 12: 982, 2006). Patients bring in pieces of lint, skin, or hair as proof ("matchbox sign"; Mayo Clin. Proc. 79: 1470, 2004); so far, they have never withstood examination by pathologists. A lone report of identification of the structures as nematodes or something similar remains unconfirmed. Delusional parasitosis in an organic psychosis from medication: World J. Gastro. 13: 2379, 2007. The drug pimozide seems to work better than the others; there's talk about a specific dopamine problem (Med. Hypoth. 68: 1351, 2007).

* Pitted keratolysis is a corynebacterial infection of macerated super-thick keratin on the soles of the feet, especially in people who go barefoot or wear wet shoes or have super-tight boots. It looks warty and smells like decomposition.

THE EXFOLIATINS

You've studied them in microbiology. Usually these poisons are produced by staph. Staphylococcal epidermolytic toxin A and B produce staph scalded-skin syndrome (the forme fruste is "bullous impetigo"). It's a pediatric disease, since most adults have antibodies. Review Arch. Dis. Child. 78: 85, 1998.
Clinically, there is spectacular blistering. Under the microscope, expect to see mostly acantholysis, especially in a cleavage plane between the spiny and granular layers, i.e., the toxin attacks filaggrin granules (Arch. Dis. Child. 78: 85, 1998), which is why mucosal surfaces are spared. The principal substrate, however, is probably desmoglein 1, the autoantigen in pemphigus (NEJM 355: 1800, 2006).

* There is a disagreement in the literature as to whether these staph toxins are also superantigens. Yes: J. Imm. 164: 2207, 2000; No: Infect. Immun. 68: 3048, 2000.

Don't confuse this with toxic shock syndrome, which during the acute phase merely looks like a sunburn despite the patient being severely and systemically ill. Late in toxic shock syndrome, there's some epidermal inflammation and necrosis and it often desquamates over the palms and soles.

* SWEET'S SYNDROME

Neutrophils invade and damage the epidermis, without any underlying vasculitis.

This is usually a paraneoplastic syndrome. Nobody understands why it happens.

HIDRADENITIS SUPPURATIVA

A deep, longstanding, troublesome, hard-to-treat inflammation of skin bearing apocrine sweat glands (i.e., armpits, crotch).

The pathology always centers around obstruction of the glands, with cyst-like change of the adnexal structures, inflammation and scarring.

Bacteria are present, at least in most cases. The most common aerobe is staph epidermidis (Br. J. Derm. 140: 90, 1999), but a host of bacteria, especially anaerobes (J. Med. Micro. 48: 103, 1999) have been demonstrated. Often there is a mixed flora. Whether the bacteria are etiologic, help the process keep going, or are simply commensals is still unclear, but once the process is underway, the response to antibiotics is very poor.

Hidradenitis suppurative often ends up requiring surgery, or more recently laser work. The results are not always satisfactory.

* There are anecdotal reports of good responses to infliximab, the immunomodulating antibody that has been so effective in Crohn's disease, which of course is another mysterious inflammatory illness. J. Derm. Treat. 16: 58, 2005.

{12230} hidradenitis suppurativa, vulva

SUPERFICIAL FUNGI ("dermatophytes")

Lots of fungi thrive in the cool, nutrient-rich environment of the epidermis. To find them, take a bit of scale and treat it with KOH, then look under your microscope.

Seborrheic dermatitis (Arch. Derm. 126: 1497, 1990; Am. Fam. Phys. 52: 149, 1995) is a flaky, oily dermatitis that tends to occur in the nasolabial folds, the center of the chest, and the scalp ("dandruff" is part of the seborrheic dermatitis picture).

Long considered "idiopathic" or "caused by excess sebum" (plain wrong: Br. J. Derm 122: 71, 1990), and even "psychogenic", we now know that a principal culprit is Pityrosporum yeast ("P. ovale", "P. orbicularis", "Malassezia furfur"), which thrives on sebum, and that people with seborrhea are those who have difficulty doing cell-mediated immunity against this yeast (J. Am. Acad. Derm. 23: 82, 739, & 1106, 1990).

Antifungals are now the mainstay of therapy. See Lancet 358: 170, 2001.

"Atopic eczema most prominent on the face" is likely to be childhood seborrhea. Babies have more sebum production than adults.

{12499} seborrheic dermatitis
{12565} seborrheic dermatitis
{12571} seborrheic dermatitis

Candida yeast infection takes a variety of forms. Especially when a skinfold in involved, satellite lesions are typical just past the edges of the main rash.

{12348} candida paronychia
{14238} candida, penis
{12507} candida exacerbating intertrigo
{08163} moniliasis of skin ("diaper rash")

Ringworm ("athlete's foot", others, depending on location) is caused by a variety of fungi in the dead layer of the epidermis.

The immune response to the fungus can look like eczema, but of course glucocorticoids can make it worse rather than better.

Fungal infections on hairy areas are especially hard to treat topically, as the preparations don't reach the hair follicles.

The curious "id reaction" is a mysterious vesicular process involving the fingers in patients with superficial fungus infection somewhere else. (Your lecturer had this as a would-be athlete with the appropriate foot infection.)

{14234} tinea capitis ("ringworm of the scalp")
{08148} tinea pedis ("athlete's foot")
{12268} tinea pedis
{14227} tinea pedis
{12270} tinea cruris ("crotch-rot")
{12477} tinea corporis ("ringworm of the body")
{14221} tinea corporis
{14223} tinea corporis, leg
{08149} ringworm, id reaction
{08152} more ringworm
{12625} pityriasis rubra pilaris (mysterious disease that simulates ringworm)

Erythrasma is a curious jock-itch caused by a corynebacterium; it fluoresces red.

Onychomycosis ("onychogryposis")

Crusty, thick nails. You've seen these in the elderly. The result of lowering the temperature and resistance of the nail by poor blood supply. (One example of A. T. Still's thinking being "right on the nail".)

Tinea versicolor ("pityriasis versicolor")



My choice as "the world's mildest disease", this is a common, faint skin eruption of the upper torso and perhaps elsewhere, caused by * Malasezia furfur / * Pityrosporum.

You might never notice it. As the name implies, it "reverses color". Skin with tinea versicolor does not tan. It is darker than untanned skin, lighter than tanned skin. The pattern resembles raindrops ("guttate pattern").

A variant involves the hair follicles, with reddening and sometimes pus formation.

There are a variety of cheap topical fungicides that work remarkably well for temporary control. Or give a single ketoconazole tablet and have the patient work up a sweat one hour later.

{12182} tinea versicolor
{12505} tinea versicolor
{12519} tinea versicolor
{14247} tinea versicolor
{14250} tinea versicolor

Pityrosporum, KOH prep
from a doctor buddy with
folliculitis of his beard area

* Throughout his teens, your instructor had pityrosporum folliculitis everyplace where his hair was starting to thicken. He was tricolored in summer -- red, tan, white (postinflammatory depigmentation) in about an even mix, like a checked tablecloth. Baffled the town's "best dermatologist", and was never appropriately treated, which was unfortunate.

Malassezial folliculitis Yutaka Tsutsumi MD

BUGS

Scabies is an epidemic, transmissible infection by the sarcoptes mite, which likes to tunnel through keratin. Favorite sites are the fingers and penis. It itches like crazy.

{09753} scabies
{43077} scabies
{43079} scabies mite
{24872} scabies

Pediculosis (head, body, and/or pubic crab lice) requires no description. Look for eggs on the hairs.

Mosquito bites you know. Spider bites look like urticaria but hurt and usually occur in pairs; brown recluse spider bites can undergo necrosis.

{12222} bug bites

Yes, there is a little mite named "Demodex" that lives head-down in your follicles. Its ability to harm us remains uncertain. It is one of the "usual suspects" in rosacea and in the itchy-eyelids problems of older folks.

Demodex folliculorum Advanced Yutaka Tsutsumi MD

"Delusional parasitosis" has long been diagnosed in people who insist they have bugs but the doctor cannot see them. I was always suspicious, and now it turns out that 18 of 20 (in one series) have collembola springtails on board (controls were negative). Click here for the article.

Botfly video
Human myiasis from Panama
Educational, some profanity

HAIR LOSS

All normally-masculinized men remodel their temporal hairlines at about age 20, losing it on their temples and accentuating the forward spike at the mid-forehead level. All but the smoothest men have progression sooner or later. Male pattern baldness has required no description since ancient times (* Lev. 13: 40 and the difficult 2 Kings 2: 23-24.)

Generally, the hairier the guy's upper body is during his 20's, the more rapidly he gets male-pattern baldness. The correlation is very close -- just look around you. In my opinion, the stuff about "diet", "how fast your hair grows", "what to put on it", and so forth is just seeing faces in the clouds. Hairy-balding guys are supposedly at increased coronary risk but it's slight (Arch. Int. Med. 160: 165, 2000); this may be because they're insulin resistant (Lancet 356: 1165, 2000; uh, is this a tie-in with Stein Leventhal? -- Ed).

The major gene for hirsutism-and-baldness seems to be the androgen receptor gene itself (J. Inv. Derm. 116: 452, 2001).

It is ironic that hundreds of thousand of U.S. men are paying $1000/year each for topical minoxidil or propecia, while many super-macho bodybuilders and fighter-types shave themselves from crown to toe. But the stuff works: Aus. Fam. Phys. 28: 248, 1999.

If you or someone you love is worried about masculine hair loss, the most effective way to halt the process was cited 2500 years ago by Hippocrates, who observed that eunuchs almost never go bald.

Alopecia areata is localized or generalized loss of hair for no obvious reason. In the most extreme cases, even the eyebrows are lost. Widespread cases are likely to remain permanent. Inconsistent evidence of autoimmunity and anecdotal accounts of the problem beginning after an episode of extreme fright are interesting, but the illness remain mysterious. Every large city has a club for these folks.

{12327} alopecia areata

To be distinguished from alopecia areata is trichotillomania, habitual tugging on hair. Some psychiatrists can treat this; don't expect much success in general medical office practice.

{12328} trichotillomania

FRECKLES ("ephelides", singular is "ephelis")

Increase in pigment production by a local group of melanocytes. A freckle can be up to 1 cm. Freckles typically occur in light-skinned (especially red-headed) kids, especially after sun exposure.

Contrary to "Big Robbins" and most other texts, a freckle (in adult or child) will indeed also contain more melanocytes than surrounding skin. What's more, freckles are likely to show some cytologic atypia and even stain with HMB-45 (the "melanoma antigen", actually a marker for any extra-turned-on melanocytes). See Cancer 67: 1990, 1991. (* I hope this never makes the "Kansas City Star"; there's enough cancer paranoia already.)

Not surprisingly, the melanocortin-1 receptor, which is the major human red-hair locus, is also the major freckle locus (Hum. Mol. Genet. 10: 1702, 2001).

{12191} ephelis

MELASMA ("raccoon eyes", "mask of pregnancy")

Increased pigmentation of the periorbital face. Seen in patients who are pregnant, taking the oral contraceptive pill, taking phenytoin, or "idiopathic".

* If it bothers you, there's a phenol thioester depigmenting agent (Arch. Derm. 127: 1528, 1991). This will work if, and only if, the pigment is primarily in the epidermis rather than in the macrophages.

LENTIGINES (singular is "lentigo")

A local hyperplasia of melanocytes, with hyperpigmentation, and generally some elongation of the rete pegs as well. Unlike freckles, they do not darken in the sunlight.

You start to acquire single lentigines as a kid (your smaller, flatter "moles" are lentigines).

As you grow older, crops of larger lentigines ("senile lentigos", "liver spots"; of course, they have nothing to do with your liver) may erupt, especially on the backs of your hands.

* Nobody's really looked at the genetic changes; since LEOPARD syndrome (a rare acronymic illness) features many lentigos, expect changes at the LEOPARD genes RAF1, PTPN11, k-RAS, and the others on the chain. Nat. Genet. 39: 1007, 2007.

* "Advertising is intended to promote unhappiness." In the 1970's, the "Gray Panthers" (outspoken older folks) made a public laughing-stock out of a skin-bleach commercial designed to cause the elderly to hate their lentigines ("Those horrible spots!....")

* Dermatosis papulosa nigra is the only name I've ever been able to find for the multiple black facial spots seen on many people of African ancestry (Sidney Poitier and Bill Cosby have them), and occasionally on East Asian folks as well. They are a non-problem.

Café au lait spots feature melanocytes with giant melanosomes. Despite their usefulness in confirming your clinical suspicions of neurofibromatosis or McCune-Albright's, several percent of normal people have at least one little one.

{09645} lentigo city! ("old age spots")
{09647} lentigo
{09648} lentigo
{12192} lentigines
{12525} lentigo city

NEVOCELLULAR NEVI ("pigmented nevi", "melanocytic nevi", "moles"; single is "nevus")

Fascinating little lesions, somewhere in the borderland between hamartomas and tumors, in which masses of "nevus cells" (chemically similar to melanocytes, and sometimes making melanin) pop up at the dermal-epidermal junction and/or the upper dermis and/or elsewhere.

Melanocytic nevus: The common, garden-variety mole (i.e., there's more to it than a lentigo.)

Most people start getting theirs as young kids, and have most of them by puberty. Apparently everybody has them; they're airbrushed out of certain photos. As we age, they tend to involute.

Nobody really knows what triggers a mole to form, but Nowell's law seems to be operating. The "West Midlands Mole Study" found more moles in whites than in non-whites, more in boys than girls, more in kids that burn rather than tan, more in frecklers, and an impressive correlation between number of moles and number of holidays in hot climates, independent of sunburn history (Arch. Derm. 128: 1201, 1992). The Vancouver study found pretty much the same thing (Arch. Derm. 126: 466 & 770, 1990). Not surprisingly, phototherapy for neonatal hyperbilirubinemia is a strong risk factor for many nevi appearing later (Arch. Derm. 142: 1599, 2006); wheter it's a melanoma risk is unclear, but