A. incontinentia pigmenti
B. delayed hypersensitivity reaction
C. naevus
D. linear darrier’s disease
Answer:
2q: in congenital dystrophic epidermolysis bullosa the defect is seen in ?
A. laminin 4
B. collagen type 7
C.
D.
answer:
to view all the 200 mcqs of AIIMS november 2008 click here
Clinical signs to elicit characteristics of blisters are a crucial part of the examination of patients with vesiculobullous disorders. It is therefore essential for dermatologists to be familiar with, or rather be expert at eliciting these signs, which include Nikolskiy sign, bulla spread sign, Sheklakov sign/false-Nikolskiy sign, and pseudo-Nikolskiy sign/epidermal peeling sign.
This sign is named after the Russian dermatologist Piotr Vasiliyevich Nikolskiy who described it in 18941. A positive Nikolskiy sign indicates intraepidermal cleavage and differentiates intraepidermal blisters from subepidermal blisters.2 It is pathognomonic of pemphigus and staphylococcal scalded skin syndrome. The sign may also be elicitable in the rare ichthyosis bullosa of Siemens, where it is termed the `mauserung phenomenon'.3
The sign is best elicited by applying lateral pressure with the thumb or fingerpad on skin over a bony prominence. This results in a shearing force that dislodges the upper layers of epidermis from the lower epidermis.4,5 A rubber eraser or any blunt object that grips the skin well may also be used. Nikolskiy sign can also be elicited on the intact oral mucosa with the help of a rubber eraser or a cotton-tipped swab.
Nikolskiy sign may be elicited over the normal looking skin of a pemphigus patient either close to existing lesions (marginal Nikolskiy sign) or over normal looking skin at a distant site (direct Nikolskiy sign).6 A positive direct Nikolskiy sign indicates severe activity of the disease in pemphigus. It is the first sign to disappear as the disease responds to therapy; the marginal Nikolskiy sign may persist for some time.
The Nikolskiy sign is positive in the active or progressive stage of pemphigus. When it becomes negative in a patient receiving immunosuppressive therapy, it indicates the end of acute stage disease. However, its reappearance during the course of treatment signals a flare up. Such a patient would require an increase in the dosage of immunosuppressants or the introduction of new drugs.
The term "Nikolskiy phenomenon" is applied when the superficial layer of the epidermis is felt to move over the deeper layer, and instead of immediately forming an erosion as in Nikolskiy's sign, a blister develops after some time. 6
Bullae may also be induced in pemphigus patients by application of suction. Unlike the usual suction-induced subepidermal blisters, these are due to intraepidermal acantholysis. Occasionally, cantharidin has also been used to induce blisters. Such induced blisters may be required for histological diagnosis in pemphigus patients with no blisters and a negative Nikolskiy sign.
The "modified Nikolskiy" sign7 is the peripheral extension of blisters on applying pressure to their surface. This is helpful in patients in whom a new vesicle or bulla is not available for biopsy.8 The advantage here is that the artificially extended blister cannot show epithelial regeneration, which is sometimes seen in the floor of older subepidermal blisters making them appear as intraepidermal.
In the traditional "bulla spread" sign or Lutz sign, the margin of an intact bulla is first marked by a pen. Slow, careful and unidirectional pressure applied by a finger to the bulla causes peripheral extension of the bulla beyond the marked margin. The bulla thus extended has an irregular angulated border in pemphigus vulgaris, while a regular rounded border is observed in bullous pemphigoid or other subepidermal blistering disorders.6
The sign may also be elicited on a burst blister if a substantial portion of the roof is intact. The Asboe-Hansen sign is a variation of the bulla spread sign. It applies to smaller, intact, tense bullae where the pressure is applied to the centre of the blister.9
This sign is positive in all varieties of pemphigus and many cases of subepidermal blisters, including bullous pemphigoid, dermatitis herpetiformis, epidermolysis bullosa acquisita, cicatricial pemphigoid, dystrophic epidermolysis bullosa, Stevens-Johnson syndrome and toxic epidermal necrolysis. Due to fragility of the roof of the blister it is usually negative in Hailey-Hailey disease and staphylococcal scalded skin syndrome.
This sign is positive in subepidermal blistering disorders, like bullous pemphigoid, cicatricial pemphigoid, herpes gestationis, dermatitis herpetiformis, linear IgA bullous dermatotis, epidermolysis bullosa acquisita, junctional and dystrophic epidermolysis bullosa, porphyrias and bullous SLE.
This involves pulling the peripheral remnant of a roof of a ruptured blister, thereby extending the erosion on the surrounding normal appearing skin. It is called the "false Nikolskiy" sign because it is a subepidermal cleavage occurring in the perilesional skin.6 The erosions thus induced are limited in size, do not exhibit tendency to subsequent spontaneous extension and heal rapidly.
This sign is positive in Stevens-Johnson syndrome, toxic epidermal necrolysis and in some cases of burns and bullous ichthyosiform erythroderma. The method and mechanism of elicitation is the same as for Nikolskiy sign. However, it can be elicited only on the involved or erythematous areas. This phenomenon has been described as Nikolskiy sign in most textbooks.10-12 However, the underlying mechanism here is the necrosis of epidermal cells and not acantholysis as in true Nikolskiy sign.
The distal 1–2-mm rim of the nail (which is still in contact with the nail bed) is pink, while the rest of the nail is white. This appears to be a non-specific sign, although in the patient shown it was associated with renal failure.
Terry's nails is a physical finding in which fingernails and/or toenails appear white with a characteristic "ground glass" appearance, with no lunula. The condition is thought to be due to a decrease in vascularity and an increase in connective tissue within the nail bed. It frequently occurs in the setting of hepatic failure, cirrhosis, diabetes mellitus, congestive heart failure, hyperthyroidism, and/or malnutrition. Eighty percent of patients with severe liver disease have Terry's nails.
In patients with Terry's nails, most of the nail plate turns white with the appearance of ground glass, and the lunula is obliterated. The condition may occur on only one finger, but more commonly all fingers are affected. This condition was described originally in relation to severe liver disease, usually cirrhosis, with 80 percent of these patients having Terry's nails. Subsequently, in another study, 25 percent of hospitalized patients with varied diseases were found to have Terry's nails. The condition is thought to be caused by a decrease in vascularity and an increase in connective tissue in the nail bed.
Hepatic failure, cirrhosis, diabetes mellitus, CHF, hyperthyroidism, malnutrition are the causes .
Other conditions where we can see red lunula are :
1. AIDS 2. Rheumatoid arthritis 3. systemic lupus erythematosus 4.alopecia areata 5.cardiac failure 6. chronic systemic diseases
The lunula, or lunulae (pl.) (nail moon), is the crescent-shaped whitish area of the bed of a fingernail or toenail. The lunula is the visible part of the nail matrix (i.e. the root of the nail).
It appears by week 14 of gestation, and has a primary structural role in defining the free edge of the distal nail plate (the part of the nail that actually grows outward).
It is located at the end of the nail that is closest to the skin of the finger but still lies under the nail. It is not actually white but only appears so when seen through the nail.
It is half-moon-shaped, and has unique histologic features.
The lunula is most noticeable on the thumb, and not everyone's lunula is visible.
The lunula and the nail itself are good places to find warning signs of certain diseases such as liver disease, kidney disease, heart problems, and lung diseases.Any colour differences or unusual lines may indicate some type of disease or insufficiency. However, vertical lines on one's fingernails are normal as one ages.
Lunular anomalies include changes in form, structure or colour. Lunular dysmorphologic features (that is, anomalies in form) can be characterized by macrolunula, microlunula or anolunula, and nonconvex lunula. Lunular dyschromias (colour anomalies) can be confluent or spotted or can be characterized by longitudinal coloured bands that traverse the lunula. Alterations in the morphologic features or colour (or both) of the lunula can be an indication of either a cutaneous or a systemic disorder. A deep red lunula and pale nails is associated with congestive heart failure.
Q: gorlin's sign is characteristic of ? 
Brocq used the term pseudopelade to describe a peculiar form of scarring alopecia resembling alopecia areata. (Pelade is the French term for alopecia areata.) This clinical entity is not a specific disease but a pattern of scarring alopecia, and the term pseudopelade of Brocq eventually should be abandoned. An additional source of confusion is the modern use of the term pseudopelade to describe a different form of scarring alopecia (ie, central, centrifugal, scarring alopecia [CCSA]).
Pseudopelade of Brocq is an end stage or clinical variant of various other forms of scarring alopecia and a diagnosis of exclusion. The same pattern of hair loss can be seen in burnt out (ie, no clinical or histologic evidence of inflammation) discoid lupus erythematosus (DLE), lichen planopilaris (LLP), and other forms of scarring alopecia. If a definitive diagnosis of DLE, LPP, or another condition can be made based on clinical, histologic, or immunofluorescent features, then the term pseudopelade of Brocq cannot be used. A primary form of traditional pseudopelade may exist, but this has yet to be established with certainty.
Pseudopelade of Brocq is a very uncommon pattern of alopecia.
Whites usually are affected more often.
Adults usually are affected more often, although the condition has been reported in children.
The typical patient is surprised to discover discrete asymptomatic areas of scalp hair loss . In many patients, the disease is slowly progressive; ie, new areas of alopecia develop over a period of months to years. However, the condition often worsens in spurts, with periods of activity followed by dormant periods. This is distinctly different from the slow but steady disease progression seen in several other forms of scarring alopecia. Disease progression in pseudopelade eventually ends spontaneously.
Lesions of pseudopelade are randomly distributed, irregularly shaped, and often clustered in patches on the scalp. Cases with exclusive crown or vertex involvement actually may represent examples of burnt-out, central, centrifugal, cicatricial (scarring) alopecia (CCCA). The individual lesion is hypopigmented (porcelain white is the classic description) and slightly depressed (atrophic). Lesions often are shaped irregularly, as opposed to the round or oval patches usually seen in alopecia areata and most cases of CCSA.
The classic description of "footprints in the snow" refers to dermal atrophy causing a slight depression below the surrounding normal scalp. In fact, many cases of pseudopelade do not demonstrate atrophy. Usually, only mild erythema and slight perifollicular scaling are present, and, often, no clinical evidence of inflammation is present. In fact, some authors would argue than any inflammation excludes traditional pseudopelade from the clinical differential diagnosis. Typical of many forms of scarring alopecia, a few isolated hairs may remain within an otherwise smooth, shiny, denuded patch. Include the nails and oral mucosa as well as the skin in physical examination to exclude evidence of other forms of scarring alopecia. Pseudopelade of Brocq is a diagnosis of exclusion.
Pseudopelade of Brocq is felt to be the end stage of several different forms of scarring alopecia, especially lichen planopilaris and chronic cutaneous lupus erythematosus. Therefore, the cause of pseudopelade of Brocq is linked to the etiology of the underlying skin disease.
Differentials:
Aplasia Cutis Congenita
Lupus Erythematosus, Discoid
Central, centrifugal, scarring alopecia
Follicular degeneration syndrome
Lichen planopilaris
Temporal triangular alopecia
·
The histopathologic findings of traditional pseudopelade have yet to be clearly defined. The criteria established by Pinkus, based on his experience and on the writings of several other authors, are not correlated in any way with clinical features. Thus, pseudopelade as described by Pinkus is a histologic and not a clinical entity. In most cases of traditional pseudopelade, the active lesion is elusive, and the typical histologic findings are those of a burnt-out scarring alopecia. The histologic findings of pseudopelade of the crown more recently described apply to CCCA and not pseudopelade of Brocq. A prospective study of pseudopelade of Brocq with sound clinical correlation has yet to be performed. In most cases, if an active lesion is sampled, the histologic findings are those of the primary process, eg, lichen planopilaris.
Treatment:
When lesions of pseudopelade of Brocq are burnt out, treatment is neither necessary nor possible. Unfortunately, the condition can reactivate episodically and unpredictably. If active inflammation is present, consider an alternative diagnosis, and potent topical corticosteroids, such as fluocinonide or clobetasol, can be tried.
Lupus Pernio is one of the few cutaneous manifestations that are characteristic of sarcoidosis. Lesions are chronic, indurated papules or plaques that affect the mid-face, particularly the alar rim of the nose. Even a few small papules in this location may be associated with granulomatous infiltration of the nasal mucosa and upper respiratory tract, resulting in masses, ulcerations, or even life-threatening airway obstruction.
Lupus pernio is a chronic raised indurated (hardened) lesion of the skin, often purplish in color. It resembles frostbite as it is seen on ears, cheeks, lips, nose, hands, fingers, and forehead. It is most often associated with sarcoidosis. Microscopically, it resembles Lupus vulgaris. Biopsy shows granulomatous infiltration.
LEOPARD syndrome is a very rare inherited disorder that is characterised by skin, heart, ear, genital, head and facial abnormalities. The mnemonic LEOPARD describes these characteristic abnormalities associated with the disorder.
The clinical features of LEOPARD syndrome vary considerably between patients, with most only manifesting 3-5 abnormalities. Lentigines are the most common feature of the syndrome and occur in more than 90% of patients. However, they do not have to be present to diagnose LEOPARD syndrome.
The clinical features of lentigines are:
Careful examination of the skin usually shows up other skin abnormalities including:
Non-cutaneous features include:
LEOPARD syndrome is nearly always due to mutations in the PTPN11 gene (protein-tyrosine phosphatase, nonreceptor type 11).
It is inherited in an autosomal dominant manner, which means that if one parent is affected there is a 50% chance that each child will be affected. About 70% of cases are inherited. The remainder are sporadic cases occurring from new mutations.
The signs and symptoms experienced by people with LEOPARD syndrome vary greatly. Some patients may have a partial form of the syndrome and suffer mild symptoms while others with the full syndrome are more severely affected.
A proposed minimum criteria for the diagnosis of LEOPARD syndrome is:
If lentigines are absent, a diagnosis of LEOPARD syndrome may be made if the patient has at least 3 of the categories listed above and has an immediate relative also with the condition.
A team of specialist doctors including a cardiologist, endocrinologist, orthopaedist and dermatologist should manage LEOPARD syndrome.
If necessary, isolated lentigines can be removed through the use of chemical peels, cryotherapy, laser treatments or surgical excision. For some patients, treatment with topical retinoids and hydroquinone cream may be helpful.
21q: epiloia is the synonym for which disease ?
answer : c .
22q: discoloration of hair in persons swimming regularly due to absorption of copper by hair is called ?
answer : b . green hair .
23q: fish odour syndrome refers to ?
answer : a . apocrine secretions .
24q: tiny café-au-lait spots in the axillae in neurofibromatosis patients is called as ?
answer : d . crowe’s sign . remember darrier’s sign is different from darrier’s disease and darrier’s sign is not seen in darrier’s disease.
25q: enamel paint appearance of skin is seen in ?
answer : a . this is also called flaky paint appearance .
q: chinese letter pattern of hyperpigmentation is seen in ?Incontinentia pigmenti is also referred to as ‘Bloch-Sulzberger syndrome’, ‘Bloch-Siemens syndrome’, ‘melanoblastosis cutis linearis’, and ‘pigmented dermatosis-Siemens-Bloch type’.
Incontinentia pigmenti is a rare genetic condition characterised by skin, eye, teeth and central nervous system (CNS) abnormalities. The characteristic skin lesions of incontinentia pigmenti are present at birth or develop in the first few weeks of life in approximately 90% of patients.
Incontinentia pigmenti is a dominant X-linked disease. This means that the abnormal incontinentia pigmenti gene is located on one of the X chromosomes, which determine the sex of a child (XY=male; XX=female). Dominant X-linked disease means that a female with only one copy of the abnormal gene will show the disease, even though they have a normal gene on their other X-chromosome. Males who inherit the abnormal gene do not survive, resulting in miscarriage or stillbirth (X-linked dominant, male lethal syndrome). Rarely incontinentia pigmenti is reported in males with Klinefelter syndrome (XXY syndrome) or as a result of spontaneous mutations.
The incontinentia pigmenti gene is localised on chromosome Xq28. This gene normally codes for the nuclear factor-KB essential modulator protein (the NEMO or NF-kappaB gene).
Progressive skin rashes are the main clinical feature of the disease. There are four recognised clinical stages but their sequence is irregular, their duration variable and they may overlap.
| Stage 1: Vesicular |
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| Stage 2: Verrucous |
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| Stage 3: Hyperpigmented |
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| Stage 4: Atrophic/ hypopigmented |
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Other organs may be affected in various ways in patients with incontinentia pigmenti. These manifestations may not be seen or recognised until infancy or early childhood.
| Teeth |
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| Nails |
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| Hair |
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| Eyes |
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| Central Nervous System |
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There is no specific treatment for incontinentia pigmenti. The main goal is to prevent secondary bacterial infection of skin lesions and to monitor closely the development of related problems. This should include regular dental care and close monitoring by an ophthalmologist for the first few years of life.
Incontinentia Pigmenti (IP) is a genetic disorder that affects the skin, hair, teeth, and nails. It is also known as Bloch Sulzberger syndrome, Bloch Siemens syndrome, melanoblastosis cutis and naevus pigmentosus systematicus.
This disorder was first reported by Bruno Bloch, a German dermatologist in 1926 and Marion Sulzberger, an American dermatologist in 1928.
The skin lesions evolve through characteristic stages:
chinese letter pattern of hyperpigmentation seen in incontinentia pigmentosa Alopecia, hypodontia, abnormal tooth shape, and dystrophic nails are observed. Some patients have retinal vascular abnormalities predisposing to retinal detachment in early childhood. Cognitive delays/mental retardation are occasionally seen.
The diagnosis of IP is established by clinical findings and occasionally by corroborative skin biopsy. Molecular genetic testing of the IKBKG gene (chromosomal locus Xq28) reveals disease-causing mutations in about 80% of probands. Such testing is available clinically. In addition, females with IP have skewed X-chromosome inactivation; testing for this can be used to support the diagnosis.
IP is inherited in an X-linked dominant manner. IP is lethal in most, but not all, males. A female with IP may have inherited the IKBKG mutation from either parent or have a new gene mutation. Parents may either be clinically affected or have germline mosaicism. Affected women have a 50% risk of transmitting the mutant IKBKG allele at conception; however, most affected male conceptuses miscarry. Thus, the expected ratio for liveborn children is 33% unaffected females, 33% affected females, and 33% unaffected males. Genetic counseling, prenatal testing, and preimplantation genetic diagnosis is available.
In females, the cells expressing the mutated IKBKG gene due to lyonization selectively die around the time of birth so the X-inactivation is extremely skewed.
A neurocutaneous syndrome characterized by cutaneous and neurologic manifestations (mental retardation and seizures), and tumors.
· 1. Intracranial Calcifications (60%)
· 2. Others
Q: koenen tumors are seen in greater than 50 % cases of ?
answer : c . tuberous sclerosis .
--- the first question that comes to mind is
Q: what are these koenen tumors?
Answer : these are asymptomatic tumors that occur in adolescence in patients with tuberous sclerosis. They are often multiple and can cause depressions in the nail plate. Surgery is the treatment for bothersome lesions. Acquired digital fibrokeratomas
( subungual or periungual fibromas) are small growths that appear around the nail which are fleshy ,asymptomatic and may have a keratotic distal tip .
Usually appear in adolescence and are located more in toes than fingers .
Q: woodlamp examination will help in the diagnosis of all the diseases except ?
answer : b. rosacea .
--- to answer this question you need to know
Q: what is woodlamp examination ?
Answer : Wood's lamp was invented in 1903 by a
Q: how does the woodlamp help in diagnosing the skin disorders?
Answer : depending on the disease the skin is affected with this woodlamp shows different colours which helps us in diagnosing that particular condition .
Erythrasma ---- gives a ---- coral red colour
Pseudomonas ---- gives a ---- greenish colour
Porphyria cutanea tarda ---- gives a ---- pinkish red colour
Tuberous sclerosis ---- gives a ---- blue white colour and visibility of ash leaf macule ( verification needed )
Tinea capitis ---- gives a ---- light cream colour
Ptyriasis versicolor ---- gives a ---- golden yellow colour
Leprosy ---- gives a ---- blue white colour ( verification needed )
· Golden Yellow (Tinea Versicolor)
· Pale Green (Trichophyton Schoenleini)
· Bright Yellowgreen (Microsporum Audouini or M. Canis)
· Aquagreen To Blue (Pseudomonas Aeruginosa)
· Pink To Pinkorange (Porphyria Cutanea Tarda)
· Ash-Leaf-Shaped Spot (Tuberous Sclerosis)
· Bluewhite (Leprosy)
· Pale White (Hypopigmentation)
· Purplebrown (Hyperpigmentation)
· Bright White, Or Bluewhite (Depigmentation, Vitiligo)
· Bright White (Albinism)
Wood's lamp was invented in 1903 by a Baltimore physicist, Robert W. Wood.[1] It was first used in dermatology practice for the detection of fungal infection of hair by Margarot and Deveze in 1925.[2] Wood's lamps are small, durable, inexpensive, safe and very easy to use. Although mainly used in the diagnosis of some infective and pigmentary dermatoses, they have recently been used as a diagnostic tool for certain skin cancers.
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Wood's lamp emits long-wave UV radiation (UVR), also called black light, generated by a high pressure mercury arc fitted with a compound filter made of barium silicate with 9% nickel oxide, the “Wood's filter.” This filter is opaque to all light rays except a band between 320 and 400 nm with a peak at 365 nm. Fluorescence of tissues occurs when Wood's (UV) light is absorbed and radiation of a longer wavelength, usually visible light, is emitted. The output of Wood's lamp is generally low (<> The fluorescence of normal skin is very faint or absent and is mainly due to constituents of elastin, aromatic amino acids and precursors or products of melanin.[3]
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The use of a Wood's lamp does not require great skill. However, some practical points should be kept in mind to avoid misinterpretation of results.[4],[5],[6]
- The lamp should ideally be allowed to warm up for about 1 minute.
- The examination room should be perfectly dark, preferably a windowless room or a room with black occlusive shades.
- The examiner should get dark adapted in order to see the contrast clearly.
- The light source should be 4 to 5 inches from the lesion.
- Washing the area before subjecting it for Wood's lamp examination should be avoided since it may yield false negative results due to dilution of the pigment.
- Topical medicaments, lint and soap residues should be wiped off from the site to be examined since these may fluoresce under Wood's light. Common sources of error are bluish or purplish fluorescence produced by ointments containing petrolatum, green fluorescence by salicylic acid containing medicaments, and light reflected from examiners white coat producing light blue fluorescence.
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Superficial fungal infections
Tinea capitis
The first use of Wood's lamp was for the detection of tinea capitis based on the fact that some dermatophyte species produce characteristic fluorescence under UV light. The chemical responsible for the fluorescence is pteridine.[7] Wood's lamp is helpful in the diagnosis and treatment of an individual patient as well as for mass screening and control of epidemics in schools.[8] It can also help to assess the length and response to treatment; the end point being emergence of non-fluorescent hair. Dermatophytes that cause fluorescence are generally members of the Microsporum genus. However, the absence of fluorescence does not necessarily rule out tinea capitis as most Trichophyton species, with the exception of T. schoenleinii, are non-fluorescent.[7] The fluorescence pattern of dermatophytes is shown in [Table - 1].
Pityriasis versicolor
Malassezia furfur emits a yellowish-white or copper-orange fluorescence. Wood's lamp can detect sub-clinical infection and the extent of infection. It can also help distinguish Pityrosporum folliculitis from other causes of folliculitis.[9]
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Pseudomonas infections
Pathogenic Pseudomonas species produce a pigment 'pyoverdin' or 'fluorescein' which shows green fluorescence under Wood's light. Fluorescence is detected when the bacterial count exceeds 105/cm2, the number required for infections.[10] Wood's lamp can detect early Pseudomonas infection of burn wounds and widespread cutaneous erosions in pemphigus, toxic epidermal necrolysis and Stevens-Johnson syndrome. The diagnosis of ecthyma gangrenosum can also be made earlier than confirmatory blood culture reports by injecting saline into the wound and examining the solution thus withdrawn under Wood's light.[11]
Erythrasma
Corynebacterium minutissimum shows coral red fluorescence under Wood's light due to water soluble coproporphyrin III produced by the organisms. Hence, washing the area will remove the fluorescence. Subclinical colonization by these organisms can also be detected using Wood's lamp, in the toe webs, scalp or the trunk.[8],[9]
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Coproporphyrin is the major porphyrin produced by P. acnes that imparts orange-red fluorescence to the comedones inhabited by P. acnes. Facial follicular fluorescence correlates well with the P. acnes population.[12]
Coral red fluorescence is frequently seen in normal individuals over facial follicular openings and the papillae of the tongue. Similar fluorescence due to proto- or coproporphyrins may be occasionally seen in squamous cell carcinomas and even non-malignant leg ulcers. Some malignant neoplasms of the gastrointestinal or respiratory tracts may show similar fluorescence.
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Hypopigmentary and depigmentary dermatoses
a) Hypopigmentation in fair skinned persons can be very difficult to discern. In hypopigmented or depigmented lesions there is less or no epidermal melanin. Consequently, there is a window through which the light induced autofluorescence of dermal collagen can be seen. Due to the abrupt cut-off in the visible emission from lesional skin, the margins of hypopigmented or depigmented spots appear sharper under Wood's light. The lesions appear bright blue-white due to autofluorescence.[6]
Wood's lamp is therefore helpful in making a diagnosis of vitiligo[13] and particularly differentiating it from pityriasis alba, leprosy and post-inflammatory hypopigmentation or for identifying evolving lesion in a fair skinned person. It is similarly useful in demonstrating evolving lesions of chemical leukoderma[13], leukoderma associated with melanoma,[14] the ash leaf macules of tuberous sclerosis,[15] and hypomelanosis,[16] especially in the fair skinned. Wood's lamp can also help to differentiate nevus depigmentosus from nevus anemicus; the latter does not
show accentuation with Wood's light. Follicular repigmentation following oral photochemotherapy can also be demonstrated earliest by the use of Wood's light.
Hyperpigmentary dermatoses
Wood's lamp can be used to determine the depth of melanin in the skin. The variations in epidermal pigmentation become more apparent under Wood's light. For dermal pigmentation, this contrast is less pronounced. However, this applies only for the fair skin types and not for type V or VI skin.[17]
Based on Wood's light findings, Sanchez et al[18] classified melasma into four subtypes: epidermal, dermal, mixed and Wood's light inapparent. Wood's light may also serve as a prognostic guide in the treatment of melasma, as the epidermal type of melasma is more likely to respond favorably to depigmenting agents than other types.
Wood's lamp can also be a very useful guide in chemical peeling. Addition of salicylic acid (in a 1:5 ratio) or fluorescein sodium (1:15 ratio) to peeling solutions and observing for green and yellow-orange fluorescence respectively under Wood's light helps to avoid overcoating of the peeling solution and ensures the even treatment of all areas.[19]
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Detection of excess porphyrins in the teeth, urine, stool samples, red blood cells and blister fluid in different forms of porphyrias can easily be done with the help of Wood's lamp. Addition of dilute hydrochloric acid to the sample being examined intensifies the fluorescence by converting porphyrinogens to porphyrins.[20] The types of fluorescence observed in the principal porphyrias are shown in [Table - 2].
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A relatively newer, non-invasive and simple technique is being developed for the diagnosis of premalignant and malignant conditions. It involves the application of 20% ALA ointment to the tumor and leaving it on for 4-6 hours under occlusion, allowing protoporphyrinogen IX to accumulate, after which the area is illuminated with Wood's light. This photodynamic diagnosis has proved very useful in the diagnosis of basal cell epithelioma, squamous cell epithelioma, Bowen's disease, solar keratosis and extramammary Paget's disease.[21]
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The other lesser recognized but useful applications of Wood's lamp include:
- Demonstration of a burrow in scabies by applying a fluorescent substance like tetracycline paste or fluorescein dye.[22]
- Detection of systemically administered drugs such as tetracycline or mepacrine in the skin and nail lunulae.[23],[24] Topical tetracycline hydrochloride demonstrates coral red fluorescence which changes to yellow after a few minutes under Wood's lamp examination.
- Assessing the protective value of sunscreen creams and barrier creams in industry.[25]
- Wood's lamp may be useful for the detection of allergens on the skin in cases of cosmetic allergies. It has been occasionally used for photo-patch testing although it is not an ideal source for this test. Use of fluorescent markers during patch tests or other tests that require identification of the skin site after 24 or 48 hours is aided by a Wood's lamp. Wood's lamp is also reported to be useful in assessing the adequacy of application of protective creams in industry to prevent contact dermatitis.[25],[26]
- Calculation of the circulation time by injecting intravenous flourescein.[22]
- Studying cutaneous penetration and epidermal turnover through fluorescent tags.[22]
- Detection of semen on the skin in cases of sexual abuse.[27]
- Wood's light has a sterilizing effect on Staphylococcus aureus and mycobacteria and may be used to sterilize culture media.[28]
- Wood's lamp has been used occasionally as a powerful suggestive treatment for warts in pediatric patients with some success.[29]
- UV lamp is also widely used by financial institutions to check fake paper currency or verify signatures and in the industry to detect cracks in ceramics or metals.[6]
Wood's lamp is a simple, non-invasive device chiefly used for the diagnosis of infective and pigmentary dermatoses by dermatologists. However, newer uses, like its application in photodynamic diagnosis of skin cancers, are being continually explored.
