Atlas of dermatology pdf

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Please enter your name here. Trauma has been implicated to play a role chronic RA undergoing treatment with MTX, even despite due to the neoangiogenesis and granulation tissue that it good clinical response to the treatment [45].

Recently, ARN causes. Diagnosis is usually based on clinical findings of has also been reported with the use of other drugs of the symmetric inflammatory polyarthritis, seropositive for RF, TNF-alpha inhibitor profiles such as etanercept Enbrel and and extra-articular manifestations are highly suggestive.

It does not require the presence of previous classic rheumatoid nodules, although histologi- cally, these lesions are the same as the classical rheumatoid nodules [32]. It has been postulated that the progression of ARN is caused by adenosine A1 receptor promotion of multinucle- ated cell formation by human monocytes.

The lesions may resolve once MTX is stopped and recur after rechallenged. The addition to other anti-inflammatory drugs such as hydroxychloroquine, d-penicillamine, colchicines, or sul- fasalazine to MTX may decrease the cases of ARN or improve the already present lesions. These lesions tend to last an average of 3 years [49].

Rheumatoid Nodulosis Rheumatoid nodulosis RN is the condition that describes a specific variant of polyarthritis associated with severe sero- positive RA, radiological subchondral bone cysts, and subcu- taneous rheumatoid nodules. In some instances, skin nodules are the predominant sign with minor or even absent joint symptoms. RN was first described in by Bywaters and later Ginsberg and coworkers received credit for the term RN for an intermittent arthritis associated with multiple rheuma- toid nodules usually involving the hands and feet with intraosseous cystic changes [50, 51].

Couret and coworkers were the first to compile the subsequent diagnostic criteria for RN: 1 multiple subcutaneous rheumatoid nodules confirmed by biopsy, 2 recurrent joint symptoms with minimal clinical or radiological involvement, 3 a benign clinical course, and 4 mild or no systemic manifestations of RA [52].

It is impor- Fig. It is not fre- quently associated with HLA-DRB1 allele as in classical laris, digital infacts and gangrene, atrophie blanche AB , and rheumatoid nodules and despite the almost exact histological nail fold telangiectasias. Despite a low preva- benign and does not lead to the progression of classic erosive lence rate, the systemic form of RV occurs more often than RA with systemic manifestations [49, 53].

RN is usually a Wegener granulomatosis or polyarterits nodosa [20, 56]. In about recorded in the literature [54]. Small vessel Rheumatoid vasculitis is an inflammatory condition of the disease is characterized by periungual infarctions, localized small, medium, and large vessels that affect a sector of petechiae or purpura and splinter hemorrhages. Splinter patients with RA. There are diverse cutaneous vasculitic hemorrhages, also called Bywater lesions, are small, brown, manifestations clinically such as palpable and non-palpable purpuric and painless lesions on the nail fold, nail edge, or purpura, erythematous nodules, ulcerations, livedo reticu- digital bulb [20] Fig.

The association with mononeuritis multi- tissue diseases such as RA, due to inflammation within the plex or bowel involvement has shown a fatal prognosis [62].

AB appears as smooth, scar-like, Due to this high mortality rate, aggressive therapeutic modal- slightly depressed ivory-white patches with telangiectasia ities should be administered without delay. Other nuria, bowel ulcers, alveolitis, hematuria, pleuritis, cerebral treatments options for mild to moderate disease include infarction, and an acute abdomen [55, 59]. The factors associated with RV include high titer of RF, Pyoderma Gangrenosum joint erosions, male gender, and the presence of other extra- Pyoderma Gangrenosum PG has four clinical variants: articular manifestations, particularly rheumatoid nodules 1 ulcerative, 2 bullous, 3 pustular, and 4 vegetative.

RV can be present before or at the time of RA diagno- PG occurs more frequently in patients with RA and is sis, although it is usually seen late in the course of the disease associated with the ulcerative form, most often with a an average of 10—14 years after the onset of arthritis. It is seronegative polyarthritis [65]. It is reported that more than a fourth of PG cases The variety of significant skin manifestations and the lack have an arthritic component, although associated PG of specific signs and symptoms make the diagnosis depen- lesions do not worsen the severity of the arthritis and is dent upon ruling out systemic conditions and on histological considered an independent disease process [68].

It occurs evidence of necrotizing vasculitis [60]. Biopies should be most often in women [66]. The pathogenesis is not well taken from the center of the lesions, except when the lesion understood because PG is also seen in other immunologic is an ulcer, for which the biopsy should be taken from the conditions such as inflammatory bowel disease and hema- border. The clinical diagnosis is established by the presence tologic diseases.

It pro- in skin pathology, and 4 evidence of systemic involvement gresses from a tender, erythematous, or violaceous papule to by RV [61].

The ulcerations can last for Histopathologically there is a spectrum of continuous months to years and leave a resultant scar.

Lesions can be as vascular involvement. RA vasculitis is an immune complex large as 10 cm in diameter [20]. Histopathology mediated vasculitis with high titers of C-reactive proteins changes show a deep neutrophilic infiltrate at the border of and immunofluorescence revealing C3 and IgM deposits in the ulcers with proliferation of vessels but no evidence of small and medium-sized vessel walls.

When the vasculitis leukocytoclastic or non-thrombotic vasculitis [62, 68]. The affects medium-sized vessel walls, it can resemble polyar- differential diagnosis includes other vasculitis, mycobacte- teritis nodosa histologically by the inflammatory necrotizing rial infections, halogenodermas skin eruptions after expo- obliterative arteritis with focal panniculitis [20, 62].

Larger vessel walls [62]. The level of RF is often cyclosporine, azathioprine, and dapsone [65, 69]. Although the etiol- ogy is unknown, the relationship between the granulomatous dermatitis and arthritis is thought to be related to autoimmu- nity; it has been associated with autoimmune thyroiditis, SLE, and lymphoproliferative disorders [72]. The clinical setup of this condition is most often charac- terized by a middle-aged woman with high RF titers and severe RA with fluctuations between remission and flares.

Interstitial granulomatous dermatitis can occur prior, during, Diffuse interstitial and focal palisading infiltrates of lymphocytes, his- tiocytes, eosinophils, and neutrophils and with the degeneration of col- or after the arthritis presents [72]. These patients usually lagen found in the reticular dermis have elevated ESR [73]. Occasionally, the lesions are pap- ules, nodules, or plaques ranging from erythematous to Palisaded Neutrophilic Granulomatous Dermatitis violaceous color in the similar linear distribution [72, 73] Rheumatoid palisaded neutrophilic granulomatous dermati- Fig.

These lesions are usually grouped, non-tender and collagen found in the reticular dermis. The eruptions appear non-pruritic and associated with severe and disabling RA. This entity has been poorly saded granulomas surrounding altered collagen and fibrin defined and been given many different names. Histologically, [62, 71, 72] Fig. The differential diagnosis includes there are extensive neutrophilic infiltrates and occasional other palisading granulomas such as granuloma annulare, scant lymphocytes, eosinophils, and histiocytes without the granulomatous slack skin, necrobiosis lipoidica, Blau syn- evidence of leukocytoclastic vasculitis [77].

The differential drome, and interstitial granulomatous drug reactions [75]. The treatment is dapsone Preliminary criteria for the classifica- or low-dose prednisone if allergic , and the clinical course tion of systemic sclerosis scleroderma. Clements PJ. Systemic sclerosis. A unifying hypothe- Conclusion sis for scleroderma: identifying a target cell for scleroderma.

Curr Rheumatol Rep. Sehgal VN, Srivastava G, et al. Connective tissue diseases present a diagnostic challenge to In J Dermatol. Cutaneous nodules in and the fact that they are diagnosed by fulfillment of specific patients with rheumatoid arthritis: a case report and review of litera- tures. Clin Rheumatol. Therefore, it Rheumatoid arthritis [comment]. Gabriel SE. The epidemiology of rheumatoid arthritis. Rheum Dis we see a patient with a skin rash to direct history and physi- Clin North Am.

The prevalence of rheumatoid arthritis in the United Kingdom: new By instituting early and adequate therapy, the serious com- estimates for a new century. Sayah A, English JC.

Rheumatoid arthritis: A review of the cutane- ous manifestations. J Am Acad Dermatol. Skin manifestations of rheumatoid arthritis: a study of Turkish References patients. Int J Dermatol. Sontheimer RD. Dermatomyositis: an overview of recent progress ogy. Philadelphia: WB Saunders; Dermatol Clin. Red lunulae in a patient with — Cutaneous manifestations of selected rheu- Ziff M. The Rheumatoid nodule. Am Fam Physician. The spectrum of cutaneous lesions in 3.

Cutaneous lupus ery- rheumatoid arthritis. A clinical and pathological study of 43 thematosus: diagnosis and management. Am J Clin Dermatol. J Cutan Pathol. Young A, Koduri G. Extra-articular manifestations and complica- 4. Cutaneous manifestations of lupus erythe- tions of rheumatoid arthritis.

Best Pract Res Clin Rheumatol. Rheum Dis Clin North Am. Systemic lupus erythe- Rheumatoid nodules. Review of matosus in Iran: a study of patients over 33 years.

Int J Rheum the spectrum of associated conditions and proposal of a new clas- Dis. Am J Med. Hypertrophic discoid ;— Dermatol Online J. The revised criteria for the allele and the development of methotrexate-induced accelerated classification of systemic lupus erythematosus.

Photoprotective effects of a Rheumatoid arthritis: clinical picture and broad-spectrum sunscreen in ultraviolet-induced cutaneous lupus its variants. New study. York: Oxford University Press; Inflammatory Rheumatoid nodules on the dis- myopathies: Clinical, diagnostic and therapeutic aspects.

Muscle tal region of the sole. J Dermatol. Ulcerating rheumatoid nodule of the Koler RA, Montemarano A. J Clin Pathol. Vascularity of the early sub- Arch Pathol. Practical rheumatology. London: Mosby; Immunohistochemical Deciphering the clinical presentations, patho- findings in rheumatoid nodules. Virchows Arch A Pathol Anat genesis, and treatment of the idiopathic inflammatory myopathies.

Immunological and Inflammatory myopathies. Curr immunohistochemical analysis of rheumatoid nodules. Ann Rheum Treat Options Neurol.

Olsen NJ. Scleroderma: the need for extreme remedies. Am J Med Macrophage migration and Sci. Epub ahead of print.

Black CM. Scleroderma, clinical aspects. J Intern Med. Cytokine profile of the rheuma- Hassoun PM. Lung involvement in systemic sclerosis. Presse Med. Gall EP. General features. Systemic rheumatoid vasculitis: Rheumatoid arthritis: an illustrated guide to pathology, diagnosis, a review.

Semin Arthritis Rheum. Philadelphia: JB Lippincott; Intravenous cyclophosphamide plus methyl- Cutaneous manifestations of rheumatoid prednisolone in treatment of systemic rheumatoid vasculitis. Am J arthritis. The safety and efficacy of the use of metho- Clinical and trexate in long-term therapy for rheumatoid arthritis. Arthritis histopathological spectrum of cutaneous vasculitis in rheumatoid Rheum. Br J Dermatol. Accelerated nodulosis and vas- Clinical and serological fea- culitis during methotrexate therapy for rheumatoid arthritis.

Ann Rheum Dis. Accelerated nodulosis Extra-articular features of and vasculitis following etanercept therapy for rheumatoid arthritis. Rheumatoid arthritis: frontiers in pathogenesis and treat- Development of rheumatoid ment.

New York: Oxford University Press; Pyoderma gangrenosum: classifica- ercept. Accelerated nodulosis during low dose metho- with follow-up. An analysis of ten cases Pyoderma gangrenosum: a reappraisal of [comment]. J Rheumatol. Garcia-Patos V. Rheumatoid nodule. Semin Cutan Med Surg. Pyoderma gangreno- ;—7. Bywaters EG. A variant of rheumatoid arthritis characterized by reference to polyarthritis. Response of atypical bullous pyoderma bling palindromic rheumatism.

Rheumatoid nodulosis: an steroids. Acta Derm Venereol. Linear subcutaneous bands in 49— Rheumatoid nodulosis: Ann Intern Med. Differential diagnosis in J Rheumatol. Dupond JL, et al. Interstitial comparative study with rheumatoid arthritis with and without granulomatous dermatitis with arthritis. Rheumatol Int. A case of rheumatoid nodulosis Interstitial granulomatous dermatitis with cutaneous cords and Factors associated with the development Dermatol.

Interstitial granulomatous dermatitis with plaques and arthritis. The incidence Clin Rheumatol. Br J The interstitial granuloma- Rheumatol. Griffen JE, et al. Palisaded neutrophilic granulomatous dermatitis Atrophie blanche-like scarring after in rheumatoid arthritis.

Rheumatoid —2. Arch Dermatol. Clinical and histo- Rheumatoid pathological spectrum of cutaneous vasculitis in rheumatoid arthri- neutrophilic dermatitis in a woman with sero-negative rheumatoid tis. Environmental factors may also modify the signs of diseases that primarily affect the pulmonary system susceptibility to sarcoidosis. The pathogenesis of this condi- may assist the clinician in diagnosis and estimation of prog- tion involves a T-helpermediated immune response to nosis.

This chapter describes selected pulmonary diseases environmental antigens in a genetically susceptible host [6]. Often times in medicine, The characteristic histologic feature of the non-infectious, findings on the skin may prove very helpful in exposing an non-caseating granulomas of sarcoidosis are the epithelioid underlying systemic condition. In all fields of other words, there are few to no plasma cells or lymphocytes medicine, especially internal medicine, pneumology, neph- associated with the granuloma [5, 7].

The variable, multi-systemic disease of sarcoidosis was first Cutaneous sarcoidosis can represent a diagnostic challenge described by Jonathan Hutchinson from England in The sarcoidosis [1—3]. The etiology remains temic involvement and the convenience of the skin as a tissue uncertain; however, several genetic polymorphisms are asso- source for histologic analysis [9, 11].

Patients with nonspecific lesions tend the time [7]. In addition, patients with lupus pernio have to have a good prognosis since these are mostly associated increased occurrence of lytic and cystic bone lesions under- with an acute form of sarcoidosis.

The most common nonspe- lying affected skin areas, especially the hands and feet, cific lesion is erythema nodosum. Other forms include nail, chronic uveitis, and fibrotic sarcoid in the kidneys and lacri- mucosal, and childhood sarcoidosis [9].

Papules, nodules, and maculopapular eruptions, as a group, are the most com- The classic specific lesion of sarcoidosis is lupus pernio, first mon cutaneous manifestations of sarcoidosis Fig.

It is characterized by rela- They may be red-brown or yellow-brown with an erythema- tively symmetric, violaceous, shiny, indurated, smooth, and tous base, or violaceous in color and the surface is smooth doughy plaques and papules.

The violaceous color has other areas of the body such as the trunk, extremities, nape of often been described as having a cyanotic hue as that seen in the neck, and upper back [5, 9, 19]. Diascopy, a procedure frostbite.

It occurs more color, which is characteristic of sarcoidal skin [9, 13]. Some plaques may show 12, 15]. This persistent lesion is not painful and does not hyperpigmentation with scales and they commonly form an disturb the epidermis causing ulceration; however, the lesions annular configuration with central clearing Figs.

Even a small amount of little papules on the nose vessels near the surface of the skin, it is called angiolupoid may be associated with granulomatous dissemination into sarcoidosis [7, 19]. Sarcoid plaques are usually distributed the nasal mucosa and upper respiratory tract, resulting in symmetrically and bilaterally [8, 9].

It is important for a phy- ulcerations, masses, or even serious airway obstruction [16]. A rare variant of the sarcoid plaques that Fig. The cyanotic hue is characteristic. The earlobes, nose, and cheeks are affected areas most prone to perniosis.

It can be distinguished from true pso- vary from about 0. They riasis by the fact that they heal with scarring [9, 13]. When the forearms are affected, the Subcutaneous Nodules Darier—Roussy dorsum of the hand and the fingers tend to swell in a fusiform pattern [13, 20—22]. The first documented case of subcutaneous sarcoidosis was These skin lesions are the only subset of sarcoidosis fre- in by Darrier and Roussy [20, 21].

Despite the associated systemic 1. The pathology of subcutaneous nodules are restricted to the Subcutaneous sarcoidosis has a consistent clinicopathologic subcutaneous tissue and does not affect the epidermis.

These presentation and usually appears at the beginning of the disease. The confirmatory diagnosis requires the detection of pannicular fat lobules sarcoid or epitheliod granulomas with minimal lymphocytic inflammation and minimal septal involvement Fig. Scar Sarcoidosis Scar sarcoidosis was first described in by Caesar Boeck. It frequently presents in West Africans [26, 27]. Scar sarcoi- dosis shows characteristic granulomatous invasion of previ- ously traumatized skin or areas with imbedded foreign material, such as tattoos [3, 5, 23].

It often occurs with other cutaneous manifestations; however, it tends to occur near the beginning of the onset of sarcoidosis when the presence of pulmonary involvement may have not yet begun [13, 26]. Red-brown nodules occur Particular attention should be given to sites on the body such predominantly around the nose as areas for venipuncture access, previous Mantoux test sites, Fig. Sarcoid granulomas in the Fig. A patient presenting with wide- inferior dermis and subcutaneous tissue spread red-brown plaques occurring on the bilateral extremities.

The trunk is a common site. Most of these patients have pulmonary involve- ment, lymphadenopathy, and splenomegaly Fig. Granulomatous invasion of old scar tissue is particularly characteristic healed herpes zoster dermatomes, tattoos, post-cutaneous laser surgery areas, post-consecutive botox injection areas, and injury scars [26, 28, 29].

The old scars, often atrophic and hypopigmented, evolve into elevated, purple or red lesions with associated new nodules or plaques Fig. It tends to commence on the fronto-parietal area and progress into the scalp as an atrophic, red, and scaly plaque Erythema nodosum EN is the most common nonspecific of alopecia. It can easily be confused with cutaneous discoid cutaneous eruption of sarcoidosis [18].

A biopsy taneously within 6 weeks [5, 9, 39]. It is a painful disorder of is needed in such situations to differentiate between these the subcutaneous fat. The characteristic lesion is a tender, two conditions histopathologically. These lesions present in erythematous, poorly delineated subcutaneous nodule usu- various morphologies including macular lesions, scaly ally distributed in a symmetric pattern. The main causes of plaques, and infiltrated nodules [9].

EN lesions typically occur on should carefully evaluate the patient to rule out systemic the anterior tibial surface, but can also be present on the sarcoidosis after the diagnosis of scalp sarcoidosis is extensor surface of the forearms, the thighs, and the trunk [3, established [30, 32]. The nodules can vary from 1 to 10 cm in diameter. The essential histologic features are those of a septal pan- niculitis where there is intense inflammation of the deep der- Ichthyosiform Sarcoidosis mis and fibrous septum with relative sparing of the fat lobules, without evidence of vasculitis [9, 40].

An acquired ichthyosis secondary to sarcoidosis was first In the s, Lofgren and Lundback discovered the asso- described by Braverman in [33].

Ichthyosis refers to ciation between EN and bilateral hilar lymphadenopathy, dry and scaly skin due to a defect in keratinization. Other symptoms may include fever or anterior lower limbs [33, 34]. Histopathology reveals the ocular involvement. This syndrome, similar to the EN sarcoid specific naked granuloma and ichthyosis vulgaris changes of patients, has a good prognosis due to the association with an the epidermis, such as compact orthokeratosis and a decrease acute or transient form of the disease [3, 8, 9, 13, 40].

Nail, Mucosal, and Childhood Sarcoidosis Some of the most unusual manifestations of sarcoidosis are Hypopigmentation those lesions involving in the nails or mucosa, as well as pre- senting with disease manifestations as a child. Nail sarcoido- The first report of sarcoidosis hypopigmented macules was sis findings include clubbing, subungual hyperkeratosis, in by Thomas et al. Oftentimes, sarcoidosis on brittleness, pitting, discoloration, and onycholysis.

Nail black or dark skin only presents with hypopigmented papules, involvement is indicative of the chronic form of the disease macules, or dermal nodules. They are most often found on and is considered a specific lesion because of the presence of the extremities. Since it may be the presenting sign of the the hallmark non-caseating granulomas upon histologic disease, it is important to recognize these lesions and rule out examination [2, 7, 9].

The most common presentation is nodules of the firmatory [9, 36]. The mechanism of action remains contro- buccal mucosa, gingival tissue, tongue, lips, hard palate, and versial; however, a nutritional deficiency in melanocytes, a salivary glands [7, 9].

In children younger than 6 years, etiology of tuberculosis, the infectious bacillus bacteria. The pulmonary manifesta- with 8—9 million new infections annually. Childhood sarcoidosis can be easily con- lives a year [45]. CDC [46, 47]. An estimated 15 million people are co- infected with HIV and Mycobacterium tuberculosis, and Treatment 6,00, of the 3 million HIV deaths in were specifi- The first-line treatment of choice is corticosteroids, either in cally ascribed to TB [45, 48].

The cutaneous lesions Tuberculosis was a major problem in the late nineteenth in sarcoidosis are not life threatening and the therapeutic century but declined due to improved hygiene, improved regimen should be dependent and adjusted according to the living standards, use of BCG immunization, and the intro- progression and severity of the disease. The most mutilated duction of chemotherapy [49]. However, there has been a skin lesions should be injected with triamcinolone acetonide resurgence of TB since the s, for which, the Centers for weekly.

The alternate day use of control programs [48, 50]. In developing countries, contrib- prednisone for maintenance therapy has proven to be just as uting issues include shortages of healthcare facilities with effective as the daily dose regimen [9, 12, 21]. The global inci- antimalarial drugs, but one must be cautious for serious side dence of TB is increasing at a rate of 1. Chloroquine can also primarily by countries in sub-Saharan Africa and the former be used intralesionally once a month.

Other treatment options Soviet Union [52]. Biologic agents, especially Lupus pernio and disfiguring skin plaques have been etanercept, infliximab, alefacept, efalizumab, and adali- treated successfully in some patients with laser treatments mumab, are known to cause reactivation TB due to the sup- such as pulsed-dye and the CO2 laser, however, as with all pression of the cell-mediated immune response [48].

The medications, not all patients respond the same. Cosmetic ability to detect tuberculosis of the skin will serve as a valu- options should be taken into consideration due to the social able skill in the rapid detection and realization of therapy for and psychological impact such cutaneous lesions can have physicians of the twenty-first century.

The disease primarily affects the lungs due to the trans- mission via droplets of respiratory secretions. Since TB-causing bacteria are obligate aerobes, they are able to Tuberculosis remain suspended in the air for hours droplet nuclei and survive in well-ventilated alveoli [53]. The pri- example of cutaneous tuberculosis [42, 43]. The German mary disease may also present with constitutional symptoms physician and scientist, Dr.

Primary infections are traditionally characterized lesions as tuberculous chancre, tuberculosis verrucosa cutis by any pneumonic infiltrate granuloma in the middle or TVC , lupus vulgaris LV , scrofuloderma, miliary tubercu- lower lung zones Ghon focus , especially a circular shape, losis, orificial tuberculosis, and gummatous tuberculosis.

A reactivation on AFB stains, culture, or PCR and are defined as cutaneous of TB, in contrast, classically has cavitary lesions in the hypersensitivity reactions to an underlying focus of tubercu- upper lobes of the lung [48].

The tuberculids include lichen scrofulosorum, Systemic involvement in tuberculosis is commonly asso- erythema induratum of Bazin EIB , tuberculonecrotic tuber- ciated with cutaneous TB. The incidence of skin tuberculo- culid, and nodular tuberculid [49, 59]. It remains to be one of the another strain of bacteria, specifically M.

The major difference is that M. Extra-pulmonary from animals to humans, most frequently through infected manifestations of TB account for approximately Cutaneous manifestations of TB are very rare and only represent 1. Several published studies have revealed that cutaneous TB is best diagnosed using a com- Endogenously Acquired Disease prehensive work up of the patient in which histologic study of the skin biopsy specimen is most essential [61].

Skin Lupus Vulgaris lesions are distinguished by whether M. Up to merase chain reaction PCR. Its pathogenesis is mul- cutaneous tuberculosis. True cutaneous tuberculosis can be tifactorial: direct inoculation, BCG vaccination, contiguous, acquired exogenously or endogenously and includes such lymphatic, and hematogenous route of infection [49, 65].

The lesions may present in a variety of morphologies from an infected lymph node, bone, joint, or epididymis to including the classic plaque or keratotic type gelatinous , the overlying skin in patients with a weak immune response the hypertrophic form tumor-like soft nodule , the ulcerative [69, 72, 73].

This is the most common cutaneous TB in chil- form necrosis , and the vegetative form papule with ulcer- dren and it is more common in girls than in boys [42, 57, 66, ation and necrosis. The plaque form is the most common 69]. It initially unpasteurized milk is a common occurrence around the presents as asymptomatic, flat, red-brown papules and world that leads to the M. It progresses into slowly expanding skin-colored or lymph nodes [49, 66, 69, 72, 73].

On diascopy, the nodules are seen as nodule overlying the site of the deeper infection. Over a period of color. The expanding plaque has an atrophic center with a months, it begins to ulcerate, eventually forming the hall- raised red-brown border, occasionally with scaling [67].

The mark sinus tracts that drain watery, purulent, or caseous ulcerative form is the most destructive and deforming of all material [49, 60, 72]. The ulcers are shallow with undermined LV lesions because the underlying tissue becomes ulcerated blue-colored borders.

Healing forms an elongated scar or and necrotic, leaving behind an atrophic scar. It can be espe- keloid, the characteristic puckered scar [49, 59, 60]. Finally, the vegetative form is similar to the ulcer- infection, especially pulmonary involvement [49, 59, 66, ative form in that it is characterized by necrosis and ulcer- 69]. The most commonly affected 59]. After many decades with the disease, squamous cell car- area is the neck, but may also occur on the axillae, chest, or cinoma may develop in the lupus vulgaris lesion [67, 68].

At times, lupus vulgaris may arise The areas in the body where these lesions appear vary from scrofuloderma. This form of cutaneous TB may take among different places in the world.

In Western countries, LV several years to spontaneously heal [49, 59, 71]. It is also referred to as [69]. In the tropics and developing countries, on the other metastatic tuberculous abscesses that arise on the trunk, hand, where kids play without protective clothing, it occurs extremities, or head [46, 47, 49, 54, 59, 74]. It occurs after most often on the lower extremities and buttocks [42, 49].

It occurs in patients with moderate to high immunity against M. Since Acute miliary tuberculosis is the extensive dissemination of lupus vulgaris is a paucibacillary form of tuberculous infec- M. The internal focus based on the histopathological appearance and the response of the active disease most commonly originates from the lungs. This rare form of TB has become increasingly common among The histopathologic examination shows the hallmark tuber- HIV-infected patients.

The first documented case that presented cles, which consist of accumulations of epithelioid histiocytes with cutaneous findings was reported in in an AIDS with Langerhans giant cells and varying amount of caseation patient [75]. Patients with acute miliary TB usually have a seri- necrosis in the center [71].

As a result, they have a with intermittent episodes of healing. Neither caseation necro- poor prognosis, with many cases leading to death [49, 59].

It is the additional clinical criteria that is pura, and uncommonly, umbilicated vesicles [49, 60, 71—73]. By the fourth week, the lesions are the apple-jelly nodules revealed by diascopy [71]. Histology confirms Scrofuloderma the diagnosis, revealing multiple microabscesses with neu- Scrofuloderma, also known as tuberculosis cutis colliqua- trophils and numerous AFB organisms surrounded by mac- tiva, arises from the extension of underlying tubercle bacilli rophages and giant cells [49, 60].

Recognizing this cutaneous sore may persist, on the upper outer arm, which imitates the lesion is significant because it indicates advanced internal TB chancre, but is referred to as a BCG granuloma. It tends disease and poor prognosis. It presents as red- or yellow- to occur 2—6 weeks after vaccination. It appears as a small colored nodules that ulcerate around the mucosal orifices, solitary brown nodule or papule that ulcerates, scabs, and such as on the lips, inside the mouth, or on the anogenital heals as a scar [62, 72].

These painful ulcers have an irregular circular shape, with an undermined border and a shallow, punched-out, and Tuberculosis Verrucosa Cutis granulomatous appearance.

It spreads to infect the mucosa or TVC results from a reinfection with M. Since this cutaneous mani- anus orifice [49, 59, 60, 74]. Perianal tuberculosis is believed festation entails reinfection, it occurs most often in those to be a consequence of auto-inoculation from swallowed who have occupational exposure, such as physicians bacilli-containing sputum through defects in the perianal especially pathologists or forensic scientists , other medical mucosa [71].

This cutaneous variant of TB occurs in patients with strong cell-mediated immunity. The lesion first appears as a small, solitary, asymptomatic, Exogenously Acquired Disease and reddish-brown papule that progresses into a large, irreg- ular verrucous plaque [49, 60]. The margins are firm while Tuberculous Chancre the center is soft, and there is a surrounding erythematous The tuberculous chancre, also known as the primary inocula- border. There are deep fissures on the surface which often tion tuberculosis, is seen following primary infection with expel pus [49, 59].

TVC is found most commonly on the M. There have been cases test [49, 59, 60]. Notify me of new posts by email. Been Medical Video Lectures Dr. Thursday, January 13, Sign in. Forgot your password? Get help. Privacy Policy. Password recovery.

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