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Disorders of Pigmentation
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Michael Joseph Lavery, Charles Cathcart, Hasan Aksoy
Differential diagnosis: These include other reticulate pigmentary disorders (Table 25.5). Galli-Galli Disease has similar features to DDD; however, there are some distinctive features, such as erythematous–brown keratotic papules with suprabasal acantholysis in histopathologic evaluation. It is considered a variant of DDD. Haber’s syndrome is also manifested by a reticulate pigmentation, comedo-like lesions, and pitted scars, but it can be distinguished by a photosensitive, facial rosacea-like rash that occurs in childhood.
Other papulonodular disorders
Published in Aimilios Lallas, Enzo Errichetti, Dimitrios Ioannides, Dermoscopy in General Dermatology, 2018
Enzo Errichetti, Aimilios Lallas, Dimitrios Ioannides
Of note, a similar pattern may also be appreciated in other dermatological conditions which may display acantholysis and dyskeratosis on histology, viz. Galli–Galli disease, acantholytic dyskeratotic acanthoma, and Grover’s disease (Darier-like subtype; see next paragraph).1–5
Histopathology
Published in Dimitris Rigopoulos, Alexander C. Katoulis, Hyperpigmentation, 2017
Galli–Galli disease may present itself with clinical features indistinguishable from those of Dowling–Degos disease, or with more maculopapular manifestations reminiscent of generalized Grover’s disease.25,26 On microscopy, the filiform proliferation of the epidermis with basal hyperpigmentation is largely identical to that seen in Dowling–Degos disease, but in addition, suprabasal acantholysis is present (Figure 23.11). The pattern can be quite similar to that seen in some variants of Grover’s disease. The observation that mutations in the keratin 5 gene and POGLUT1 gene have been identified in patients diagnosed with Galli–Galli disease led to the view that it may represent a variant of Dowling–Degos disease, rather than a distinct entity.
Current status and prospects for the diagnosis of pemphigus vulgaris
Published in Expert Review of Clinical Immunology, 2021
Ali Nili, Ali Salehi Farid, Masoud Asgari, Soheil Tavakolpour, Hamidreza Mahmoudi, Maryam Daneshpazhooh
The diagnosis of PV is not challenging if this disease is suspected. PV is traditionally diagnosed with a multi-step approach as one of the AIBDs. This approach begins with clinical evaluation, biopsy, and DIF combined with Dsg ELISA as a pivotal adjunct. The diagnosis will be challenging if DIF is negative and since DIF is considered the gold standard for the immunologic diagnosis of pemphigus, many experts recommend repeating the test; if the re-test is negative or whenever DIF is unavailable or feasible, serological evaluation as either IIF or Dsg ELISA are suitable substitutes [122]. Anti-Dsg ELISA, or to a far lesser extent IIF, may also give a rough estimate of the severity of the disease and help in the monitoring of the disease. Dsg ELISA is also encouraged if the clinical and histological findings are not concordant regarding the type of pemphigus (PV versus PF). If DIF was suggestive of other AIBDs, other investigations are suggested either as multi-step diagnostic tests or multivariant tests based on BIOCHIP or ELISA. Whenever both linear and intercellular IgG deposits are noted, particularly in the face of lichenoid histopathological findings, PNP is suspected, and besides the usual serological tests for PV, IIF on rat bladder, envoplakin ELISA, BP230 antibodies, and immunoblot tests for antibodies against the plakin family are mandatory. In the challenging case with repeated negative DIF results, high values of anti-Dsg or even high intercellular IIF antibodies on ME or recombinant Dsg substrate may be acceptable. Finally, if DIF, IIF, and Dsg ELISA results are negative, the diagnosis of PV should only be kept if clinical (especially mucosal involvement) and histopathological (suprabasal cleft and acantholysis) findings are unequivocal. Hailey-Hailey disease, Galli-Galli disease, superficial types of epidermolysis bullosa, and impetigo are among diseases that may display acantholysis pathologically and can be ruled out clinically. Infrequently, Dsg antibodies are undetectable in PV despite positive immunofluorescence findings; in these cases, antibodies against other antigens (such as acetylcholine receptors and Dscs) may be involved. These antibodies are not screened in routine practice. Only in very rare cases, DIF and IIF are negative and Dsg antibodies undetectable. In these cases, repeating the tests may lead to the correct diagnosis. Drug-induced PV may also be implicated. Figure 5 illustrates the diagnostic assays for pemphigus based on availability, accuracy, and validity.