Focusing on Pemphigus vulgaris, a blistering auto-immune disease, during acantholysis, circulatingautoantibodies cause disruption of cell-cell and cell-matrix adhesion.[5] The antibodies circulate against intercellular adhesion structures and demosomal protein desmoglein (DSG), which causes the disruption.[6] Acantholytic cells also known asTzanck cells are a distinguishing feature when diagnosing Pemphigus vulgaris.[7] The Tzanck test can be used to diagnosis Pemphigus vulgaris for patients who are uncomfortable with a biopsy.[8] he test can be used to identify acantholytic cells which are classified as large roundkeratinocytes characterized by an enlargednucleus, indistinct or missingnucleoli and plentiful basophilic cytoplasm.[9] Thishistological feature is also seen inherpes simplex infections (HSV 1 and 2) andvaricella zoster infections (chicken pox and shingles).
The incidence of acantholysis varies according to the condition it is associated with.
In Pemphigus vulgaris, the incidence ranges from 0.076 to 5 per 100,000 person-years.[10] The occurrence of Pemphigus vulgaris is most common in adults between ages of 50 and 60 years old.[11] Approximately 70% of cases of this condition come fromIndia,China,Malaysia and theMiddle East. While Pemphigus vulgaris affects all, the highest incidence occurs inAshkenazi Jews.[12] Some common factors that cause this condition arestress,medication, surgical and dental procedures, physical trauma or other illnesses.[13] Genetics is also a strong factor in inheriting Pemphigus vulgaris. This has been showed in Ashkenazi Jews with Pemphigus vulgaris.[14]
Grover’s disease, which is also caused by acantholysis, is most common in older adults with older adults likely to have more extensive and longer duration of the disease.[15] The disease is around 1.6 to 2.1 times more common in males than females.[16] Some factors that are associated with causing Grover’s disease are environmental factors like extensive sunlight exposure or heat and preexisting illnesses such as cancer and infections.[17]
^Parsons, Jerome Michael (1 November 1996). "Transient acantholytic dermatosis (Grover's disease): A global perspective".Journal of the American Academy of Dermatology.35 (5):653–666.doi:10.1016/S0190-9622(96)90715-X.PMID8912557.
^Parsons, Jerome Michael (1 November 1996). "Transient acantholytic dermatosis (Grover's disease): A global perspective".Journal of the American Academy of Dermatology.35 (5):653–666.doi:10.1016/S0190-9622(96)90715-X.PMID8912557.
^Parsons, Jerome Michael (1 November 1996). "Transient acantholytic dermatosis (Grover's disease): A global perspective".Journal of the American Academy of Dermatology.35 (5):653–666.doi:10.1016/S0190-9622(96)90715-X.PMID8912557.
