Prevalence of rare dermtoses manifesting at intertrigenous areas – a prospective study
Corresponding Author(s) : Praneeth NG
ngpraneethreddy@gmail.com
International Journal of Allied Medical Sciences and Clinical Research,
Vol. 2 No. 4 (2014): 2014 Volume 2- Issue -4
Abstract
Background
Intertrigo, or intertriginous dermatitis, may be defined as inflammation resulting from moisture trapped in skin folds subjected to friction
Several infections, predominantly fungal, bacterial and mixed infections, eczemas, vesicobullous disorders, papulosquamous diseases can manifest at the intertrigenous areas, when left unattended may lead to chronicity of the illness, serious complications and morbidities.
Aims & objectives
To study the rare dermatoses at intertrigenous areas with predisposing factors and clinical presentations and to correlate the dermatoses with obesity.
Results
In our study of 180 patients, candidal intertrigo was present in 42 patients, mechanical intertrigo was diagnosed in 30 cases, irritant contact dermatitis was present in 16 patients and acanthosis nigricans in 20 patients.Eleven patients in the study were diagnosed with tinea cruris, 9 with bacterial intertrigo 8 cases with atopic dermatitis. Tinea pedis was present in 7cases. Intertrigo with both bacterial and fungal infections was diagnosed in 6 cases, seborrhoeic dermatitis in 5 patients and tinea versicolor in 4 patients. Rarer dermatoses like inverse psoriasis were present in 7 cases, Hailey Hailey disease was diagnosed in 3 cases and Darier’s disease in 2 cases. 1 case each of hidradenitis suppurativa, pemphigus vegetans and trichomycosis axillaris were present in the study.
Conclusion
There was no significant difference in the distribution of dermatoses age group, sex of these patients. Even though a few patients were categorized as grade I and II obese, majority occurred in non obese category. Factors like climate, environment, occlusion and tight dressing were the other predisposing factors. Hence most of the intertrigenus dermatoses could be prevented by taking all measures to prevent occlusion and improving skin hygiene.
Keywords
Intertrigo
obesity
Intertrigenous dermatoses
1.
Praneeth NG. Prevalence of rare dermtoses manifesting at intertrigenous areas – a prospective study. Int. J. of Allied Med. Sci. and Clin. Res. [Internet]. 2020 Aug. 2 [cited 2026 Feb. 26];2(4):459-67. Available from: https://ijamscr.com/ijamscr/article/view/119
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References
-
[1] Patriek Mistiaen, Meike van Halm-Walters, Prevention and treatment of intertrigo in large skin folds of adults: a systematic review. Mistiaen and Van Halm-Walters BMC Nursing. 2010; 9: 1-9
[2] Vary Jay C, O’Connor Kim M. Common dermatologic conditions. MCNA. 2011; 98: 445-485.
[3] Richard AF, Clark and Terrence T Hopkins. The other eczemas. From Moschella and Hurley Dermatology, Vol. 1, 3rd Edition, 1992; 486.
[4] Griffiths CEM, Barker JNWN. Psoriasis. In: Burns T, Breathnach S, Cox N, Griffiths C (eds). Rook’s Textbook of Dermatology, 8th edition. West Sussex: Wiley Blackwell Publishers; 2010: 20.11-5.
[5] James WD, Berger TG, Elston DM (eds). Andrew’s Disease of the Skin, 10th edition. Canada: Saunders Elsevier; 2009.
[6] Guglielmetti Antonio, Conlledo Rodrigo, Bedoya Juliana, Ianiszewski Correa Francisco Julio. Inverse psoriasis involving genital skin folds: Successful therapy with Dapsone. DermatolTher. 2012; 15: 1-9.
[7] Kim de Winter, Hessel H. van der Zee and Errol P Prens. Is mechanical stress an important pathogenic factor in hidradenitis suppurativa?. Experimental Dermatology: 2012; 21: 176–177.
[8] Jemec GBE, Heidenheim M, Nielson NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. 1996; 35:191–4.
[9] Fitzsimmons JS, Fitzsimmons EM, Bilbert G. Familial hidradenitis suppurativa: evidence in favour of single genetransmission. J Med Genet 1984;21: 281–285.
[10] Fitzsimmons JS, Guilbert PR, Fitzsimmons EM. Evidence of genetic factors in hidradenitis suppurativa. Br J Dermatol1985;113: 1–8.
[11] Von der Werth J, Williams HC. The natural history ofhidradenitis suppurativa. J Eur Acad Dermatol 2000; 14:389–393.
[12] König A, Lehman C, Rompel R, et al. Cigarette smoking as a triggering factor of hidradenitis suppurativa. Dermatology 1999;198: 261–264.
[13] Jemec GBE. Hidradenitis suppurativa. J Cutan Med Surg 2003: 7 : 47–56.
[14] Jemec GBE, Faber M, Gutschick E. Microbiology of hidradenitis suppurativa. Dermatology 1996: 193: 203–206.
[15] Buimer MG, Wobbes T, Klinkenbijl HG. Hidradenitis suppurativa. Br J Surgery 2009; 96: 350-60.
[16] Cullen DR. Genetic features of familial benign pemphigus. Br JDermatol. 1965; 77:20–23.
[17] Hu Z, Bonifas JM, Beech J. Mutations in ATP2C1, encodinga calcium pump, cause Hailey–Hailey disease. Nat Genet.2000; 24:61–65.
[18] Dhitavat J, Fairclough RJ, Hovnanian A. Calcium pumps and keratinocytes: lessons from Darier’s disease and Hailey–Hailey disease. Br J Dermatol. 2004;150:821–8.
[19] Palmer DD, Perry HO. Benign familial chronic pemphigus. ArchDermatol. 1962;86:493–502.
[20] Burge SM. Hailey–Hailey disease: the clinical features, responseto treatment and prognosis. Br J Dermatol. 1992;126:275–82.
[21] Munro CS. The phenotype of Darier’s disease: penetrance and expressivity in adults and children. Br J Dermatol. 1992;127:168–171.
[22] Burge SM, Wilkinson JD. Darier–White disease: a review of the clinical features in 163 patients. J Am Acad Dermatol. 1992; 27:40–50.
[23] Miyauchi Y, Daiho T, Yamasaki K. Comprehensive analysis of expression and function of 51 sarco(endo)plasmic reticulum Ca2+-ATPase mutants associated with Darier disease. J Biol Chem. 2006; 281:22882–95.
[24] Burge SM. Bullous eruptions. In: Champion RH, Burton JL, Burns DA. Textbook of dermatology. Oxford (UK): Blackwell Scientific Publications; 1998. p. 1874–90.
[25] Cohen LM, Skopicki DK, Harrist TJ. Lever’s histopathology of the skin. Philadelphia: Lippincott-Raven, 1997.
[26] Crissey JT, Rebell GC, Laskas JJ. Studies on the causative organisms of trichomycosis axillaris. J Invest Dermatol 1952; 19: 187–97.
[27] Freeman RG, McBride ME, Knox JM. Pathogenesis of trichomycosis axillaris. Arch Dermatol. 1969;100:90–5
[28] McBride ME, Duncan WC. Trichomycosis axillaris. Arch Dermatol. 1972; 105:459–60.
[29] Zawar V. Photoletter to the editor: Trichomycosis (trichobacteriosis) axillaris. J Dermatol Case Rep.2011;5:36–7.
[30] Mondal Ashim kumar, Kumar Piyush, Chowdhury Satyendra Nath, Pal Subrata, Debbarman Panchami, Barbhuiya J N, et al. Erythematous plaques in axillae- a report of two cases. J Pak Asso Dermatol. 2011;21: 219-22.
[31] Gregor BE, Jemec, Heidhenheim Maichel, Neilson Neils Henrik. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol.1996; 35: 191-4.
References
[1] Patriek Mistiaen, Meike van Halm-Walters, Prevention and treatment of intertrigo in large skin folds of adults: a systematic review. Mistiaen and Van Halm-Walters BMC Nursing. 2010; 9: 1-9
[2] Vary Jay C, O’Connor Kim M. Common dermatologic conditions. MCNA. 2011; 98: 445-485.
[3] Richard AF, Clark and Terrence T Hopkins. The other eczemas. From Moschella and Hurley Dermatology, Vol. 1, 3rd Edition, 1992; 486.
[4] Griffiths CEM, Barker JNWN. Psoriasis. In: Burns T, Breathnach S, Cox N, Griffiths C (eds). Rook’s Textbook of Dermatology, 8th edition. West Sussex: Wiley Blackwell Publishers; 2010: 20.11-5.
[5] James WD, Berger TG, Elston DM (eds). Andrew’s Disease of the Skin, 10th edition. Canada: Saunders Elsevier; 2009.
[6] Guglielmetti Antonio, Conlledo Rodrigo, Bedoya Juliana, Ianiszewski Correa Francisco Julio. Inverse psoriasis involving genital skin folds: Successful therapy with Dapsone. DermatolTher. 2012; 15: 1-9.
[7] Kim de Winter, Hessel H. van der Zee and Errol P Prens. Is mechanical stress an important pathogenic factor in hidradenitis suppurativa?. Experimental Dermatology: 2012; 21: 176–177.
[8] Jemec GBE, Heidenheim M, Nielson NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. 1996; 35:191–4.
[9] Fitzsimmons JS, Fitzsimmons EM, Bilbert G. Familial hidradenitis suppurativa: evidence in favour of single genetransmission. J Med Genet 1984;21: 281–285.
[10] Fitzsimmons JS, Guilbert PR, Fitzsimmons EM. Evidence of genetic factors in hidradenitis suppurativa. Br J Dermatol1985;113: 1–8.
[11] Von der Werth J, Williams HC. The natural history ofhidradenitis suppurativa. J Eur Acad Dermatol 2000; 14:389–393.
[12] König A, Lehman C, Rompel R, et al. Cigarette smoking as a triggering factor of hidradenitis suppurativa. Dermatology 1999;198: 261–264.
[13] Jemec GBE. Hidradenitis suppurativa. J Cutan Med Surg 2003: 7 : 47–56.
[14] Jemec GBE, Faber M, Gutschick E. Microbiology of hidradenitis suppurativa. Dermatology 1996: 193: 203–206.
[15] Buimer MG, Wobbes T, Klinkenbijl HG. Hidradenitis suppurativa. Br J Surgery 2009; 96: 350-60.
[16] Cullen DR. Genetic features of familial benign pemphigus. Br JDermatol. 1965; 77:20–23.
[17] Hu Z, Bonifas JM, Beech J. Mutations in ATP2C1, encodinga calcium pump, cause Hailey–Hailey disease. Nat Genet.2000; 24:61–65.
[18] Dhitavat J, Fairclough RJ, Hovnanian A. Calcium pumps and keratinocytes: lessons from Darier’s disease and Hailey–Hailey disease. Br J Dermatol. 2004;150:821–8.
[19] Palmer DD, Perry HO. Benign familial chronic pemphigus. ArchDermatol. 1962;86:493–502.
[20] Burge SM. Hailey–Hailey disease: the clinical features, responseto treatment and prognosis. Br J Dermatol. 1992;126:275–82.
[21] Munro CS. The phenotype of Darier’s disease: penetrance and expressivity in adults and children. Br J Dermatol. 1992;127:168–171.
[22] Burge SM, Wilkinson JD. Darier–White disease: a review of the clinical features in 163 patients. J Am Acad Dermatol. 1992; 27:40–50.
[23] Miyauchi Y, Daiho T, Yamasaki K. Comprehensive analysis of expression and function of 51 sarco(endo)plasmic reticulum Ca2+-ATPase mutants associated with Darier disease. J Biol Chem. 2006; 281:22882–95.
[24] Burge SM. Bullous eruptions. In: Champion RH, Burton JL, Burns DA. Textbook of dermatology. Oxford (UK): Blackwell Scientific Publications; 1998. p. 1874–90.
[25] Cohen LM, Skopicki DK, Harrist TJ. Lever’s histopathology of the skin. Philadelphia: Lippincott-Raven, 1997.
[26] Crissey JT, Rebell GC, Laskas JJ. Studies on the causative organisms of trichomycosis axillaris. J Invest Dermatol 1952; 19: 187–97.
[27] Freeman RG, McBride ME, Knox JM. Pathogenesis of trichomycosis axillaris. Arch Dermatol. 1969;100:90–5
[28] McBride ME, Duncan WC. Trichomycosis axillaris. Arch Dermatol. 1972; 105:459–60.
[29] Zawar V. Photoletter to the editor: Trichomycosis (trichobacteriosis) axillaris. J Dermatol Case Rep.2011;5:36–7.
[30] Mondal Ashim kumar, Kumar Piyush, Chowdhury Satyendra Nath, Pal Subrata, Debbarman Panchami, Barbhuiya J N, et al. Erythematous plaques in axillae- a report of two cases. J Pak Asso Dermatol. 2011;21: 219-22.
[31] Gregor BE, Jemec, Heidhenheim Maichel, Neilson Neils Henrik. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol.1996; 35: 191-4.
[2] Vary Jay C, O’Connor Kim M. Common dermatologic conditions. MCNA. 2011; 98: 445-485.
[3] Richard AF, Clark and Terrence T Hopkins. The other eczemas. From Moschella and Hurley Dermatology, Vol. 1, 3rd Edition, 1992; 486.
[4] Griffiths CEM, Barker JNWN. Psoriasis. In: Burns T, Breathnach S, Cox N, Griffiths C (eds). Rook’s Textbook of Dermatology, 8th edition. West Sussex: Wiley Blackwell Publishers; 2010: 20.11-5.
[5] James WD, Berger TG, Elston DM (eds). Andrew’s Disease of the Skin, 10th edition. Canada: Saunders Elsevier; 2009.
[6] Guglielmetti Antonio, Conlledo Rodrigo, Bedoya Juliana, Ianiszewski Correa Francisco Julio. Inverse psoriasis involving genital skin folds: Successful therapy with Dapsone. DermatolTher. 2012; 15: 1-9.
[7] Kim de Winter, Hessel H. van der Zee and Errol P Prens. Is mechanical stress an important pathogenic factor in hidradenitis suppurativa?. Experimental Dermatology: 2012; 21: 176–177.
[8] Jemec GBE, Heidenheim M, Nielson NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. 1996; 35:191–4.
[9] Fitzsimmons JS, Fitzsimmons EM, Bilbert G. Familial hidradenitis suppurativa: evidence in favour of single genetransmission. J Med Genet 1984;21: 281–285.
[10] Fitzsimmons JS, Guilbert PR, Fitzsimmons EM. Evidence of genetic factors in hidradenitis suppurativa. Br J Dermatol1985;113: 1–8.
[11] Von der Werth J, Williams HC. The natural history ofhidradenitis suppurativa. J Eur Acad Dermatol 2000; 14:389–393.
[12] König A, Lehman C, Rompel R, et al. Cigarette smoking as a triggering factor of hidradenitis suppurativa. Dermatology 1999;198: 261–264.
[13] Jemec GBE. Hidradenitis suppurativa. J Cutan Med Surg 2003: 7 : 47–56.
[14] Jemec GBE, Faber M, Gutschick E. Microbiology of hidradenitis suppurativa. Dermatology 1996: 193: 203–206.
[15] Buimer MG, Wobbes T, Klinkenbijl HG. Hidradenitis suppurativa. Br J Surgery 2009; 96: 350-60.
[16] Cullen DR. Genetic features of familial benign pemphigus. Br JDermatol. 1965; 77:20–23.
[17] Hu Z, Bonifas JM, Beech J. Mutations in ATP2C1, encodinga calcium pump, cause Hailey–Hailey disease. Nat Genet.2000; 24:61–65.
[18] Dhitavat J, Fairclough RJ, Hovnanian A. Calcium pumps and keratinocytes: lessons from Darier’s disease and Hailey–Hailey disease. Br J Dermatol. 2004;150:821–8.
[19] Palmer DD, Perry HO. Benign familial chronic pemphigus. ArchDermatol. 1962;86:493–502.
[20] Burge SM. Hailey–Hailey disease: the clinical features, responseto treatment and prognosis. Br J Dermatol. 1992;126:275–82.
[21] Munro CS. The phenotype of Darier’s disease: penetrance and expressivity in adults and children. Br J Dermatol. 1992;127:168–171.
[22] Burge SM, Wilkinson JD. Darier–White disease: a review of the clinical features in 163 patients. J Am Acad Dermatol. 1992; 27:40–50.
[23] Miyauchi Y, Daiho T, Yamasaki K. Comprehensive analysis of expression and function of 51 sarco(endo)plasmic reticulum Ca2+-ATPase mutants associated with Darier disease. J Biol Chem. 2006; 281:22882–95.
[24] Burge SM. Bullous eruptions. In: Champion RH, Burton JL, Burns DA. Textbook of dermatology. Oxford (UK): Blackwell Scientific Publications; 1998. p. 1874–90.
[25] Cohen LM, Skopicki DK, Harrist TJ. Lever’s histopathology of the skin. Philadelphia: Lippincott-Raven, 1997.
[26] Crissey JT, Rebell GC, Laskas JJ. Studies on the causative organisms of trichomycosis axillaris. J Invest Dermatol 1952; 19: 187–97.
[27] Freeman RG, McBride ME, Knox JM. Pathogenesis of trichomycosis axillaris. Arch Dermatol. 1969;100:90–5
[28] McBride ME, Duncan WC. Trichomycosis axillaris. Arch Dermatol. 1972; 105:459–60.
[29] Zawar V. Photoletter to the editor: Trichomycosis (trichobacteriosis) axillaris. J Dermatol Case Rep.2011;5:36–7.
[30] Mondal Ashim kumar, Kumar Piyush, Chowdhury Satyendra Nath, Pal Subrata, Debbarman Panchami, Barbhuiya J N, et al. Erythematous plaques in axillae- a report of two cases. J Pak Asso Dermatol. 2011;21: 219-22.
[31] Gregor BE, Jemec, Heidhenheim Maichel, Neilson Neils Henrik. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol.1996; 35: 191-4.