STUDY Incidence of Cancer Among Patients With Suppurativa

Jan Lapins, MD; Weimin Ye, MD; Olof Nyre´n, MD; Lennart Emtestam, MD

Background: On the basis of some case reports, a re- Results: The risk of developing any cancer in the lationship has been suggested between hidradenitis cohort with HS increased 50% (95% confidence interval suppurativa (HS) and the development of nonmela- of SIR, 1.1-1.8, based on 73 observed cases). Statisti- noma skin cancer. cally significant risk elevations were observed for non- melanoma skin cancer (5 cases; SIR, 4.6; 95% confi- Objectives: To confirm this relationship and to ex- dence interval, 1.5-10.7), buccal cancer (5 cases; SIR, plore the risk of other cancers among patients with HS. 5.5; 95% confidence interval, 1.8-12.9), and primary liver cancer (3 cases; SIR, 10.0; 95% confidence inter- Patients: Patients with a discharge diagnosis of HS were val, 2.1-29.2). obtained from the computerized database of hospital dis- charge diagnoses from January 1, 1965, through December Conclusions: This study confirms an increased risk of 31, 1997. A total of 2119 patients with HS were identified. nonmelanoma skin cancer among patients with HS. The risk for buccal cancer and primary liver cancer was also Setting: All hospitals in Sweden. elevated among this cohort, but these associations should be interpreted cautiously because the combination of mul- Design: With record linkage to the Swedish National tiple significance testing and the few observed cases may Cancer Registry, standardized incidence ratios (SIR [the have generated chance findings. ratio of the observed to expected incidence]) were cal- culated to estimate relative risk. Arch Dermatol. 2001;137:730-734

IDRADENITIS suppurativa 29 among men). The average age at diag- (HS) is a chronic, suppu- nosis of cancer was 51.2 years for women rative, and cicatricial in- and 55.0 years for men (Table 1). Among flammatory disease, all 2119 patients, 134 (6%) had a diagno- mainly affecting apo- sis of alcoholism and 152 (7%) had a di- Hcrine gland–bearing areas of the skin.1 Sev- agnosis of diabetes mellitus. About one eral case reports of co-occurrence of HS third (652) of the patients had ever un- and nonmelanona skin cancer2-16 have im- dergone surgical excision of the affected plied a causal relationship, but firm epi- skin areas. demiological data are lacking. In an at- After excluding 8 cancer cases accu- tempt to confirm this association and to mulated during the first year of fol- look for other cancer associations as well, low-up (SIR, 1.9; 95% CI, 0.8-3.8), in- we performed a retrospective cohort study cluding 1 case of squamous cell carcinoma of patients hospitalized for HS in Swe- of the skin, the risk for any cancer (all sites) den. The patients were followed up for up was increased by 50% among patients hos- From the Department of to 32 years to examine the subsequent risks pitalized for HS, compared with the age- Medicine, Section of of cancer. and sex-matched general Swedish popu- Dermatology and Venereology, lation during the time of the study Karolinska Institute at RESULTS (Table 2). The estimated relative risks for Huddinge University Hospital, cancers of different sites with at least 2 ob- Stockholm, Sweden (Drs Lapins and Emtestam); and the On average, the patients with HS were fol- served cases are also listed in Table 2. Department of Medical lowed up for 9.8 years, yielding 20801 ac- There was a significantly increased rela- Epidemiology, Karolinska cumulated patient-years at risk. During the tive risk for nonmelanoma skin cancer Institute, Stockholm (Drs Ye observation period, we ascertained a to- (5 cases; SIR, 4.6; 95% CI, 1.5-10.7), but and Nyre´n). tal of 81 cases of cancer (52 among women, no excess risk was observed for mela-

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©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 PATIENTS AND METHODS or incomplete national registration numbers. We also ex- cluded 67 patients with prevalent cancers (ie, those who had a previously registered diagnosis of cancer) and 51 pa- STUDY COHORT tients with inconsistencies uncovered during medical record linkage. Thus, a total of 2119 patients, 1495 women In 1964-1965, the National Board of Health and Welfare and 624 men, were enrolled in the study cohort, which is started collecting data on individual hospital discharges in further characterized in Table 1. the Inpatient Register. In addition to the national registra- tion number (unique personal identifiers assigned to all STATISTICAL ANALYSIS Swedish residents), each record—corresponding to one in- hospital episode—contains administrative and medical data Follow-up time (person-years) was calculated from the date such as hospital department and discharge diagnoses. The of enrollment in the cohort (date of the first discharge from diagnoses are coded according to the International Classi- the hospital having a diagnosis of HS) until the occur- fication of Diseases, 7th Revision (ICD-7) through 1968, the rence of a first cancer diagnosis, emigration, death, or the eighth revision until 1987 (ICD-8), the ninth revision end of the study (December 31, 1997). To avoid possible (ICD-9) until 1996, and the 10th revision (ICD-10) there- ascertainment bias associated with differential autopsy rates after. The number of hospitals providing data to the reg- between the cohort members and the general population, ister has increased steadily: the register covered 60% of the we did not count cancers found incidentally at autopsy. Rela- Swedish population in 1969, 75% in 1978, and 85% by the tive risk of cancer was estimated as the standardized inci- end of 1983. From 1987, the register attained complete na- dence ratio (SIR), defined as the ratio of the observed num- tionwide coverage. ber of cancers to that expected. The expected number of All patients recorded in the Inpatient Register with a cancers was calculated by multiplying the number of ob- discharge diagnosis of HS (ICD-7=714.07, ICD-8=705.91, served person-years, divided into age- (in 5-year groups), ICD-9=705W, and ICD-10=L732) were initially selected for sex-, and calendar year–specific strata, by the correspond- inclusion in the study. A total of 2259 unique national reg- ing cancer incidence rates. These incidence rates, derived istration numbers were registered at least once with this di- from the relevant strata in the entire Swedish population agnosis between January 1, 1965, and December 31, 1997. and aggregated by 5 calendar years to avoid instability in During the period 1987 through 1996, the ICD-9 code, 705W, rates of rare cancers, were calculated by dividing number contains also other diseases, namely, pompholyx, bromhi- of the first primary cancers excluding those discovered in- drosis, and chromhidrosis. However, the incidence of these cidentally at autopsy by person-years at risk (number of 3 diagnoses in Swedish inpatients is very low. midyear population without reported cancer). The 95% con- fidence interval (CI) of the SIR was calculated on the as- FOLLOW-UP DATA sumption that the observed number follows a Poisson dis- tribution.18 For selected cancer sites, stratified analyses were Record linkage of the study cohort to the nationwide Reg- also performed to detect any difference of risk pattern across ister of Causes of Death, using the national registration num- sex, duration of follow-up, period at discharge, status of bers as identifiers, provided information on dates and causes comorbidities, and whether patients had ever undergone of death among those deceased through 1997. Correspond- surgical excision of the affected skin areas. An approxi- ing linkage to the emigration register identified dates of emi- mate ␹2 test was used to test the difference between 2 SIRs.19 gration. The National Swedish Cancer Register, founded We also calculated standardized mortality ratios for se- in 1958 and close to 98% complete,17 was used to ascer- lected causes of death. Patients with prevalent cancers tain all incident cancers until December 31, 1997. The can- (ie, those who had a previously registered diagnosis of cer register coded malignant neoplasm according to the cancer) were included in the mortality analyses. In the main ICD-7 classification during the entire study period. analyses, we excluded cancers and person-years accumu- To remove records with incorrect national registra- lated during the first year of follow-up to minimize the tion numbers, which would otherwise contribute person- possible influence of selection bias. Such bias occurs if years at no risk of cancer, we also linked the cohort file to patients with HS and a subclinical cancer are more likely the register of the total population. If a national registra- to be hospitalized than those without a subclinical cancer. tion number could not be found in this register or in the If this is the case, these cancers are most likely to be diag- death and emigration registers, we concluded that it did nosed within the first year of follow-up. This study is not correspond to an existing person. We, thus, excluded approved by ethics committee of Huddinge University from the cohort 22 medical records because of erroneous Hospital, Stockholm, Sweden.

noma. Significantly elevated relative risks were also ob- No obviously increased risk was observed for colon, rec- served for buccal cancer (5 cases; SIR, 5.5; 95% CI, 1.8- tum, breast, female genital system, and brain cancers in 12.9) and primary liver cancer (3 cases; SIR, 10.0; 95% our cohort (Table 2). Nine cancers are not accounted for CI, 2.1-29.2). Although not statistically significant, in- in Table 2 and they occurred in the following sites: stom- creased risks were noted for esophageal cancer (2 cases; ach (1 patient), ampulla of Vater (1 patient), pancreas SIR, 7.4; 95% CI, 0.9-26.8), lung cancer (5 cases; SIR, (1 patient), prostate (1 patient), testis (1 patient), thy- 1.7; 95% CI, 0.6-4.1), kidney cancer (2 cases; SIR, 1.7; roid (1 patient), and unspecified (3 patients). 95% CI, 0.2-6.3), cancers in urinary tract organs other Stratified analyses for selected cancer types among than kidney (3 cases; SIR, 1.9; 95% CI, 0.4-5.5), and he- patients hospitalized for HS from January 1, 1965, through matopoietic cancers (6 cases; SIR, 1.8; 95% CI, 0.7-4.0). December 31, 1997, in Sweden by sex, follow-up dura-

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©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Table 1. Characteristics of the Patient Cohort Hospitalized Table 2. Standardized Incidence Ratio (SIR) and for , 1965-1997, Sweden Its 95% Confidence Interval (CI) for Major Cancer Types Among Patients Hospitalized for Hidradenitis No. of Women No. of Men Total No. Suppurativa, 1965-1997, Sweden* Patient Characteristics (n = 1495) (n = 624) (N = 2119) Age at enrollment, mean, y 34.3 41.0 36.3 No. of Observed Calendar year at entry, mean 1987 1987 1987 Cancer Type ICD-7 Code† Cases SIR 95% CI Follow-up, mean, y 10.1 9.2 9.8 Person-years at risk 15 074 5726 20 801 All-site 140-209 73 1.5 1.1-1.8 No. of cancers 52 29 81 Cancers of the skin Age at diagnosis of 51.2 55.0 52.6 Nonmelanoma 191 5 4.6 1.5-10.7 cancer, mean, y Melanoma 190 3 1.0 0.2-2.9 Cancers other than skin Buccal 140-148 5 5.5 1.8-12.9 Esophagus 150 2 7.4 0.9-26.8 tion, and calendar period of hospitalization are given in Colon 153 2 0.8 0.1-2.8 Table 3. Small numbers of observed and expected can- Rectum 154 2 1.2 0.2-4.3 cers hampered interpretation of these data. Men seemed Liver 155.0 3 10.0 2.1-29.2 to have a higher relative risk for all-site cancer, but a lower Trachea, bronchus, 162 5 1.7 0.6-4.1 or lung relative risk for nonmelanoma skin cancer and buccal can- Breast 170 15 1.2 0.7-2.1 cer than women, although these differences were not sta- Female genital system 171-176 8 1.3 0.6-2.6 tistically significant. The observed excess risk for pri- Kidney 180 2 1.7 0.2-6.3 mary liver cancer was seemingly confined to men, with a Urinary tract organ 181 3 1.9 0.4-5.5 borderline significant difference between sex (P=.07). Ex- excluding kidney cept for buccal cancer, where the excess became more ob- Brain 193 3 1.3 0.3-3.9 Hematopoietic 200-209 6 1.8 0.7-4.0 vious after more than 10 years of observation (P=.05), there system was no clear tendency of increasing or decreasing relative risks with time. Nor did the relative risks vary materially *Data exclude the first year of follow-up. with calendar period of enrollment. The findings re- †ICD-7 indicates International Classification of Diseases, Seventh mained practically unaltered after removal of patients with Revision. a co-diagnosis of alcoholism, and the excesses seemed to be essentially independent of whether a surgical excision The earliest inflammatory event in HS is a rupture of the hidradenitis had been carried out (although only of the follicular epithelium, followed by the spilling of one case of buccal and no cases of primary liver cancers foreign body material such as corneocytes, bacteria, se- were observed among operated on patients). Cancer cases bum products, and hair into the dermis. The dumping were clearly overrepresented among patients with a co- of foreign products initiates an inflammatory response diagnosis of diabetes mellitus (P=.01 for all-site cancer and to cause a foreign body granuloma. Epithelial strands PϽ.01 for buccal cancer), but the excesses of all-site can- form sinuses in this inflammatory tissue. Secondary cer, nonmelanoma skin cancer, and primary liver cancer bacterial colonization in this milieu can intensify the remained (the latter nonsignificantly) after removal of the chronic ,1 a similar picture as seen with patients with diabetes mellitus. intravascular catheters20 and prosthetic devices,21 but in HS the process is long standing, and the presence of a COMMENT foreign body enhances the pathogenetic properties of coagulase-negative staphylococci that are found in a To our knowledge, no other large-scale follow-up study high proportion of hidradenitis lesions.22 Thus, al- of patients with HS has been published. The association though it is not fully understood why HS predisposes to between HS and the risk of nonmelanoma skin cancer has, skin cancer, the suspicion has centered on the role of however, been suggested in some case reports.2-16 The lack chronic irritation and infections that may lead to prolif- of proper denominators in measures of occurrence and of erative epidermal changes, including cancer. The rea- correct unexposed comparison groups make case reports son for the greater risk among female patients than a shaky basis for qualitative or quantitative inferences re- among male patients, although not clearly ascertained garding cause-and-effect relationships. In our cohort of pa- statistically in our data, is unclear. It may be related to tients with HS, we observed a 4.6-fold increase of non- hormonal factors or to the fact that HS has an earlier de- melanoma skin cancer 1 to 32 years after enrollment. This but among females than males, leading to a longer du- supports the clinical impression voiced in the previous case ration of the chronic disease in females. reports. There seems to have been no obvious concentra- In our study, for the first time, it was possible to in- tion of missed preclinical cancers in our cohort, as only vestigate other cancer risks in a relatively large group of one case with skin cancer was ascertained within the first patients with HS over 3 decades. Increases were found year of follow-up. In the National Swedish Cancer Regis- for several cancer types, most importantly buccal can- ter neither cases of basal cell carcinoma nor actinic kera- cer and primary liver cancer. We have no information tosis are reported. Thus, the nonmelanoma skin cancer cat- of the alcohol-drinking habits of our cohort, and, to our egory includes only squamous cell carcinoma and not knowledge, no such studies exist, but the increased in- squamous intraepidermal neoplasia or Bowen disease. cidence of primary liver and buccal cancer might be an

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©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Table 3. Standardized Incidence Ratio (SIR) and Its 95% Confidence Interval (CI) for Selected Cancer Types Among Patients Hospitalized for Hidradenitis Suppurativa, 1965-1997, Sweden, Stratified by Various Cofactors*

Nonmelanoma All-Site Cancer Skin Cancer Buccal Cancer Primary Liver Cancer

Characteristics Obs† SIR 95% CI Obs† SIR 95% CI Obs† SIR 95% CI Obs† SIR 95% CI Sex Male 26 1.7 1.1-2.5 1 1.7 0.04-9.2 2 4.0 0.5-14.6 3 20.6 4.2-60.1 Female 47 1.4 1.0-1.8 4 8.2 2.2-21.0 3 7.3 1.5-21.4 0 ...... Follow-up duration, y 1-9 43 1.4 1.0-1.9 2 3.0 0.4-10.8 1 1.8 0.04-9.9 2 10.9 1.3-39.3 10+ 30 1.5 1.0-2.2 3 7.1 1.5-20.7 4 11.6 3.2-29.8‡ 1 8.6 0.2-47.7 Period of enrollment in the cohort 1965-1986 55 1.5 1.1-2.0 3 4.0 0.8-11.7 4 6.1 1.7-15.7 2 9.3 1.1-33.6 1987-1997 18 1.3 0.8-2.1 2 5.9 0.7-21.2 1 3.9 0.1-21.8 1 11.7 0.3-65.2 Alcohol abuse No 70 1.5 1.2-1.9 5 4.9 1.6-11.5 4 4.8 1.3-12.3 3 10.8 2.2-31.5 Yes 3 1.0 0.2-2.9 0 ...... 1 13.3 0.3-74.1 0 ...... Diabetes mellitus No 61 1.3 1.0-1.7 4 4.0 1.1-10.3 2 2.5 0.3-8.8 2 7.4 0.9-26.8 Yes 12 2.8 1.5-5.0‡ 1 10.6 0.3-59.1 3 33.7 6.9-98.4§ 1 32.7 0.8-182.0 Surgical excision No 40 1.5 1.1-2.1 1 1.4 0.04-8.0 4 7.9 2.2-20.3 3 16.7 3.4-48.8 Yes 33 1.4 1.0-2.0 4 10.2 2.8-26.2 1 2.5 0.1-13.8 0 ......

*Data exclude the first year of follow-up. Ellipsis indicates not applicable. †Observed (Obs) cases of cancer. ‡Differences of SIRs between 2 strata, PϽ.05. §Difference of SIRs between 2 strata, PϽ.01.

indication of excessive drinking among patients with HS. cers in this cohort make the risk estimates highly sensi- Although the excesses remained practically unaltered in tive to chance effects. Second, because we used hospital the stratum of patients with no recorded alcoholism, the discharge data to identify our cohort, we may have se- possibility of residual confounding of alcohol abuse can- lected patients with the most severe form of HS26 and, not be excluded, since probably only a small proportion thus, artificially increased the likelihood of finding other of alcohol abusers will be given a co-diagnosis of alco- serious diseases. Moreover, hospitalized patients may have holism when they are hospitalized for other reasons. Ac- an excess of comorbidities, in turn, associated with can- cording to epidemiological data, cigarette smoking seems cer risk. The closer surveillance of hospitalized patients to be involved in many skin diseases as reviewed previ- may also introduce some ascertainment or detection bias ously.23 We have no information on the smoking habits for skin, breast, and prostate neoplasms. However, the of our patients, but in a questionnaire study of 63 pa- excess risk for all-site cancer, buccal cancer, liver can- tients with HS, 89% were smokers compared with 46% cer, and nonmelanoma skin cancer persisted after 10 years in a matched-pair control group.24 Similar results regard- of observation, which argues for a true relation with HS. ing smoking habits and HS were found in a recent ret- Third, information on potential confounding factors, such rospective study.25 Therefore, substantial confounding by as cigarette smoking, alcohol drinking, and occupa- smoking cannot be ruled out, since the risk of lung can- tional exposures was unavailable for adjustment. Fi- cer (SIR, 1.7; 95% CI, 0.6-4.1) and mortality from lung nally, we could not separate HS from some other skin cancer (standardized mortality ratio, 1.7; 95% CI, 0.5- diseases (ie, pompholyx, bromhidrosis, and chromhi- 3.9) were increased. The reason for this relationship be- drosis) during the 1987-1996 period. Thus, our cohort tween the presence of HS, buccal cancer, liver cancer, and may contain some patients who did not have HS. How- cancer in general, if true, and causal, is unclear. How- ever, no material difference of cancer risk pattern be- ever, microbial or lifestyle factors or genetic predisposi- tween the 2 periods (1965-1986 vs 1987-1997) was ob- tion are suggested to be included in the considerations. served, which suggests no important influence on our The major strength of our study is the internal validity, results by this misclassification of exposure. that is, the stringent cohort design with no losses to fol- low-up and virtually complete cancer ascertainment. The CONCLUSIONS epidemiological approach ensured that our patients were representative of hospitalized Swedish patients with HS, We have shown a statistically significant 50% excess of thus benefiting the external validity. Moreover, the re- malignant neoplasms among patients with HS. The great- striction to patients admitted to hospitals probably mini- est relative excess among patients with HS was for non- mizes misclassification of the studied condition. How- melanoma skin cancer, buccal cancer, and primary liver ever, several limitations should also be noted in the cancer, but the confounding by smoking and possibly al- interpretation of our findings. First, owing to the rarity cohol abuse might explain some or most of these excess of HS, the small numbers of expected cases of some can- risks. The increased frequency of skin cancers, the site

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©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 of the chronic inflammation, and bacterial colonization, and perianal squamous cell carcinoma. Australas J Dermatol. 1997;38:209- support a possible etiopathologic link between the dis- 211. 10. Lin MT, Breiner M, Fredricks S. Marjolin’s ulcer occurring in hidradenitis sup- ease and neoplasia. Clinicians caring for patients with HS purativa. Plast Reconstr Surg. 1999;103:1541-1543. should be aware of their propensity to develop these 11. Malaguarnera M, Pontillo T, Pistone G, Succi L. Squamous cell cancer in Ver- tumors. Whenever atypical clinical manifestations of neuil’s disease (hidradenitis suppurativa) [letter]. Lancet. 1996;348:1449. HS occur, histopathologic examination of representa- 12. Manolitsas T, Biankin S, Jaworski R, Wain G. Vulval squamous cell carcinoma arising in chronic hi dradenitis suppurativa. Gynecol Oncol. 1999;75:285-288. tive skin biopsy specimens are recommended. 13. Perez-Diaz D, Calvo-Serrano M, Martinez-Hijosa E, et al. Squamous cell carci- noma complicating perianal hidradenitis suppurativa. Int J Colorectal Dis. 1995; Accepted for publication January 31, 2001. 10:225-228. This study was supported by grants from the Edvard 14. Shukla VK, Hughes LE. A case of squamous cell carcinoma complicating hidrad- Welander Foundation, Stockholm, Sweden (Dr Lapins) and enitis suppurativa. Eur J Surg Oncol. 1995;21:106-109. 15. Sparks MK, Kuhlman DS, Prieto A, Callen JP. Hypercalcemia in association with the Finsen Foundation, Stockholm (Dr Lapins). cutaneous squamous cell carcinoma: occurrence as a late complication of hi- Corresponding author: Jan Lapins, MD, Department dradenitis suppurativa. Arch Dermatol. 1985;121:243-246. of Medicine, Section of Dermatology and Venereology, 16. Zachary LS, Robson MC, Rachmaninoff N. Squamous cell carcinoma occurring I43, Karolinska Institutet at Huddinge University Hospi- in hidradenitis suppurativa. Ann Plast Surg. 1987;18:71-73. 17. Mattsson B, Rutqvist LE, Wallgren A. Undernotifaction of diagnosed cancer cases tal, SE-14186 Stockholm, Sweden (e-mail: Jan.Lapins to the Stockholm Cancer Registry. Int J Epidemiol. 1985;14:64-69. @dermat.hs.sll.se) 18. Bailar JC, Ederer F. Significance factors for the ratio of Poisson variable to its expectation. Biometrics. 1964;20:639-643. 19. Breslow NE, Day NE. The Design and Analysis of Cohort Studies. Lyon, France: REFERENCES International Agency for Research on Cancer; 1987. 20. Raad II, Bodey GP. Infectious complications of indwelling vascular catheters. Clin 1. Jansen T, Plewig G. inversa. Int J Dermatol. 1998;37:96-100. Infect Dis. 1992;15:197-208. 2. Anstey AV, Wilkinson JD, Lord P. Squamous cell carcinoma complicating hi- 21. Dougherty SH. Pathobiology of infection in prosthetic devices. Rev Infect Dis. dradenitis suppurativa. Br J Dermatol. 1990;123:527-531. 1988;10:1102-1117. 3. Black SB, Woods JE. Squamous cell carcinoma complicating hidradenitis sup- 22. Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the purativa. J Surg Oncol. 1982;19:25-26. most common bacteria found in cultures from the deep portions of hidradenitis 4. Camisa C. Squamous cell carcinoma arising in . Cutis. 1984;33: suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Dermatol. 185-187, 190. 1999;140:90-95. 5. Curry SS, Gaither DH, King LE. Squamous cell carcinoma arising in dissecting 23. Smith JB, Fenske NA. Cutaneous manifestations and consequences of smoking. perifolliculitis of the scalp: a case report and review of secondary squamous cell J Am Acad Dermatol. 1996;34:717-732. carcinomas. J Am Acad Dermatol. 1981;4:673-678. 24. Konig A, Lehmann C, Rompel R, Happle R. Cigarette smoking as a triggering 6. Dufresne RG, Ratz JL, Bergfeld WF, Roenigk RK. Squamous cell carcinoma aris- factor of hidradenitis suppurativa. Dermatology. 1999;198:261-264. ing from the follicular occlusion triad. J Am Acad Dermatol. 1996;35:475-477. 25. Rompel R, Petres J. Long-term results of wide surgical excision in 106 patients 7. Gordon SW. Squamous cell carcinoma arising in hidradenitis suppurativa: case with hidradenitis suppurativa. Dermatol Surg. 2000;26:638-643. report. Plast Reconstr Surg. 1977;60:800-802. 26. Hurley HJ. Axillary , apocrine bromhidrosis, hidradenitis suppu- 8. Kaplan RP. Cancer complicating chronic ulcerative and scarifying mucocutane- rativa and familial benign pemphigus: surgical approach. In: Roenigk RK, Roenigk ous disorders. Adv Dermatol. 1987;2:19-46. HH Jr, eds. Dermatologic Surgery: Principles and Practice. 2nd ed. New York, 9. Li M, Hunt MJ, Commens CA. Hidradenitis suppurativa, Dowling Degos disease NY: Marcel Dekker Inc; 1996:623-645.

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