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International Wound Journal logoLink to International Wound Journal
. 2023 Feb 6;20(6):2215–2223. doi: 10.1111/iwj.14099

Risk factors associated with keloid infections: A five‐year retrospective study

Zhengyun Liang 1,2, Mingzi Zhang 1, Yan Hao 1,2, Mengjie Shan 1,2, Hao Liu 1, Yijun Xia 1,2, Qiao Chen 1, Guojing Chang 1, Youbin Wang 1,
PMCID: PMC10333032  PMID: 36746767

Abstract

Keloid infections reduce patient‐reported quality of life greatly. Characteristics and risk factors of keloid infections have not been thoroughly studied. So, a retrospective cohort study was conducted focusing on the potential risk factors, microbiologic cultures and histological findings. Keloid patients consulting for surgical interventions were included in this study. Data were collected from their electronic medical records. 564 patients were recruited with the keloid infection rate being 22.4%. For adult patients, age above 40 years (OR, 2.84; P = .000), disease duration of 12 years or more (OR, 3.03; P = .000), the number of keloids over 3 (OR, 1.59; P = .050) and the presence of family history (OR, 1.91; P = .027) were significantly associated with keloid infections. Suppurative keloids were located mostly in thorax (61.79%). For the under‐age subgroup(n = 25), family history was frequently seen in patients with infections. Microbiologic cultures revealed a mixed spectrum of bacteria including Staphylococcus (25%), Actinomyces (30%) and Prevotella (10%). The rate of epidermoid cysts was 19.7% in histological examination. Age > 40 years, disease duration ≥12 years, the number of keloids >3 and the presence of family history are risk factors for keloid infections.

Keywords: infections, keloid, multivariate analysis, risk factors, suppuration

1. INTRODUCTION

Characterised by abnormal activity of fibroblasts and redundant deposition of extracellular matrix, keloids are a type of pathological scars caused by reticular dermis injuries or no obvious triggers. Keloids are considered to be the combined result of nature and nurture. Other than pain and pruritus, keloids can cause cosmetic issue and psychological trauma. 1 The decrease of patient‐reported quality of life is particularly pronounced in keloid with infections. Keloid infections, also known as suppurative keloids, suppurative keloidosis and keloid suppuration, can give rise to redness, agonising pain, tenderness, sinus and pus discharge. Harmful as keloid infections are, studies regarding characteristics and risk factors of keloid infections are rather scarce. Therefore, we conducted a retrospective cohort study focusing on the potential risk factors, microbiologic cultures and histological findings of keloids with infection.

2. MATERIAL AND METHODS

2.1. Patient recruitment and data collection

From July 2017 to July 2022, keloid patients consulting for surgical interventions were enrolled in this study in the plastic surgery department of Peking Union Medical College Hospital (PUMCH). Diagnostic criteria for keloids were as follows: elevated fibrous masses, which extend beyond the original wound borders with no sign of regression. The diagnoses were later confirmed by pathological examination of surgically removed tissues. Surgical contraindications such as severe heart, liver and brain diseases, were not seen in any of the enrolled patients. Following the Declaration of Helsinki principles, this study was approved by the Ethics Committee of Peking Union Medical College Hospital, China. Informed consent was obtained from all patients or their legal guardians.

Electronic medical records were accessed and the following data were collected: gender, age, disease duration, onset age, body mass index, keloid‐triggering events, keloid symptoms, presence of keloid infection, the number of keloids, keloid distribution, family history, habits of smoking or drinking, comorbidities (hypertension and its grading, diabetes and rheumatism), blood routine (WBC, neutrophil, lymphocyte, platelet and haemoglobin count), creatinine, alanine aminotransferase and preoperative temperature. Preoperative temperature was defined as the core temperature taken in the morning one day prior to surgery. The microbiologic culture results of pus swabs taken from keloids with infections were extracted as well. Suppurative keloid tissues excised from operation were read by experienced pathologists to detect any abnormalities.

2.2. Statistical analysis

Continuous variables were presented as means with standard deviations except for the number of keloids, which would be displayed as medians, while categorical variables were expressed as frequencies. For the univariable analysis, continuous variables were analysed using student's t test or Mann–Whitney tests as appropriate and chi‐square test was utilised to analyse categorical variables.

For the multivariate analysis, logistic regression was conducted on potential variables with a P‐value less than .05 in the univariable analysis. Since increased preoperative temperature, pronounced pain and pruritus might be caused by keloid infections, these three factors were excluded from the multivariate analysis. Keloid distribution and triggering factors were eliminated too, for some patients had several keloids at different locations, with variable triggering factors and not all of these lesions had infection outbreaks. A P‐value less than .05 suggested statistical significance. Statistical analysis was carried out by applying IBM SPSS (version 24.0).

3. RESULTS

564 patients in total were included in this cohort study, 22.4% (127 patients) of which had experienced at least one infection outbreak from a least one of their keloids (Figure 1). Female patients predominated over male patients in groups with or without infections. The adult group comprised 539 patients while 25 patients were assigned to the under‐age group (younger than 18 years old).

FIGURE 1.

FIGURE 1

Photographs of keloids with infections. (A) Chest keloid with ulcer and surrounded by pigmentation. (B) Umbilical keloid with ulcer and pus. (C) Sinus formation in a chest suppurative keloid. (D) Chest keloid with redness, ulcer and crust

3.1. Characteristics of adult patients with and without infections

For the adult group (Table 1), patients with infections were significantly older than in those without infections (44.88 ± 15.17 versus 34.85 ± 13.41, P = .000) with a longer disease duration (15.32 ± 10.08 versus 8.22 ± 7.20, P = .000). More patients with keloid infections complained of pain and pruritus (respectively 87.0% versus 54.8%, P = .000; and 90.2% versus 81.5%, P = .022). Keloid‐triggering events differed between the two groups with a higher frequency of surgery (27.7% versus 17.3%, P = .011) and lower frequency of piercing (1.6% versus 10.3%, P = .002) in patients with infections. The number of keloids tended to be greater in patients with infections than those without infections (3 versus 2, P = .042). Patients with suppurative keloids tended to have keloid lesions more distributed in thorax, waist and abdomen, arms and legs, and perineum (thorax: 77.2% versus 63.9%, P = .006; waist and abdomen: 30.9% versus 15.9%, P = .000; arms and legs: 20.3% versus 12.3%, P = .024; perineum: 21.1% versus 9.6%, P = .001) but less in ears (8.1% versus 16.6%, P = .020). Suppurative keloid distribution was also recorded in Table 2. 5 patients had more than one suppurative keloid. Keloid lesions with infections were located mostly in thorax (61.79%), followed by waist and abdomen (17.89%) and perineum (10.57%).

TABLE 1.

The comparison of clinical characteristics between adult patients with and without infections

Keloids with infection Keloids without infection Univariate analysis (P value)
No. of patients 123 416
Gender .685
Female 72 (58.5%) 252 (60.6%)
Male 51 (41.5%) 164 (39.4%)
Sex‐ratio (F:M) 1.41:1 1.54:1
Age (years) 44.88 ± 15.17 34.85 ± 13.41 .000**
Disease duration (years) 15.32 ± 10.08 8.22 ± 7.20 .000**
Onset age (years) 29.56 ± 14.34 26.62 ± 12.83 .062
Body mass index (kg/m2) 25.12 ± 4.00 24.26 ± 4.43 .055
Cause .006**
Trauma 3 (2.5%) 27 (6.5%) .085
Surgery 34 (27.7%) 72 (17.3%) .011*
Piercing 2 (1.6%) 43 (10.3%) .002**
Acne 26 (21.1%) 96 (23.1%) .652
Folliculitis 8 (6.5%) 20 (4.8%) .456
Others 2 (1.6%) 11 (2.7%) .755
Spontaneous 48 (39.0%) 147 (35.3%) .455
Symptoms
Pain 107 (87.0%) 228 (54.8%) .000**
Pruritus 111 (90.2%) 339 (81.5%) .022*
Number of keloids 3 2 .042*
Keloid distribution
Thorax 95 (77.2%) 266 (63.9%) .006**
Waist&abdomen 38 (30.9%) 66 (15.9%) .000**
Back & shoulders 40 (32.5%) 129 (31.0%) .751
Head & neck 14 (11.4%) 55 (13.2%) .592
Arms & legs 25 (20.3%) 51 (12.3%) .024*
Ears 10 (8.1%) 69 (16.6%) .020*
Perineum 26 (21.1%) 40 (9.6%) .001**
Family history 27 (22.0%) 49 (11.8%) .004**
Smoking 12 (9.8%) 46 (11.06%) .682
Alcohol 4 (3.3%) 18 (4.33%) .597
Comorbidities
Hypertension 24 (19.5%) 47 (11.3%) .018*
Grade I 9 (7.3%) 13 (3.1%)
Grade II 7 (5.7%) 16 (3.9%) Inline graphic.089
Grade III 8 (6.5%) 18 (4.3%)
Diabetes 10 (8.1%) 12 (2.9%) .010**
Rheumatism 1 (0.8%) 2 (0.5%) .664
Preoperative temperature (°C) 36.67 ± 0.25 36.31 ± 0.25 .000**
WBC count (×10 9/L) 6.24 ± 1.64 6.52 ± 1.71 .113
Neutrophil count (×10 9/L) 3.69 ± 1.30 3.85 ± 1.33 .219
Lymphocyte count (×10 9/L) 2.00 ± 0.58 2.10 ± 0.59 .112
Neutrophil:Lymphocyte 1.95 ± 0.80 1.95 ± 0.86 .971
Plt count (×10 9/L) 234.56 ± 55.72 250.19 ± 60.51 .011*
Hgb count (g/L) 139.30 ± 16.33 141.31 ± 16.18 .229
ALT (U/L) 19.79 ± 11.05 21.77 ± 16.55 .840
Cr (μmol/L) 66.02 ± 13.34 65.82 ± 12.79 .887

Abbreviations: ALT, alanine aminotransferase; Cr, creatinine; Hgb, haemoglobin; Plt, platelet.

*

P < 0.05.

**

P < 0.01.

TABLE 2.

Suppurative keloid distribution in adult patients (n = 123)

Keloid distribution n Percentage(%)
Thorax 76 61.8
Waist & abdomen 22 17.9
Back & shoulders 6 4.9
Head & neck 3 2.4
Arms & legs 4 3.3
Perineum 13 10.6
Ears 4 3.3

Moreover, the rate of a positive keloid family history was significantly higher in patients with infections (22.0% versus 11.8%, P = .004). Hypertension and diabetes were more frequently seen in patients with suppurative kelois (respectively 19.5% versus 11.3%, P = .018; and 8.1% versus 2.9%, P = .010), but hypertension grading was not significantly different between the two groups. Preoperative temperature was higher in groups with infections (36.67 ± 0.25 versus 36.31 ± 0.25, P = .000). A lower count of platelet in the circulating blood was observed in patients with infections than those without infections (234.56 ± 55.72 versus 250.19 ± 60.51, P = .011).

No gender difference was detected between the two groups. The following factors did not differ between groups with and without infections: onset age, body mass index, habits of smoking, habits of drinking, rheumatism, WBC, neutrophil, lymphocyte and haemoglobin count, creatinine and alanine aminotransferase.

Seven potential risk factors were included in the multivariable regression analysis (Table 3), after screening in compliance with the above criteria. Age above 40 years (OR, 2.84; P = .000), disease duration of 12 years or more (OR, 3.03; P = .000), the number of keloids over 3 (OR, 1.59; P = .050) and presence of family history (OR, 1.91; P = .027) were significantly associated with keloid infections. The difference between the two groups regarding hypertension, diabetes and platelet count was not statistically significant.

TABLE 3.

Multivariable regression analysis of factors associated with keloid infections

Variables OR 95% Confidence interval P value
Disease duration ≥12 years 3.03 1.882–4.862 .000
>40 years old 2.84 1.689–4.785 .000
>3 keloids 1.59 1.000–2.532 .050
Family history 1.91 1.077–3.381 .027
Hypertension 1.02 0.538–1.944 .946
Diabetes 1.22 0.457–3.238 .694
Platelet ≤234 (×109/L) 1.3 0.829–2.027 .256

3.2. Characteristics of under‐age patients with and without infections

For the under‐age (Table 4), presence of family history was more frequently seen in patients with infections (25% versus 0%, P = .036). Patients with keloid infections were prone to have increased preoperative temperature (36.95 ± 0.25 versus 36.28 ± 0.23, P = .000). Other variables including keloid distribution were not significantly different between the two groups. Out of 4 patients with infections, 2 had their suppurative keloids located in thorax, 1 in right shoulder and 1 in right ear. Since only one variable, family history, was left after screening according to criteria, multivariable regression analysis was not conducted for the under‐age.

TABLE 4.

The comparison of clinical characteristics between under‐age patients with and without infections

Keloids with infection Keloids without infection Univariate analysis (P value)
No. of patients 4 21
Gender .796
Female 2 (50%) 12 (57.1%)
Male 2 (50%) 9 (42.9%)
Sex‐ratio (F:M) 1.00:1 1.33:1
Age (years) 14.08 ± 1.27 12.10 ± 3.71 .413
Disease duration (years) 7.25 ± 3.86 3.95 ± 3.37 .092
Onset age (years) 6.83 ± 2.72 8.14 ± 3.70 .507
Body mass index (kg/m2) 21.69 ± 5.18 21.66 ± 7.15 .994
Cause .56
Trauma 0 6 (28.6%)
Surgery 3 (75%) 9 (42.9%)
Piercing 0 0
Acne 0 1 (4.7%)
Folliculitis 0 0
Others 0 0
Spontaneous 1 (25%) 5 (23.8%)
Symptoms
Pain 3 (75%) 9 (42.9%) .248
Pruritus 4 (100%) 13 (61.9%) .229
Number of keloids 3 1 .261
Keloid distribution
Thorax 2 (50%) 5 (23.8%) .295
Waist&abdomen 0 1 (4.8%) .81
Back & shoulders 1 (25%) 4 (19.1%) .789
Head & neck 0 2 (9.5%) .932
Arms & legs 1 (25%) 1 (4.8%) .18
Ears 1 (25%) 8 (38.1%) .624
Perineum 0 2 (9.52%) .932
Family history 1 (25%) 0 .036*
Smoking 0 0 NA
Alcohol 0 0 NA
Comorbidities
Hypertension 0 1 (4.8%) .81
Grade I 0 0
Grade II 0 1 (4.8%) Inline graphic .81
Grade III 0 0
Diabetes 0 0 NA
Rheumatism 0 0 NA
Preoperative temperature(°C) 36.95 ± 0.25 36.28 ± 0.23 .000 **
WBC count (×10 9/L) 8.94 ± 2.91 6.50 ± 1.33 .192
Neutrophil count (×109/L) 5.85 ± 3.35 3.20 ± 0.82 .212
Lymphocyte count (×109/L) 2.35 ± 0.75 2.72 ± 0.85 .426
Neutrophil:Lymphocyte 3.13 ± 3.03 1.27 ± 0.46 .103
Plt count (×109/L) 245.25 ± 49.31 286.57 ± 54.52 .173
Hgb count (g/L) 138 ± 4.55 135.86 ± 11.37 .718
ALT (U/L) 12 ± 3.61 25.11 ± 25.76 .399
Cr (μmol/L) 51.33 ± 2.08 49.89 ± 13.65 .86

Abbreviations: ALT, alanine aminotransferase; Cr, creatinine; Hgb, haemoglobin; Plt, platelet.

*

P < .05.

**

P < .01.

3.3. Microbiologic cultures of suppurative keloid pus

Swabs of pus were taken for further microbiologic cultures from 20 patients with suppurative keloids. Microbiologic cultures indicated 6 patients had polymicrobial infections. 11 g‐positive Cocci (11/20; 55%) including different types of Staphylococcus (5/20, 25%) were found in these cultures. 8 g‐positive bacilli (8/20; 40%) were detected, the majority of which were various Actinomyces (6/20; 30%). Gram‐negative bacteria found in the cultures were all bacilli (7/20,35%), 2 of which were Prevotella (2/20,10%). 7 out of these bacteriological cultures yielded negative results. Details of microbiologic culture results was shown in Table 5.

TABLE 5.

Microbiologic culture results of suppurative keloid pus (n = 20)

Microbial population n Percentage(%)
Gram‐positive
Cocci 11 55.0%
Oxacillin‐sensitive Staphylococcus aureus 1 5.0%
Staphylococcus epidermidis 2 10.0%
Oxacillin‐resistant Staphylococcus epidermidis 1 5.0%
Coagulase negative Staphylococcus 1 5.0%
Enterococcus faecalis 1 5.0%
Anaerobic bacteria 1 5.0%
Finegoldiamagna 1 5.0%
Others 3 15.0%
Bacilli 8 40.0%
Corynebacterium 1 5.0%
Actinomyces 6 30.0%
Actinomyces europaeus 2 10.0%
Actinomyces turicensis 1 5.0%
Others 1 5.0%
Gram‐negative
Bacilli 7 35.0%
Prevotella 2 10.0%
Prevotella.buccae 1 5.0%
Pseudomonas aeruginosa 1 5.0%
Haemophilus parainfluenzae 1 5.0%
Porphyromonas 1 5.0%
Others 2 10.0%
Negative 7 35.0%

For the under‐age, 1 out of 4 microbiologic cultures yielded positive results. Oxacillin‐resistant Staphylococcus epidermidis was found in this microbiologic culture.

3.4. Histological findings of suppurative keloid tissues

All surgically removed keloid tissues displayed an acute and/or chronic inflammatory infiltrate. Abscess areas were seen in 9 samples and ulcer formation in 5 samples. Histological examination showed that epidermoid cysts were present in 25 suppurative keloid tissues (25/127;19.7%), most of which were accompanied by abscess, rupture and giant cell reaction. Glandular dysplasia and adenocarcinoma were found in 1 sample. Squamous epithelium hyperplasia was also seen in 1 keloid tissue.

4. DISCUSSION

Although the pathogenesis of keloids still remains inconclusive, ample evidences indicate that keloids are the result of continuous local inflammation in the reticular dermis. 2 Characterised by imbalance of multiple cytokines and dysregulation of immune cells, such as macrophages, 3 , 4 keloids could be labelled as one of the immunocompromised cutaneous districts (ICDs). 5 Like all ICDs, this regional immune defect renders keloids vulnerable to opportunistic infection outbreaks. Episodes of infections are associated with more diminished quality of life compared with patients without infections. The rate of keloids with infection is rather high;22.4% in our study and 26% in a 114‐patient cohort. 6 Thus characteristics and risk factors of keloid infections should be thoroughly investigated to achieve better clinical results.

By examining demographic characteristics and keloid‐related characteristics, we found that age, disease duration, symptoms, the number of keloids, family history, hypertension, diabetes, preoperative temperature and platelet count are possible factors associated with keloid infections. Besides, the majority of keloid infections occurred in the thorax, one of the high‐tension areas. Females predominated over males with or without infections but surprisingly, no sex difference was detected in the univariate analysis. Several researches have suggested male gender predominance in suppurative keloids. 6 , 7 This discrepancy may be due to the different patient groups. Patients with infections seemed to display more pain and pruritus with a higher basic body temperature, which is quite understandable. Since infection could cause pain, pruritus and raise in body temperature, these three variables were eliminated, leaving only seven variables in the multivariate regression analysis.

Diabetes is anticipated to affect keloid formation, progress and infection, because diabetic wounds demonstrate pronounced NLRP3 inflammasome activity, 8 which is considered to play an essential role in keloid fibrosis. 9 Additionally, infection predisposition in diabetes mellitus is plain to see. However, diabetes is not a risk factor for keloid infection in this study though a significantly higher proportion of DM was observed in patients with suppurative keloids. Similarly, hypertension is not significantly associated with keloid suppuration in the multivariable analysis, even though both hypertension and infection are factors in severe keloids. 10 , 11 As for platelets, a lower level of circulating platelets in patients with keloid infections was detected in the univariate but not multivariate analysis. This trend might be explained by the ability of human keloid fibroblasts to directly promote platelet aggregation. 12 Plus, platelets take an active part in the immune response to microbial organisms, 13 which means when infections occur in a keloid lesion, platelets are gathered at the site of infection but not in the circulating blood.

In our study, the multivariable analysis revealed that age above 40 years, disease duration of 12 years or more, the number of keloids over 3 and the presence of family history are independent risk factors for keloid infections. Firstly, because aging leads to dysregulation of the immune system, 14 it would not be a surprise to find that middle age (over 40 years old) is associated with greater susceptibility to infections in keloid patients. Secondly, it has been reported that longer duration of keloid correlates with low growth rate and high keloid recurrence. 15 Our study indicated that long keloid duration also increases the risk of lesion infection, adding to the importance of early and systematic intervention of keloids. Thirdly, a greater number of keloids usually means more severe keloid condition. 11 If there are lots of keloids, personal hygiene could be a huge challenge, increasing susceptibility to infections. Patients with multiple keloids should be educated to clean every single keloid daily and properly to minimise infections. Lastly, keloid family history not only significantly correlates with keloid distribution, 16 keloid formation 17 and progression 18 but also, according to our results, is a risk factor for one of the keloid complications. Shan et al. demonstrated significantly reduced expression of CCR7, a member of the chemokine receptor superfamily responsible for immune response mediation, in patients with keloid family history. Co‐stimulatory molecules such as CD80 and CD86 also tended to decrease in family‐history‐positive keloid patients. 19 These genetic abnormalities lead to impaired immune response against infections and inflammation in patients with keloid family history, thus explaining why the presence of family history negatively affect keloid lesion in many ways.

Microbiologic cultures revealed that keloid suppuration is mostly opportunistic infections caused by members of the human microbiota. The bacterial spectrum of suppurative keloids is rich and mixed. It includes bacteria with various biological features, such as Staphylococcus, one of the gram‐positive cocci commonly seen in clinical infections, Actinomyces, gram‐positive bacilli which are found in the breast abscesses and gangrene, 20 , 21 and Prevotella, the causative gram‐negative bacilli for oral as well as musculoskeletal and skin infections. 22 Because regional immune dysregulation might be the cause of these opportunistic infections in keloid lesion, extra caution should be taken on the application of corticosteroids for suppurative keloids, especially polymicrobial ones, which is rather not rare in keloid suppuration. Usage of antibiotics should be adjusted according to prior antimicrobial susceptibility testing, since these pathogens could be resistant to empirical antibiotic therapy.

By examining keloid tissues from patients with infections, we discovered that the presence of epidermoid cysts (ECs) is more common in suppurative keloids (19.7%) than previously thought. ECs in keloids may be of traumatic origins. 23 In ECs, epidermal fragments are trapped within scar tissues, giving rise to cyst formation along with activated inflammation. It is similar to the basic mechanism of suppurative keloids;that is fibrous entrapment, cyst formation, rupture and drainage, subsequent foreign body reaction and inflammatory infiltrate. 24 The relationship between ECs and keloid suppuration has not yet been explored. It might be a histopathologic parameter worth looking into in future researches.

For the juvenile age group, similar female preponderance was observed (Female: Male = 14:11) in the current study, which is partially consistent with the work of Michael et al. 25 Unlike the adult group, only family history and preoperative temperature were found to be significantly different between keloid infection and non‐infection subgroups. Pain and pruritus are common complaints of the under‐age with or without infection. Multimodal approach should be implemented as early as possible since the disfigurement of keloids might hinder children's psychological development.

At last, close follow‐ups, more detailed patient educations and more active interventions, such as surgery combined with radiotherapy, are highly recommended for keloid patients with one or more of the aforementioned risk factors. For those in the acute phase of keloid infection, the dressing should be changed once a day or more frequently to drain the wound. Pus sample, if any, should be taken for antimicrobial susceptibility testing to guide the usage of antibiotics. Antibiotics are applied only when infections deteriorate after regular dressing change. Since infections are prone to recur, patients with previous outbreaks of infections are indicated for surgical excision to thoroughly remove the source of infections.

5. CONCLUSION

Close follow‐ups and active interventions are recommended for keloid patients with one or more of the following risk factors: age above 40 years, disease duration of 12 years or more, the number of keloids over 3 and the presence of family history. Microbiologic cultures revealed that the bacterial spectrum of suppurative keloids is rich and mixed. Acute and/or chronic inflammatory infiltrate were present in all suppurative keloid samples. Epidermoid cysts were commonly seen in keloid infections.

AUTHOR CONTRIBUTIONS

Zhengyun Liang and Youbin Wang designed the research study. Yan Hao, Mengjie Shan, Qiao Chen and Hao Liu collected data from electronic medical records. Yijun Xia and Guojing Chang participated in clinical patient management and medical photography. Zhengyun Liang and Mingzi Zhang analysed the data. Zhengyun Liang wrote the paper. Zhengyun Liang and Youbin Wang revised the paper. Zhengyun Liang, Mingzi Zhang, Yan Hao, Mengjie Shan, Hao Liu, Yijun Xia, Qiao Chen, Guojing Chang and Youbin Wang have read and approved the final manuscript.

CONFLICT OF INTEREST

All authors declare that they have no conflicts of interest to disclose.

ETHICS STATEMENT

This study has been approved by the Ethics Committee of Peking Union Medical College Hospital, China (I‐22PJ261).

ACKNOWLEDGEMENT

This project was supported by The National Natural Science Foundation of China (Grant No. 81871538) and the 2019 Grant of Research and Application of Clinical Diagnosis and Treatment Technology in Beijing from Beijing Municipal Science and Technology Commission. (Z191100006619009).

Liang Z, Zhang M, Hao Y, et al. Risk factors associated with keloid infections: A five‐year retrospective study. Int Wound J. 2023;20(6):2215‐2223. doi: 10.1111/iwj.14099

DATA AVAILABILITY STATEMENT

Author elects to not share data.

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Data Availability Statement

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