Conflicts of interest: none declared.
Senile gluteal dermatosis: a clinical study of 137 cases
Article first published online: 15 MAY 2013
© 2013 The International Society of Dermatology
International Journal of Dermatology
Volume 53, Issue 1, pages 51–55, January 2014
How to Cite
Liu, H.-N., Wang, W.-J., Chen, C.-C., Lee, D.-D. and Chang, Y.-T. (2014), Senile gluteal dermatosis: a clinical study of 137 cases. International Journal of Dermatology, 53: 51–55. doi: 10.1111/j.1365-4632.2012.05702.x
- Issue published online: 18 DEC 2013
- Article first published online: 15 MAY 2013
Senile gluteal dermatosis (SGD) is a common genital dermatosis but has gained little attention before. A large-scale clinical study of this disease is lacking.
Materials and methods
We examined 162 consecutive outpatients with gluteal skin diseases of different causes. Fourteen skin biopsies were performed. Patient's age, gender, body mass index (BMI), way of sitting or lying, treatment response, and underlying systemic diseases were recorded.
About 137 (85%) patients could be defined as SGD. These patients, with a mean age of 79.4 ± 40.7 years and a mean BMI of 21.7 ± 10.8, presented with either partial (n = 43, 31%) or full-blown (n = 94, 69%) SGD lesions characterized by the sign of so-called “three corners of a triangle”: brownish plaques on the gluteal cleft and each side of the buttocks. Male/female ratio was 130/7. Itching or pain of varying intensity was reported by 50 patients (36%) and 14 patients (10%), respectively. Eighty-six patients (53%) presented with horizontal hyperkeratotic ridges, a characteristic sign of SGD. Most patients spent most of the day sitting but reported no special way of sitting or lying. More than half of patients with SGD claimed no response to topical steroids and/or keratolytics. In comparison with patients with SGD, SGD-free patients were younger (61.3 ± 36 years, P = 0.0005) and heavier (BMI 26.2 ± 15.6, P < 0.0001) but showed no significant difference in the frequency of underlying systemic diseases.
SGD is a common dermatosis, mostly affecting the thinner elderly. Friction, pressures and long hours sitting seemed to be important factors to trigger this dermatosis.
Senile gluteal dermatosis (SGD) was first reported in Japan in 1979 as hyperkeratotic lichenified skin lesions of the gluteal cleft and seemed to be a common genital dermatosis, but there has been limited reporting in the West as well as minimal presence in major dermatology textbooks.[1-5]
In addition to skin lesions on the gluteal cleft, as we pointed out recently in a study involving 12 patients with SGD, scaly brownish plaques may also occur on each side of the buttocks and display a pattern of so-called “three corners of a triangle”. However, a large-scale clinical study of this disease is still lacking.
Materials and methods
It was difficult to recruit willing patients for examination as it required them to expose their gluteal area. We then opted to examine 162 consecutive outpatients who came to our OPD for their skin lesions on the gluteal area. SGD was defined as brownish scaly plaques on the gluteal cleft and each side of the buttocks forming complete or partial “three corners of a triangle”. Patients with tinea, candidiasis, or cutaneous amyloidosis were excluded from the study. Patient's age, gender, body weight, the way they sit or lie on a chair or bed, and the response to the treatments were recorded. Fourteen skin biopsies were performed. Special attention was given to the types of chair or bed used by patients daily.
Underlying systemic diseases
Retrospective or concurrent patient chart review was performed to see if there was any significant association between SGD and underlying systemic illness. Relevant systemic diseases were arbitrarily defined as those that might have made patients more prone to long periods of sitting or lying, such as neurogenic disorders, malignant neoplasms, heart failure, chronic joint problems (spine or knee joints), and nutrition deficiencies. These diseases were included for analysis only if they had been present for at least five years before SGD was identified with multiple hospitalizations or with occasional hospitalization but frequent outpatient visits for the same problem.
For comparison of continuous and categorical variables between SGD and SGD-free groups, the independent t- test, Fisher's exact test, Odds ratio, and corresponding 95% confidence intervals were performed using IBM SPSS 19 (SPSS, Chicago, IL, USA).
One-hundred and thirty-seven patients (85%) could be defined as SGD (Fig. 1a), with a mean age of 79.4 ± 40.7 years (age range, 53–92 years) and a male/female ratio of 130/7. Patients' body mass index (BMI) ranged from 15.0 to 28.6 (mean, 21.7 ± 10.8). The buttock lesions corresponded well with the tuberosity of ischium, but the gluteal cleft lesions did not necessarily match the coccygeal apex. About two-thirds of patients with SGD (n = 94, 69%) showed full-blown skin lesions on their gluteal cleft and the buttocks. Twenty-four patients (17%) presented with lesions on the gluteal cleft only. Fourteen patients (10%) presented with skin lesions on each side of their buttocks without involving the gluteal cleft. The remaining five patients (4%) presented with lesions on the gluteal cleft and a unilateral lesion on one side of the buttocks. In contrast to the darker, non-inflammatory plaques in almost all patients, inflammatory psoriasiform plaques with erosions were noted in 10 patients (Fig. 1b). Eighty-six patients (53%) presented with horizontal hyperkeratotic ridges (Fig. 1c), a characteristic sign of SGD. Ulcers of varying depth were noted in four patients.
Most patients spent most of the day sitting but reported no special way of sitting or lying. However, 13 patients did regularly sit on unpadded rattan or wooden chairs for long hours, and three patients slept on a hard-surfaced bed without a mattress. Two patients who developed concurrent keratotic plaques on the hips (Fig. 1d) slept more often on their sides than on their backs. Forty-six patients (33.6%) complained of modest itching. Nine patients (6.6%) complained of pain during sitting or lying, which could be relieved by cushions. Sixty patients (43.7%) reported modest response to topical steroids plus keratolytics (2% salicylic acid ointment or 10% urea cream), and pressure-relieving devices seemed to be more helpful.
There were 25 (15%) patients showing no SGD, with a mean age of 61.3 ± 36 years (age range, 20–95 years) and a male/female ratio of 21/4. Their BMI ranged from 21.6 to 32 (mean 26.2 ± 15.6). They visited our hospital for a variety of skin diseases on the buttocks, including herpes simplex, perianal pruritus, prurigo, verruca, and benign neoplasms. In comparison with patients with SGD, SGD-free patients were younger (P = 0.0005) and heavier (P < 0.0001).
The vast majority of our patients with SGD had certain underlying diseases, such as hypertension, benign prostate hyperplasia, and diabetes mellitus, among others. However, only systemic diseases probably relevant to the development of SGD were included for analysis. In the SGD group (n = 137), there were seven patients suffering from neurogenic disorders, 13 patients from cancers, four patients from congestive heart failure, 10 patients from advanced spine or knee joint problems, two patients from respiratory problems, one patient from nutrient deficiency, and six patients from coronary artery disease (CAD). Five of them suffered from double diseases. In the SGD-free group (n = 25), one patient had neurogenic disorders, three patients had cancers, four patients had advanced spine or knee joint problems, and no patient had double diseases (Table 1). Although Fisher's exact test showed no significant association between the systemic diseases and SGD, the estimated odds were higher (odds ratio > 1) for the patients with neurogenic disorder (1.292), congestive heart failure (1.719), and CAD (2.521; Table 1).
|Systemic diseases||No. of SGD patients with the disease||No. of SGD-free patients with the disease||P-valuea||Odds ratio||95% CI for odds ratio|
|Neurogenic disorderb||7||1||N/S (1.00)||1.292||0.15, 10.99|
|Cancer||13||3||N/S (0.72)||0.769||0.20, 2.92|
|Congestive heart failure||4||0||N/S||1.719c||0.09, 32.92|
|Joint problemsd||10||4||N/S (0.24)||0.413||0.12, 1.44|
|Respiratory probleme||2||0||N/S||0.941c||0.04, 20.18|
|Nutrient deficiencyf||1||0||N/S||0.560c||0.02, 14.15|
|Total||43||8||N/S (1.00)||0.972||0.39, 2.43|
In most SGD cases, the histopathological changes were constant but rather nonspecific: psoriasiform epidermal hyperplasia with vascular dilatation in the papillary dermis and sparse lymphohistiocytic infiltration (Fig. 2a). When advanced, the skin lesions became more inflamed: papillary dermal edema, small-vessel dilatation/proliferation extending down to the reticular dermis, dense lymphohistiocytic infiltration, and occasional erosion. There was no interface change or incontinence of pigment (Fig. 2b).
Our study suggested that SGD is a common dermatosis because most patients we examined had genital dermatosis fulfilling the definition of SGD. This dermatosis, when first reported, seemed to be common among Japanese and was thought to be due to constant friction and chafing from the custom of sitting and lying on “tatami”, straw mats used as flooring in Japan.[1-3] However, SGD seemed to be rarely reported in Westerners. Our patients with SGD presented with similar lesions on the gluteal cleft, as described previously, but the associated skin lesions on the buttocks were also an important part of the disease, forming the so-called “three corners of a triangle” pattern, as we reported recently. In addition, lesions on the hips can also occasionally happen, reinforcing the important role of pressure and friction. Because none of our patients used straw mats at home, other regular furniture, especially those providing hard surface, was capable of inducing SGD. In this sense, we speculate that SGD should not be limited to Japanese or Taiwanese but be common in aged people of all races.
Most of our patients with SGD were male, but the majority (about 60%) of patients visiting our hospital were veterans who tend to be elderly. Further study to look into the incidence of SGD in younger populations, especially wheelchair-bound individuals, may be warranted.
Most of our patients with SGD presented with dark non-inflammatory plaques, but 10 patients were noted to have inflammatory psoriasiform plaques with occasional erosions (Fig. 1b). These 10 patients had multiple admissions for several systemic diseases. However, we could not conclude that severe underlying diseases had triggered the development of erosions based on two reasons: (1) patients with SGD tended to be old, thus connected to some systemic diseases; and (2) several other patients with SGD suffering from severe systemic diseases did not show erosion or ulcer.
The clinical and histopathological features of SGD may mimic early stages of decubitus ulcer in some ways. Most of our patients showed sacral skin lesions, and four of them developed ulcers. In addition, two patients showed concomitant skin lesions on the hips corresponding with the greater trochanter (Fig. 1d). All salient histopathological features of early decubitus ulcer could be found in patients with SGD: dilated capillaries and venules in the papillary dermis as well as mild to moderate papillary dermal edema.
Although about half of our patients reported modest response to topical steroids and/or keratolytics, they were mostly unsatisfied with the treatments. On the contrary, pressure-relieving devices such as life buoy-shaped loop or air- or water-filled cushion could actually offer more help.
The histopathological changes of SGD were nonspecific, but the diagnosis can be made on purely clinical grounds based on the sign of “three corners of a triangle” and horizontal hyperkeratotic ridges. SGD should be differentiated from friction melanosis (FM), a skin disease with localized hyperpigmentation over bony prominences such as the clavicle, scapula, or vertebrae following repetitive rubbing in predisposed, usually dark-skinned individuals.[8-10] Although there is potential to develop FM on the gluteal area, the pigmentation in a ripple pattern is not seen in SGD. In addition, postinflammatory melanin deposits characteristic of FM were not found in SGD.[8-10]
In comparison with patients with SGD, SGD-free patients were younger and heavier. This finding could have implications for the development of SGD, as aged persons spend most of their time sitting, and thinner persons' fat could less likely cushion the impact of friction and pressure.
Theoretically, patients' underlying systemic diseases could play a role in the development of SGD. However, we found no significant difference in the frequency of underlying systemic diseases between SGD and SGD-free groups. The reason remains unclear. Perhaps the limited number of patients enrolled in our study may count. The other possibility is that we do not know how long is necessary for certain systemic diseases or how severe the disease is to trigger the development of SGD. Further study with more patients and long-term follow-up would help delineate the role of underlying systemic diseases in the development of SGD, especially those diseases showing higher odds ratio (>1) in our study, such as neurogenic disorder, congestive heart failure, and CAD (Table 1).
In conclusion, SGD is a common dermatosis mostly affecting the thinner elderly. Friction, pressures, and long hours sitting seemed to be important factors to trigger this dermatosis. The role of underlying systemic diseases needs further clarification.
The authors thank Prof. Benjamin Ing-Tiau Kuo and his team for assistance with statistics and data analysis.
- 1Hyperkeratotic lichenified skin lesion of gluteal region. Nishinihon J Dermatol 1979; 41: 798., .
- 2Hyperkeratotic lichenified skin lesion of gluteal region. Pract Dermatol 1985; 7: 1143–1146., .
- 4A senile gluteal dermatosis caused by friction. Eur J Dermatol 1992; 2: 157–159., .
- 5Mechanical and thermal injury. In: Burns T, Breathnach S, Cox N, Griffiths C, eds. Rook's Textbook of Dermatology, 8th edn. Singapore: Blackwell, 2010: 28:15., , .