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Bilateral localized lipoatrophy secondary to a single intramuscular corticosteroid injection

  • Author(s): Avilés-Izquierdo, JA
  • Longo-Imedio, MI
  • Hernánz-Hermosa, JM
  • Lázaro-Ochaita, P
  • et al.
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Bilateral localized lipoatrophy secondary to a single intramuscular corticosteroid injection
JA Avilés-Izquierdo MD, MI Longo-Imedio MD, JM Hernánz-Hermosa MD, P Lázaro-Ochaita MD
Dermatology Online Journal 12 (3): 17

Dermatology Service, Hospital "Gregorio Marañón", Madrid. Spain. dermaviles@gmail.com

Abstract

A 15-year-old boy developed two, almost symmetric, asymptomatic, depressed plaques, localized to both buttocks after receiving a single intramuscular corticosteroid injection in his right buttock for treatment of lumbar pain. He suffered from asthma since early childhood, and had been repeatedly treated with corticosteroid injections for many years as a young child. A skin biopsy from both lesions was performed, showing a decrease in the number and size of adipocytes. We describe a case of acquired localized lipoatrophy with a particular bilateral distribution secondary to a single intramuscular corticosteroid injection.


Atrophy of the subcutaneous fat may result from two different processes from a pathogenic point of view, lipoatrophy and lipodystrophy. Lipoatrophy refers specifically to a loss of subcutaneous fat attributed to a previous inflammatory process involving the subcutis. In contrast, lipodystrophy refers to an absence of subcutaneous fat with no evidence of inflammation.

Localized acquired lipoatrophies constitute a poorly defined group of diseases clinically characterized by focal loss of fat. Their development has been linked to trauma (drug injection) or inflammatory diseases such as panniculitis. Usually they are not associated with metabolic or systemic disorders and they tend to resolve spontaneously.


Clinical synopsis

A 15-year-old boy developed two almost symmetric, asymptomatic, round, depressed plaques localized to both gluteal areas (Fig. 1). His medical history was significant for severe asthma for which he received multiple intramuscular corticosteroid injections in early childhood.

He consulted a dermatologist because of lack of regression of the plaques 4 months after their onset. The patient received a single intramuscular corticosteroid injection (40 mg methylprednisolone) in his right buttock to treat an acute episode of lumbar pain, and few weeks later he noticed an erythematous and depressed plaque at the site of the injection. Interestingly, another similar plaque appeared in the following days localized to the left buttock, where he denied having received any trauma or injection.

Physical examination revealed two, almost symmetric, depressed plaques, 4 cm in diameter, localized to the upper-outer quadrant of both buttocks. Their surface was slightly erythematous, with partial alopecia, suggesting a previous inflammation process. The skin lesions were soft to palpation and no inflammation signs were present in the perilesional skin. A skin biopsy from both depressed plaques showed similar findings, a decrease in the number and size of adipocytes without any other significant findings in the epidermis or the dermis (Fig. 2). No treatment was prescribed. A followup visit at 2 months revealed signs of spontaneous resolution in both lesions. After 4 months complete recovery with normal hair regrowth was observed.

Based on the presence of inflammation, the histological findings, the evolution, and previous reports, we diagnosed of our case as a bilateral localized lipoatrophy secondary to corticosteroid injection.


Figure 1Figure 2
Figure 1. Almost bilateral atrophic round plaques localized on external sides of both buttocks.
Figure 2. H&E stained photomicrograph (power magnification × 120) from skin biopsy of the injection side, characterized by the small size of the lobules and the atrophy and the reduced number of adipocytes.

Discussion

Lipoatrophies are a heterogeneous group of diseases clinically characterized by partial or diffuse loss of fat that can be congenital or acquired. Acquired localized lipoatrophies can be classified based on whether an underlying cause is identified (Table 1). Secondary lipoatrophies are linked to preexisting inflammation induced by infections, connective tissue diseases (lupus erythematosus, morphea, dermatomyositis, or overlap disease), neoplasms, or trauma.

Table 1. Classification of acquired localized lipoatrophies
Primary or idiopathicSecondary
A) Lipoatrophia semicircularis
B) Lipodystrophia centrifugalis abdominalis infantilis
C) Involutional lipoatrophy
A) Pyogenic abscesses
B) Localized connective tissue diseases
C) T-cell lymphoma
D) Iatrogenic (subcutaneous, intramuscular, and dermal injections)

Localized lipoatrophy has received different names according to its clinical appearance and location, including annular lipoatrophy, abdominal lipoatrophy, semicircular lipoatrophy, and postinjection localized lipoatrophy. Localized lipoatrophy secondary to pressure and compression by tight-fitting clothes has also been described.

Lesions of localized lipoatrophy have been described as residual lesions of different types of panniculitis, but most cases are associated with intramuscular injections, mainly of corticosteroids and antibiotics [1, 2] but they have also been described after injections of insulin, vasopressin, recombinant growth hormone [3], adrenal cortex hormones [4], and methotrexate [5].

In those cases of lipoatrophy secondary to subcutaneous injections of corticosteroids, two different histopathologic patterns have been described. Both patterns are characterized by the small size of the lobules and by the atrophy of the reduced number of adipocytes. The first pattern consists of faintly acidophilic or albuminous small adipocytes that are retracted from the surrounding connective tissue of the septa. Inflammatory cells are sparse and blood vessels appear prominent, congestive, and dilated. The second histopathologic pattern seen in lesions of lipoatrophy secondary to subcutaneous injections of corticosteroids is characterized by small atrophic fat cells surrounded by a prominent vasculature [6].

Lipoatrophy refers specifically to a loss of subcutaneous fat attributed to a previous inflammatory process involving the subcutis. In contrast, lipodystrophy refers to an absence of subcutaneous fat with no evidence of clinical inflammation. However, in fully developed lesions of lipodystrophy, some authors have described an early inflammatory stage in lesions of lipodystrophy, with lymphocytes and vascular involvement in the fat lobule [6].

Although infrequently reported, some authors suggest that localized lipoatrophies are relatively common. Because of the absence of reported cases, these entities remain poorly understood. Most cases are considered idiopathic. In cases linked to insulin injections, an immune response mediated by tumor necrosis factor-α has been hypothesized [7].

The development of localized lipoatrophy associated with corticosteroid injections is a well-described phenomenon. It has been reported with the use of triamcinolone. The buttocks and proximal extremities the areas most frequently involved [8], especially in children who have received multiple injections for treatment of severe asthma or allergic rhinitis [9]. Other cases have developed in atopic patients receiving only topical steroids [10].

Upon a clinical diagnosis of acquired localized lipoatrophy, appropriate medical history and physical examination should indicate whether a deep incisional biopsy is necessary to rule out treatable underlying conditions such as tumors or connective tissue diseases.

Primary localized lipoatrophies usually resolve spontaneously and are not associated with systemic disorders. If the lesions persist and are of cosmetic concern, a combination of liposuction and localized fat transplantation may be performed [11].

We have reported a case of acquired localized lipoatrophy with symmetric distribution secondary to a single intramuscular corticosteroid injection in a patient who received multiple injections during his childhood. We believe that prior sensitization from repeated intramuscular corticosteroid injections during childhood, including several previous injection in both buttocks, might explain the development of a second, symmetric, contralateral lipoatrophic lesion after a new injection. Further reports will be appreciated to elucidate the exact mechanism responsible of this curious side effect.

References

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6. Panniculitis. Part II. Mostly lobular panniculitis. Requena L, Sánchez Yus E. J Am Acad Dermatol 2001;45:325-61

7. Atlan-Gepner C, Bongrand P, Farnarier C, et al. Insulin-induced lipoatrophy in type I diabetes. A possible tumor necrosis factor-alpha-mediated dedifferentiation of adipocytes. Diabetes Care 1996 ; 19: 1283-1285.

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9. Yamamoto T, Yokozeki H, Nishioka K. Localized involutional lipoatrophy: report of six cases. J Dermatol. 2002;29:638-643.

10. Hisamichi K, Suga Y, Hashimoto Y, Matsuba S, Mizoguchi M, Ogawa H. Two Japanese cases of localized involutional lipoatrophy. Int J Dermatol 2002;41:176-177.

11. Andre P. Post-cortisone lipoatrophy treated by an autologous graft of adipose cell islets. Ann Dermatol Venereol 1990; 117: 733-734.

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