Linear scleroderma after contusion and injection of mepivacaine hydrochloride
- Author(s): Ueda, Takashi;
- Niiyama, Shiro;
- Amoh, Yasuyuki;
- Katsuoka, Kensei
- et al.
Published Web Locationhttps://doi.org/10.5070/D336k88174
Linear scleroderma after contusion and injection of mepivacaine hydrochlorideDepartment of Dermatology, Kitasato University School of Medicine, Sagamihara, Japan. firstname.lastname@example.org
Takashi Ueda MD, Shiro Niiyama MD, Yasuyuki Amoh MD PhD, Kensei Katsuoka MD PhD
Dermatology Online Journal 16 (5): 11
A 36-year-old woman initially was treated for a contusion by local injection of mepivacaine hydrochloride into the left dorsum of the foot. Approximately 3 months after the injury and injection, linear sclerotic plaques originating from the site of contusion and injection were recognized. These progressed in extent and severity over a period of 3 years, when she presented to our clinic. By biopsy, swelling of collagen fibers in the lower dermis was revealed and the condition was diagnosed as linear scleroderma. Our present case had multiple linear sclerotic plaques of the left lower extremity, the distribution of which was consistent with Blaschko lines. It was also revealed that the initial sclerotic plaque was at the site of the contusion and local mepivacaine hydrochloride injection. Our present case is interesting in that the findings suggest a correlation between linear scleroderma plaque occurrence and the contusion or injection of mepivacaine.
We encountered a patient with multiple linear sclerotic plaques of the skin, which were localized to the left lower extremity and had manifested shortly after she suffered a contusion treated by injection of local anesthesia.
In 2004, a 36-year-old woman had sustained a contusion of the left dorsum of the foot and received a local injection of mepivacaine hydrochloride (carbocain®) into the site of injury. She was aware of red plaques at the site of injection approximately 3 months after this treatment. Thereafter, the plaque lesions spread in an ascending direction. She had no past history of contact with any organic solvent or of cosmetic surgery.
|Figure 1||Figure 2|
|Figure 1. Linear brownish sclerotic relatively well-demarcated plaque.|
Figure 2. Similar linear changes occurred in parallel with the plaques.
A linear brownish sclerotic relatively well-demarcated plaque, which was approximately 10 cm in length, was observed on the left dorsum of the foot. An ovoid plaque with more severely sclerotic and atrophic changes was present in the center of the liner plaque (Figure 1). This plaque site was consistent with the contusion and injection site. There were also linear brownish sclerotic plaques present in the area ranging from the medial side of the left knee to the lateral side of the femur. Similar linear changes occurred in parallel with the plaques (Figure 2). Portions of the margins of the some sclerotic plaques were dark red in color.
The patient was negative for rheumatoid factor, antinuclear antibodies, and anti-single-stranded DNA antibody. Superficial ultrasonography exhibited a hypoechoic image at the sclerotic site.
|Figure 3. Swelling of collagen fibers was recognized in the lower dermis.|
A biopsy specimen was collected from the dark-red portion of the margin of the sclerotic femoral plaque. The epidermis showed slight atrophy with increased melanin in the basal layer. Slight lymphocyte infiltration was recognized around the blood vessels and the appendages in the upper dermis. Swelling of collagen fibers was recognized in the lower dermis (Figure 3). Direct immunofluorescence was negative.
In our present case there was a possibility that injection of mepivacaine hydrochloride had induced the sclerotic condition. Therefore, an administration test was conducted with the patient’s consent. Local injection of 0.5 ml of the drug was conducted at intervals of approximately 3 cm on the full circumference of the rash-free portion of the left crus. Evaluation by superficial ultrasonography approximately 3 months later, in a manner similar to that conducted during the course of our present case, demonstrated no distinct changes as compared to the normal areas. Topical corticosteroid was used for treatment, however, no remarkable improvement has been observed.
One theory concerning the origin of linear scleroderma is that the eruption appears along Blaschko lines ; another theory suggests that linear scleroderma has nothing to do with the lines of . Thus, there is as yet no consensus on the reason for the distinct distribution. In our present case, all linear plaques of the left lower extremity were arranged along the Blaschko lines. The pattern has been considered to show a line of progression of proliferation and migration of cells comprising the skin, which occurs during fetal development [3, 4]. Many forms of congenital cutaneous disease are distributed along the Blaschko lines, but there are also some acquired diseases that follow these same patterns. For the acquired diseases the following possibility has been raised: inflammatory and immune responses trigger cells with genetic variations, rendering the subject susceptible to the development of cutaneous abnormalities at the sites of genetic abnormalities, which may be present in a mosaic form . In our present case, the sclerotic plaques initially spread from the site of contusion and mepivacaine hydrochloride injection, suggesting that the contusion or injection had triggered this spread.
Injection of a variety of chemical substances or drugs, such as paraffin, bleomycin, methysergide, pentazocine, vitamin K1, and corticosteroids, has been reported as a cause of scleroderma or scleroderma-like illness . There have been no reports confirming a correlation between mepivacaine hydrochloride and localized scleroderma. However, Rose et al. reported a familial case  in which a child developed dermatomyositis following local anesthesia (with an amide anesthetic) and the child’s grandmother developed systemic sclerosis after local anesthesia (details unknown). In our present case, no sclerotic lesions were reproduced by the re-administration of mepivacaine hydrochloride at a different site. Possible reasons are that there is no causal relationship between the sclerotic lesion and mepivacaine hydrochloride, the dose of the administered drug was low, or the site of administration was outside of the mosaic area. Very few instances of scleroderma after injection have been reported in the literature. Desmons et al.  described a progressive band-like scleroderma-like condition of the limbs in a 7-month-old infant shortly after DTP vaccination.
Trauma has been implicated as an important trigger of scleroderma. Christianson et al.  reviewed 191 patients with linear scleroderma and morphea and found 14 cases associated with trauma. Falange et al.  reported 53 patients with linear scleroderma and found 23 percent to have a history of trauma to the involved site. The injury often precedes the onset of the disease by weeks or months. Localized scleroderma following a surgical procedure, irradiation, vaccination, chicken pox, an ischemic injury, and local trauma has been reported. The role trauma plays in the development of linear scleroderma is unknown. Biological stress or trauma may trigger the production and release of inflammatory mediators and fibrogenic cytokines. This results in the synthesis of excess collagen in susceptible individuals. Linear scleroderma has occurred following traumatic nerve damage, including spinal cord injury. It is hypothesized that neuropeptides stimulate fibroblast production through mediators such as IL-1, causing sclerosis . We hypothesize that the contusion or injection of mepivacaine hydrochloride triggered scleroderma in our patient. However,this event is so unusual and suggests some underlying predisposition to the development of scleroderma in our patient.
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