Janin and colleagues [1] described 14 patients with fasciitis who had chronic graft-versus-host disease. Their patients had a disease that resembled eosinophilic fasciitis. Biopsy specimens showed that the earliest histologic changes were edema and fibrosis in the intermediate septa separating the fat lobules and in the muscular fascia beneath the fat lobules.

After the characteristics of eosinophilic fasciitis (a disorder of unknown cause) were described, similar clinical and histologic features were noted to occur in patients with various diseases, such as morphea profunda, lupus erythematosus panniculitis, the toxic oil syndrome, the eosinophilia-myalgia syndrome, postirradiation injury, infections, cancer, venous or lymphatic diseases, and graft-versus-host disease [2-4]. When any of these disorders are referred to, the term "fasciitis" has been used based on the assumption that the inflammatory reaction arises in the fascia, spreading to the septa of the subcutaneous fat tissue.

In a series of 32 patients [3], the histologic features of eosinophilic fasciitis were compared with those features of extensive subcutaneous induration as a manifestation of other diseases (infectious, paraneoplastic, post-traumatic, and circulatory disorders). Evidence from this investigation [3] challenges the notion that the first histologic alteration takes place in the fascia. Indeed, all biopsy specimens showing features of fasciitis also showed evidence of septal panniculitis. However, cutaneomuscular biopsy specimens obtained from the periphery of a lesion often showed septal panniculitis but a normal fascia [3]. When multiple indurative lesions coexisted, cutaneomuscular biopsy specimens taken from small lesions indicated either septal panniculitis or panniculitis and fasciitis. Samples from larger lesions always showed panniculitis and fasciitis. These data [3] suggest that the intermediate septa are the first to be affected by the inflammatory sclerosing process, whereas the fasciitis is secondary to the spread of inflammation to the fascia. Other authors [5] believe that simultaneous involvement of the fascia and the subcutaneous septa occurs from the onset. If this hypothesis is correct, then, in view of our findings, the fasciitis has a segmental distribution, "skip lesions" alternating with segments of normal fascia.

Many noxious agents may induce panniculitis associated with fasciitis. Hence, the term "fasciitis-panniculitis syndrome" has been proposed [3] when referring to the clinical manifestations and histologic alterations in the subcutaneous fascial layers shared by eosinophilic fasciitis and various other disorders. Fasciitis-panniculitis in graft-versus-host disease Figure 1 in reference 1) rather than fasciitis in graft-versus-host disease is one of those disorders.