Erythema induratum of Bazin presenting as peripheral neuropathy.

Erythema induratum of Bazin (EIB) is a rare tuberculid that typically affects middle-aged women. We report a unique case of EIB in a 57-year-old Hispanic woman who presented with recurrent painful plaques and nodules on the lower extremities, specifically on the pretibial area of the legs and dorsal aspect of the feet, with a severe burning sensation on the feet that resolved after antituberculosis therapy. We review the characteristics of EIB and examine how the unique presentation of peripheral neuropathy may relate to the pathophysiology of this disease.

Neutrophilic panniculitis: algorithmic approach to a heterogeneous group of disorders.

CONTEXT: Neutrophilic panniculitis encompasses an etiologically and morphologically heterogeneous group of disorders. Correct histopathologic diagnosis is important in identifying certain systemic diseases and guiding appropriate treatment. OBJECTIVE: To review the clinical and histopathologic features of different types of neutrophilic panniculitis, and to provide a diagnostic algorithm for these disorders. DATA SOURCES: A review of the literature with emphasis on the distinguishing features of different entities was performed. CONCLUSIONS: Evaluation for neutrophilic panniculitis entails paying close attention to the pattern of inflammation, the type of fat necrosis present, any evidence of vascular damage, and other relevant histopathologic features. An algorithmic approach integrating all histopathologic, clinical, and laboratory findings is required for correct diagnosis.

Erythema nodosum and erythema induratum (nodular vasculitis): diagnosis and management.

Erythema nodosum is the most common type of panniculitis; it may be due to a variety of underlying infectious or otherwise antigenic stimuli. The pathogenesis remains to be elucidated, but both neutrophilic inflammation and granulomatous inflammation are implicated. Beyond treating underlying triggers, therapeutic options consist mainly of nonsteroidal anti-inflammatory drugs, symptomatic care, potassium iodide, and colchicine. Erythema induratum (nodular vasculitis) is a related but distinctly different clinicopathologic reaction pattern of the subcutaneous fat. It is classically caused by an antigenic stimulus from Mycobacterium tuberculosis but may be associated with several other underlying disorders. After appropriate antimicrobial treatment in tuberculous cases, therapy for erythema induratum is similar to options for erythema nodosum.

A 30 year history of panniculitis.

The differential diagnosis of panniculitis may be challenging due to the uniform clinical presentation of different panniculitis subsets. We describe a 45-year-old woman with a 30 year history of panniculitis, who had repeatedly failed to fulfill diagnostic criteria for various panniculitis subsets. Finally, erythema induratum was diagnosed and she was successfully treated with antituberculous chemotherapy. The wide spectrum of histological alterations of chronic erythema induratum as well as the sensitivity of polymerase chain reaction for Mycobacterium tuberculosis in erythema induratum lesions is discussed.

Panniculitis: recent developments and observations.

Dermatopathologists rarely greet a biopsy of panniculitis with total confidence that a specific, definitive diagnosis will be rendered. As with many other areas in dermatopathology, our understanding of the pathogenesis of many forms of panniculitis is incomplete. This article examines a subset of panniculitis primarily from a pathogenetic standpoint, with the intention of providing a differential diagnosis for those cases in which ischemic changes are seen in the subcutis. The diverse group of conditions evoked by this approach also shares the distinction of having been the focus of nosologic and causative controversy, both historically and currently. In particular, stasis-associated sclerosing panniculitis, vascular calcification-cutaneous necrosis syndrome (calciphylaxis), oxalosis, and nodular vasculitis-erythema induratum are examined in depth. Erythema nodosum and variants, other granulomatous panniculitides, and panniculitides showing cytophagocytosis are also discussed with current perspectives.

[Immunohistochemistry of nodular vasculitis. A possible role of delayed cellular hypersensitivity]. / Etude immunohistochimique de la vasculite nodulaire. Rôle possible d'une hypersensibilité retardée cellulaire.

The physiopathogenesis of nodular vasculitis is still unknown: there is probably an initial Arthus' phenomenon responsible for the lesions of the deep vessels, but the frequent recurrences and the long time duration of the hypodermic nodules are still not understood. Dendritic protein S100 positive cells had previously been observed within hypodermal granulomas. The purpose of this study was to confirm these observations in a large group of nodular vasculitis, and to compare the expression of S100 protein in other vascular diseases and in pure panniculitis. Immunohistochemical staining for S100 protein was performed on paraffine-embedded samples: 45 cases of nodular vasculitis, 21 of panniculitis, 10 of superficial leucocytoclastic vasculitis, 10 of periarteritis nodosa, and 10 of erythema nodosum were analyzed by means of optic microscopy. Numerous dendritic S100 protein positive cells were found within hypodermal granulomas in most of the cases of nodular vasculitis, but these cells were absent in the 3 cases of initial deep leucocytoclastic vasculitis lesions of nodular vasculitis. The mean percentage of these cells was 4.5 p. 100 in the hypodermal inflammatory areas; they were observed mainly around vascular lesions. Hypodermal dendritic cells were absent or less numerous in all other cases, and a high number of such cells seems to be observed only in nodular vasculitis. Because of their dendritic morphology, and the high expression of S100 protein, these cells could be interdigitated cells, which are known to present antigens to T-lymphocytes. They could play an important role in generating the chronicity of nodular vasculitis, by a mechanism of delayed cell-mediated hypersensitivity, after the initial lesions caused by immune complexes.