Inflammation in subcutaneous fat often poses a diagnostic problem for clinician and pathologist alike, since the clinical and histopathological findings in the various inflammatory disorders of adipose tissue (AT) have overlapping features. Specificity in diagnosis is potentially difficult since similar clinical presentations are sometimes associated with disparate histopathological features. Diagnostic problems may also relate to the corollary observation that a range of clinical presentations may have similar histopathologic findings.
There is no universally accepted classification of panniculitis, but from the point of view of many pathologists, a useful classification begins by dividing panniculitis into septal and lobular forms, “septal” signifying inflammation confined predominantly to the septa, and “lobular” indicating inflammation predominantly involving the fat lobule itself. The septal form has been most classically associated with erythema nodosum (EN) and the lobular form with all or most other types of panniculitides. But even this beginning point has not been proven adequate since lobular granulomatous panniculitis may be seen in clinically classic EN,1 and lobular panniculitides may have mixed lobular and septal inflammation.2 This classification has been expanded by making note of the presence or absence of vasculitis in the septa or lobules,3 by the composition of the inflammatory infiltrate, and by additional specific features when present (Fig. 70-1).
Approach to the patient with panniculitis.
Since diverse clinical conditions may be expressed by similar histopathologic features, and the spectrum of histopathologic features in EN and other panniculitides may be variable,4 it may not be possible to make a specific diagnosis of panniculitis based on histopathology alone. This necessitates correlation with clinical features, including location of lesions, systemic symptoms, laboratory findings, and etiological factors. A significant aid to success in the diagnosis of inflammation in AT is obtaining a tissue sample that will adequately represent the histopathologic changes in the lesion. This can only be done with large excisional biopsies, as small punch biopsies are unlikely to obtain adequate AT, and the inflammatory infiltrate can be missed. An additional consideration is that inflammation in AT is not a static process, and as samples taken at different stages of an evolving lesion will present with different histopathologic features, more than one biopsy may be necessary to come to a conclusive diagnosis.
Under the best of circumstances, with optimal histopathologic sampling and clinical correlation, there may be no specific etiology for many inflammatory reactions in AT. But even with a specific diagnosis or etiology, underlying questions remain. Why were the inflammatory cells accumulating in the AT? What were they doing there?
In the past 20 years, research into obesity has led to a great deal of information about the function of adipocytes and AT, and to the understanding that adipocytes are central not only to energy homeostasis but also as cellular components of the innate immune system and mediators ...