“…An immune mechanism may initiate or perpetuate the adipose damage. It has been described in association with tuberculosis (Tilden et al, 1940;Beerman, 1953;Macdonald and Feiwel, 1968), glomerulonephritis (Spain and Foley, 1944), myositis (Kiernan and Burger, 1960), intrahepatic sclerosing cholangitis, vasculitis, and positive LE cells (Hellstrom and Perez-Stable, 1966), leucopenia (Friedman, 1945), leucopenia and leucagglutinins (Rosenstock, 1968), pancytopenia (Wyatt 1969), hypersplenism, megaloblastosis, and pancytopenia (Mitsutani et al, 1973), and following withdrawal of steroids given in treatment of rheumatic fever (Smith and Good, 1956). A histologically similar condition (lupus erythematosus profundus) has also been described in association with systemic lupus erythematosus (Macoul, 1967), and Tuffanelli (1971) has demonstrated IgG antivascular antibody, IgM, and complement at the dermal epidermal junction in this condition.…”