Cases reported "Fat Necrosis"

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1/5. Vasculitis-induced membranous fat necrosis.

    Membranous fat necrosis (MFN) a distinct degenerative process of adipose tissue, is characterised by the presence of membranocystic lesions (MCLs) superimposed on a background of typical traumatic-type fat necrosis. MCLs are cysts, of varying size and shape, that are lined by an eosinophilic, crenulated membrane, having the staining properties of ceroid. Although MFN has been documented in varying systemic adipose tissue sites and in tumours, the pathogenesis of this pathological curiosity is unknown. To date, an ischemic basis for MFN has been the most proximate, and atherosclerosis and venous insufficiency, due to large and medium vessel disease, have been the most popular underlying clinical disorders. Although systemic vasculitis has been quoted as the underlying ischemic disorder in some patients, vasculitis has not been commented on nor demonstrated in tissue sections in association with MFN. In,reporting vasculitis-induced MFN, we document the occurrence of MFN in association with uncommon causes of vasculitis, namely: 1) Granulomatous vasculitis in a post-herpetic zosteriform scar; 2) cytomegalovirus-induced vasculitis in the clinical setting of systemic lupus erythematosus; and 3) Lymphocytic vasculitis in a tetanus toxoid immunization site reaction.
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2/5. Acute skin and fat necrosis during sepsis in a patient with chronic renal failure and subcutaneous arterial calcification.

    Calcification of small subcutaneous arteries and arterioles is commonly found in patients with chronic renal failure (CRF), but the syndrome of acute ischemic necrosis of the skin and subcutaneous fat supplied by these vessels is relatively uncommon. The necrosis occurs during dialysis and after successful renal transplantation, and it is often fatal. Occlusion of the calcified arteries and associated microvessels by thrombi is reported infrequently, but it is relevant to the necrosis. However, the pathogenesis remains enigmatic. In the patient described here, who had CRF, bacteremia, and laboratory evidence of disseminated intravascular coagulation (DIC), the distribution of thrombi and necrosis was mainly that of the calcified arteries which, therefore, probably played a role in the localization of the thrombi. An increased susceptibility of the endothelium of calcified vessels to the procoagulant effects of sepsis may be a contributing factor.
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3/5. Studies on subcutaneous fat necrosis of the newborn.

    biopsy specimens from the skin and subcutaneous fat tissue of four cases with neonatal subcutaneous fat necrosis were made and investigated by light and electron microscopy at 2, 4, and 6 weeks, and 5 months (Case 2) from the onset of the disease. Three stages of ultrastructural change of fat cells were observed. The evolution of crystal formation in the fat cells was seen and phagocytosis of crystals and fat droplets by macrophages and foreign-body giant cells was also noted. In the light microscope accumulation of calcium concretions in the spaces between and inside the fat cells was found. In the electron microscope we detected foci of highly electron-dense granules, which were similar in distribution and structure to calcium salts stained with the von Kossa method. Changes in small and medium size blood vessels were observed.
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4/5. Pancreatic duct arteriovenous fistula and the metastatic fat necrosis syndrome.

    This report summarizes the course of a patient with asymptomatic chronic pancreatitis associated with hemorrhage into the pancreatic duct and metastatic fat necrosis. Retrograde cannulation of the pancreatic duct and superior mesenteric arteriography established the presence of a pseudocyst with a pancreatic duct-arteriovenous (DAV) fistula as the cause of the syndrome. ligation of feeder vessels with external drainage of the cyst as the initial surgical procedure stopped the bleeding but failed to prevent recurrence of the pancreatic duct-venous fistula. A pancreaticoduodenectomy with resection of the cyst and fistula was required to arrest destruction of distant tissues. Although serum and urine amylase concentrations were markedly elevated, serum lipase levels were normal throughout the patient's course. Elevation of serum lipase does not seem to be a necessary condition for the development of the metastatic fat necrosis syndrome.
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5/5. Hairy-cell leukaemia with polyarteritis nodosa.

    In four patients a systemic vasculitis similar to polyarteritis nodosa developed within 2 years of the onset of hairy-cell leukaemia. Arteriographic studies in two patients revealed microaneurysms, and biopsy specimens in three patients revealed a vasculitis affecting medium-sized vessels. Blood neutrophilia and neutrophilic vascular infiltrate were absent. One patient had circulating immune complexes. Two patients responded to corticosteroids alone, one required cyclophosphamide as well as steroids, and one improved without chemotherapy. The association of vasculitis with hairy-cell leukaemia may provide insight into the pathogenesis of arteritis.
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