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Fat necrosis.

Fat necrosis has been found to be associated with many forms of pancreatitis, carcinoma of the pancreas and pancreatic trauma. The causative agents seem to be pancreatic lipase and colipase, which presumably escape from the pancreas during the development of the disease. The precise mechanism by which these factors attack the adipose tissue, leading to the formation of foci of fat necrosis, is not known. The pathologic finding of fat necrosis is not restricted to the peritoneal-retroperitoneal region, where a direct contact with these factors is the most likely cause. In other patients, fat necrosis involves peripheral tissues, notably in subcutaneous adipose tissue throughout the body, in joints of the hand and foot and in bone marrow. This is associated with additional complications dependent upon the sites involved and is manifested as skin lesions, polyarthritis and osteolytic defects in patients who sometime suffer from a primary pancreatic disease.

Acute Disease↗

Case report: soft tissue and perivisceral calcification occurring in an infant: a case of brown fat necrosis.

Fat necrosis is a well described cause of widespread subcutaneous calcification occurring in a young infant. In this condition the radiographic demonstration of soft tissue calcification is often dramatic but is clinically irrelevant since the diagnosis is usually evident without recourse to radiology. Visceral fat necrosis and calcification, in the absence of hypercalcaemia, have been reported occasionally in association with subcutaneous fat necrosis. We report a case with calcification largely confined to deep perivisceral sites without clinical signs of subcutaneous fat necrosis.

Adipose Tissue, Brown↗

Acute hemorrhagic pancreatitis (massive necrosis) with fat necrosis induced in mice by DL-ethionine fed with a choline-deficient diet.

Female, albino mice were fed a choline-deficient diet containing 0.5% DL-ethionine. All animals died within 5 days due to the development of an acute hemorrhagic pancreatis with fat necrosis throughout the peritoneal cavity. The apancreatitis was characterized by a massive necrosis of the exocrine parenchyma with intense hemorrhage and inflammatory reaction of the stroma. The sequence of histologic and ultrastructural alterations occurring in the acinar cells of the pancreas were studied in mice fed the diet for 1, 2, and 3 days. Major findings consited of accumulation of zymogen granules, vacuolation due to foci of cytoplasmic degradation, and alterations in the morphology of the zymogen granules. The pancreatitis appears to be due to intraparenchymal activation of zymogens, resulting from a synergistic action of choline deficiency with the basic toxicity of ethionine toward the acinar cells of the pancreas. The experimental model simulates closely the acute hemorrhagic pancreatitis with fat necrosis occurring in humans and may prove useful for exploring the pathogenesis of this condition.

Acute Disease↗

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.

Adolescent↗

Pericardial fat necrosis.

Pericardial fat necrosis has a highly characteristic clinical picture that enables a preoperative diagnosis to be made on clinical grounds. Surgical therapy, which remains the treatment of choice for this curable entity, confirms the diagnosis. This report reviews the literature and adds a thirteenth documented case to the previously reported 12 cases.

Adult↗

The mammographic spectrum of fat necrosis of the breast.

Fat necrosis of the breast is a benign condition that most commonly occurs as the result of minor breast trauma. The radiographic and clinical significance of fat necrosis of the breast is that it may mimic a breast malignancy, requiring biopsy for diagnosis. The mammographic appearance of fat necrosis ranges from a lipid cyst to findings suspicious for malignancy, including clustered microcalcifications, a spiculated area of increased opacity, or a focal mass. The changes of fat necrosis may be seen following blunt trauma, cyst aspiration, biopsy, lumpectomy, radiation therapy, reduction mammoplasty, breast reconstruction with a transverse rectus abdominis myocutaneous (TRAM) flap, implant removal, and anticoagulant therapy, as well as in patients without a relevant history. Fat necrosis may also be detected mammographically as an incidental finding in benign lipomas. It is important to recognize the mammographic spectrum of appearances of fat necrosis to avoid unnecessary biopsy and to avoid overlooking breast cancer.

Breast Diseases↗

An unusual case of cutaneous pancreatic fat necrosis.

BACKGROUND: Cutaneous pancreatic fat necrosis is a pathognomonic sign for pancreatic disease and usually presents as subcutaneous nodules in the pretibial region. OBJECTIVE: A case of cutaneous pancreatic fat necrosis is presented in which the clinical presentation of diffuse erythema was unusual. This disease is discussed and its possible etiologies are reviewed. METHODS: A MEDLINE search for cases of cutaneous pancreatic fat necrosis presenting as diffuse erythema without nodules was conducted. RESULTS: Diffuse erythema is an unusual presentation of cutaneous pancreatic fat necrosis. CONCLUSION: This may be the first case of cutaneous pancreatic fat necrosis presenting as diffuse erythema.

Adolescent↗

Visceral brown fat necrosis in postperinatal mortality.

Fat necrosis was present in 22 of 400 cases of consecutive postperinatal mortalities investigated to assess the presence and pattern of deep fat necrosis. In just over 50% of the cases of fat necrosis the cause of death was categorised as sudden infant death syndrome, which also showed more severe degrees of necrosis. The mechanism of necrosis may be vascular hypoperfusion, possibly related to shock, and brown adipose tissue, on account of its high metabolic activity and rich capillary plexus, may be particularly vulnerable to infarction. The occurrence of fat necrosis in association with other causes of death did not provide any definite clue as to the nature of the alleged shock.

Adipose Tissue, Brown↗

Subcutaneous pseudomembranous fat necrosis: new observations.

BACKGROUND: Pseudomembranous fat necrosis is a peculiar manifestation of necrosis of adipose tissue characterized by formation of pseudocystic cavities lined by crenulated membranes. The underlying mechanism for the formation of pseudomembranes is unknown and numerous hypotheses have been proposed. Despite divergent interpretations, most authors consider necrotic fat cells to be the anatomic substrate for the formation of pseudomembranes. METHODS: A total of 341 panniculitides were reviewed for the presence of pseudomembranous fat necrosis. The specific diagnoses were established after correlation of all available clinical and laboratory data with the histopathology. Special attention was given to the time in the evolution of the disease when the biopsy was taken. Additional immunohistochemical studies were performed in 12 cases. RESULTS: Thirty of 341 cases of different types of panniculitides were found to show pseudomembranous fat necrosis, namely: 10 of 15 cases of sclerosing panniculitis (lipodermatosclerosis), 6 of 95 cases of erythema nodosum, 7 of 34 cases of traumatic panniculitis, 1 of 7 cases of lupus panniculitis, 1 of 20 cases of erythema induratum Bazin (nodular vasculitis), 1 of 9 cases of necrobiosis lipoidica, 1 of 4 cases of sclerotic lipogranuloma, 1 of 9 cases of infectious panniculitis (erysipelas), 1 of 2 cases of pancreatic panniculitis, and 1 of 4 cases of subcutaneous sarcoidosis. Pseudomembranous fat necrosis labelled strongly for the histiocytic markers CD68 and lysozyme. CONCLUSIONS: Our series provides data suggesting that pseudomembranous fat necrosis represents a dynamic process that varies according to the evolution of the lesion at the time of the biopsy. In biopsies taken from early foci of panniculitides pseudomembranes show vescicular or picnotic nuclei. Later, pseudomembranes retain their crenulated appearance but lack nuclear elements. Furthermore, we present histopathologic, histochemical, and immunohistochemical evidence that pseudomembranous fat necrosis results from the interaction of residual products of disintegrated fat cells and macrophages. Histiocytic markers such as CD68 and lysozyme may be used as reliable tools in order to detect pseudomembranes in panniculitides.

Adipose Tissue↗

Fat necrosis of the breast.

Fat necrosis of the breast is an uncommon entity but may mimic malignancy on both mammographic and clinical examination. Seven patients had recent excisional breast biopsy specimens that showed fat necrosis. The mammographic appearance is a reflection of the reparative phase of the lesion, with a cystic appearance representing early or incomplete healing. Progression to connective tissue invasion appears as an irregular, dense, spiculated mass. Clinically, these tumors may be firm, fixed, and produce overlying skin or nipple retraction. No matter how strong the clinical suspicion that a breast lesion represents fat necrosis, an excisional biopsy is necessary for confirmation in all cases.

Adult↗

Pamidronate: Treatment for severe hypercalcemia in neonatal subcutaneous fat necrosis.

BACKGROUND: Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon disorder that occurs in the first weeks of life after foetal distress. It can be complicated by potentially life-threatening hypercalcemia. Treatments of hypercalcemia have included hydration, furosemide and corticosteroids. Only one report has described the use of intravenous bisphosphonates for this condition. We propose that pamidronate could be the first line therapy for severe hypercalcemia in SCFN. PATIENTS AND RESULTS: Four newborns presented between 2001 and 2004 with SCFN complicated by severe hypercalcemia. At diagnosis, ionized calcium levels were higher than 1.4 mmol/l and were associated with high urinary calcium/creatinine ratios and high 1,25-dihydroxyvitamin D levels. Despite treatment with IV fluids, low calcium diet and furosemide, calcium levels remained high. The patients were given 3-4 doses (0.25-0.50 mg/kg/dose) of pamidronate. Urinary calcium/creatinine ratios and calcium levels decreased within 48-96 h. 1,25-dihydroxyvitamin D levels normalized with resolution of the skin lesions. No persistent nephrocalcinosis was observed. CONCLUSION: Pamidronate is effective, well-tolerated in the short-term and obviates the need for prolonged treatment with furosemide and corticosteroids. To prevent nephrocalcinosis, pamidronate might be considered as first line treatment for severe hypercalcemia in SCFN.

Bone Density Conservation Agents↗

Membranous fat necrosis in lipomas.

Membranous fat necrosis (MFN) is an under-recognized variant of fat necrosis (FN) that is characterized by the presence of membranocystic foci in which cysts are lined by an eosinophilic, homogeneous membrane with pseudo-papillary luminal projections. Although MFN has been described in systemic adipose tissue, it has not been described in lipomas. We report the rare occurrence of MFN in four lipomas. The lipomas ranged in size between 9 and 22 cm and occurred in menopausal women in the left shoulder, right upper back, right thigh, and gluteal regions. In two cases the membranocystic foci were identified macroscopically, whereas in the other two cases MFN was only identified on histologic assessment. Apart from the typical histologic appearance of the membranocystic foci, the membranes have a distinct histochemical profile that includes consistent Sudan black positivity and either periodic acid-Schiff or Ziehl-Neelsen positivity. In all cases, there was autofluorescence of the membranes on immunofluorescent examination of unstained sections. These membranocystic foci have the typical staining reactions of ceroid pigment. The exact cause of MFN in lipomas is not known, but in view of their large sizes, traumatic and ischemic etiologies are proposed.

Aged↗

Nodular cystic fat necrosis with systemic sclerosis.

Nodular cystic fat necrosis is a distinct spectrum characterized clinically by mobile subcutaneous nodules and histologically by encapsulated fat necrosis. We describe herein a case of nodular cystic fat necrosis in a patient with systemic sclerosis in the atrophic stage. Several mobile, firm nodules were surgically removed from the flexural aspect of the forearm and lower leg. Histopathology showed features of nodular cystic fat necrosis with lipomembranous changes and calcification. Of interest, lipomembranous changes were seen also in the biopsied specimen from the extensor aspect of the forearm of scleroderma. We speculate that multiple, chronic, local or systemic events causing a compromise in the blood supply of the subcutaneous tissues may contribute to the induction of lipomembranous changes in the affected skin as well as nodular cystic fat necrosis in this case.

Calcinosis↗