Membranous Fat Necrosis

Rj, Poppiti; Margulies, Milton; Cabello, Belén; Am, Rywlin

doi:10.1097/00000478-198601000-00007

Cited by 46 publications

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“…These histopathological features were identical to those of MFN. [14][15][16][17][18] Hence, MFN-like bodies are true MFN of non-cystic type, 16 implying a necrotic form of preceding fat cells. Only MFNlike bodies correspond to extensive necrosis of AV fat cells.…”

Section: Discussionmentioning

confidence: 99%

“…Other than generalized Nasu-Hakola disease, 16,20 MFN most commonly involves the subcutaneous tissue 14,16,17 and breast, 15 and could be found in bone marrow 24 and intraarticular loose bodies. 25 In the current study, MFN was identified in 58 d-AVs (83%) and in 63% of nd-AVs, which are higher than or almost equal to the reported incidences (38-75%) of MFN in subcutaneous tissues affected by some underlying diseases.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9][10][11] However, the clinicopathological features of non-tumorous AV fat cells remain poorly understood, 11,12 although they may be scarce and represent a metaplastic condition associated with calcified or ossified valves. 12,13 Recently, our routine examination of stenotic AVs incidentally disclosed not only fat cells, but also small bodies with eosinophilic serpiginous membranes closely resembling the histological features of membranous fat necrosis (MFN) [14][15][16] (unpublished data). MFN, also called membranous lipodystrophy-like changes, membranocystic changes, membranocystic fat necrosis, or lipomembranous fat necrosis, [16][17][18][19] was initially considered a morphologic hallmark of 'membranous dystrophy,' 'lipomembranous polycystic osteodysplasia,' or 'Nasu-Hakola disease,' 12,[16][17][18][19][20] and is now known to be a peculiar form of fat necrosis.…”

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confidence: 90%

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Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Matsukuma

Takeo

Kono

et al. 2013

Pathology International

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We examined 152 aortic valves (AVs), which included 82 postmortem non-dysfunctional AVs (nd-AVs) and 70 surgically removed dysfunctional AVs showing aortic stenosis (AS), aortic regurgitation (AR), or combined AS and AR (AS-R). Fat cells, membranous fat necrosis (MFN), and fat-MFN-related lesions composed of fat cells and/or MFN were found in 127 (83.6%), 110 (72.4%), and 140 (92.1%) of 152 AVs, respectively, and all were associated with older age (P = 0.010, P = 0.022, and P = 0.003, respectively). MFN was associated with fibrous thickening and calcification (both, P = 0.001). Nd-AV fat cells and fat-MFN-related lesions were not correlated with body mass index. Compared with ageand sex-matched control cases, MFN in AS and AS-R cases was more frequent (P = 0.030 and P = 0.045, respectively), but MFN in AR cases showed no significant differences. Fat-MFN-related lesions, possibly representing true preceding fat cells, showed no differences in AVs with and without dysfunction or in dysfunctional types. These data suggest that AV fat cells are age-related, obesity-independent, and AV dysfunction-unrelated common phenomenon. MFN is also age-dependent and could be caused by AS and AS-R, which is probably concerned with AV thickening and calcification.Key words: aortic valve, fat, fat necrosis, heart, membranous dystrophy, membranous fat necrosis, valvular dysfunction Lipid deposits or accumulation of aortic valves (AVs) has been reported to be related to aging and/or calcific changes 1-6 and tumorous fatty lesions of AVs have been rarely reported.7-11 However, the clinicopathological features of non-tumorous AV fat cells remain poorly understood, 11,12 although they may be scarce and represent a metaplastic condition associated with calcified or ossified valves. 12,13Recently, our routine examination of stenotic AVs incidentally disclosed not only fat cells, but also small bodies with eosinophilic serpiginous membranes closely resembling the histological features of membranous fat necrosis (MFN) [14][15][16] (unpublished data). MFN, also called membranous lipodystrophy-like changes, membranocystic changes, membranocystic fat necrosis, or lipomembranous fat necrosis, [16][17][18][19] was initially considered a morphologic hallmark of 'membranous dystrophy,' 'lipomembranous polycystic osteodysplasia,' or 'Nasu-Hakola disease,' 12,[16][17][18][19][20] and is now known to be a peculiar form of fat necrosis. 16 However, to the best of our knowledge, MFN has not been mentioned previously in AVs with or without valvular dysfunction. We questioned whether or not AV fat cells and/or MFN-like bodies are concerned with AV dysfunction. Therefore, we examined the clinicopathological characteristics of these lesions in postmortem non-dysfunctional AVs (nd-AVs) and surgically removed dysfunctional AVs (d-AVs). MATERIALS AND METHODSEighty-two postmortem nd-AVs were available from 10% buffered formalin-fixed heart specimens in 82 patients without AV dysfunction (52 men and 30 women with a mean age of 70.6 years; range, 40-95 years), ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 90%

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Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Matsukuma

Takeo

Kono

et al. 2013

Pathology International

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“…The presence of lipofuscin has been reported in cases of fat necrosis [17], Hermansky-Pudlack syndrome [18], in age-related macular degeneration [19] and in patients receiving amiodarone [20, 21] or clofazimine. This substance can also be found in many human tissues with aging interpreted as an accumulation of waste products resulting from an intracellular autophagy, and the granules are considered as degradation products of lysosomes [22].…”

Section: Discussionmentioning

confidence: 99%

Orange Palpebral Spots

Assouly¹,

Cavelier‐Balloy²

2008

Dermatology

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We report 27 cases of adults (23 females/4 males, average age 53 years old) presenting yellow-orange pigmented symmetric spots in the internal part of their superior eyelids, different from xanthelasma. Most of them were not aware of their orange palpebral spots (OPS). A systematic observation of adults showed OPS on 15 out of 326 patients. Laboratory investigation carried out in 11 patients did not show particular results except a high level of vitamin E or of total carotenoids in single cases and of β-cryptoxanthin in 5 cases attributed to the high consumption of citrus fruit during winter. In 9 out of the 10 biopsies performed, high-situated fat cells were observed in the reticular dermis, and Fontana pigments (+) in the superficial dermis and sometimes basal keratinocytes. In 1 case yellow-brown autofluorescent microgranular deposits that may correspond to lipofuscin were identified in the superficial dermis. The origin of OPS remains unclear; more than high-situated adipocytes colored by carotenoids, lipofuscin deposit could explain this color, easily visible due to the thinness of the skin in this part of the body. Identifying OPS avoids being mistaken about other pathologies, but further investigations are necessary to understand this entity better.

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“…Many researchers have described metaplastic, proliferative, and degenerative changes in ILBs, such as the formation of cartilaginous and/or osseous lamellae, resorptive changes of mineralized tissues, and enchondral ossification [2][3][4][5][6][7][8][9][10][11][12][13]. Our recent examination of ILBs incidentally found focal fat cells with lipomembranous changes, which are known to be a unique form of fat necrosis [14,15]. We speculated that these fatty lesions may represent remnants of necrotic bone marrow, but they were not accompanied by bone marrow structures.…”

Section: Introductionmentioning

confidence: 99%

Fatty lesions in intra-articular loose bodies: a histopathological study of non-primary synovial chondromatosis cases

et al. 2011

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Intra-articular loose bodies (ILBs) are not uncommon conditions in patients with various joint diseases. Their morphological alterations have been investigated in detail, but little attention has been paid to their fatty lesions. In this study, we examined fatty bone marrow, fat cells without bone marrow structures (extramedullary fat cells), and their necrotic changes in 55 ILBs surgically removed from 42 patients, excluding primary synovial chondromatosis cases. The presence of viable re-vascularized vessels with or without enchondral ossification could discriminate 19 re-attached ILBs from 36 true free ILBs. Fatty bone marrow was found in 25 ILBs, and its necrosis was recognized in 11 (44.0%) of them. Extramedullary fat cells, characterized by single or clustered fat cells focally or multifocally distributed in fibrous or cartilaginous stroma, were identified in seven true free ILBs (7of 55, 12.7%), and all of them were focally necrotic. Unique lipomembranous changes were detected in 7 (12.7%) of 55 ILBs; they were found in 4 (36.4%) of 11 ILBs of necrotic bone marrow and were associated with 3 (42.9%) of 7 necrotic extramedullary fatty lesions. These changes were highlighted by periodic-acid Schiff and Masson's trichrome stain more clearly. We concluded that extramedullary fat cells represent lipometaplasia in ILBs with no blood supply. We considered that lipomembranous changes in ILBs can be a useful hallmark for necrotic bone marrow or necrosis of extramedullary lipometaplastic lesions.

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Membranous Fat Necrosis

Cited by 46 publications

References 0 publications

Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Orange Palpebral Spots

Fatty lesions in intra-articular loose bodies: a histopathological study of non-primary synovial chondromatosis cases

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