Fig 1 - available via license: Creative Commons Attribution-NonCommercial 3.0 Unported
Content may be subject to copyright.
Source publication
Membranous lipodystrophy is characterized by the presence of microcysts lined by amorphous, eosinophilic material with an arabesque appearance. We experienced a case of a 72-year-old man who had dark brownish, pruritic papules on the arms, legs, and back. Histopathologic examination of a biopsied lesion showed homogeneous, eosinophilic material in...
Context in source publication
Context 1
... 72-year-old man presented with multiple, dark brown- ish, hyperkeratotic papules on the arms, legs, and back ( Fig. 1), which had been present for the last 8 months. These lesions were severely pruritic. The patient had not- ed gradual progression of the lesions, especially in recent times. His medical history was significant for a cerebral in- farction occurring 10 years prior to presentation. On phys- ical examination, the patient had neither ...
Similar publications
An 83-year-old Caucasian male presented with a history of asymptomatic yellow-orange macules and plaques concentrated on his trunk and proximal extremities that have been slowly progressing for the past three years. A punch biopsy revealed the presence of eosinophilic amorphous and fissured material within the superficial and interstitial dermis co...
Citations
... LFN was initially considered a specific morphology of Nasu-Hakola disease (35,38,39). However, subcutaneous LFN has occasionally been discovered in patients without this hereditary disease 35,36,47,48). Machinami (31) reported subcutaneous LFN within necrotic legs caused by impaired arterial blood supply, such as thromboangiitis obliterans, arteriosclerotic obliterans, and progressive systemic sclerosis (LFN incidence rates: 38, 75, and 50%, respectively). Poppiti et al (22) observed LFN in the thoracic subcutaneous tissues of a 66-year-old man without Nasu-Hakola disease or other underlying diseases and identified LFN in 7 (21%) of 33 consecutive cases of subcutaneous fat necrosis. ...
Lipomembranous fat necrosis (LFN) is an uncommon but distinct form of fat necrosis, which is characterized by eosinophilic, crenulated and/or serpiginous membranes. LFN exhibits macrocystic, microcystic and/or crushed features. LFN is routinely detectable on hematoxylin and eosin (H&E)-stained sections, and is present both in the acute phase and in the later or fibrous stage of necrotic fatty lesions. Smaller crushed LFN embedded within fibrous tissues may be difficult to recognize on H&E-stained sections, but can be highlighted by some staining techniques, including Masson trichrome, periodic acid-Schiff, orcein, long Ziehl-Neelsen stain, silver impregnation, phosphotungstic acid-hematoxylin and luxol fast blue staining. LFN was initially considered a specific feature of Nasu-Hakola disease, but has since been identified in various subcutaneous or intraabdominal lesions related to ischemic conditions or venous insufficiency. In addition, LFN is detectable in intra-articular loose bodies and aortic valves with or without dysfunction, suggesting that LFN is also associated with ischemia-like hypoxic conditions or malnutrition. LFN is considered to be a histological hallmark of hidden ischemic or hypoxic/malnourished conditions in various diseases; however, the exact mechanisms of LFN remain poorly understood. The present review described the clinicopathological features of this interesting, but poorly characterized, condition.
... Initially, it was described as polycystic lipomembranous osteodysplasia. 1 Various clinical conditions, such as lupus erythematosus, diabetes mellitus, erythema nodosum, morphea, as well as trauma and vascular disorders have been found to exhibit similar membranous lipodystrophies and lipodystrophy-like changes. [2][3][4][5] We report a case of secondary membranous lipodystrophy associated with hypertension and venous insuffi ciency. ...
... 2 Similar changes were also detected in diabetes mellitus, multiple myeloma, atypical mycobacterial infection, erythema nodosum, and vascular disorders, including arterial ischemia of lower limbs, varicose veins, thrombophlebitis and deep venous thrombosis. [3][4][5] The pathogenesis of membranous lipodystrophy is unknown. Idiopathic processes, enormous proliferation of the fat cell membranes, physiochemical interaction between the ground substance in connective tissue and fat droplets, free fatty acids released from degenerated fat cells processed by macrophages, metabolic disorders of lipids in mesenchymal cells, loops and fold in the basal laminae of fat cells in varying stages of lipid depletion at the time of necrosis; and ischemic injury of adipose tissue resulting from venous insuffi ciency are various mechanisms that have been proposed. ...
... 3 It often projects into cysts, creating a pseudopapilla or arabesque appearance. 5 Our histopathological examination revealed similar fi ndings, as well as dermal vascular hyperpla- High blood pressure and venous insuffi ciency led us to think that ischemia -the most important cause of membranous lipodystrophy -was the underlying etiology. Hypertension increases the medial thickness and narrows th e vascular lumen, resulting in impaired capillary perfusion. ...
Membranous lipodystrophy is a distinct type of membranocystic fat necrosis. It is
associated with many local and systemic diseases, including vascular disorders. The
histopathological changes which characterize this phenomenon are variably sized cysts
in the fat lobules of the subcutaneous tissue, which are surrounded by eosinophilic
membranes projecting into the cystic space. We report a case of secondary membranous
lipodystrophy associated with both hypertension and venous insufficiency.
Alzheimer's Disease (AD) is a highly complex disease involving a broad range of clinical, cellular, and biochemical manifestations that are currently not understood in combination. This has led to many views of AD, e.g. the amyloid, tau, presenilin, oxidative stress, and metal hypotheses. The amyloid hypothesis has dominated the field with its assumption that buildup of pathogenic β-amyloid (Aβ) peptide causes disease. This paradigm has been criticized, yet most data suggest that Aβ plays a key role in the disease. Here, a new loss-of-function hypothesis is synthesized that accounts for the anomalies of the amyloid hypothesis, e.g. the curious pathogenicity of the Aβ42/Aβ40 ratio, the loss of Aβ caused by presenilin mutation, the mixed phenotypes of APP mutations, the poor clinical-biochemical correlations for genetic variant carriers, and the failure of Aβ reducing drugs. The amyloid-loss view accounts for recent findings on the structure and chemical features of Aβ variants and their coupling to human patient data. The lost normal function of APP/Aβ is argued to be metal transport across neuronal membranes, a view with no apparent anomalies and substantially more explanatory power than the gain-of-function amyloid hypothesis. In the loss-of-function scenario, the central event of Aβ aggregation is interpreted as a loss of soluble, functional monomer Aβ rather than toxic overload of oligomers. Accordingly, new research models and treatment strategies should focus on remediation of the functional amyloid balance, rather than strict containment of Aβ, which, for reasons rationalized in this review, has failed clinically.
In Korean medicine, pulse diagnosis is one of the important methods for determining the health status of a patient. For over 40 years, electromechanical pulse diagnostic devices have been developed to objectify and quantify pulse diagnoses. In this paper, we review previous research and development for pulse diagnostic devices according to various fields of study: demand analysis and current phase, literature studies, sensors, actuators, systems, physical quantity studies, clinical studies, and the U-health system. We point out some confusing issues that have been naively accepted without strict verification: original pressure pulse waveform and derivative pressure pulse waveform, pressure signals and other signal types, and minutely controlled pressure exertion issues. We then consider some technical and clinical issues to achieve the development of a pulse diagnostic device that is appropriate both technically and in terms of Korean medicine. We hope to show the history of pulse diagnostic device research in Korea and propose a proper method to research and develop these devices.
The deficient and excess pulse qualities (DEPs) are the two representatives of the deficiency and excess syndromes, respectively. Despite its importance in the objectification of pulse diagnosis, a reliable classification model for the DEPs has not been reported to date. In this work, we propose a classification method for the DEPs based on a clinical study. First, through factor analysis and Fisher's discriminant analysis, we show that all the pulse amplitudes obtained at various applied pressures at Chon, Gwan, and Cheok contribute on equal orders of magnitude in the determination of the DEPs. Then, we discuss that the pulse pressure or the average pulse amplitude is appropriate for describing the collective behaviors of the pulse amplitudes and a simple and reliable classification can be constructed from either quantity. Finally, we propose an enhanced classification model that combines the two complementary variables sequentially.
