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Devesh Mishra Pathology Pdf 14 [WORK]



The approval was obtained from Institutional Review Board and ICH-GCP 2008 Seoul amendment and ICMR 2006 guidelines were followed during the study procedure. The study was registered in clinical trial registry of India (CTRI/2010/091/000416, 21-07-2010) . The subjects with confirmed diagnosis of OA were examined by an orthopaedician to exclude other causes of knee joint pathology. The trial patients were subjected to biochemical investigations [Random Blood Sugar (RBS), Liver Function Tests (LFT) and Renal Function Tests (RFT), Uric acid] prior to and after administration of study medications to assess the safety profile of study medications.




Devesh Mishra Pathology Pdf 14


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Peeling Skin Syndrome (PSS) is a rare genodermatoses characterized by asymptomatic, localized or generalized, continuous exfoliation of the stratum corneum; it may present at birth or in adulthood. We describe a patient having the type A non-inflammatory variant of PSS showing asymptomatic and continuous skin peeling from the neck, trunk, back, and extremities. Friction appeared to be an aggravating factor, but there was no seasonal variation. Histopathology in this condition reveals hyperkeratosis and splitting of the epidermis between the granular layer and the stratum corneum. No treatment for this disorder has been found to be effective so far.


Two main subtypes of PSS based on the presence or absence of inflammatory changes have been suggested: Type A is a non-inflammatory variant characterized by asymptomatic, generalized, continuous skin peeling with intact general health, whereas Type B patients exhibit ichthyotic erythroderma that evolves into pruritic, scaly, and erythematous patches with rare vesiculations, easily removable hair, and summer flaring [3, 6]. In some patients sparing of the face, palms, and soles has been reported [7] as is present in this patient. The condition is life-long and is usually generalized. However, a few localized forms such as acral and facial types have also been described [8, 9]. (Figure 4) Histopathology of PSS usually reveals hyperkeratosis and splitting of the epidermis between the granular layer and the stratum corneum or sometimes shows an intracorneal split. Intracellular, cytoplasmic splitting may also be found in the lower stratum corneum [6]. Electron microscopy demonstrates abnormal and cribriform keratohyalin granules indicating a severe disturbance of keratinization. In a few patients, reduced desmosomal plates or intercellular electrondense globular deposits in the stratum corneum were also found [3, 6, 8].


Peeling skin syndrome is largely a cosmetic disability causing substantial emotional stress to the patient whose diagnosis relies upon the presence of peeling skin without any underlying pathology and characteristic histology showing a split between the stratum corneum and the stratum granulosum. Understanding of the pathogenic events leading to the development of PSS will go a long way in formulating treatment for this presently untreatable lifelong disease. Homozygous missense mutation G113C, in TGM5, which encodes for Transglutaminase 5 in the acral form of PSS but not in generalized types of PSS, requires further investigation and may hold the key to unraveling the pathogenic event in other acantholytic disorders and formulating new treatments for such conditions.


Peeling Skin Syndrome (PSS) is a rare genodermatoses characterized by asymptomatic, localized or generalized, continuous exfoliation\n of the stratum corneum; it may present at birth or in adulthood. We describe a patient having the type A non-inflammatory\n variant of PSS showing asymptomatic and continuous skin peeling from the neck, trunk, back, and extremities. Friction appeared\n to be an aggravating factor, but there was no seasonal variation. Histopathology in this condition reveals hyperkeratosis\n and splitting of the epidermis between the granular layer and the stratum corneum. No treatment for this disorder has been\n found to be effective so far.\n


Two main subtypes of PSS based on the presence or absence of inflammatory changes have been suggested: Type A is a non-inflammatory\n variant characterized by asymptomatic, generalized, continuous skin peeling with intact general health, whereas Type B patients\n exhibit ichthyotic erythroderma that evolves into pruritic, scaly, and erythematous patches with rare vesiculations, easily\n removable hair, and summer flaring [3, 6]. In some patients sparing of the face, palms, and soles has been reported [7] as is present in this patient. The condition is life-long and is usually generalized. However, a few localized forms such\n as acral and facial types have also been described [8, 9]. (Figure 4) Histopathology of PSS usually reveals hyperkeratosis and splitting of the epidermis between the granular layer\n and the stratum corneum or sometimes shows an intracorneal split. Intracellular, cytoplasmic splitting may also be found in\n the lower stratum corneum [6]. Electron microscopy demonstrates abnormal and cribriform keratohyalin granules indicating a severe disturbance of keratinization.\n In a few patients, reduced desmosomal plates or intercellular electrondense globular deposits in the stratum corneum were\n also found [3, 6, 8].\n


Peeling skin syndrome is largely a cosmetic disability causing substantial emotional stress to the patient whose diagnosis\n relies upon the presence of peeling skin without any underlying pathology and characteristic histology showing a split between\n the stratum corneum and the stratum granulosum. Understanding of the pathogenic events leading to the development of PSS will\n go a long way in formulating treatment for this presently untreatable lifelong disease. Homozygous missense mutation G113C,\n in TGM5, which encodes for Transglutaminase 5 in the acral form of PSS but not in generalized types of PSS, requires further\n investigation and may hold the key to unraveling the pathogenic event in other acantholytic disorders and formulating new\n treatments for such conditions.\n 350c69d7ab


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