8 research outputs found

    Immunohistochemical expression of p16INK4a in premalignant lesions and malignant tumours of cervix

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    Background: Cervical carcinoma is the third most common cancer in women worldwide and firth most common cause of cancer related deaths. Human Papilloma virus, the most common cause of cervical cancer, causes functional inactivation of pRb, resulting in overexpression of p16INK4a. The overexpression of p16INK4a correlates well with the degree of cervical dysplasia and neoplasia. The present study is done to determine the IHC expression of p16INK4a so that it may be used as a biomarker for HPV and may play a role in the prevention, diagnosis and prognosis of cervical neoplasm. Methods: The present study was conducted on 60 formalin-fixed, paraffin-embedded specimens of cervical neoplasms, which comprised 47 cases of squamous cell carcinoma followed by 8 cases of adenocarcinoma, 3 cases of HSIL and 2 cases of LSIL. These were then subjected to IHC by p16INK4a. Cytoplasmic and nuclear positivity for p16INK4a was noted. Results: Overall 95% cases were positive for p16INK4a expression, 100% cases of adenocarcinoma, 98% cases of squamous cell carcinoma, 100% cases of HSIL and 0% cases of LSIL were positive for p16 expression. Conclusions: The present study showed statistical correlation of immunoreactivity of p16INK4a with histological type was clinically significant (p value <0.0001). In our study, p16INK4a immunohistochemical expression increased with increasing degree of dysplasia and with presence of cervical carcinoma

    Healthcare Disparities in Lupus Nephritis: Findings from the Southern California Lupus Registry

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    Lupus nephritis (LN) is a major cause of among systemic lupus erythematosus (SLE) patients. Despite therapeutic advancements, LN patients continue to have a poor prognosis related to socioeconomic status (SES). We sought to establish the correlation between SES and LN prevalence in San Bernardino and Riverside counties of Southern California

    Vitamin D and Lupus: Are we doing enough?

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    The aim of this study is to identify rheumatology practice care gaps in evaluating for vitamin D deficiency in systemic lupus erythematosus (SLE), as well as adherence to vitamin D replacement in SLE patients currently on corticosteroid therapy. Data for this study were collected from the Southern California Lupus Registry in addition to data extraction from medical health records. Evaluation of serum vitamin D level within 6 months of patient encounter, current or prior use of systemic corticosteroids, and vitamin D replacement in patients receiving corticosteroid therapy were noted. Vitamin D deficiency was defined as serum 25(OH)D3 less than 30 ng/ml. Of 182 patients in the cohort, data were available for 176. Evaluation of vitamin D deficiency was noted in 49 patients (28%), 27 (55%) of whom had abnormal values. Current corticosteroid use was noted in 56 (32%) patients and prior use in 73 (41%). Vitamin D replacement was prescribed to 30 (54%) patients with current corticosteroid use. In an academic rheumatology clinic, we have identified underevaluation for vitamin D deficiency in SLE patients despite increasing awareness of its contribution to disease activity. Further, routine supplementation of vitamin D is particularly lacking in individuals receiving systemic corticosteroids. This presents a practical opportunity for improvement in SLE clinical care

    Atypical manifestations of sarcoidosis in a Hispanic male

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    Sarcoidosis is a multisystem granulomatous disease of unknown etiology that can present with nonspecific features, often resulting in delayed diagnosis. The diagnosis requires the demonstration of non-caseating granulomas on biopsy. While the prevalence of sarcoidosis in the USA is rare, the disease is rarer yet in Hispanics. It is for this reason that we report herein the case of a Hispanic gentleman with a unique clinical manifestations of sarcoidosis. With what began as a two-month history of joint pain and skin rash, this 55-year-old man was hospitalized with multiple joint pain, weight loss, fatigue and a pruritic rash with leonine facies in the setting of anemia, leukopenia, hypercalcemia, elevated serum creatinine, and urine Bence-Jones proteinuria. CT imaging of the chest was nonspecific, but skin biopsy revealed non-caseating granulomatous disease. After completing an infectious and malignancy evaluation, the patient was diagnosed with sarcoidosis, which was treated successfully with low-dose steroid therapy

    Sarcoidosis and Systemic Sclerosis: Strange Bedfellows

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    Coexistence of systemic sclerosis and sarcoidosis is rare. Both have predominant lung manifestations, each with distinctive features on computed tomography (CT) of the chest. We present herein a 52-year-old male with limited systemic sclerosis manifested primarily by sclerodactyly and subsequently by shortness of breath. A series of CT scans of the chest were reviewed. Initial CT chest one year prior to sclerodactyly onset revealed bilateral hilar and right paratracheal, prevascular, and subcarinal adenopathy. Five-year follow-up demonstrated thin-walled cysts, mediastinal lymphadenopathy, and nonspecific nodules. Due to progression of dyspnea, follow-up CT chest after one year again demonstrated multiple cysts with peripheral nodularity and subpleural nodules, but no longer with hilar or mediastinal adenopathy. Diagnostic open lung biopsy was significant for noncaseating granulomas suggestive of sarcoidosis. This is the first known case of a patient with systemic sclerosis diagnosed with sarcoidosis through lung biopsy without radiographic evidence of hilar or mediastinal lymphadenopathy at the time of biopsy. A review of cases of concomitant sarcoidosis and systemic sclerosis is discussed, including the pathophysiology of each disease with shared pathways leading to the development of both conditions in one patient

    Genetic studies of body mass index yield new insights for obesity biology

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    Note: A full list of authors and affiliations appears at the end of the article. Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P 20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.</p
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