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Cavernous sinus thrombosis following dental extraction : a rare case report and forgotten entity
Karun Aggarwal,Sanjay Rastogi,Atul Joshi,Ashish Kumar,Archana Chaurasia,Rajat Prakash 대한구강악안면외과학회 2017 대한구강악안면외과학회지 Vol.43 No.5
Prior to the advent of efficacious antimicrobial agents, the mortality rate from cavernous sinus thrombosis (CST) was effectively 100%. There have been very few reports of CST associated with tooth extraction. A 40-year-old female presented to the emergency room with swelling over the right side of the face and history of extraction in the upper right region by an unregistered dental practitioner. The patient presented with diplopia, periorbital ecchymosis, and chemosis of the right eye. A computed tomography scan revealed venous dilatation of the right superior ophthalmic vein. The patient was immediately treated with incision and drainage, intravenous antibiotics, and heparin (low molecular weight). Unfortunately, the patient died two days after surgery due to complications from the disease. CST is a rare disease with a high mortality rate. Therefore, dental health education in rural areas, legal action against unregistered dental practitioners, early diagnosis, and aggressive antibiotic treatment can prevent future mortality resulting from CST.
Tuberculosis of the Spleen as a Cause of Fever of Unknown Origin and Splenomegaly
( Biju Pottakkat ),( Ashok Kumar ),( Archana Rastogi ),( Narendra Krishnani ),( Vinay K. Kapoor ),( Rajan Saxena ) 대한소화기기능성질환·운동학회 2010 Gut and Liver Vol.4 No.1
Background/Aims: Splenic involvement of tuberculosis, which is rare, warrants better definition in the current era of resurgence of tuberculosis. Methods: Out of 339 splenectomies performed between January 1989 and December 2008 for indications other than trauma, histopathologic analysis of the spleen revealed tuberculosis in 8 patients. Results: All eight patients were referred for splenectomy due to fever of unknown origin (FUO). No patient was infected with HIV, and all had at least moderate splenomegaly and hepatomegaly. Three patients had hypersplenism with bleeding manifestations. Radiologic evaluations demonstrated that splenic lesions were present in five patients. Five patients had evidence of tuberculosis manifested as enlarged splenic hilar lymph nodes, cystic lymph nodes, or liver. Two patients exhibited tubercle bacilli in their sputum during the postoperative period. Conclusions: In areas where tuberculosis is prevalent, tuberculosis should be considered in the differential diagnosis of patients presenting with FUO and splenomegaly. Extrasplenic involvement is usually seen in splenic tuberculosis, although it may not be apparent at presentation. Splenic tuberculosis can present in isolation without extrasplenic involvement, and even in immunocompetent individuals. (Gut Liver 2010;4:94-97)
( Ashish Kumar Vyas ),( Sharda Patra ),( Archana Rastogi ),( Shiv Ku-mar Sarin ),( Nirupma Trehanpati ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: Vertical transmission of Hepatitis B virus (HBV) from infected mother to the newborn is the major cause of HBV chronicity. Asialoglycoprotein receptor (ASGPR) expression on hepatocytes has been associated with HBV entry and endocytosis. However, there is a big lacuna regarding expression of ASGPR expression on placental cells and its role in HBV vertical transmission. Methods: 34 HBsAg+ve and 13 healthy pregnant mothers were enrolled along with their newborns. QHBsAg, HBV DNA and liver-function-test were performed among the groups. HBsAg+ve women were grouped into transmitting and non-transmitting mothers on the basis of newborns HBsAg and HBVDNA. Expression of ASGPR and HBsAg were analyzed in placental tissue using Immunohistochemistry and immunofluorescence staining. Peripheral and cord blood-mononuclear cell together with dendritic cells (mDCs and pDCs) were analyzed for the expression of DC-ASGPR, using flow cytometry and QPCR in all subjects. Results: The incidence of HBV vertical transmission to the newborn was 18% among the HBsAg positive pregnant females. HBV transmitting mothers showed increased expression of ASGPR in trophoblasts of placenta. Immunofluorescence microscopy revealed co-localization of HBsAg and ASGPR in placenta as well as in DCs of HBV transmitting mothers. HBV transmitting mothers and their HBsAg+ve newborns showed increased mRNA levels of DC-ASGPR in PBMCS. However, flowcytometry revealed no significant difference in the expression of ASGPR on PBMCs or CBMCs cells between the 2 groups. The HBV transmitting mothers and their HBsAg+ve newborns also showed an increased expression of DC-ASGPR on both myeloid and plasmocytoid dendritic cells compared to HBV non-transmitting mothers and their HBsAg negative newborns. Conclusions: The present work highlights for the first time a role of ASGPR in the intrauterine mother to baby HBV transmission. Blocking of ASGPR appears to be novel therapeutic strategy for prevention of HBV mother to baby vertical transmission.