Nay Thi Tun is currently in Residency Training of Internal Medicine Program in Easton Hospital, PA. She has obtained M.B.B.S in Yangon, Myanmar. She has done her residency training in Central Women’s Hospital in Yangon, Myanmar for Obstetrics and Gynecology. At present she is a committee member of “Blood Blank” in Easton Hospital and “Instiutional Review Board” in Easton Hospital as well as she is an acting as a student coordinator. She has participated in many medical meetings and publishes number of research works.

Epithelioid hemangioendothelioma (EHE) is a variant of epitheloid vascular tumors that originates from the vascular endothelium. EHE was first described by Weiss and Enzinger in 1982, and has been found in skin, lung, pleura, liver, bone, brain, heart, and other organs. The etiology of EHE remains unclear. Genetically, the translocation t (1;3)(p36.3,q25) has been found in two EHE cases. Although EHE is considered an intermediate malignancy between hemagioma and angiosarcoma, the clinical behavior of this vascular tumor is unpredictable. Management of EHE remains a therapeutic challenge due to the extremely low incidence of this vascular tumor, variable disease courses with different responses to surgery, chemotherapy or anti-angiogenic agents. We are presenting the case of a young woman who was diagnosed with metastatic EHE to liver and lung at the age of 26 years old. She was initially treated with Adriamycin without response, and subsequently chemo-embolization of bulky left hepatic disease that was causing intractable abdominal pain and left shoulder pain. Further progressive disease was managed with left lateral segmental hepatectomy, which was combined with aggressive loco-regional management of additional metastatic lesions with cryoablation and radiofrequency ablation. Unfortunately, the tumor relapsed about two years and nine months after this aggressive surgical approach. She then began treatment with interferon alpha 2b for approximately seven years, attaining a complete hepatic clinical remission on PET/CT after the first three years of treatment. She has been off treatment since March 2010, and to-date she remains free of disease with a Karnofsky scale of 100. The patient has therefore had a durable clinical response to interferon alpha 2b for more than ten years, with a complete hepatic clinical response for more than seven and a half years, since May 2006. One of the mechanisms of action for alpha interferon has been shown to be anti-angiogenesis, and it is possible that it is this mechanism of action that has successfully controlled this patient's aggressive metastatic EHE. Therefore, alpha interferon should be considered as a potential treatment for metastatic or recurrent metastatic EHE, since our patient has had a durable clinical response to alpha interferon for more than a decade since the treatment was initiated.

Dr. Ramakrishna Pai Jakribettu and Dr. Rekha Baloor M.D are affiliated with Father Muller Medical College - Department of Microbiology, Dr. Manoj P Rai - has been working as a research assistant Weill Cornell Medical College NY from past 1 year, Dr. Shridhar Avabrata M.D - Associate professor of Pediatrics, Father Muller Medical College, India. Andrew Thaliath is currently an Intern in Father Muller Medical College and Dr. Manjeshwar Shrinath Baliga Phd is the research chair for Father Muller Medical College, India.

During the course of Dengue infection, IgM is detected around 3-5 days following the onset of illness, reaching peak levels around 10th day to reach undetectable levels at 2-3 months. IgG dengue-antibody appears during first week of illness and has been noted to persist lifelong (WHO - 1997). Levels of Dengue IgM antibody during secondary dengue infection is significantly lower and undetectable compared to primary dengue infection. Hence, both dengue IgM and IgG antibody profiling are required for identification of secondary dengue infection (WHO.1997). A total of 69 of dengue positive and 93 dengue negative children aged <18 from Father Muller medical college, Mangalore with serological diagnosis based on Dengue NS1Ag and differential of IgM and IgG antibody results and IgM ELISA confirmatory test are enrolled. Correlation - Hemoglobin (p = 0.0003 r = 0.236), Total Count (p =< 0.001 r = -0.504), Platelet (p=<.001 r= -0.741). The results show statistically significant negative correlation for Total Count and platelet counts with stage of dengue determined on the basis of antibody type. Thus careful monitoring of hematological parameters at different time points of illness and its correlation with antibody typing could be helpful for evaluation of prognosis and careful interventions to curtail the complications would result in reduction of morbidity and mortality.

Sustained TFR has been reported in clinical trials ofpatients withCML-CP who achievedsustaineddeep MR on imatinib therapy. Nilotinib treatmentresults in high rates of sustained deep MR, a key eligibility criterion for TFR studies.The randomized, phase 2 ENESTgoal study(NCT01744665) will evaluate TFR among patients with CML-CP who achievesustained MR4.5 (BCR-ABL≤0.0032% on the International Scale [IS] by real-timequantitative polymerase chain reaction [RQPCR]) after switching tonilotinib.ENESTgoal will enrollapproximately 300 patients with major molecular response (BCRABLIS≤ 0.1%)but with detectable disease (BCR-ABLIS>0.0032%), as assessed by a central laboratory, after ≥1 year ofimatinib therapy. Patients will switch to nilotinib 300 mg twice dailyonstudy entry andbe monitored quarterly for up to 2 years; those who achieveconfirmed MR4.5 during the monitoring phase will be randomized to enter a 1- or 2-year consolidation phaseof continuednilotinib treatment. Patients will then stop nilotinib therapy and enter the 3-year TFR phase if MR4.5is maintained throughout the consolidation phase. RQ-PCR assessments will be performed monthly for the first 6 months of the TFR phase, then every 2 months for 18 months and then quarterlythereafter. Patients with molecular relapse, defined in ENESTgoalas confirmed loss of MR4 (or BCR-ABLIS>0.01%), will re-initiate nilotinibtherapy. The primary endpoint of the study is the molecular relapse-free rate at 6 months after suspension of nilotinib therapy. ENESTgoal is currently open for enrollment in the United States.

Introduction: Coumadin anticoagulation therapy is indicated in a variety of thromboembolic conditions. Close INR monitoring is required to maintain therapeutic range in order to decrease complications, emergency room visits, and medical costs associated with Coumadin therapy. To achieve this, tight quality control in primary health care systems is undeniably important. Using finger stick device measurement of the international normalized ratio (INR) is increasingly common in outpatient, inpatient, nursing home, and home care environments. The purpose of this study is to comparison with INR provided by the new finger stick device and Laboratory-based Venipuncture in our primary care center managed anticoagulation clinic. Methods: The INR data was collected from 8 patients receiving Coumadin during a period of 4 months. INR was collected by the lab draw for 2 months and finger stick device for next 2 months. The venous plasma INR was measured from a single laboratory coagulation analyzer and the capillary whole blood INR were obtained from a single finger stick device. Results: The total number of blood samples collected for INR analyses were 101, 53 samples were collected by the lab draw and 48 samples were obtained for finger stick analysis. In this study, the difference between the two methods currently used for monitoring INR, each for a 2 months period was evaluated. It was noticed that 55% (29/53) of INRs were in the therapeutic range when collected by the lab draw as compared with 67% (32/48) of INRs in the therapeutic range when collected by the finger stick device. However, this difference was not statistically significant (P>0.05). Discussion: In a finger stick measurement of INR, the patient applies a small amount of blood to a test strip and then feeds the strip into the device. The benefits of by using finger stick device for INR measurement include convenient, low cost, and fewer medical complications. Additionally, off-target INR values can be adjusted more regularly and more quickly. In contrast, previous clinical study has shown that the capillary whole blood INR was not significantly different from the laboratory-based venipuncture. The capillary whole blood INR has the potential advantage of obtaining an INR result in general practice, thus allowing direct assessment and management of INR instantaneously. Conclusion: Results suggest that there is no statistically significant difference between the finger stick device and Laboratory-based Venipuncture for INR measurement in our ambulatory center managed anticoagulation clinic.

Dr Deobrat Mallick is a second year Internal medicine resident at Wright Center for Graduate medical education (WCGME) at Scranton. He has done his Medical school from Guwahati Medical College, Assam, India in 1997. He has begun his Post-graduate training program (MD) in Internal Medicine in the year 1999 at Jiwaji University at Gwalior. In 2004 he had moved to United Kingdom and trained and worked in Emergency Medicine for several years before moving to USA in 2012 to start his residency in Medicine. He has now worked for several years in UK, India and USA. During which period he has worked in both large city hospitals and smaller district general hospitals with different levels of capabilities and this has helped him to hone his clinical knowledge and various skills.

Introduction: Cold agglutinin disease is a rare, most often affecting females in the seventh decade of life, with an incidence of one case per million people per year. It is characterized by the presence of IgM antibodies (rarely IgA or IgG) directed against polysaccharide antigens on the red blood cell surface. These antibodies transiently bind erythrocytes in the colder extremities, generally below 30 degrees C. They dissociate after returning centrally, but frequently sublytic quantities of the opsonin C3b will be bound the erythrocyte surface. This interaction causes the affected blood cells to be removed by the spleen, liver, and bone marrow. Hemolysis is not necessarily severe.Cold agglutinin disease is often caused by infection by pathogens such as Mycoplasma pneumoniae, cytomegalovirus, influenza virus, or Ebstein-Barr Virus.It can also reflect the presence of an underlying lymphoproliferative disorder, encompassing a wide range of disorders. Case: The patient was a 91 year old female presented to hospital after her outpatient workup showed sever anemia and a positive Stool for occult blood test. She was recently started on Naproxen and steroid for back pain by her PCP. Her hemoglobin upon presentation to the emergency department was 6.1 g/dl, for which she received one unit of PRBCs. She underwent EGD and a bleeding gastric lesion was identified. Biopsy was taken from the lesion. The cause of anemia at this time was suspected to be GI bleed; however a workup of the patient's anemia also raised the possibility of hemolytic anemia with evidence high indirect bilirubin and LDH. Haptoglobin was low normal. Further workup for auto-immune hemolysis with direct Coombs test was positive for C3B and 3D, but Negative for IgG. Hematology evaluation with cold agglutinin titers and thermal amplitude test revealed a cold agglutinin autoimmune hemolytic anemia secondary to Anti-I antibody. Meanwhile, thegastric biopsy was analyzed and was found to contain high-grade diffuse B cell lymphoma. CT showed a large retroperitoneal soft tissue mass, most likely lymphadenopathy, displacing nearby organs and extending into the left psoas and L3 vertebral body. An MRI found extension of this mass into the neural foramina on the left at L2-3 & L3-4 and on the right at L3-4. There were also linear signal alterations consistent with pathologic fracture in the body of L3.After discussion with the patient and her family, chemoimmunotherapy was started. Rituximab was begun after hepatitis B serology was found to be negative. Oncovin, adriamycin, and dose-reduced cylcophosphamide were added to her regimen 2 days later. Discussion: Treatment of mildly symptomatic cold agglutinin disease (e.g., mild degrees of acrocyanosis or anemia) is mainly supportive, and consists of avoidance of exposure to cold and additional sources of complement. In the presence of severe signs and symptoms, treatment with rituximab with or without fludarabine was recommended. When there is evidence for its presence, treatment of an underlying lymphoma is often successful in reducing signs and symptoms of cold agglutinin disease. Conclusion: The many pathogeneses of anemia can be overwhelming and may prompt the physician to settle for the first explanation that comes to hand. However the astute clinician faced with cold agglutinin autoimmune hemolytic anemia should always consider underlying lymphoproliferative disorder in addition to infectious causes.