K CT scan: multiple enlarged left-sided level II to V lymph
K CT scan: multiple enlarged left-sided level II to V lymph nodes with central necrosis and peripheral enhancement, lymphadenopathy in the left supraclavicular region69 195 40 Not performed (deceased) 156,303 84 195 Not performed (deceased) Chest/abdominal/pelvic CT scan: massive lymphadenopathy in the neck, left supraclavicular and paratracheal regions, bilateral hilum, retroperitoneum, paraaortic, peripancreatic, and retrograstric regions, extending into the splenic hilum and left kidney, with bilateral renal vessels displaced anteriorly. Multiple masslike bilateral pulmonary nodules27 Not performed 33 Not performed 17,767 Not performed Undetectable Not performed Neck CT scan: bilateral level II lymphadenopathy and a 6 mm nodule in the left apex with mild surrounding inflammationHuhn et al. AIDS Research and Therapy 2010, 7:44 http://www.aidsrestherapy.com/content/7/1/Page 4 ofTable 1 Clinical, immunologic, and virologic characteristics among subjects diagnosed with NHL after starting newerclass antiretroviral regimens (Continued)Biopsy site and Right medial specimen temporal brain biopsy Pathology Diffuse large B-cell lymphoma Positive Yes Died August 2008 Left axilla lymph node excisional biopsy Left cervical lymph node excisional biopsy Left neck lymph node fine needle aspirate Right lateral oropharyngeal wall biopsy via larynoscopy Plasmablastic large Bcell lymphoma PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27488460 Positive Yes SurvivedAtypical Burkitt Diffuse large B-cell lymphoma Diffuse large B-cell lymphoma with lymphoma translocation (8,14) Positive Yes Survived Tissue preparation inadequate Yes Survived Not performed Yes Died MarchEBV in situ hybridization Chemotherapy Outcomepatients achieving viral suppression with undetectable VL, Valsartan/sacubitril solubility compared to patients without NHL. A striking characteristic in NHL cases was the rapid onset of symptomatic disease which occurred at a median of 5 weeks after starting new HAART regimens. Our analysis suggests that the development of NHL may be attributable to either severe immunosuppression in these patients or complications from IRIS. The degree of immunosuppression in HIV infection has long been linked with risk of developing NHL [7,23,24]. In early reports assessing immunologic and virologic parameters associated with NHL, nadir CD4 count or low time-weighted mean CD4 count appeared to correlate with a high risk of NHL, which would support hypotheses that a long-term immunocompromised state may promote emergence of NHL [3,25]. Contemporary studies, however, have demonstrated that cumulative HIV viremia, particularly recent exposure to viremia, and the latest CD4 count measured before the onset of symptomatic NHL may be the most HIV-specific predictive factors for NHL oncogenesis [11,12,14,15,24,26,27]. Our analysis correlates with prior studies documenting low CD4 counts in patients with virologic failure immediately before the onset of NHL. An important feature of our cohort was the finding of symptomatic NHL occurring in the setting of profoundHIV viral load decline following initiation of HAART. This phenomenon raises the question of whether the degree and velocity of virologic response we can now achieve due to the simultaneous availability of new agents or possible unique properties of newer-class antiretrovirals may have facilitated an abnormal lymphoproliferative pathway. Clinically, in the PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28242652 largest cohort study of IRIS among 180 patients, the intensity of the viral load decrease within 90 days of starting HAART in antiretroviral na.
