Initial Institutional Experience With Cryoablation Therapy for Breast Fibroadenomas: Technique, Molecular Science, and Post-Therapy Imaging Follow-up
Sheth, Monica; Lodhi, Umairullah; Chen, Brandon; Park, Young; McElligott, Suzanne
Cryoablation is a safe and effective nonsurgical treatment for breast fibroadenomas (FAs). The treatment response is inversely related to the tumor size, with lesions less than 2â€‰cm showing an optimal response. Ultrasound (US) imaging follow-up of the ablated tumor is recommended at 6-month intervals for 2â€‰years at our institution. Although a decrease in the size of the FA clinically and on US imaging is the expected treatment response, variations can be seen. Knowledge of typical US changes over time is imperative to prevent unnecessary rebiopsy or excision in patients who have undergone cryoablation. We will review the initial patient selection criteria, cryoablation technique, and US findings at regular follow-up intervals after cryoablation of FAs through a series of cases treated at our institution.
Multisystem Radiologic Manifestations of Erdheim-Chester Disease
Lodhi, Umairullah; Sarmast, Uzair; Khan, Saadullah; Yaddanapudi, Kavitha
Erdheim-Chester Disease is a rare form of multiorgan non-Langerhans' cell histiocytosis that affects individuals between the ages of 50 and 70 with an equal distribution among males and females. It is associated with significant morbidity and mortality that is mostly due to infiltration of critical organs. Some of the sites that Erdheim-Chester Disease affects include the skeletal system, central nervous system, cardiovascular system, lungs, kidneys (retroperitoneum), and skin. The most common presenting symptom of Erdheim-Chester Disease is bone pain although a large majority of patients are diagnosed incidentally during a workup for a different disease process. Diagnosing Erdheim-Chester Disease is challenging due its rarity and mimicry to other infiltrative processes. Therefore, a multimodality diagnostic approach is employed with imaging being at the forefront. As of date, a comprehensive radiologic review of the manifestations of Erdheim-Chester Disease has rarely been reported. Here we present radiologic findings of an individual suffering from Erdheim-Chester Disease.
Interferon-Î± accelerates murine systemic lupus erythematosus in a T cell-dependent manner
Liu, Zheng; Bethunaickan, Ramalingam; Huang, Weiqing; Lodhi, Umairullah; Solano, Ingrid; Madaio, Michael P; Davidson, Anne
OBJECTIVE:To investigate the mechanism by which interferon-Î± (IFNÎ±) accelerates systemic lupus erythematosus (SLE) in (NZBÃ—NZW)F1 (NZB/NZW) mice. METHODS:NZB/NZW mice were treated with an adenovirus expressing IFNÎ±. In some mice, T cells were depleted with an anti-CD4 antibody. The production of anti-double-stranded DNA (anti-dsDNA) antibodies was measured by enzyme-linked immunosorbent assay and enzyme-linked immunospot assay. Germinal centers and antibody-secreting cells (ASCs) in spleens and IgG deposition and leukocyte infiltrates in kidneys were visualized by immunofluorescence staining. The phenotype of splenic cells was determined by flow cytometry. Finally, somatic hypermutation and gene usage in VH regions of IgG2a and IgG3 were studied by single-cell polymerase chain reaction. RESULTS:IFNÎ±-accelerated lupus in NZB/NZW mice was associated with elevated serum levels of IgG2 and IgG3 anti-dsDNA antibodies and accumulation of many IgG ASCs in the spleen, which did not develop into long-lived plasma cells. Furthermore, IgG2a and IgG3 antibodies in the mice were highly somatically mutated and used distinct repertoires of VH genes. The induction of SLE in the mice was associated with an increase in B cell Toll-like receptor 7 expression, increased serum levels of BAFF, interleukin-6 (IL-6), and tumor necrosis factor Î±, and induction of T cells expressing IL-21. Although IFNÎ± drove a T cell-independent increase in serum levels of IgG, autoantibody induction and the development of nephritis were both completely dependent on CD4+ T cell help. CONCLUSION/CONCLUSIONS:These findings demonstrate that, although IFNÎ± activates both innate and adaptive immune responses in NZB/NZW mice, CD4+ T cells are necessary for IFNÎ±-driven induction of anti-dsDNA antibodies and clinical SLE.