We describe a case of a homosexual male with human immunodeficiency virus (HIV) and CD4 count of 246 presenting with acute severe bloody diarrhea. Infectious work up was negative, and colonoscopy revealed severe diffuse colonic ulcerations. Histopathologic analysis and Treponemal pallidum immunostaining confirmed the diagnosis of intestinal spirochetosis. There was no evidence of co-infection with other pathogens. His symptoms completely resolved after a 14-day course of metronidazole. This case is notable as colonic ulceration of any severity in patients living with HIV is rarely identified with intestinal spirochetosis. Hence, it should be considered in the differential diagnosis of colonic ulcerations.

Introduction: Autoimmune hemolytic anemia (AIHA) is a rare and diverse group of acquired hemolytic anemias which results from increased destruction of red blood cells (RBCs) due to autoantibodies directed against antigens on the RBC surface. Currently, there are no clearly defined evidence-based guidelines on the management of AIHA, and current treatment options are based on small retrospective studies, case reports, as well as expert experiences and recommendations. We report a case of severe idiopathic mixed AIHA that responded to a combination of steroids, intravenous immunoglobulin (IVIG) and bortezomib. Case Report: A 25-year-old African American female presented with jaundice, shortness of breath, and abdominal pain. She had splenomegaly on examination and initial work-up was significant for severe anemia (hemoglobin, 3.3 g/dl) and hyperbilirubinemia (total bilirubin, 26.7 mg/dl; direct bilirubin, 21.9 mg/dl). Direct antiglobulin test (DAT) was microscopically positive for anti-IgG and anti-C3d, and cold autoantibodies were identified. An extensive workup for a possible secondary cause of her anemia was non-revealing. She was sequentially treated with prednisone, IVIG, and bortezomib. Marked response was noted as evidenced by improvement in the hemoglobin from a nadir of 3.2 g/dl on admission to 10.1 at discharge. Patient has remained clinically in remission since then. Conclusion: The first line treatment for warm AIHA (w-AIHA) includes glucocorticoids and transfusion of least incompatible RBCs. Steroids are rarely necessary or effective in cold agglutinin AIHA in which case high dose IVIG and plasmapheresis have been used albeit with inconsistent results. Bortezomib is an inhibitor of the 26S proteasome and is approved for the treatment of multiple myeloma. It has been reported to have some activity in rituximabresistant cold agglutinin disease (CAD) due to its activity against the CD20-negative plasma cell compartment that may be responsible for IgG anti-RBC autoantibody production.

Primary hyperparathyroidism (PHPT) typically occurs in persons above 45 years, with a female predominance. PHPT induces a state of hypercalcemia, but acute pancreatitis is a rare sequelae of this hypercalcemia. We report a case of a 31-year-old man with no known medical history who presented in diabetic ketoacidosis with electrolyte abnormalities. His clinical course progressed to multi-organ dysfunction despite correction of metabolic derangements. Further workup led to the discovery of the uncommon triad by which previously undiagnosed PHPT precipitated severe diabetic ketoacidosis.

We describe a case of a homosexual male with human immunode ciency virus (HIV) and CD4 count of 246 presenting with acute severe bloody diarrhea. Infectious work up was negative, and colonoscopy revealed severe di use colonic ulcerations. Histopathologic analysis and Treponemal pallidum immunostaining con rmed the diagnosis of intestinal spirochetosis. ere was no evidence of co-infection with other pathogens. His symptoms completely resolved a er a 14-day course of metronidazole. is case is notable as colonic ulceration of any severity in patients living with HIV is rarely identi ed with intestinal spirochetosis. Hence, it should be considered in the di erential diagnosis of colonic ulcerations.

Dear Editor, BioMed Central, Advances in Rheumatology. We read with great interest the article "Effect of food intake and ambient air pollution exposure on ankylosing spondylitis disease activity" [1] by Narjes Soleimanifar et al. The authors touch on an important aspect of managing patients with ankylosing spondylitis (AS), especially given the increasing interest in the role of genetic, environmental and dietary factors in the pathogenesis and severity of disease. However, we would like the authors to clarify certain aspects of their work, which we strongly believe will be beneficial for the readership of Advances in Rheumatology.