Suprasellar Plasmacytoma Leading to the Diagnosis of Multiple Myeloma.

Plasmacytomas are a collection of plasma cells that occur as a solitary lesion or in conjunction with multiple myeloma. Intracranial location is uncommon but should be considered as management differs. Plasmacytomas in the suprasellar region are rare but should be considered in the differential diagnosis of suprasellar masses. Clinical presentation and imaging findings have similarities and overlap between pituitary adenomas and plasmacytomas, so the diagnosis depends on biopsy and pathological evaluation. Immunohistological staining is often necessary due to structural similarities to adenomas. Isolated cases may be treated with radiation alone and surgery is reserved for symptoms due to mass effect. Systemic therapy is given if there is evidence of multiple myeloma. In this case report, we present a 52-year-old male who presented with worsening blurry vision associated with headaches and epistaxis of four months duration. CT of the head showed a large mass involving the sella and skull base. Labs showed normal calcium, creatinine, and intact pituitary function. Biopsy of the mass was initially diagnosed as a pituitary adenoma but repeat pathology revealed plasmacytoma. Body imaging revealed diffuse lytic lesions. Bone marrow biopsy and serum electrophoresis were consistent with a diagnosis of multiple myeloma. The patient underwent radiation therapy to the suprasellar mass followed by systemic therapy for multiple myeloma with bortezomib, lenalidomide, and dexamethasone. The patient achieved a very good partial response.

Iron Deficiency Anemia Associated With Acid-Modifying Medications: Two Cases and Literature Review.

Iron deficiency anemia is often listed among potential adverse effects of gastric acid-suppressive medications, given that gastric acidity promotes intestinal absorption of nonheme iron. Additionally, the antacid calcium carbonate can inhibit iron absorption. However, there is little direct clinical evidence that proton-pump inhibitors, histamine-2 receptor antagonists, or calcium carbonate cause iron deficiency anemia. Most case reports have had substantial limitations (e.g., minimal follow-up and presence of other causes of iron deficiency), and retrospective cohort studies have lacked sufficient patient-specific detail to make strong causal inferences. We present 2 cases-both with detailed, prospective 10-year follow-up-in which combinations of proton-pump inhibitors, histamine-2 receptor antagonists and calcium carbonate were clearly associated with development of iron deficiency anemia. Overt iron-deficiency anemia is probably uncommon in patients who use acid-modifying medications and who have no other conditions that predispose to iron deficiency. Nevertheless, clinicians should be aware of this potential complication, given widespread use of these agents.

Lymph node-derived donor encephalitogenic CD4+ T cells in C57BL/6 mice adoptive transfer experimental autoimmune encephalomyelitis highly express GM-CSF and T-bet.

Experimental autoimmune encephalomyelitis (EAE) is a relevant animal model for the human demyelinating inflammatory disorder of the central nervous system (CNS), multiple sclerosis (MS). Induction of EAE by adoptive transfer allows studying the role of the donor T lymphocyte in disease pathogenesis. It has been challenging to reliably induce adoptive transfer EAE in C57BL/6 (H-2b) mice. The goal of this study was to develop a reproducible and high yield protocol for adoptive transfer EAE in C57BL/6 mice. A step-wise experimental approach permitted us to develop a protocol that resulted in a consistent relatively high disease incidence of ~70% in recipient mice. Donor mice were immunized with myelin oligodendrocyte glycoprotein (MOG)p35-55 in complete Freund's adjuvant (CFA) followed by pertussis toxin (PT). Only lymph node cells (LNC) isolated at day 12 post immunization, and restimulated in vitro for 72 hours with 10 µg/mL of MOGp35-55 and 0.5 ng/mL of interleukin-12 (IL-12) were able to transfer disease. The ability of LNC to transfer disease was associated with the presence of inflammatory infiltrates in the CNS at day 12. Interferon gamma (IFNγ) was produced at comparable levels in cell cultures prepared from mice at both day 6 and day 12 post immunization. By contrast, there was a trend towards a negative association between IL-17 and disease susceptibility in our EAE model. The amount of GM-CSF secreted was significantly increased in the culture supernatants from cells collected at day 12 post immunization versus those collected at day 6 post-immunization. Activated CD4+ T cells present in the day 12 LNC cultures maintained expression of the transcription factor T-bet, which has been shown to regulate the expression of the IL-23 receptor. Also, there was an increased prevalence of MOGp35-55-specific CD4+ T cells in day 12 LNC after in vitro re-stimulation. In summary, encephalitogenic LNC that adoptively transfer EAE in C57BL/6 mice were not characterized by a single biomarker in our study, but by a composite of inflammatory markers. Our data further suggest that GM-CSF expression by CD4+ T cells regulated by IL-23 contributes to their encephalitogenicity in our EAE model.