Only seen was a positive blood culture for candida on day eighteen. CT guided lung biopsy was positive for Thioflavin T amyloid deposits. Brain biopsy was positive for eosinophilic material (similar to the lungs) but unfavorable for Thioflavin T stain. The patient’s clinical status continued to deteriorate with cold cyanotic fingers developing on day 12 and a health care acquired pneumonia, respiratory failure, and fungemia on day 18. On day 29, family withdrew life support and denied any autopsies. em Conclusion /em . Described is an atypical course of MGUS complicated by amyloidosis of the lung and nonamyloid eosinophilic deposition in the brain. As MGUS might be complicated by diseases such as amyloidosis and multiple myeloma, a scheduled follow-up of these patients is usually usually necessary. Further research is needed in order to better define the optimal treatment and management strategies of MGUS and its complications. 1. Introduction B cell dyscrasias are characterized by a clonal proliferation of B cells (benign or malignant). The spectrum of B cell dyscrasia is usually broad and includes the monoclonal gammopathy of undetermined significance (MGUS) [1]. MGUS is found in more than 1% of persons who are 50 years or older and is defined by the presence of a serum monoclonal protein concentration less than 3?g/dL, with Myelin Basic Protein (68-82), guinea pig absence of lytic bone lesions, of M proteins in urine, of hypercalcemia and of renal failure [1C3]. Amyloidosis is usually a rare complication of MGUS which is usually secondary to excessive production of a monoclonal immunoglobulin (Ig) and deposition of the single Ig isotype or subunits in various tissues. Aggregomas, on the other hand, are tumoral non-amyloidotic monoclonal immunoglobulin light chain deposits [4]. In this paper, we describe an unusual presentation of MGUS combining amyloid deposition in the lung and non-amyloid eosinophilic deposition in the Brain. 2. Case A-66-year-old male, who was exsmoker, presented to the ER for a change in mental status. As per the family, the patient who had a normal mental status in the past was noticed to be progressively worsening for the last couple of months, with disorientation mainly found over phone discussions. At the time of presentation he was awake and alert, but disoriented to time and place. He denied any pain and was unable to provide any history. Physical exam was Myelin Basic Protein (68-82), guinea pig normal except for the presence of facial ecchymosis. The neurological part showed a normal motor, sensory, and cranial nerve exam. Also, his gait was stable. Past medical history was Myelin Basic Protein (68-82), guinea pig significant for hypertension, hypercholesterolemia, aortic valve replacement (nonmetallic), atrial fibrillation (on warfarin), incomplete heart Rabbit Polyclonal to IKK-alpha/beta (phospho-Ser176/177) block, pacemaker, and IgG- IgA, kappa type Monoclonal Gammopathy of Undetermined Significance (MGUS). Family history was not relevant. MGUS was diagnosed 9 months ago on serum protein electrophoresis (SPEP) as patient was referred to our institution’s center for cancer and blood related diseases for hyperglobulinemia on routine blood work. At that time the patient underwent extensive work up to rule out any plasma cell dyscrasias. The Urine protein electrophoresis (UPEP) was unfavorable for M spike. Immunohistochemistry and flow cytometry from peripheral smear as well as from bone marrow biopsy were unfavorable for a clonal plasma cell or malignant B-cell. Chromosomal analysis and cytogenetics were also normal. In the ER, a head CT scan revealed multiple parenchymal hemorrhagic lesions suspicious for metastases mainly in the frontal part bilaterally and in the left parieto-temporal region, with edema and compression mainly around the left lateral ventricle. Also, an interventricular lesion at.