S. Narreddy 1 , M. Snyder 1 , P. Khan 1 , N. Lekas 1 , R.D. Hobbs 1 ; 1 Oakwood Healthcare System, Dearborn, MI LEARNING OBJECTIVE: To recognize the dilemma posed by multiple enhancing ring lesions in the brain and emphasize the need for brain biopsy in equivocal cases. CASE INFORMATION: A 67 year-old Arabic male presented with a one-month history of progressive weakness and sensory changes of the left arm and leg. He had lived in the US for thirty years before returning to Yemen two years ago to work on a farm. On examination, he had right homonymous hemianopia, left hemipareisis and left hemianesthesia but nothing that would suggest either an infectious process or a malignancy. Basic work-up including HIV test was negative. An MRI revealed multiple enhancing ring lesions in the left and right occipital lobes, the right parietal lobe, and left cerebellar hemisphere. The findings were interpreted as metastatic lesions from an unknown primary. When no primary focus was found a brain biopsy was performed. Gross pus was aspirated. Histology was consistant with abscess. Smears revealed filamentous gram-positive organisms and cultures grew Nocardia asteroides. DISCUSSION: Multiple ring enhancing lesions in the brain typically represent either metastatic lesions (3 ± 15% of brain tumors; bronchogenic, breast, melanoma, renal, lymphoma are most common primaries) or abscesses. Differentiating between the two by clinical or radiographic means has been difficult, even with the development of CT and MRI scanning. Although advanced radiographic technologies (i.e., diffusion-weighted echo planar imaging, technetium-99m labeled leukocyte scintigraphy) accurately image brain appearance, to clarify treatment it is important to recognize that a brain biopsy is warranted when the diagnosis is in question and a primary focus cannot be identified. A 44 year old Hispanic male presented to clinic with multiple complaints including: red itchy eyes, productive cough with occasional blood, rhinorrhea, nasal congestion, myalgias, abdominal pain, and subjective fevers and chills. Except for a gastric ulcer diagnosed 1 month earlier, he was otherwise healthy. He was diagnosed with a viral syndrome, reassured, and given symptomatic treatment. The patient returned for a second visit 2 weeks later without improvement in his symptoms. A CXR, PPD, and HIV test were all negative. An ophthalmology exam confirmed the diagnosis of viral conjunctivitis. The patient, concerned that his symptoms were not improving, returned a week later, appearing very ill, and was admitted for further work up. On physical exam, notable findings included a T = 38.8 C, scleral injection, nasal and oropharyngeal erythema, decreased breath sounds at both lung bases, and mild abdominal tenderness in the right upper quadrant. Labs were significant for proteinuria, hematuria, and elevated liver function tests. To work up his abdominal symptoms, a CT of the abdomen was obtained which showed gastric thickening and a right lung nodule. Subsequent testing included an EGD showing diffuse erythematous mucosa; a repeat CXR and CT of the chest revealing multiple opacities in both lungs with hilar lymphadenopathy; bronchoscopy showing erythematous friable mucosa; and a repeat slit lamp examination revealing bilateral episcleritis. C-ANCA titers were 1:160. A nasal biopsy was performed showing granulomatous disease with giant cells and chronic vasculitis confirming the diagnosis of Wegeners Granulomatosis. The patient was treated with Cytoxan and Prednisone with resolution of symptoms. DISCUSSION: Wegeners Granulomatosis is a form of small vessel vasculitis with prevalence of 3:100,000. The mean age of onset is 40 years, with men affected slightly more than women. It classically involves upper and lower respiratory tracts and kidneys, but can involve virtually any organ system. This case illustrates how Wegeners can mimic colds and sinusitis, obscuring the diagnosis and delaying treatment. Early diagnosis is crucial because untreated Wegeners has a poor prognosis with median survival of 5 months and up to 90% mortality. Furthermore, renal failure can progress rapidly even in the absence of symptoms. Timely initiation of therapy with Cytoxan and Prednisone can be life saving and may markedly decrease morbidity and mortality. On the morning of admission, he was unable to arise from bed. The weakness involved both upper and lower extremities and was associated with mild abdominal pain. After 5 hours, he alerted a family member who assisted him to his feet. Upon standing the patient lost consciousness. He denied vomiting or recent illness but noted decreased food intake for the 2 days prior to admission. His only past medical history was a penetrating knife wound to the forehead 20 years prior to admission. He was taking no medications and did not use intravenous drugs. The blood pressure was 90/54 mmHg, the heart rate 110 beats/min and the temperature 36C. He had a normal thyroid exam and there were no carotid bruits. Examination of the heart, lung and abdomen were normal. Reflexes were decreased throughout; proximal and distal muscle strength was diminished. There were no focal deficits; sensation and cerebellar functions were normal. His sodium, potassium, calcium, magnesium, and creatinine were normal. The blood glucose was 54 mg/dL, and despite multiple ampules of dextrose he remained hypoglycemic. Persistent hypotension and refractory weakness prompted an evaluation of his adrenal function. The random cortisol was 1.6 mg/dl; the ACTH was low. DISCUSSION: The diagnosis of adrenal insufficiency should be considered when refractory hypoglycemia, orthostatic hypotension, and weakness simultaneously present. The causes of acute adrenal insufficiency include iatrogenic withdrawal of steroids, adrenal hemorrhage, tuberculosis and autoimmune disease. An important and under-recognized cause of adrenal insufficiency is inhibition of the hypothalamic-pituitary-adrenal axis by heavy alcohol ingestion. A repeat history revealed that the patient had a 6-day period of heavy alcohol and cocaine use. The normal electrolytes were clues that the adrenal insufficiency was not due to Addison's disease. The functional aldosterone axis and lack of hyperpigmentation implied a pituitary etiology which was confirmed by the low ACTH and robust rise in cortisol following cortrosyn stimulation. The weakness and hypoglycemia corrected with administration of hydrocortisone. Clinical reasoning identified the specific etiology of this patient's Addisonian syndrome and prevented unnecessary therapy.