The symptoms and signs of IE often are constitutional and, when localized, result from a complication of IE. Consequently, if physicians are to avoid overlooking the diagnosis of IE, a high index of suspicion must be maintained. This is especially true in cases of IE that have a subacute course. Subacute endocarditis is characterized by an insidious onset and by nonspecific signs and symptoms of chronic illness, such as low grade fever, fatigability, and malaise. Immunologic phenomena occur when the disease is protracted. Musculoskeletal symptoms, as was described in this patient, are common. Although fever is the most common sign in patients with IE, it is typically low grade. Heart murmurs are noted in 80 to 85 percent of patients with native value endocarditis (NVE) and are emblematic of the lesion predisposing to IE. Enterococci, which comprise normal gut flora, account for 5 to 15 percent of cases of NVE. There are no specific clinical manifestations nor is there a single lab test that establishes the diagnosis of IE unequivocally. A combination of major and minor clinical findings, outlined in the Duke criteria, makes the diagnosis highly probable. In the absence of surgical indication, optimal therapy for enterococcal endocarditis requires synergistic bactericidal interaction of antimicrobial agents targeted against the bacterial cell wall (penicillin, ampicillin, or vancomycin) and an aminoglycoside. Because of her overall clinical and laboratory presentation, the pituitary-adrenal axis was evaluated. The AM Cortisol was level 1.4 and ACTH was 5. Brain MRI and CT abdomen were unremarkable. The diagnosis of secondary adrenal insufficiency, potentially secondary to Megace 1 , was made. Patient was started on hydrocortisone 20 mg PO qAM, and 10 mg PO qPM. She had marked improvement in her symptoms. Megace 1 was discontinued and hydrocortisone was ultimately tapered. IMPLICATIONS/DISCUSSION: Findings in adrenal failure are nonspecific, and, without a high index of suspicion, the diagnosis of this potentially lethal but readily treatable disease is missed easily. Symptoms due to cortisol deficiency include anorexia, nausea, vomiting, weight loss, weakness, and fatigue. Although orthostatic hypotension is more marked in primary than secondary adrenal insufficiency because of aldosterone deficiency, it does occur in the latter. Hyperpigmentation (due to increase ACTH), hyperkalemia and volume depletion (due to aldosterone deficiency) occur only in primary adrenal failure. Hyponatremia is seen in both. In patients in whom adrenal insufficiency is merely to be ruled out, plasma cortisol is measured between 8 and 9 AM. Concentrations of <3 Ag/dl are indicative of adrenal insufficiency and obviate the need for other tests. Concentrations greater than 19 Ag/dl rule out the disorder. The short cosyntropin stimulation test is the most commonly used test for the diagnosis of primary adrenal insufficiency. Secondary adrenal insufficiency is characterized by low blood cortisol and ACTH levels, a low baseline rate of steroid excretion, and abnormal ACTH and metyrapone responses. Megace 1 is a progestational agent with activity in advanced breast and endometrial cancer and AIDS-related cachexia. Long-standing Megace 1 therapy can result in marked suppression of serum cortisol levels and decreased ACTH .The depressing effect of megestrol acetate on the pituitary-adrenal axis does not cause clinically evident problems in the overwhelming majority of cancer patients. However physicians should be aware of the possibility of adrenal insufficiency while taking or upon withdrawal of this drug. This is especially important in severely ill patients, in whom the subtle signs and symptoms of adrenal insufficiency can be attributed to their primary disease. LEARNING OBJECTIVES: 1) To recognize some causes of gait disorder in the elderly 2) To recognize the importance of a detailed history and 3) To recognize the role of genetic testing in appropriate elderly patients with gait disorders. CASE INFORMATION: 64-year-old female patient with past medical history of diabetes, mild osteoarthritis, and hypercholesterolemia developed gait problems over the last year and a half. She started losing balance around that time and her gait had become slow. She denied headaches, seizures, swallowing problems, memory disturbances or any sensory involvement. Her family history is significant for one sister and all male members in her father's family who developed gait disorders in their sixties. On examination, slurring of speech was present. Extraocular movements were intact. Strength in all extremities was normal and there was no pronator drift. Sensory examination was intact. Reflexes were symmetric and brisk. Gait was wide-based and she could not walk on her heels or toes. Her handwriting was small and she had difficulty with rapid alternating movements. An MRI showed mild cerebellar atrophy. Tests for Lyme disease, rheumatoid factor and anti-nuclear antibody were negative. Vitamin B12 level and sedimentation rate were normal. Genetic testing revealed that she possessed the CAG/ CAA repeat expansion mutation associated with spinocerebellar ataxia 17. Genetic counseling has been offered to her family members. IMPLICATIONS/DISCUSSION: There are many potential causes for gait disorders in the elderly. The most common are related to the presence of a sensory-motor polyneuropathy such as seen with diabetes, or strokes related to cerebrovascular disease. Also common are disorders secondary to compressive myelopathy. In this patient the presence of slurred speech made myelopathy and neuropathy unlikely and the absence of structural lesions on MRI suggested a progressive degenerative disorder. Spino-cerebellar ataxia(SCA) type 17 is a rare autosomal dominant neurodegenerative disease caused by an abnormal CAG expansion in the TATAbinding protein (TBP) gene. SCA 17 was identified in 4 Japanese pedigrees and first reported in 2001. Most individuals present between the ages of 20 and 30 with gait ataxia and dementia, progressing over several decades to include bradykinesia, dysmetria, dysdiadokokinesis, hyperreflexia, and paucity of movement. Neuroimaging shows cortical and cerebellar atrophy. Even the small number of SCA 17 patients identified so far suggests that there would be substantial phenotypic variability, probably secondary to incomplete penetrance. This case emphasizes the details of the differential diagnosis of gait disorders in the elderly and the importance of the family history even in the elderly patient. This has become especially important with the greater availability of genetic testing that will provide the basis for genetic counseling. 2) The importance of a complete history in pinpointing a rare diagnosis; CASE INFORMATION: A 37 yo white female with no significant PMH presented to the ER with a chief complaint of constant, progressive weakness over the past ten days. The patient initially noted swelling, paresthesias, and muscle tenderness in her legs, followed by progressive weakness from the ankles to the hips. She described difficulty in standing from a seated position, climbing stairs, and ambulating. She denied any alleviating or exacerbating factors or similar past symptoms. She had taken only acetaminophen as needed and had no known drug allergies. She denied any ingestions, exposures, or recent travel. On ROS, she denied fever, changes in appetite, weight, urine output or color, any GI upset, recent illness, or rashes. She was a smoker, but denied any alcohol or drug use. Exam revealed a thin, well-developed female laying in bed in no apparent distress. Her temperature was 98.28F, pulse was 100, BP was 139/ 82, RR was 20, weight was 115 lbs., and height was 5 H 7 HH . HEENT exam revealed poor dentition, otherwise normal. Cardiac, lung, neck, and abdominal exams were normal. Musculoskeletal exam showed strength to be 5/5 in the upper extremities, 3/5 in the proximal lower extremities, 4/5 in distal lower extremities. A positive Trousseau's sign (carpopedal spasm) was noted upon inflation of BP cuff. DTRs were slightly brisk in all 4 extremities but no spasticity was noted. Otherwise, neurologic exam was normal. Skin exam showed no rashes. Laboratory evaluation revealed significant hypokalemia of 1.7 mmol/L (normal 3.5±5.0), plasma chloride of 94, plasma CO2 of 31, serum calcium of 7.4, serum magnesium of 1.3, and serum phosphorus of 3.3. Other electrolytes, BUN/Cr, and glucose were normal. Serum CPK was significantly elevated at 5,098 U/L (normal 24±170). Urine sodium was 177 mmol/L, urine potassium was 8 mmol/L, and 24 hour urine potassium was 14 mmol/L. MCV was 104 fL, folate level 3.3 ng/mL, and albumin 3.7 g/dL. Toxicology and diuretic screens were negative. The profound hypokalemia, hypokaliuria, macrocytic anemia, and hypoalbuminemia were consistent with the suspicion of a 18 dietary disorder; i.e, low intake vs. eating disorder. The patient consistently denied an eating disorder or distorted body image. Upon obtaining further dietary history, the patient's daily consumption of 5±6 L of Pepsi 1 stood out as an apparent etiology. The patient stated that she had been drinking caffeinated colas heavily for several years. Upon cessation of cola consumption and replacement with a total of over 820 meq of KCL, the patient's weakness improved. IMPLICATIONS/DISCUSSION: Colas and other caffeinated beverages have been reported to be causes of significant hypokalemia, likely due to caffeine toxicity and/or phosphatepotassium binding. Although a rare diagnosis, this case of cola induced myopathy was made by using fairly simple, bedside physician-patient discussion.