LEARNING OBJECTIVES: 1) Expand the differential for abdominal pain; 2) Diagnose an atypical presentation of herpes zoster in the absence of skin lesions; 3) Recognize that zoster sine herpete is a clinical diagnosis. CASE INFORMATION: A 58 year-old male with history of nephrolithiasis presented with abdominal pain, fever, and chills. Physical exam was significant for low-grade fever and left upper quadrant tenderness. Radiographic studies revealed a 5.3 Â 4.6 cm dissecting aortic aneurysm at the level of the diaphragm, and a separate dissection of the right common iliac artery. The patient was admitted with a diagnosis of an infected aortic aneurysm and evaluated by vascular surgery. The patient continued to complain of left upper quadrant pain, described in a definite dermatomal distribution along the left lower costal margin with radiation to the left flank. Despite absence of any physical evidence of rash, the description was suggestive of herpes zoster. Varicella titers were then ordered and positive IgM titers were revealed. Zoster sine herpete was diagnosed, and the pain spontaneously resolved without medical intervention. On follow-up, the patient remains asymptomatic, never having developed a rash, and repeat CT scans reveal stable aneurysms. IMPLICATIONS/DISCUSSION: Herpes Zoster (Shingles) is a reactivation of varicellazoster virus, which lies dormant in the dorsal or cranial nerve ganglia. Upon recurrence, patients typically have a prodrome of fever, along with pain or tingling in the affected dermatome (50% thoracic, 20% cervical, and 10% lumbosacral). In most cases, the virus creates vesicles along the dermatome after three days, which then crust and resolve within two to three weeks. A small percentage of patients, however, develop acute segmental neuralgia, with a concomitant rise in varicalla IgM antibodies in the absence of skin lesions. This is zoster sine herpete, and as our case illustrates, patients can be initially misdiagnosed with a host of other illnesses, including myocardial infarction, cholecystitis, appendicitis, or diverticulitis. Very little has been published concerning zoster sine herpete since many cases spontaneously resolve without ever having reached the diagnosis. In this particular case, a CT of the abdomen revealed a dissecting aortic aneurysm, which was unrelated to the patient's chief complaint. By relying more on physical exam, the patient's description of the pain, and prior radiographic studies, the diagnosis might have been made more efficiently. This case stresses the importance of history and physical exam in the clinical diagnosis of zoster sine herpete. Otherwise, the diagnosis can be masked by confounding information. ventricular response. CXR (photo to be included) disclosed severe tension pneumothorax with complete collapse of the left lung and slight mediastinal shift to right. Emergent placement of a chest tube resulted in re-expansion of the lung, and stabilization. The patient did well and was discharged from the hospital 2 days later. IMPLICATIONS/DISCUSSION: Use of complementary/alternative medicine, often in concert with``mainstream'' medical treatment, is common and widely practiced in the United States. Acupuncture is effective as sole or adjunctive therapy for management of many types of pain, and is generally regarded as safe. The current vignette describes a case of tension pneumothorax directly attributable to acupuncture treatment. Traumatic injury from acupuncture is rare, but review of the medical literature discloses numerous reports of adverse events resulting from acupuncture treatments. Pneumothorax is the most commonly reported traumatic injury, especially among patients predisposed by presence of COPD; other risks include cardiac tamponade, peripheral nerve injury, and injury to blood vessels including pseudoaneurysm formation. Non-traumatic adverse effects of acupuncture include infections (hepatitis and other blood-borne diseases, as well as reports of septicemia and endocarditis.) The overall safety profile of acupuncture is positive, but patients and physicians should be aware of potential risks of treatment. State laws vary widely regarding requirement for certification; referral to licensed or certified medical acupuncturists is recommended. year-old woman presented with one month of fevers, evanescent rash, myalgias and arthralgias, severe fatigue, and anorexia with 20 pound weight loss. Examination disclosed T 39.48C, tender posterior cervical lymphadenopathy, no obvious synovitis, and a salmon-colored macular exanthem on the lower extremities. CBC showed normocytic anemia (Hgb 9.8,) slight leukocytosis (WBC 11.1 with 82.3% granulocytes,) normal LFTs except for slight elevation of AST, normal BUN/Cr, UA, and CXR. Further tests revealed ESR 90, negative ANA and RhF, and ferritin >2000. Further diagnostic workup included negative PPD, negative blood cultures, normal echocardiogram, normal CT scan except borderline mediastinal lymphadenopathy and mild hepatosplenomegaly, and negative titers for HIV, EBV, CMV, and Lyme disease. Lymph node biopsy disclosed reactive node with no evidence of a clonal population of cells. The patient was diagnosed with AOSD and had minimal response to aspirin. She was treated with steroids and is presently minimally symptomatic on hydroxychloroquine and NSAID. IMPLICATIONS/DISCUSSION: AOSD is a rare disease (incidence 1.6 cases/million persons/yr) that highlights the importance of clinical history and physical examination, since there is no definitive test to make the diagnosis. Diagnostic criteria have been proposed (will be delineated.) ASOD usually follows one of three patterns: self-limited (monophasic) disease with complete resolution of symptoms within one year, intermittent (polyphasic) course with complete remission between flares, or persistent active disease, with chronic destructive arthritis. First line treatment is aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs;) patients with more severe disease may respond to steroids. There are no controlled trials of immune modulating drugs in ASOD. Reports exist of success using methotrexate to control systemic symptoms; other agents used (all off-label) include gold salts, azathioprine, cyclophosphamide, cyclosporine, sulfasalazine, and intravenous immune globulin. Recent reports suggest etanercept and infliximab may have benefit in patients not responding to other therapies. A 74 year old white female presented with a 3 day history of`d ifficulty getting out of a chair'', dyspnea on exertion and``tea colored'' urine. Her past medical history was significant for depression and hypercholesterolemia. Her past medications included simvastatin (40 mgs po qd) and nefazodone (150 mgs po bid). She had been started on the nefazodone 3 months ago for treatment of depression and shortly thereafter developed a fever, nausea/vomiting and muscle spasms. Physical examination revealed significant weakness of the proximal musculature: 3/5 strength in the shoulder abductors and 2/5 strength in the hip flexors. Her laboratory data revealed: CK 37,050, AST 1,744, ALT 1,029, BUN 17, Creatinine 0.8 , Urinalysis: SpGr 1.020, pH 6.0, protein 100, large blood, granular casts. The nefazodone and simvastatin were discontinued and a forced bicarbonate diuresis was initiated. Polymyositis was suspected and steroids were started empirically pending the outcome of testing. An EMG showed no evidence of an underlying myopathy). ANA and an anti-Jo-1 antibody tests were negative. A muscle biopsy showed age-appropriate atrophy but no necrosis of myocytes and no evidence of lymphocytic infiltrate, thus ruling out the diagnosis of polymyositis. Her renal function remained normal throughout the hospitalization. Her CPK was 1,776 eight days after admission and she gradually regained strength in her proximal muscle groups. She was thought to have developed rhabdomyalyis secondary to a drug interaction between simvastatin and nefazodone. IMPLICATIONS/DISCUSSION: To our knowledge, this is the second case report of an adverse event associated with the concomitant use of simvastatin and nefazodone. Simvastatin is metabolized via the CYP3A4 system and nefazodone is a direct inhibitor of CYP3A4 enzymes. While myositis and rhabdomyolysis are adverse events associated with simvastatin monotherapy, we speculate that the introduction of nefazodone into this patient's regimen sufficiently inhibited the CYP3A4 system to cause an increase in serum simvastatin concentration that was adequate to cause rhabdomyolysis. Therefore, we would recommend avoidance of CYP3A4 inhibitors such as nefazodone in those receiving simvastatin therapy.