DIFFICULT DYSURIA. S.B. Fazio 1 ; 1 Harvard University, Brookline, MA LEARNING OBJECTIVES: 1. Characterize the differential diagnosis of dysuria 2. Distinguish prostatitis from other causes of rectal pain 3. Recognize atypical presentations of appendicitis CASE INFORMATION: A 21 year old male presented to urgent care complaining of three weeks of dysuria and rectal pain. The pain was sharp and intermittent, brought on by urination or defecation, and radiated into the right inguinal area. He denied fever, nausea, vomiting, abdominal pain or tenesmus. Past medical history was unremarkable; he was on no LEARNING OBJECTIVES: (1) Recognize thyroid disease as an extrahepatic manifestation of chronic hepatitis C. (2) Manage thyroiditis associated with hepatitis C when the disease is either subclinical or mild. (3) Realize that thyroiditis can occur in patients with hepatitis C with or without the use of interferon therapy. CASE INFORMATION: A 29 year old woman with a 15 year history of hepatitis C (HCV) presented to general internal medicine clinic to establish primary care. She had undergone initial evaluation of her HCV disease 3 years earlier but had declined liver biopsy or interferon therapy at that time and discontinued followup. She had recently returned to hepatology and had proceeded with liver biopsy. On questioning and complete review of systems, the patient had no complaints. Notable findings on exam included a symmetric, smooth, nontender goiter, 6 cm with no palpable nodules. Exam of the liver was normal. Studies from 3 years and 6 months earlier were reviewed. At both time points, TSH was below normal, ALT was moderately elevated and HCV viral quantitative measurements were low. Genotype was 1A. Liver biopsy revealed minimal disease with Grade I lobular inflammation and Stage 0 fibrosis. Updated studies were ordered and revealed a normal TSH, mildly elevated total T3, normal free T4 and elevated anti-thyroid antibodies. No treatment was prescribed. At followup 1 month later, she remained asymptomatic and her goiter had markedly resolved to a minimally palpable and visible gland. Repeat laboratories revealed an isolated mildly elevated total T3. DISCUSSION: Chronic HCV infection has been associated with several extrahepatic conditions including thyroiditis. The mechanism may be related to HCV infection of mononuclear cells but the exact mechanism is still largely unknown. Recent case-control studies have found the prevalence of thyroid abnormalities and anti-thyroid antibodies significantly higher in patients than controls. Most commonly, there is no associated thyroid enlargement. Approximately 50% of those with anti-thyroid antibodies have subclinical thyroid disease and 50% have overt symptoms. Thyroid dysfunction has also been noted during interferon-alpha therapy in up to 12% of HCV patients but studies have found disease in both interferon-treated and untreated patients. Prospective studies show thyroid dysfunction may develop in patients on interferon therapy with or without antibodies. Those with antibodies do not show a significantly higher propensity to develop thyroid dysfunction during interferon therapy. In summary, as in the general population, management includes timely recognition of signs and symptoms of thyroid disease. In the HCV population, these symptoms can often be subtle or may be attributed to HCV itself. HCV patients with thyroiditis should be followed closely; however, they may not necessarily require intervention if thyroid disease is subclinical and the thyroiditis or goiter may remit spontaneously. Finally, pre-existing thyroiditis is not a contraindication to interferon therapy.