PATIENT. D. Lehman 1 , J. Mills 1 , C. Sorensen 1 , J. Whitesel 1 , R. Reves 1 ; 1 Denver Health and Hospital Authority, Denver, CO (Tracking ID #75102) LEARNING OBJECTIVES: To recognize that tuberculosis can present with unusual clinical manifestations, often sub-acute or chronic, especially in the immunocompromised context, such as HIV infection. CASE INFORMATION: 48 y/o male with heterosexually acquired HIV infection and a CD4 count of 306, presented with a 1-month history of penile and rectal pain and 1 week of no urethral voiding. He noted urine coming from the rectum with feces. Voiding cystourethrogram showed a prostatic-rectal fistula and a Foley catheter was placed. He was born in Mexico and had a negative PPD 10 years earlier. Four months earlier he had presented with dysuria, an enlarged prostate, pyuria and microscopic hematuria. CT scanning then showed a 2.7 by 3.0 cm hypodensity within an enlarged prostate that, in the absence of fever and toxicity, appeared clinically not consistent with a prostatic abscess. No urine culture was done, but he received 10 days of levofloxacin. Fistula evaluation by GI with colonoscopic biopsy showed chronic inflammation and necrosis. Transrectal ultrasound showed a large prostate with prostatic calculi with no cyst or abscess. Granulomas and acid-fast bacilli (AFB) were found in biopsies obtained during an unsuccessful surgical attempt to repair the fistula. Bilateral infiltrates were found on a post-operative chest X-ray. AFB were found in urine and sputum and cultures grew Mycobacterium tuberculosis (TB). Standard 4-drug therapy for TB was successful and the fistula closed without further surgery after 6 months of directly observed treatment and Foley drainage. IMPLICATIONS/DISCUSSION: Delayed and missed diagnoses of active pulmonary and extrapulmonary TB are common due to the relative rarity of the disease and a lack of familiarity with its protean manifestations. TB of the genitourinary tract accounts for about 1% of reported cases of TB in the US. Extrapulmonary forms (27% of US cases) are more common among children and patients with HIV-infection or other disorders of immunity. The keys to earlier recognition of active TB are awareness of: 1) the manifestations of the disease, 2) risk factors for previous exposure and latent TB infection, and 3) risk factors for progression from latent TB infection to active disease. In retrospect this patient had all three of these features. The clinical features of active TB, both pulmonary and extrapulmonary are variable, but chronic and sub-acute presentations are common. Signs of systemic toxicity are helpful if present but are commonly absent. TB of the urinary tract should be suspected in patients with unexplained``sterile'' pyuria and/or hematuria and in those with unexplained chronic inflammation and fibrosis. This patient had a common risk factor for infection, having been born in Mexico, and had HIV infection as a risk factor for progression to active TB. Although the GU tract is a relatively common extra-pulmonary site for TB, there is little mention in the literature of fistula as a complication of TB prostatitis. The most likely etiology of a prostaticrectal fistula is surgery, rarely by infection. Radiological studies revealed what appeared to be a solid posterior occipital mass consistent with a malignant lesion and surgical intervention was pursued. At craniotomy he was found to have an abscess; smears revealed yeast forms and cultures grew Cryptococcus neoformans. CSF results were WBC 255, protein 112, glucose 27 and cryptococcal antigen 1:64. Serum cryptococcal antigen was 1:128. He disclosed no risk factors for immunodeficiency which was confirmed by negative studies for HIV-1 and 2 antibody, HIV-1 and 2 PCR, HTLV-1 and 2 antibody and HTLV-1 and 2 PCR. Of note, his CD4 count was 79 and his total IgG, IgG1 subclass and IgG2 subclass levels were low. IgA and IgM levels were at the lower limits of the normal range. He received two weeks of amphotericin B and improved appropriately. Lumbar puncture at that time revealed: WBC 440, protein 111, glucose 30 and cryptococcal antigen 1:2. Repeat CD4 count was 191 and serum cryptococcal antigen was 1:64. His therapy was changed to fluconazole and he continued to improve. IMPLICATIONS/DISCUSSION: Although possible in immunocompetent hosts, cryptococcal meningoencephalitis presents most commonly in patients with HIV infection, drugassociated immunosuppression, leukemia and complement deficiency. This infection has rarely been reported in cases of hypogammaglobulinemia. Cryptococcus neoformans infects through aerosolization producing a primary respiratory infection that spreads hematogenously to distant sites. In hypogammaglobulinemia of the type shown in this patient, the proposed host defect stems from dysfunctional T-cell activity resulting in fundamental difficulties with complement fixation, opsonization and reduction of circulating antigens. We propose the possibility that the hypogammaglobulinemia facilitated the development of this patient's CNS disease. These immunosuppressed patients present with fever, headache and malaise similar to, but typically more intense and shorter in duration than infections in the immunocompetent host. Response to treatment with amphotericin B and fluconazole are similar to those in immunocompetent hosts.Close monitoring and medication adjustments per clinical response are essential. Thus, this case provided an unusual initial presentation of hypogammaglobulinemia as cryptococcal meningoencephalitis. LEARNING OBJECTIVES: To recognize filariasis in the differential diagnosis of nephrotic syndrome. CASE INFORMATION: A 46 year old man who had recently emigrated from West Africa presented with a three month history of lower extremity pitting edema. His physical examination was significant for anasarca. Laboratory data revealed a white blood cell count of 9900 with 58% eosinophils, an albumin level of 1.2 g/dl as well as a BUN and creatinine of 16 and 1.0 respectively. An initial urinalysis revealed protein level of greater than 300 mg/dl and microhematuria. A subsequent 24-hour urine collection revealed 7.6 grams of protein confirming a diagnosis of nephrotic syndrome. The differential diagnosis of nephrotic syndrome with eosinophilia includes lymphoma and various parasite infections. While parasitic serologies were pending, chest and abdominal CT scans were normal ruling out a diagnosis of lymphoma. A renal biopsy showed membranous glomerulonephritis with diffuse IgG deposits in the subepithelium. Subsequent peripheral blood smears showed obvious microfilariae of the Loa loa species, indicating active infection. Further laboratory studies revealed the absence of other conditions associated with membranous glomerulopathy. Therefore, it was concluded that the nephrotic syndrome and the membranous glomerulonephritis were most likely caused by the filarial infection. The patient was treated with metolazone and lisinopril to treat the anasarca/ nephrotic syndrome and given ivermectin to treat the filariasis. At follow-up two months later, the edema had resolved and his urinalysis had almost normalized. IMPLICATIONS/DISCUSSION: Loa loa is one of eight filarial species and occurs mainly in the rain forests of Africa. Adult worms develop and mate to form microfilariae, which appear in the blood. Whereas other filarial species cause the classic symptoms of lymphedema, the loaisis species is more commonly associated with pruritus and localizd areas of subcutaneous swelling. Various nephropathies, including nephrotic syndrome, are rare and likely result from immune complex deposition within the glomerulus. In tropical countries, infectious diseases are common causes of the nephrotic syndrome. As demonstrated in this case, one should consider the diagnosis of filariasis in patients that present with anasarca and/or nephrotic syndrome and who have a history of travel to endemic countries for filariasis. year-old white female with a history of von Willebrand disease presented with 3 weeks of severe fatigue. She denied history of trauma or abnormal bleeding although she reported easy skin bruising. On physical examination, her temperature was 37.4 degrees Centigrade and BP 102/72 mmHg. She appeared thin and pale. Neck was supple, without thyromegaly. Lungs were clear. Heart was regular, without murmurs or gallops. Abdomen was benign without masses, tenderness or hepatosplenomegaly. Extremities had no cyanosis, clubbing or edema. Neurological examination was non-focal. CBC revealed a hemoglobin of 10g/dl, platelet of 33,000/mm3, and WBC of 3500/mm3 with 13% blasts. Bone marrow biopsy found 40% blasts with positive CD33 and CD34. She was diagnosed with acute myeloid leukemia. Chemotherapy with cytarabine was started. Five hours later, she developed severe stabbing left upper quadrant abdominal pain radiating to the back and left shoulder, aggravated by body movement, only slightly relieved by intravenous hydromorphone. One hour later she became hypotensive with a BP of 90/50 mmHg. Hemoglobin dropped from 9.0 to 7.1g/dl in 4 hours. Electrocardiogram showed sinus tachycardia and no acute ischemic changes. Abdominal series was unremarkable. An abdominal CT scan was reported unremarkable initially, but further review demonstrated blood surrounding the spleen. Emergent laparotomy found acute rupture of a normal sized spleen (8.0 Â 5.5 Â 2.3 cm). Splenectomy was performed. She was transfused a total of 6 units of packed red blood cells. Hemoglobin remained stable after the surgery. She developed acute respiratory distress syndrome and died of respiratory failure and cardiac arrest within a week. IMPLICATIONS/DISCUSSION: The spleen is an immunologic organ commonly involved in hematologic diseases. Splenic rupture can be classified into 1) traumatic; 2) spontaneous; and 3) pathologic. Pathologic splenic rupture occurs in a spleen affected by a disease without previous trauma. The presentations of splenic rupture are the result of intra-abdominal hemorrhage, hypotension, tachycardia, peritoneal irritation signs, and fever. The abdominal pain could radiate to the left shoulder (Kehr's sign). Pathologic rupture of a spleen affected by a hematologic malignancy is a rare event and it is especially unusual for a normal sized spleen to rupture. The risk of splenic rupture increases with age and size of the spleen. The release of the enzymatic content of cells shortly after induction chemotherapy may lead to splenic damage, followed by rupture of the spleen. The present patient had received cytarabine just 5 hours before the abrupt onset of abdominal pain. Other risk factors of bleeding such as thrombocytopenia and von Willebrand disease might also have contributed to her catastrophic event. The diagnosis of pathologic splenic rupture begins with a high index of suspicion. A patient with risk factors presenting with left upper abdominal pain should be observed closely and investigated. Plain abdominal X-ray, ultrasound and CT scan are valuable tests. Aspiration of blood by abdominal puncture could confirm the diagnosis. For insidious rupture, liverspleen scintigraphy is of value. The only therapy is splenectomy. A 67-year-old male was well until 6 weeks prior to presentation, when he developed diffuse extremity deep aching pain and difficulty with walking, maintaining his balance and doing buttons. He denied diplopia, but had trouble looking to the left. He denied weakness, numbness, sensory loss, trouble with speech or articulation, or bowel or bladder dysfunction. On physical examination, he had normal vital signs. He was alert, cooperative, but somewhat slow. A 2 Â 2 cm non-tender supraclavicular lymph node was palpable. Heart, lungs and abdomen were unremarkable. Extremities had no cyanosis, clubbing or edema. Eyes could not move past the midline on leftward gaze. Motor strength was 5/5 in all muscle groups tested. Vibratory sense was diminished distally in the right lower extremity. A heel-to-shin testing was ataxic. He could not sit nor stand unaided. Romberg's sign was noninterpretable even with the eyes open. Plantar responses were flexor bilaterally. Cerebral spinal fluid reveaked glucose 93, lymphocyte 4, IgG 15.1, and protein 100. Anti-Hu antibody was positive. Brain MRI showed a small old lacunar infarct. Chest CT scan identified a 1 ± 2 cm right suprahilar pulmonary nodule, 3 right upper lobe nodular densities less than 1 cm each, and a prominent 3.5 cm nodule in the right pretracheal area. EMG and nerve conduction studies demonstrated a sensory motor polyneuropathy. Lymph node biopsy showed neoplastic cells staining with synaptophysin and chromogranin, supporting the diagnosis of large cell neuroendocrine carcinoma. The patient was treated with carboplatin and etoposide for three doses and IVIgG for five doses. The symptoms were stabilized. IMPLICATIONS/DISCUSSION: Paraneoplastic encephalomyelitis (PEM) is a frequent remote effect of cancer characterized by neuronal loss and inflammatory infiltrates in the nervous system. The onset is usually subacute and causes severe neurological dysfunction which antedates the diagnosis of cancer. The presenting neurological syndrome is usually sensory neuropathy, cerebellar dysfunction and cortical encephalitis. Diagnosis of the primary cancer remains challenging and requires a high index of suspicion. Usually, it is made by the demonstration of specific paraneoplastic antibodies. Anti-Hu antibody recognizes a family of RNA-binding proteins expressed in the nuclei of neurons and cancer cells. It has been used as a diagnostic marker, but no evidence suggests it causes neuronal damage. Effective treatment of the tumor with chemotherapy is an independent predictor for stabilization of PEM. Large cell neuroendocrine carcinoma is a highly aggressive tumor that usually occurs in smokers, and may be either central or peripheral. It has been suggested that surgically resectable tumors be excised and that advanced stage lesions be treated with combination chemotherapy. Immunotherapy has been proven effective in some patients in tumor regression and PEM stabilization or improvement. The prognosis is poor, with a median survival of 11 months. LEARNING OBJECTIVES: Recognize that the clinical manifestations and radiologic findings of peritoneal tuberculosis (TB) may mimic ovarian carcinoma. Recognize that an elevated CA-125 level may be more suggestive of tuberculous peritonitis than ovarian carcinoma in certain populations such as young women, HIV-infected women and women from areas endemic for tuberculosis. CASE INFORMATION: A 29 year-old Vietnamese woman with no significant past medical history presented to the emergency department with a 10 day history of fever, non-productive cough, abdominal pain, and increasing abdominal girth. A PPD placed as an outpatient was reactive to 16mm. She emigrated from Vietnam ten years prior, had no recent travel history, and had no recent sick or TB contacts. Family history was negative for cancer. On physical examination, the patient was febrile to 102.6F with a pulse of 111 BPM. Pulmonary exam was clear to auscultation. Abdominal exam was significant for mild distention, and tenderness in the epigastric and right upper quadrant regions without rebound or guarding. Gynecologic exam was normal. Chest x-ray was normal. A CT scan of the abdomen and pelvis showed diffuse intraabdominal ascites with omental caking, strongly suggestive of metastatic disease from ovarian carcinoma. Pelvic ultrasound was negative for adnexal masses. Ascitic fluid analysis showed a predominantly lymphocytic exudate. There were no malignant cells, acid-fast bacilli (AFB) or other organisms detected in the fluid. Fluid culture yielded no growth. Multiple sputum smears were negative for AFB. A CA-125 level was elevated to 546 U/ml. A CT guided biopsy of the omentum revealed granulomatous inflammation and well-defined granulomas with central necrosis ± histology consistent with tuberculous peritonitis. The patient was started on a regimen of isoniazid, rifampin, ethambutol and pyrazinamide. On follow-up two weeks after discharge, the patient reported feeling well with complete resolution of the fever and abdominal pain. IMPLICATIONS/DISCUSSION: Peritoneal tuberculosis is an uncommon entity. The common clinical presentation is ascites or an abdominal mass. The elevated CA-125 and radiologic appearance of the omentum, as in the case of our patient, can be highly suggestive of ovarian carcinoma. However, it is well established that many other conditions, including peritonitis can elevate the CA-125. When these features are present in a patient who is at high risk for developing tuberculosis and who is at low risk for developing ovarian cancer then the diagnosis of tuberculosis must be considered. Establishing the diagnosis of peritoneal tuberculosis can be difficult as ascitic fluid is rarely positive for AFB and even culture of biopsy specimens may be negative. Diagnosis is often made on the basis of suggestive histopathology and clinical features. Clinicians must maintain a high index of suspicion for tuberculous peritonitis in patients presenting with ascites and abdominal masses, especially in young women (in whom ovarian carcinoma is uncommon), HIV-infected patients and patients from areas endemic for tuberculosis. In these cases, empiric antituberculosis therapy can be considered while further workup is pending. CA-125, while nonspecific for peritoneal tuberculosis, can be useful in monitoring response to therapy and would be expected to return to normal levels.