Euforia, a supplement containing a variety of natural ingredients, is widely used as an antioxidant and anti-inflammatory formula. It is not approved by the US Food and Drug Administration and its side effects are unknown. We report a 45-year-old woman with limited systemic sclerosis who presented with jaundice and marked elevation of serum transaminases. One month before, she started taking Euforia juice. A liver biopsy disclosed submassive hepatocellular necrosis with histopathological changes consistent with toxic hepatitis. The patient's symptoms resolved with cessation of Euforia. Six months later, she persisted with abnormal liver function tests, but these resolved 18 months after discontinuation of Euforia. The mechanism by which Euforia causes liver injury is unknown. Some ingredients contained in this supplement (green tea, Aloe vera, noni and goji) are linked to hepatic injury. To our knowledge, this is the first report of hepatotoxicity associated with Euforia.

SUMMARYEhlers-Danlos syndrome (EDS) comprises a group of hereditary connective tissue disorders in which collagen synthesis and fibrogenesis are impaired. Patients with EDS type III have a bleeding tendency manifested by ecchymoses and haematomas. However, thrombotic events are rare in this entity. Herein, we present a 48-year-old Hispanic man with EDS type III who had recurrent cephalic vein thrombophlebitis and thrombosis, and brachial vein thrombosis. Tests for hypercoagulable disorders including antithrombin III activity, protein C activity, protein S activity, anticardiolipin antibodies, homocysteine levels, factor V Leiden mutation and prothrombin gene mutation were negative. The patient required long-term anticoagulation with warfarin. After 3 years follow-up, he did not present further thrombotic events. Clinicians should be aware that patients with EDS might be at risk for hypercoagulable disorders. BACKGROUND

Disseminated histoplasmosis (DH) is an acquired immunodeficiency syndromeYdefining condition, yet, esophageal involvement is an uncommon presentation of histoplasmosis but has been recognized in 2 clinical settings: as a result of contiguous histoplasmosis with mediastinal lymphadenopathy secondary to midesophageal compression, and in cases of disseminated histoplasmosis where esophageal lesions are the usual clinical manifestation. We report a case of a 32-year-old male patient with disseminated histoplasmosis presenting with esophageal narrowing that was initially misdiagnosed as esophageal candidiasis. The final diagnosis was established with a fine needle aspiration of an enlarged cervical lymph node, which showed fungal structures within macrophages consistent with histoplasmosis. Fungal stains were also positive, supporting the diagnosis. The patient was then successfully treated with antifungal therapy. Disseminated histoplasmosis should always be considered in the differential diagnosis of dysphagia in immunocompromised patients, although a more common entity such as candidiasis might be present. Failure to do so may be fatal.

Nocardia is an ubiquitous microorganism found in soil, organic matter, and water. It is particularly common in immunocompromised patients. A 51-year-old man, nonsmoker with medical history of hypertension and chronic alcoholism, presented with a 2-week history of a right upper quadrant pain, right-side chest pain, general malaise, fatigue, anorexia, 20-lb weight loss, night sweats, unquantified fever, and visual/auditory hallucinations. An abdominal and chest computed tomography reported a right pleuraYbased mass that eroded into the chest wall. The patient was admitted with diagnosis of suspected primary lung malignancy with a postobstructive pneumonic infection. Intravenous antibiotic was started with vancomycin and piperacillin/tazobactam. Computed tomographyYguided needle biopsy was done and pathology reported a gram-positive filamentous branching bacteria, weakly acid-fast positive, consistent with a Nocardia infection. Trimethoprim/sulfamethoxazole therapy, together with pleural effusion management, ensured further resolution of this invasive pleuropulmonary infection. FIGURE 3. Pulmonary nocardiosis pathology and stain with Papanicolaou at original magnification Â40.FIGURE 4. Pulmonary nocardiosis pathology and stain with Papanicolaou at original magnification Â20.FIGURE 5. Chest CT scan before (left) and after (right) treatment showing resolution of pleuraparenchymal changes. Campos-Santiago et al

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