Lymphoepithelioma-like carcinoma of the lung: radiologic features of an uncommon primary pulmonary neoplasm.

OBJECTIVE: The purpose of this study was to review the chest radiographic, CT, and MRI appearances of primary pulmonary lymphoepithelioma-like carcinoma (LELC). CONCLUSION: Primary pulmonary LELC is histopathologically identical to nasopharyngeal carcinoma. The radiographic, CT, and MRI features of primary pulmonary LELC are nonspecific, often resembling those of bronchogenic carcinoma. Primary pulmonary LELC usually presents as a poorly circumscribed, enhancing, peripheral solitary pulmonary nodule on CT; necrosis may be present and is considered a poor prognostic sign. MRI shows isointense to low-intensity signal on T1-weighted images and mildly increased signal on T2-weighted images; enhancement of abnormal tissue is typical. Most patients present with early-stage disease. Primary pulmonary LELC should be suspected in selected patients and requires differentiation from bronchogenic carcinoma and metastatic nasopharyngeal carcinoma.

Think global, act local: chronic dysuria and sterile pyuria in an Eritrean-American woman.

A 70-year-old female Eritrean immigrant living in the USA presented with classic findings of genitourinary (GU) tuberculosis (TB), including risk of tuberculosis exposure based on country of origin, chronic urinary tract symptoms and persistent sterile pyuria despite antibacterial therapy. Furthermore, this patient had the hallmark radiographical findings of ureteral stricture, a dilated pelvic calyceal system, hydroureteronephrosis and bladder wall thickening, as well as a bladder wall biopsy that revealed granulomatous disease. The patient was evaluated multiple times over the course of 3 years in outpatient and inpatient medical settings before a diagnosis was made and appropriate treatment initiated. As with many cases of GU TB, a protracted diagnosis allowed for advanced disease progression and significant morbidity from obstructive uropathy and chronic kidney disease.

Acquired A amyloidosis from injection drug use presenting with atraumatic splenic rupture in a hospitalized patient: a case report.

INTRODUCTION: Little is known about splenic rupture in patients who develop systemic acquired A amyloidosis. This is the first report of a case of atraumatic splenic rupture in a patient with acquired A amyloidosis from chronic injection drug use. CASE PRESENTATION: A 58-year-old Caucasian man with a long history of injection drug use, hospitalized for infective endocarditis, experienced atraumatic splenic rupture and underwent splenectomy. Histopathological and microbiological analyses of the splenic tissue were consistent with systemic acquired A amyloidosis, most likely from injection drug use, that led to splenic rupture without any recognized trauma or evidence of bacterial embolization to the spleen. CONCLUSION: In patients with chronic inflammatory conditions, including the use of injection drugs, who experience acute onset of left upper quadrant pain, the diagnosis of atraumatic splenic rupture must be considered.

Case 117: actinomycosis of left kidney with sinus tracts.

A 39-year-old Samoan man presented to the emergency department with fever, progressive weakness, and left flank pain of 1-month duration. For several months, he had also experienced progressive weight loss. There was no history of recent trauma, and he was not taking any medication. His medical history was notable for a large left groin abscess and left lower lobe pneumonia of unknown cause 1 year prior to the current admission. Furthermore, he had undergone exploratory laparotomy and gastric surgery for peptic ulcer disease approximately 10 years ago. Physical examination findings were positive for a tender firm mass in the left flank with no associated skin changes. Laboratory findings revealed an elevated white blood cell count of 18 x 10(9)/L. The urine cultures were negative. A computed tomographic (CT) image obtained 1 year prior to the current admission was unremarkable. CT of the abdomen and pelvis (section thickness, 5 mm) was performed after ingestion of 900 mL of 2% diatrizoate meglumine and diatrizoate sodium (Gastrografin; Bracco Diagnostics, Princeton, NJ). A 150-mL dose of iohexol (300 mg of iodine per milliliter) (Omnipaque; Nycomed, New York, NY) was administered intravenously at a rate of 4 mL/sec with a 70-second scan delay. Unenhanced CT images (not shown) did not reveal any areas of high attenuation.

Sustained expression of homeobox D10 inhibits angiogenesis.

Homeobox (Hox) genes are master regulatory genes that direct organogenesis and maintain differentiated tissue function. As HoxD3 and HoxB3 promote angiogenesis, we investigated whether endothelial cells use other Hox genes to maintain a mature quiescent phenotype. HoxD10 expression was higher in quiescent as compared to tumor-associated angiogenic endothelium. Microarray analysis of HoxD10-overexpressing endothelial cells revealed a pattern of gene expression consistent with a nonangiogenic phenotype. Moreover, sustained expression of HoxD10 impaired endothelial cell migration and blocked angiogenesis induced by basic fibroblast growth factor and vascular endothelial growth factor in the chick chorioallantoic membrane in vivo. HoxD10-overexpressing human endothelial cells also failed to form new vessels when implanted into immunocompromised mice. These results indicate a role for HoxD10 in maintaining a nonangiogenic state in the endothelium.

Sevoflurane degradation by carbon dioxide absorbents may produce more than one nephrotoxic compound in rats.

PURPOSE: Degradation of sevoflurane by carbon dioxide absorbents produces compound A, a vinyl ether. In rats, compound A can produce renal corticomedullary necrosis. We tested whether other compounds produced by sevoflurane degradation also could produce corticomedullary necrosis. METHODS: Two groups of rats were exposed for four hours to sevoflurane 2.5% delivered through a container filled with fresh Sodasorb and heated to 30 degrees C or to 50 degrees C, respectively. Compound A was added to produce an average concentration of 120 ppm in both groups. A third (control) group received 2.5% sevoflurane that did not pass through absorbent, and no compound A was added. RESULTS: As determined by gas chromatography, the higher temperature produced more volatile breakdown products, including compound A. Median necrosis of the corticomedullary junction in the 50 degrees C group [10% (quartiles 1.0%-7.8%); n = 20] exceeded that in the 30 degrees C group [5% (6.5%-15%); n = 18; P < 0.02], and both exceeded the median necrosis in the control group [0% (0.0%-0.2%); n = 10; P < 0.02]. The respective mean +/- SD values for these three studies were: 12.8 +/- 16.7%, 5.3 +/- 4.4%, and 0.3 +/- 0.5%. CONCLUSION: Degradation products of sevoflurane other than compound A can cause or augment the renal injury in rats produced by compound A.

Thoracic complications of illicit drug use: an organ system approach.

Illicit drug use constitutes a major health problem and may be associated with various thoracic complications. These complications vary depending on the specific drug used and the route of administration. Commonly abused drugs that may play a role in causing thoracic disease include cocaine, opiates, and methamphetamine derivatives. Intravenously abused oral medications may contain filler agents that may be responsible for disease. Thoracic complications may be categorized as pulmonary, pleural, mediastinal, cardiovascular, and chest wall complications. Pulmonary complications of drug abuse include pneumonia, cardiogenic edema, acute lung injury, pulmonary hemorrhage, and aspiration pneumonia. Filler agents such as talc may result in panacinar emphysema or high-attenuation upper-lobe conglomerate masses. The primary pleural complication of illicit drug use is pneumothorax. Mediastinal and cardiovascular complications of illicit drug use include pneumomediastinum, cardiomyopathy, myocardial infarction, aortic dissection, and injection-related pseudoaneurysms. Chest wall complications include diskitis and vertebral osteomyelitis, epidural abscess, necrotizing fasciitis, costochondritis, and septic arthritis. Categorization of thoracic complications of illicit drug use may facilitate understanding of these disorders and allow accurate diagnosis.