Pulmonary Histoplasmosis Mimicking Metastatic Lung Cancer: A Case Report.

Histoplasmosis is a well-known endemic fungal infection but experience in non-endemic regions is often limited, which may lead to delayed diagnosis and extensive testing. The diagnosis can be especially challenging, typically when the disease first presents with pulmonary nodules accompanied by hilar and mediastinal lymphadenopathy, suggesting a much more common malignant disease. In this situation, a greater FDG uptake in draining lymph nodes in comparison with the associated lung nodule seen in [18F]FDG-PET/CT, the so-called "flip-flop fungus" sign, can help to orientate further diagnostic measures. We report a case of a 56-year-old woman living in Switzerland, a non-endemic region, whose diagnosis of imported histoplasmosis was delayed since the findings had been initially misinterpreted as pulmonary malignancy. Further, histological workup was inconclusive due to lack of specific fungal staining, leading to ineffective treatment and non-resolving disease. This paper intends to highlight the pitfalls in diagnosing Histoplasma capsulatum and presents images of particularities of fungal infections in [18F]FDG-PET/CT, which in our case showed a "flip-flop fungus" sign.

Obstructive sleep apnea in patients with abdominal aortic aneurysms: highly prevalent and associated with aneurysm expansion.

RATIONALE: Abdominal aortic aneurysms (AAA) are associated with life-threatening complications. The likelihood that an AAA will rupture is influenced by the aneurysm diameter and its expansion rate; reasons for rapid expansion are largely unknown. OBJECTIVES: To determine the prevalence of obstructive sleep apnea (OSA) in patients with AAA, and investigate a possible association between OSA and rate of AAA expansion. METHODS: A total of 127 patients (11 females), included in an AAA surveillance program, agreed to participate and underwent a sleep study. Annual AAA expansion was determined retrospectively from available ultrasound measurements. OSA was characterized using both oxygen desaturation index (ODI) and apnea-hypopnea index (AHI). Univariate and multivariate analysis was performed to assess the effect of OSA severity on AAA expansion. MEASUREMENTS AND MAIN RESULTS: Mean age was 67.9 (SD, 6) years. Median interval between the first and last AAA measurements was 18 (range, 2-113) months. An ODI or AHI of greater than 10 was found in 40.5% and 41.5% of the patients, respectively. Patients with an ODI greater than 30 (n = 12) had a significantly faster median yearly AAA expansion rate (2.9; quartiles 2/5.7 mm/y) than patients with an ODI 0-5 (n = 47; 1.2; quartiles 0/3.1 mm/y) or 6-15 (n = 43; 1.3; quartiles 0/2.7 mm/y) (P < 0.05). In multivariate regression analysis, controlling for cardiovascular risk factors and medications, ODI greater than 30 remained an independent risk factor for AAA expansion. CONCLUSIONS: In patients with AAA, OSA is highly prevalent. Severe OSA may be a causal factor for faster AAA expansion, but this needs to be proved in a randomized controlled intervention trial.

Augmentation index and central aortic blood pressure in patients with abdominal aortic aneurysms.

OBJECTIVE: Abdominal aortic aneurysm (AAA) is a life-threatening disease as rupture of the aneurysm is associated with high mortality. The likelihood that an AAA will rupture is particularly influenced by the diameter of the aneurysm and the rate of expansion; the reasons for fast expansion are largely unknown. Applanation tonometry (APT) can predict outcome in certain cardiovascular diseases by measuring arterial stiffness (augmentation index, AIx) and central aortic blood pressure (CABP). We tested the hypothesis that AIx and CABP would be higher in patients with fast-progressing AAA. METHODS: We performed APT and peripheral blood pressure measurements in 114 patients with AAA (11 women) with a mean ± SD age of 67.4±6.1 years. Annual AAA progression rate was determined by ultrasound. Patients were grouped into fast progressors (progression ≥2 mm/year) and slow progressors (progression <2 mm/year). RESULTS: Mean follow-up time after inclusion into the AAA surveillance programme was 22.1 ± 16.3 months. AIx was similar in fast progressors (27.3 ± 13.0%) and slow progressors (26.5 ± 12.6%) (P = 0.73). Fast progressors had a significantly higher CABP during systole (116.0 ± 16.0 mmHg) and diastole (95.7 ± 12.6 mmHg) than slow progressors (109.5 ± 16.3 and 90.0 ± 13.2 mmHg) (P = 0.04 and P = 0.02, respectively). Mean peripheral blood pressure was significantly higher in fast progressors (102.7 ± 12.8 mmHg) than in slow progressors (97.7 ± 12.9 mmHg) (P = 0.04). CONCLUSION: Augmentation index did not differ in patients with fast and slow-progressing AAA. However, fast progressors had higher central aortic blood pressures suggesting that elevated aortic blood pressure is a risk factor for faster AAA progression, but this needs to be proven in controlled interventional studies.