Publications by authors named "Ayesu K"

BACKGROUND Ludwig angina is a cellulitis of the soft tissues of the neck and floor of the mouth. It is most commonly caused by Viridans streptococcal species, but other bacterial species have been shown to lead to this severe infection. Clostridium sporogenes is an anaerobic gram-positive, spore-producing bacillus found in soil and the human gastrointestinal tract.

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BACKGROUND Degenerative disc disease of the lumbar spine can be associated with spinal canal and neuroforaminal stenosis, resulting in severe pain. Conservative approaches to treatment are generally recommended initially, especially in the elderly. Epidural corticosteroid injections can provide significant but temporary pain relief and are a commonly performed procedure in pain management.

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BACKGROUND Primary effusion lymphoma (PEL) is a rare and aggressive non-Hodgkin lymphoma (NHL) that is responsible for 1% of all lymphomas not related to human immunodeficiency virus (HIV). PEL is characterized by human herpesvirus-8 (HHV-8) positivity in the absence of overt tumor burden that does not exhibit typical B cell or T cell immunophenotype characteristics. The exact mechanism of development is unknown, but it is hypothesized to develop from post-germinal B cell origin.

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: Congenital deficiency of factor II is a very rare autosomal recessive disorder that can result in a bleeding diathesis. Genotypically, individuals are either homozygous for a defective prothrombin gene or a compound heterozygote with different mutated prothrombin genes inherited from each parent. Phenotypically, it is characterized by either a low production of normal prothrombin or a near-normal production of dysfunctional prothrombin.

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Purpose: Further examination of clinical outcomes and inflammatory response of bacteremic pneumococcal community-acquired pneumonia (CAP) is of great interest to enhance the care of patients with pneumococcal CAP.

Methods: This is a secondary analysis of the Community Acquired Pneumonia Organization (CAPO) to compare the time to clinical stability (TCS), length of hospital stay (LOS), and in-hospital mortality of hospitalized pneumococcal CAP patients with and without bacteremia. To measure the effect of bacteremia in pneumococcal CAP patients on outcomes, we modeled all-cause in-hospital mortality using a Poisson regression model, and TCS and LOS using Cox proportional hazards models.

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Background: Outcomes of community-acquired pneumonia (CAP) in relation to CD4+ cell counts have not been established. We examined the correlation of CD4+ cell count and HIV-RNA level with the clinical outcomes of CAP in hospitalized HIV-infected patients.

Methods: This was a retrospective study of 127 adult hospitalized patients with HIV infection enrolled with the CAP Organization (CAPO), examining the time to clinical stability (TCS), length of hospital stay (LOS), and all-cause mortality.

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Background: Community-acquired pneumonia (CAP) severity scores can identify patients at low risk for mortality who may be suitable for ambulatory care. Here, we follow the clinical course of hospitalized patients with CAP due to 2009 H1N1 influenza.

Objective: To evaluate the role of CAP severity scores as predictors of mortality.

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We report the resistance rates of Staphylococcus aureus to non-beta-lactam antimicrobials from The Surveillance Network Database-USA (Eurofins-Medinet, Chantilly, VA). Specimens studied were from lower respiratory tract, wounds, and blood. Patients were stratified by age group and patient setting.

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Twelve patients with active duodenal ulcer disease and Helicobacter pylori infection were treated with 1 g sucralfate q.d.s.

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Patients with duodenal ulcers and Helicobacter pylori infection have elevated plasma gastrin concentrations which fall after suppression of the organism. This may be due to H. pylori elevating the pH of the antral mucous layer, therefore preventing luminal acid from inhibiting gastrin release.

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The effects of nifedipine and propranolol, alone and in combination, on collagen-induced platelet aggregation were studied in healthy volunteers using whole blood impedance aggregometry. No significant inhibition of platelet aggregation was found after the in vitro addition of propranolol, nifedipine or nifedipine vehicle or after nifedipine ex vivo. No interaction was found between in vitro propranolol and nifedipine, either in vitro or ex vivo.

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