Internists, Pulmonologist (lungs)
17 years of experience

Accepting new patients
Garden Acres Area
11803 South Fwy
Ste 311
Burleson, TX 76028
817-908-8411
Locations and availability (5)

Education ?

Medical School
Gondar College Of Medical Sciences (1993)
Foreign school

Awards & Distinctions ?

Associations
American Board of Internal Medicine

Affiliations ?

Dr. Ayo is affiliated with 19 hospitals.

Hospital Affilations

Score

Rankings

  • Texas Health Harris Methodist Hospital Azle
    Pulmonary Disease
    108 Denver Trl, Azle, TX 76020
    • Currently 4 of 4 crosses
    Top 25%
  • Baylor Medical Center at Southwest Fort Worth
    Pulmonary Disease
    1400 8th Ave, Fort Worth, TX 76104
    • Currently 4 of 4 crosses
    Top 25%
  • Baylor All Saints Medical Centers
    Pulmonary Disease
    1400 8th Ave, Fort Worth, TX 76104
    • Currently 4 of 4 crosses
    Top 25%
  • Kindred Hospital Tarrant County
    Pulmonary Disease
    1000 N Cooper St, Arlington, TX 76011
    • Currently 3 of 4 crosses
    Top 50%
  • Texas Health Harris Methodist Hospital Southwest Fort Worth
    Pulmonary Disease
    6100 Harris Pkwy, Fort Worth, TX 76132
    • Currently 3 of 4 crosses
    Top 50%
  • Harris Methodist H E B
    Pulmonary Disease
    1600 Hospital Pkwy, Bedford, TX 76022
    • Currently 2 of 4 crosses
  • LifeCare Hospital Plano
    Pulmonary Disease
    6800 Preston Rd, Plano, TX 75024
    • Currently 1 of 4 crosses
  • LifeCare Hospital of Fort Worth
    Pulmonary Disease
    6201 Overton Ridge Blvd, Fort Worth, TX 76132
    • Currently 1 of 4 crosses
  • Texas Health Presbyterian Hospital Of Dallas
    Pulmonary Disease
    8200 Walnut Hill Ln, Dallas, TX 75231
    • Currently 1 of 4 crosses
  • Regency Hospital - Ft. Worth
    Pulmonary Disease
    6801 Oakmont Blvd, Fort Worth, TX 76132
    • Currently 1 of 4 crosses
  • Baylor All Saints Sw
  • Kindred Hospital Sw
  • Harris Methodist - Springwood
    1608 Hospital Pkwy, Bedford, TX 76022
  • Texas Health Harris Sw
  • Texas Health Southwest Fort Worth
  • Harris Continued Care Hospital
    1301 Pennsylvania Ave, Fort Worth, TX 76104
  • TX Health Southwest Fw
  • Regency Hospital
  • Huguley Memorial Hospital
  • Publications & Research

    Dr. Ayo has contributed to 4 publications.
    Title Cystic Lung Disease in Birt-hogg-dube Syndrome.
    Date October 2007
    Journal Chest
    Excerpt

    BACKGROUND: To describe the clinical, radiologic, and histopathologic aspects of cystic lung disease occurring in patients with Birt-Hogg-Dubé (BHD) syndrome, a rare, inheritable, multisystem disorder. METHODS: We retrospectively reviewed five patients with BHD syndrome evaluated at the Mayo Clinic Rochester from 1998 through 2005. RESULTS: Mean age (+/- SD) at the time of pulmonary evaluation was 56.4 +/- 4.8 years; four patients were men. Three patients had not received a diagnosis of BHD syndrome at the time of initial CT of the chest. Three patients had a smoking history, and two were nonsmokers. Two patients had a history of recurrent pneumothoraces. Pulmonary function tests available in four patients revealed normal results in one patient and mild airflow obstruction or nonspecific pattern of abnormalities in three patients. CT of the chest revealed cystic lung disease in all five patients; cysts were round to oval in shape, ranged widely in size, and were randomly distributed throughout the lungs, except for a predilection to involve the lung bases more extensively. Three patients with a smoking history had more severe cystic changes compared to nonsmokers and included both patients with recurrent pneumothoraces. Surgical lung biopsy available in one patient revealed emphysema-like changes. Follow-up CT scans available in four patients revealed relative stability over a median interval of 20 months (range, 3 to 66 months). CONCLUSION: We conclude that cystic lung disease in BHD syndrome varies widely in severity, mimics pulmonary lymphangioleiomyomatosis, and may be worsened by smoking.

    Title Assessing Need for Long-term Oxygen Therapy: a Comparison of Conventional Evaluation and Measures of Ambulatory Oximetry Monitoring.
    Date May 2003
    Journal Respiratory Care
    Excerpt

    BACKGROUND: Appropriate identification of hypoxic patients with chronic obstructive pulmonary disease (COPD) is important because of the demonstrated survival benefit of long-term oxygen therapy (LTOT) and its associated cost. Resting oxygen saturation (measured via pulse oximetry [S(pO2)]) and lowest exercise S(pO2) (during a 6-min walk test) is the standard method of determining LTOT requirements, but that method does not measure the patient's oxygenation during sleep or activities of daily living. We hypothesized that values obtained via the standard method would correlate poorly with values obtained via ambulatory oximetry monitoring. METHODS: We conducted a prospective, cohort study in an out-patient pulmonary clinic in a tertiary care referral center, with 20 stable COPD patients who were being evaluated for LTOT with conventional evaluation versus 16-24 hours of ambulatory oximetry. RESULTS: The resting S(pO2) did not correlate well with mean ambulatory S(pO2) (r = 0.64) or the percent of monitored time spent with S(pO2) < 88% (r = 0.49). The lowest exercise S(pO2) also did not predict mean ambulatory S(pO2) (r = 0.39) or the percent of monitored time spent with S(pO2) < 88% (r = 0.32). Conventional evaluation overestimated LTOT requirements with 16 of the 20 patients developing an S(pO2) < 88%, most of them with exercise only (ie, most had normal resting S(pO2)). With ambulatory monitoring, however, only 3 of the 16 patients spent > 10% of the monitored time with S(pO2) < 88%. CONCLUSION: There was a poor relationship between the conventional oxygenation assessment method and continuous ambulatory oximetry during LTOT screening with COPD patients.

    Title Routine Measurement of Pleural Fluid Amylase is Not Indicated.
    Date March 2001
    Journal Archives of Internal Medicine
    Excerpt

    BACKGROUND: The routine measurement of pleural fluid amylase is frequently recommended, but the cost-effectiveness of this procedure is unknown. METHODS: To assess the utility of routine measurement of pleural fluid amylase in evaluating pleural effusions, we measured amylase, glucose, lactate dehydrogenase, and protein levels and blood cell counts in 379 patients undergoing thoracentesis during a 22-month period from 1997 to 1999. Of these, 199 had effusions after cardiac surgery; 61, malignant; 48, transudative; 28, parapneumonic; 2, chylous; 2, rheumatoid; 1, tuberculous; and 1, from chronic pleuritis. There were 37 exudates of unknown origin. RESULTS: Measurement of pleural fluid amylase levels did not assist in determining the origin of the effusion in any of the patients. Amylase levels greater than 100 U/L (normal serum level in our laboratory is 30-110 U/L) were found in 5 (1.3%) of 379 patients: 1 patient with congestive heart failure (amylase, 173 U/L), 2 with post-cardiac surgery effusions (144 U/L and 130 U/L), 1 with pneumonia (109 U/L), and 1 with lung cancer (105 U/L). CONCLUSIONS: The routine measurement of pleural fluid amylase levels is neither clinically indicated nor cost-effective. We suggest that pleural fluid serum amylase levels be measured only if there is a pretest suspicion of acute pancreatitis, chronic pancreatic disease, or esophageal rupture.

    Title Transforming Growth Factor Beta(2) (tgf Beta(2)) Produces Effective Pleurodesis in Sheep with No Systemic Complications.
    Date February 2001
    Journal Thorax
    Excerpt

    BACKGROUND: We have recently shown that transforming growth factor (TGF)beta(2) induces effective pleurodesis in rabbits. However, rabbits have a thin pleura while humans have a thick visceral pleura. The effect of intrapleural administration of TGF beta(2) in animals with a thick pleura and its associated systemic effects have not been investigated. This study was undertaken (1) to develop a new animal model for the study of pleurodesis using sheep which have a thick pleura resembling that of humans; (2) to study the efficacy of TGF beta(2) as a pleurodesis agent in the sheep model; and (3) to assess whether histological changes occur in extrapulmonary organs after intrapleural administration of TGF beta(2). METHODS: Twelve sheep were divided into four groups and were given a single intrapleural injection of TGF beta(2) in a concentration of 1.0 microg/kg, 0.5 microg/kg, 0.25 microg/kg or 0.125 microg/kg to the right pleural cavity via a chest tube. The left pleural cavity served as the control. Any pleural fluid that accumulated after the intrapleural TGF beta(2) injection was collected and analysed. The degree of pleurodesis was graded from 1 (no adhesions) to 8 (complete symphysis >50% of chest wall) at day 14 when the sheep were killed. Biopsy specimens were taken from the lungs and extrapulmonary organs. RESULTS: All sheep that received > or = 0.25 microg/kg TGF beta(2) developed excellent pleurodesis (score = 8) while those that received 0.125 microg/kg had a median score of 6. The pleurodesis score did not exceed 2 in the control (left) side of any sheep. Sheep receiving > or = 0.50 microg/kg TGF beta(2) developed large exudative pleural effusions while those receiving a lower dose did not. The production of effusions neither hindered nor was necessary for inducing pleurodesis. There were no significant fibrotic changes in any of the extrapulmonary organs. CONCLUSION: Intrapleural injection of 0.25-1.0 microg/kg TGF beta(2) produces excellent pleurodesis in a new sheep model with no evidence of extrapulmonary fibrosis.


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