PubMed Health⌕ Search

Biomedical subjects

Craig E Daniels

Publications and source records attributed to Craig E Daniels.

9 recordsLinked to original sources

The utility of fluorodeoxyglucose positron emission tomography in the evaluation of carcinoid tumors presenting as pulmonary nodules.

BACKGROUND: Fluorodeoxyglucose positron emission tomography (FDG-PET) is sensitive for detection of neoplastic solitary pulmonary nodules but may have decreased sensitivity for detection of carcinoid tumors. Our purpose was to determine the sensitivity of FDG-PET to detect pulmonary carcinoid tumors. METHODS: We performed a retrospective review of our institutional results regarding FDG-PET in the setting of thoracic carcinoid neoplasms. We identified 16 patients with a pathologic diagnosis of bronchial carcinoid who had an antecedent FDG-PET (from 2000 to 2004). All patients but one presented with pulmonary nodule(s). RESULTS: Sixteen patients had a diagnosis of carcinoid tumor, typical in 11 patients and atypical in 5 patients. The mean greatest pathologic dimension was 2.08 cm (range, 1.0 to 8.3 cm). Overall positron emission tomography (PET) sensitivity was 75% (12 true-positive and 4 false-negative results). The mean (+/- SD) size of carcinoids with false-negative PET results was not significantly different from carcinoids with true-positive results (1.6 +/- 0.81 cm and 2.35 +/- 1.87 cm, p = 0.54). Fifteen of 16 patients were staged pathologically, and positive nodes were found in 2 of these patients. PET lymph node staging agreed with pathologic staging in one stage 4 patient with positive lymph nodes and distant metastasis, but PET results were false negative in the other patient who had N2 with micrometastatic disease; stage IIIA. CONCLUSIONS: FDG-PET imaging is useful for evaluation of typical and atypical thoracic carcinoid tumors. Although overall PET sensitivity for detection of carcinoid tumors is somewhat reduced as compared to non-small cell lung cancer, it is much higher than prior reports suggest.

Adult↗

Organizing pneumonia in patients with hematologic malignancies: a steroid-responsive lesion.

BACKGROUND: Organizing pneumonia (OP) is a distinct histopathologic lesion that occurs in a variety of clinical contexts. There have been occasional reports of OP occurring in patients with hematologic malignancies. STUDY OBJECTIVES: To examine the association of OP with hematologic malignancies and to assess the clinical course of affected patients. DESIGN: A retrospective review of our institutional experience of unexplained OP developing in patients with hematologic malignancies. SETTING: Tertiary care, referral medical center. PATIENTS: We identified 6 patients with a verified histopathologic diagnosis of OP and antecedent or concomitant diagnosis of a hematologic malignancy from the Mayo Clinic database (1995-2003). Clinical, radiologic, and outcome data were abstracted from records. RESULTS: Underlying hematologic disorders included lymphoma (2), acute leukemia (2), cutaneous T-cell lymphoma (1), and myelodysplastic syndrome (1). OP was diagnosed by surgical lung biopsy in 4 and bronchoscopic biopsy in 2. Four of the 6 patients had previously been exposed to chemotherapeutic agents, two had not. Three of the 6 patients had bone marrow transplantation prior to development of OP. Five patients were treated with prednisone and all experienced symptomatic improvement with documented radiologic resolution in 4. One patient experienced symptomatic and radiologic resolution with observation alone. Three patients ultimately died from complications of their underlying hematologic disorder and 1 patient died of unknown causes. Two patients were alive without respiratory complaints more than 1 year after lung biopsy. CONCLUSIONS: OP occurs in patients with underlying hematologic malignancies who may or may not have been treated with chemotherapy and responds favorably to corticosteroid therapy.

Acute Disease↗

Treatment of idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive lung disease in most cases, and effective treatment is still lacking. This review examines the current status of treatment options and complexities in the management of patients with IPF. Although optimal therapy for IPF has not been identified, ongoing research efforts warrant reason for optimism. Current management of IPF includes not only judicious use of available pharmacological agents tailored to individual circumstances but also patient education through realistic assessment of prognosis, discussion of pros and cons of pharmacotherapy, early consideration of lung transplantation when applicable, treatment of complications, supportive care, and encouragement to participate in clinical trials.

Adrenal Cortex Hormones↗

B-type natriuretic peptide in the assessment of acute lung injury and cardiogenic pulmonary edema.

OBJECTIVE: The role of plasma B-type natriuretic peptide (BNP) in critically ill patients with acute pulmonary edema is controversial. We postulated that a low BNP level would exclude cardiac dysfunction as the principal cause of pulmonary edema and therefore help in the diagnosis of acute lung injury. DESIGN: A retrospective derivation cohort was followed by a prospective validation cohort of consecutive patients with acute pulmonary edema admitted to three intensive care units. BNP was measured within 24 hrs from onset. Critical care experts blinded to BNP results integrated clinical data with the course of disease and response to therapy and served as the reference standard. SETTING: Three intensive care units at the tertiary center. PATIENTS: Consecutive critically ill patients with acute pulmonary edema. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: In a derivation cohort of 84 patients, a BNP threshold of <or=250 pg/mL had a specificity of 87% and sensitivity of 48% for the diagnosis of acute lung injury. High specificity of BNP (90%, likelihood ratio of 3.9) was confirmed in a validation cohort of 120 consecutive patients, 52 (43%) of whom had acute lung injury. Notably, 32% of patients with acute lung injury had concomitant cardiac dysfunction. The median time from the onset of pulmonary edema to BNP testing was 3 hrs. The accuracy of BNP (area under receiver operator curve, 0.71) was comparable with pulmonary artery occlusion pressure (area under receiver operator curve, 0.66) and superior to ejection fraction (area under receiver operator curve, 0.60) in subgroups of patients in whom these tests were performed. The accuracy of BNP improved when patients with renal insufficiency were excluded (area under receiver operator curve, 0.82). CONCLUSION: When measured early after the onset of acute pulmonary edema, a BNP level of <250 pg/mL supports the diagnosis of acute lung injury. The high rate of cardiac and renal dysfunction in critically ill patients limits the discriminative role of BNP. No level of BNP could completely exclude cardiac dysfunction.

Acute Disease↗

Does interstitial lung disease predispose to lung cancer?

PURPOSE OF REVIEW: This review examines the evidence for the causality and pathogenesis of lung cancer associated with interstitial lung disease. RECENT FINDINGS: Although cigarette smoking is the leading cause of lung cancer, several other conditions either predispose to lung cancer or increase the risk of lung cancer in smokers. The evidence supports an increased risk of lung cancer due to specific fibrotic and inflammatory lung diseases (termed interstitial lung diseases), including idiopathic pulmonary fibrosis, systemic sclerosis, and certain pneumoconioses. The potential pathogenetic mechanisms indicate that recurrent injury and inflammation result in genetic alterations that predispose to lung cancer. SUMMARY: Idiopathic pulmonary fibrosis, systemic sclerosis, and certain pneumoconioses are associated with an independent increased risk of lung cancer; however, a unifying pathogenetic mechanism to explain the causality of this association has not been described. In addition, the inconsistently reported lung cancer frequencies call attention to the need for prospective studies of good quality.

Causality↗

Alkaptonuria diagnosed by flexible bronchoscopy.

A 68-year-old white man was evaluated for failure to wean from mechanical ventilation after cardiac surgery. Bronchoscopy performed prior to percutaneous dilatational tracheotomy revealed circumferential strikingly dark-colored airways, most prominent in the trachea and mainstem bronchi, extending distally into all airways with overlying desiccated black secretions. Histologic examination of bronchial mucosal biopsy samples and the desiccated secretions showed acute bronchitis and necrotic debris, respectively. This finding and the patient's history led to testing for plasma homogentisic acid, which was found to be elevated at 12.6 mug/mL, establishing the first diagnosis of alkaptonuria made using flexible bronchoscopy.

Aged↗

Imatinib mesylate inhibits the profibrogenic activity of TGF-beta and prevents bleomycin-mediated lung fibrosis.

Idiopathic pulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology. Prior efforts to treat idiopathic pulmonary fibrosis that focused on anti-inflammatory therapy have not proven to be effective. Recent insight suggests that the pathogenesis is mediated through foci of dysregulated fibroblasts driven by profibrotic cytokine signaling. TGF-beta and PDGF are 2 of the most potent of these cytokines. In the current study, we investigated the role of TGF-beta-induced fibrosis mediated by activation of the Abelson (Abl) tyrosine kinase. Our data indicate that fibroblasts respond to TGF-beta by stimulating c-Abl kinase activity independently of Smad2/3 phosphorylation or PDGFR activation. Moreover, inhibition of c-Abl by imatinib prevented TGF-beta-induced ECM gene expression, morphologic transformation, and cell proliferation independently of any effect on Smad signaling. Further, using a mouse model of bleomycin-induced pulmonary fibrosis, we found a significant inhibition of lung fibrosis by imatinib. Thus, Abl family members represent common targets for the modulation of profibrotic cytokine signaling.

Animals↗

Effect of publication bias on retrieval bias.

Publication bias is the main etiologic factor in retrieval bias. The authors measured the influence a positive study outcome had on housestaff's selecting the study for presentation.

Clinical Trials as Topic↗