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Biomedical subjects

U B Prakash

Publications and source records attributed to U B Prakash.

At least 19 recordsLinked to original sources
PubMed1999

Radiation-induced pneumonitis in the "nonirradiated" lung.

OBJECTIVE: To describe six cases of radiation-induced organizing pneumonitis occurring outside the direct radiation field and to review clinical, radiologic, and histologic aspects of this entity. MATERIAL AND METHODS: We present detailed case reports of six women, with a mean age of 62.8 years (range, 50 to 75), who had received radiation therapy (mean dose, 6,560 cGy) for breast cancer. RESULTS: From 6 to 17 months (mean, 8.8) after the completion of radiotherapy, recurrent and migrating lung infiltrates were detected outside the radiation field in the six study patients. Three patients had pronounced respiratory symptoms, whereas the rest were minimally symptomatic or asymptomatic. Thoracic computed tomography showed dense alveolar infiltrates. Bronchoalveolar lavage in two patients revealed lymphocytosis (25% and 19%), and lung biopsy in five patients demonstrated a histologic pattern consistent with bronchiolitis obliterans organizing pneumonia. Even though the symptomatic patients showed prompt resolution of their symptoms and roentgenographic abnormalities after systemic corticosteroid therapy, the lung infiltrates recurred after corticosteroid therapy was discontinued. CONCLUSION: These six cases, including their prompt response to corticosteroid therapy, provide additional evidence that irradiation damages lung tissue outside of the direct treatment field and suggest that an immunologically mediated lymphocytic alveolitis may be responsible for the recurrent migratory organizing pneumonitis.

Adenocarcinoma↗
PubMed1999

Rapidly growing mycobacterial lung infection in association with esophageal disorders.

Esophageal or other swallowing disorders complicated by lipoid pneumonia are reported to be associated with pulmonary infections caused by rapidly growing mycobacteria. Herein we describe a 63-year-old woman with achalasia of the esophagus complicated by lung infection with Mycobacterium chelonae and a 47-year-old man in whom long-term ingestion of mineral oil was complicated by lipoid pneumonia and M. fortuitum lung infection. A MEDLINE search of English language publications from 1966 to 1997 revealed 18 cases of lung infections caused by rapidly growing mycobacteria in patients with esophageal disorders. Of these 18 patients and our 2 patients, 11 were men and 9 were women (mean age, 50 years). Achalasia was present in 11 patients, and 6 had lipoid pneumonia without evidence of esophageal disorders. Three patients had lipoid pneumonia caused by lipoid ingestion in the setting of achalasia or another swallowing disorder. In 14 patients, lung infection was caused by M. fortuitum; in 5, M. chelonae; and in 1, a non-M. fortuitum rapidly growing mycobacterial infection. The most common clinical feature was fever, and the most common roentgenologic abnormality was the presence of unilateral or bilateral and patchy or dense infiltrates. The sputum was the most common source of isolation of rapidly growing mycobacteria. Achalasia and lipoid pneumonia are important risk factors for the development of lung infections caused by rapidly growing mycobacteria. Treatment of the esophageal disease might prevent occurrence of and facilitate recovery from these infections.

Diagnosis, Differential↗
PubMed1998

Respiratory complications in mixed connective tissue disease.

The term mixed connective tissue disease is used to identify the patients with combined clinical features of systemic lupus erythematosus, scleroderma or progressive systemic sclerosis, and polymyositis-dermatomyositis. A prerequisite for the diagnosis of mixed connective tissue disease is the presence, in the serum, of high titers of antibodies against uridine-rich RNA-small nuclear ribonucleoprotein (snRNP). Respiratory and nonrespiratory features of the disease follow those seen in systemic lupus erythematosus, scleroderma, or progressive systemic sclerosis, and polymyositis-dermatomyositis. Respiratory involvement is observed in 20% to 80% of patients. Major respiratory manifestations and their incidences described include interstitial pneumonitis and fibrosis (20% to 65%), pleural effusion (50%), pleurisy (20%), and pulmonary hypertension (10% to 45%). Other pulmonary features consist of pulmonary vasculitis, pulmonary thromboembolism, aspiration pneumonia, pulmonary hemorrhage, pulmonary nodules, pulmonary cysts, obstructive airways disease, mediastinal lymphadenopathy, pulmonary infections, hypoventilatory respiratory failure, and diaphragmatic dysfunction. Pulmonary hypertension is a serious complication; rapid deterioration and death have occurred in spite of corticosteroid and cytotoxic chemotherapy.

Adult↗
PubMed1998

Chest roentgenography after outpatient thoracentesis.

OBJECTIVE: To evaluate the clinical utility of posteroanterior chest roentgenograms after thoracentesis in the outpatient setting. DESIGN: We undertook a retrospective study of clinical records of outpatient thoracentesis performed between January and December 1996 by the Division of Pulmonary and Critical Care Medicine at Mayo Clinical Rochester. MATERIAL AND METHODS: The medical records of 54 men and 39 women who underwent 123 outpatient thoracentesis were reviewed. Exclusion criteria were the need for pleural biopsy at time of thoracentesis or the need for ultrasound-guided assistance for completion of the procedure. Indications for thoracentesis and postthoracentesis chest roentgenography were analyzed. RESULTS: Of 123 thoracentesis performed in the outpatient setting during the specified study period, 104 met the inclusion criteria. Of these 104 thoracentesis, 54 (52%) were followed by chest roentgenography. Pneumothorax occurred in only 5 of these 104 procedures (5%), in 5 separate patients. Three of these patients were asymptomatic and did not require therapeutic intervention; the two symptomatic patients required hospitalization and chest tube drainage. Of the two pneumothoraces in patients with symptoms, one was detected on the same day as the thoracentesis, and the other was diagnosed 2 days later. The patients who did not undergo postthoracentesis chest roentgenography had no reported complications. Of the 54 chest roentgenograms, 52 were obtained in asymptomatic patients, with no suspicion of pneumothorax. These x-ray studies led to a total cost of $4,862 and detection of three pneumothoraces that did not require therapy. CONCLUSION: Routine performance of chest roentgenography after outpatient thoracentesis can incur substantial cost. A more selective approach to this practice is needed, both to optimize patient care and to manage limited medical resources efficiently. Postthoracentesis chest roentgenograms should be limited to patients with symptoms indicative of thoracentesis-induced pneumothorax.

Aged↗
PubMed1997

alpha1-antitrypsin gene mutation hot spot associated with the formation of a retained and degraded null variant [corrected; erratum to be published].

Null alpha1-antitrypsin (alpha1AT) alleles represent the end of a continuum of variants associated with profound alpha1AT deficiency and an increased risk of emphysema. This study characterizes the molecular basis of QOclayton, a new example of an alpha1AT null allele arising from a mutational hot spot in the alpha1AT gene. The QOclayton allele is identical to the normal M1(V213) alpha1AT allele except for an insertion of a cytosine. This insertion occurs in the alpha1AT sequence which normally has seven cytosines corresponding to amino acid residues 360 to 362. The QOclayton mutation is located in the same reiterated DNA sequence as the alpha1AT QObolton deletion mutation and the insertion mutation allele QOsaarbruecken. The QOclayton cytosine insertion causes a 3' frameshift and results in the formation of a termination codon at residue 376, the same consequence as the alpha1AT QOmattawa mutation (L353 T-insertion with a 3' frameshift). To determine the molecular mechanisms responsible for the absence of alpha1AT associated with the QOclayton gene, an in vitro model of QOclayton was established using Chinese hamster ovary cells (CHO) transfected with the QOclayton gene. These cells were evaluated for alpha1AT mRNA expression, protein synthesis and secretion. Although the QOclayton gene expresses a similar amount of alpha1AT mRNA as compared with the normal alpha1AT gene, no QOclayton protein is secreted. Protein trafficking and double-label immunofluorescence demonstrate that the QOclayton protein is retained in the rough endoplasmic reticulum or pre-Golgi compartment and is degraded (t1/2 = 6.5 h). Since QOmattawa, QObolton, and QOsaarbruecken have similar termination sites in the alpha1AT mRNA, they may share a similar intracellular fate.

Animals↗
PubMed1997

Baseline characteristics of enrollees in the National Heart, Lung and Blood Institute Registry of alpha 1-antitrypsin deficiency. Alpha 1-Antitrypsin Deficiency Registry Study Group.

OBJECTIVE: alpha 1-Antitrypsin (alpha 1-AT) deficiency is a hereditary disorder characterized by a high risk for the development of emphysema at an early age. In 1988, the National Heart, Lung and Blood Institute, National Institutes of Health, initiated a registry of individuals with alpha 1-AT deficiency to help define the natural history and clinical course of this disorder. This article describes demographic and clinical characteristics of subjects enrolled in the Registry at baseline. DESIGN: Prospective longitudinal natural history study. SETTING: Thirty-seven clinical centers in the United States (36 centers) and Canada (one center). PATIENTS: There were 1,129 subjects 18 years of age or older with severe deficiency of alpha 1-AT, defined as having serum alpha 1-AT levels < or = 11 mumol/L confirmed by a Central Phenotyping Laboratory, or a ZZ or ZNull genotype identified by genomic DNA analysis. RESULTS: Most enrollees were symptomatic white subjects in their fourth to sixth decade, with a ZZ phenotype, a history of having smoked cigarettes, and pulmonary function tests demonstrating a pattern consistent with emphysema. Interestingly, only a small percentage were current smokers on enrollment, suggesting that this population is amenable to smoking cessation. A subgroup of individuals in the Registry with relatively normal lung function were younger, more likely to have never smoked and more likely to have come to medical attention owing to a family history of alpha 1-AT deficiency rather than symptomatic involvement. CONCLUSIONS: These results emphasize the need for increased awareness and early detection of alpha 1-AT deficiency. In this endeavor, dissemination of the information contained in the Registry to health-care professionals and the general population, along with initiation of appropriate preventative measures before significant lung damage has occurred, could have considerable benefits for individuals with this condition.

Adult↗
PubMed1996

Pulmonary hamartomas.

OBJECTIVE: To analyze the clinical and pathologic features of biopsy-proven pulmonary hamartomas at a tertiary referral center. DESIGN: We retrospectively reviewed institutional data on pulmonary hamartomas for a 17-year study period. MATERIAL AND METHODS: The Mayo Clinic computerized medical records database was searched for patients who had biopsy, excision, or autopsy diagnosis of pulmonary hamartomas from 1976 through 1992. Medical records and all available histologic sections were reviewed. RESULTS: Of the 215 patients with histologically confirmed pulmonary hamartoma, 141 were men and 74 were women (approximately a 2:1 ratio). Two hundred eight patients were asymptomatic, 54 of whom were undergoing assessment for a comorbid disease process. Only four patients had new onset of respiratory symptoms. The peak incidence of occurrence was in the seventh decade of life. The mean size of the hamartomas were 1.5 cm (range, 0.2 to 6.0); no lobe was predominantly involved. Most hamartomas were resected by simple or wedge excision. Sixty-three patients (29.3%) had a concurrent neoplasm (most commonly, lung carcinoma). Follow-up ranged from 2 to 192 months (mean, 61). Eight postoperative deaths occurred. No recurrent pulmonary hamartomas developed. In one patient, lung carcinoma developed 33 months after excision of a hamartoma. In a second patient, sputum cytologic findings were abnormal 9 years later. A third patient had biopsy-proven adenocarcinoma metastatic to bone and an indeterminate lung nodule 2 years after resection of a pulmonary hamartoma. CONCLUSIONS: Pulmonary hamartomas are benign lung neoplasms that, in our referral population occurred most commonly in asymptomatic older men. A substantial number of our patients had concurrent neoplasms; however, many had been referred for cancer treatment. We found no evidence of either a malignant transformation or an unexplained association with other lung neoplasms.

Adult↗
PubMed1996

The documentation of thoracic endoscopy.

Thoracic endoscopy encompasses bronchoscopy, esophagoscopy, laryngoscopy, mediastinoscopy, and thoracoscopy (pleuroscopy). In this article, the role of documentation as it applies to bronchoscopy is discussed. However, the discussion is generally applicable to other thoracic endoscopy procedures.

Bronchoscopy↗
PubMed1995

Tracheobronchial involvement in Wegener's granulomatosis.

This study was designed to characterize the clinical spectrum and course of tracheobronchial involvement in Wegener's granulomatosis (WG). Of the 51 patients with biopsy-proven WG who underwent bronchoscopy at least once at our institution between January 1982 and November 1993, 30 (59%) had endobronchial abnormalities due to WG. Initial findings included subglottic stenosis in five (17%), ulcerating tracheobronchitis with or without inflammatory pseudotumors in 18 (60%), tracheal or bronchial stenosis without inflammation in four (13%), and hemorrhage without identifiable source in two (4%) patients. Nine patients with ulcerating tracheobronchitis on initial study had subsequent bronchoscopies for continued symptoms, which in seven cases documented the progression from ulcerating tracheobronchitis to stenosis without inflammation. Bronchoscopic interventions included dilation by rigid bronchoscope in three, YAG-laser treatment in one, and placement of silastic airway stents in three patients. Only the stents provided persistent airway patency. Endobronchial biopsies were performed on 21 occasions in 17 patients. Half of the specimens were helpful in establishing the diagnosis and in all but three in assessing disease activity. While antineutrophil cytoplasmic antibody titers reflect overall disease activity, no correlation with endobronchial inflammatory activity was apparent.

Adult↗
PubMed1994

Alpha 1-antitrypsin deficiency in intracranial aneurysms and cervical artery dissection.

The pathogenesis of ruptured intracranial aneurysms and cervical artery dissections is poorly understood but may be similar in these two disorders. We report four patients with alpha 1-antitrypsin deficiency who developed a ruptured intracranial aneurysm or spontaneous dissection of the cervical internal carotid artery. Three patients were heterozygous for the deficient allele (PiMZ or PiGZ) and one was homozygous (PiZZ). A deficiency of alpha 1-antitrypsin or one of the other protease inhibitors could result in degradation of the arterial wall through an imbalance between proteolytic enzymes and their inhibitors, thereby predisposing the arterial wall to dissection or aneurysm formation.

Adult↗
PubMed1994

Arterial fibromuscular dysplasia associated with severe alpha 1-antitrypsin deficiency.

OBJECTIVE: To elucidate the putative arteriopathy associated with alpha 1-antitrypsin (alpha 1-AT) deficiency. DESIGN: We retrospectively studied the frequency of occurrence of fibromuscular dysplasia (FMD) in patients with alpha 1-AT deficiency in whom a postmortem examination had been done during a 10-year period at the Mayo Clinic. MATERIAL AND METHODS: The medical records of all patients in whom an autopsy was done at the Mayo Clinic between 1983 and 1992 were reviewed to identify all those with a diagnosis of alpha 1-AT deficiency or FMD. RESULTS: Arterial FMD was found in 2 of 6 patients with alpha 1-AT deficiency (33.3%; 95% confidence interval, 4.3 to 77.7%) in comparison with 23 of 6,690 patients without alpha 1-AT deficiency (0.3%; 95% confidence interval, 0.2 to 0.5%). In both patients with alpha 1-AT deficiency and FMD, the arterial media was thickened and composed of irregular arrays of muscular and connective tissue fibers in a background of mucoid ground substance. CONCLUSION: These findings provide further evidence for an underlying arteriopathy in patients with alpha 1-AT deficiency and suggest that FMD may be a non-specific disorder.

Adult↗