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T V Colby

Publications and source records attributed to T V Colby.

At least 37 records · Page 2Linked to original sources
PubMed2001

Pathologic approach to pulmonary hemorrhage.

The pathologist's approach to pulmonary hemorrhage is outlined. Most cases fall into those examples of pulmonary hemorrhage caused by localized sites of bleeding, and those examples that fall within the spectrum of diffuse alveolar hemorrhage. The histologic evaluation of pulmonary hemorrhage is outlined including assessment of fresh hemorrhage in alveolar spaces (including exclusion of traumatic hemorrhage related to the procedure) and the presence of hemosiderin and its various causes. The most common causes of diffuse alveolar hemorrhage and clues to their clinically pathologic diagnosis are discussed.

Hemorrhage↗
PubMed2001

Pulmonary Langerhans' cell histiocytosis: molecular analysis of clonality.

Pulmonary Langerhans' cell histiocytosis (LCH) is a form of Langerhans' cell disease that primarily affects smokers in the third to fifth decade. Extrapulmonary manifestations are rare. Its clinical course is typically characterized by stabilization or regression of bilateral micronodular infiltrates seen on chest radiographs; progression to honeycomb fibrosis is rare. Because the clinical course of pulmonary LCH is distinct from systemic multiorgan LCH, currently thought to be a clonal proliferative disorder, we examined the X-linked polymorphic human androgen receptor assay (HUMARA) locus to assess clonality in female patients with one or more discrete LCH cell nodules in open lung biopsies. Langerhans' cells (LCH cells) were excised from formalin-fixed, paraffin-embedded tissue by microdissection to assure a relatively pure cellular population, and studies for differential methylation patterns at the HUMARA locus were performed. Twenty-four nodules in 13 patients were evaluated. Seven (29%) were clonal and 17 (71%) were nonclonal. Of six cases with multiple discrete nodules, three (50%) showed a nonclonal LCH cell population. In one biopsy with five nodules, two nodules were clonal with one allele inactivated, one nodule was clonal with the other allele inactivated, and two nodules were nonclonal. In contrast to systemic LCH, pulmonary LCH appears to be primarily a reactive process in which nonlethal, nonmalignant clonal evolution of LCH cells may arise in the setting of nonclonal LCH cell hyperplasia. Cigarette smoking may be the stimulus for pulmonary LCH in contrast to other forms of LCH.

Adult↗
PubMed2001

Historical cohort study of US man-made vitreous fiber production workers: II. Mortality from mesothelioma.

As part of our ongoing mortality surveillance program for the US man-made vitreous fiber (MMVF) industry, we examined mortality from malignant mesothelioma using data from our 1989 follow-up of 3478 rock/slag wool workers and our 1992 follow-up of 32,110 fiberglass workers. A manual search of death certificates for 1011 rock/slag wool workers and 9060 fiberglass workers revealed only 10 death certificates with any mention of the word "mesothelioma." A subsequent review of medical records and pathology specimens for 3 of the 10 workers deemed two deaths as definitely not due to mesothelioma and one as having a 50% chance of being caused by mesothelioma. Two other deaths, for which only medical records were available, were given less than a 50% chance of being due to mesothelioma. Eight of the 10 decedents had potential occupational asbestos exposure inside or outside the MMVF industry. We also estimated the mortality risk from malignant mesothelioma in the cohort using two cause-of-death categorizations that included both malignant and benign coding rubrics. Using the more comprehensive scheme, we observed overall deficits in deaths among the total cohort and fiberglass workers and an overall excess among rock/slag wool workers. The excess in respiratory system cancer is largely a reflection of elevated lung cancer risks that we attributed mainly to confounding by smoking, to exposures outside the MMVF industry to agents such as asbestos, or to one or more of the several co-exposures present in many of the study plants (including asbestos). The second scheme, which focused on pleural mesothelioma in time periods when specific malignant mesothelioma coding rubrics were available, classified only one cohort death as being caused by malignant mesothelioma, compared with 2.19 expected deaths (local county comparison). We conclude that the overall mortality risk from malignant mesothelioma does not seem to be elevated in the US MMVF cohort.

Adult↗
PubMed2001

Nonspecific interstitial pneumonia and usual interstitial pneumonia: comparative appearances at and diagnostic accuracy of thin-section CT.

PURPOSE: To compare the morphologic abnormalities on thin-section computed tomographic (CT) images in a group of patients with histopathologically confirmed nonspecific interstitial pneumonia (NSIP) or usual interstitial pneumonia (UIP) and a clinical presentation of idiopathic pulmonary fibrosis. MATERIALS AND METHODS: Thin-section CT imaging patterns and distribution of disease in 53 patients with histologic diagnoses of NSIP (n = 21) or UIP (n = 32) were quantified retrospectively and independently by four observers. The appearances of NSIP and UIP at CT were compared with univariate and multivariate techniques. RESULTS: The use of thin-section CT proved to have moderate sensitivity (70%), specificity (63%), and accuracy (66%) in the diagnosis of NSIP. An increased proportion of ground-glass attenuation was the cardinal feature of NSIP at CT (odds ratio: 1.04 for each 1% increase in the proportion of ground-glass attenuation). A histologic diagnosis of NSIP was most frequent (in 24 of 35 observations [69%]) when ground-glass attenuation predominated, and was more frequent with mixed (35 of 79 observations [44%]) than with predominantly reticular disease (25 of 98 [26%] observations, P < .005). Logistic regression analysis of the data indicated that misdiagnosis of UIP in patients with NSIP was associated with less ground-glass attenuation (P < .005) at CT and a subpleural disease distribution (P = .02), with the converse being true for UIP cases misdiagnosed as NSIP. CONCLUSION: In patients with a clinical presentation of idiopathic pulmonary fibrosis, the accuracy of thin-section CT in identifying NSIP is considerably higher than previously reported. At CT, NSIP is characterized by more ground-glass attenuation and a finer reticular pattern than is UIP. Nevertheless, considerable overlap in thin-section CT patterns exists between NSIP and UIP.

Biopsy↗
PubMed2001

Chronic bronchiolitis with associated eosinophilic lung disease (eosinophilic bronchiolitis).

We encountered an adult patient with dyspnea, eosinophilia and bronchiolitis. He was diagnosed as having diffuse panbronchiolitis, and was treated with erythromycin for 3 years, but his symptoms had gradually worsened. Bronchoalveolar lavage showed marked eosinophilia, and video-assisted thoracoscopic lung biopsy revealed chronic bronchiolitis with associated eosinophilic lung disease (eosinophilic bronchiolitis). To our knowledge, no case of eosinophilic bronchiolitis has been reported in the literature.

Bronchiolitis↗
PubMed2001

The new World Health Organization classification of lung tumours.

Tumour classification systems provide the foundation for tumour diagnosis and patient therapy and a critical basis for epidemiological and clinical studies. This updated classification was developed with the aim to adhere to the principles of reproducibility, clinical significance, and simplicity in order to minimize the number of unclassifiable lesions. Major changes in the revised classification as compared to the previous one (WHO 1981) include the addition of two pre-invasive lesions to squamous dysplasia and carcinoma in situ; atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Another change is the subclassification of adenocarcinoma: the definition of bronchioalveolar carcinoma has been restricted to noninvasive tumours. There has been substantial evolution of concepts in neuroendocrine lung tumour classification. Large cell neuroendocrine carcinoma (LCNEC) is now recognized as a histologically high grade non small cell carcinoma showing histopathological features of neuroendocrine differentiation as well as immunohistochemical neuroendocrine markers. The large cell carcinoma class has been enriched with several variants, including the LCNEC and the basaloid carcinoma, both with a dismal prognosis. Finally, a new class was defined called carcinoma with pleomorphic, sarcomatoid, or sarcomatous elements, which brings together a number of proliferations characterized by a spectrum of epithelial to mesenchymal differentiation. Immunohistochemistry and electron microscopy are invaluable techniques for diagnosis and subclassification, but our intention was to render the classification simple and practical to every surgical laboratory, so that most lung tumours could be classified by light microscopic criteria.

Adenocarcinoma↗
PubMed2001

Smoking-related interstitial lung diseases: a concise review.

Interstitial lung diseases (also known as diffuse infiltrative lung diseases) are a heterogeneous group of parenchymal lung disorders of known or unknown cause. These disorders are usually associated with dyspnoea, diffuse lung infiltrates, and impaired gas exchange. The majority of interstitial lung diseases are of unknown cause. Known causes of interstitial lung disease include inhalation of organic and inorganic dusts as well as gases or fumes, drugs, radiation, and infections. This review summarizes the clinical, radiological, and histopathological features of four interstitial lung disorders that have been linked to smoking. These disorders include desquamative interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease, pulmonary Langerhans' cell histiocytosis, and idiopathic pulmonary fibrosis. Available evidence suggests most cases of desquamative interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease, and pulmonary Langerhans' cell histiocytosis are caused by cigarette smoking in susceptible individuals. Smoking cessation should be a main component in the initial therapeutic approach to smokers with these interstitial lung diseases. In addition, smoking appears to be a risk factor for the development of idiopathic pulmonary fibrosis.

Bronchiolitis Obliterans↗
PubMed2001

Diffuse pulmonary disease caused by nontuberculous mycobacteria in immunocompetent people (hot tub lung).

The clinicopathologic spectrum of infections due to nontuberculous mycobacteria (NTM) includes cavitary disease, opportunistic infection, and nodular disease associated with bronchiectasis. We report a less well-described manifestation of NTM infection: 10 immunocompetent patients without preexisting bronchiectasis had radiographic evidence of diffuse infiltrative lung disease. The most common symptoms were dyspnea, cough, hypoxia, and fever. All 10 patients had used a hot tub. Histologic examination revealed exuberant nonnecrotizing, frequently bronchiolocentric, granulomatous inflammation in all cases. In 1 case, necrotizing granulomas were also noted. The inflammation often was associated with patchy chronic interstitial pneumonia and organization. Cultures revealed NTM in all cases (Mycobacterium avium complex in all but 1 case), but staining for acid-fast bacilli was positive in only 1 case. Four patients received corticosteroids alone for presumed hypersensitivity pneumonia, 4 were treated with antimycobacterial therapy, and 2 received both. All patients demonstrated significant improvement at the time of follow-up. These findings suggest that disease due to NTM may manifest as diffuse infiltrates in immunocompetent adults and that hot tub use may be an important risk factor for this disease pattern.

Adult↗
PubMed2001

Wegener's granulomatosis.

Wegener's granulomatosis (WG) is currently categorized as one of the antineutrophil cytoplasmic antibody (ANCA)-associated small-vessel vasculitides distinguished by its predilection to affect the upper and lower respiratory tracts and kidneys clinically and histologically by the presence of necrosis, granulomatous inflammation, and vasculitis. However, small biopsies, especially from the head and neck region, often lack all these diagnostic histologic findings. Other common histologic features of WG include microabscesses and scattered multinucleated giant cells in a highly inflammatory background. Support from distinctive clinical setting or positive cytoplasmic (C)-ANCA testing may help establish the diagnosis of WG in cases lacking all the typical pathologic findings. The histopathologic differential diagnosis of WG includes nonspecific inflammatory conditions, infections, angiocentric lymphomas, collagen vascular diseases, and other forms of angiitis and granulomatosis. The prognosis of WG has dramatically improved from the 18% 5-month survival rate before the era of immunosuppressive therapy to the current remission rate of over 75% with a regimen of cyclophosphamide and glucocorticoids. A significant rate of relapse and profound disease- and/or treatment-related morbidity still occur. The cause of WG remains unknown, but circumstantial evidences suggest the potential roles of ANCA and infection in the pathogenesis.

Adolescent↗
PubMed2000

Occupational and environmental risk factors for idiopathic pulmonary fibrosis: a multicenter case-control study. Collaborating Centers.

Occupational exposures were investigated in a multicenter case-control study of clinically and histologically diagnosed idiopathic pulmonary fibrosis (IPF), a chronic diffuse interstitial lung disease of unknown etiology. Results are based on 248 cases, aged 20-75 years, diagnosed at 16 referral centers between January 1989 and July 1993. There were 491 controls ascertained by random digit dialing and matched to cases on sex, age, and geographic region. Data were collected using a standard telephone questionnaire. Occupational factors were based on a detailed history of jobs lasting 6 months or more and job activity, hobby, and specific substance checklists. Several occupational factors, adjusted for age and smoking in conditional multivariate logistic regression analyses, were significantly associated with IPF: farming (odds ratio (OR) = 1.6, 95% confidence interval (CI): 1.0, 2.5); livestock (OR = 2.7, 95% CI: 1.3, 5.5); hairdressing (OR = 4.4, 95% CI: 1.2, 16.3); metal dust (OR = 2.0, 95% CI: 1.0, 4.0); raising birds (OR = 4.7, 95% CI: 1.6, 14.1); stone cutting/polishing (OR = 3.9, 95% CI: 1.2, 12.7); and vegetable dust/animal dust (OR = 4.7, 95% CI: 2.1, 10.4). Interaction was detected between smoking and exposure to livestock (p = 0.06) and farming (p = 0.08). Results confirm previous studies showing increased risk associated with dusty environments.

Adult↗
PubMed2000

Matrix metalloproteinases and tissue inhibitors of metalloproteinases in bronchial squamous preinvasive lesions.

Metalloproteinases and their inhibitors are known to play an important role in the extracellular matrix remodeling associated with preinvasive lesions and invasive carcinomas; however, little is known about their role in early lung carcinoma. Immunohistochemical studies were made of the reactivity of bronchial squamous preneoplastic lesions from cigarette smokers, including basal cell hyperplasia, squamous metaplasia, dysplasia, carcinoma in situ, and invasive squamous cell carcinoma for matrix metalloproteinases (MMPs), their tissue inhibitors (TIMPs), and type IV collagen in 13 patients. Staining for type IV collagen disclosed discontinuities in basement membranes from basal cell hyperplasia to dysplasia, progressing to destruction in carcinoma in situ and invasive carcinoma. Reactivity for MMP-9 was mild in basal cell hyperplasia and squamous metaplasia, increasing in carcinoma in situ and invasive carcinoma. In contrast, reactivity for MMP-1 was strong in basal cell hyperplasia and squamous metaplasia, decreasing in carcinoma in situ and invasive carcinoma. Some neoplastic cells in carcinoma in situ and invasive carcinoma were MMP-3 positive. Staining for MMP-2 and TIMP-1 was moderate to strong in all squamous preinvasive lesions. Confocal microscopy showed MMP-9-positive cells passing through fragmented basement membranes in which type IV collagen and MMP-9 were colocalized. Type IV collagen colocalized with MMP-2 in all lesions and with TIMP-1 in basal cell hyperplasia and squamous metaplasia. The inverse relationships between the reactivity for MMP-1 and MMP-9 with progression of bronchial squamous preinvasive lesions suggest important roles for these MMPs in basement membrane remodeling in these lesions.

Aged↗
PubMed2000

Methotrexate pneumonitis: review of the literature and histopathological findings in nine patients.

Pneumonitis is a serious and unpredictable side-effect of treatment with methotrexate (MTX) that may become life-threatening. The clinical and histological features of nine cases of MTX pneumonitis are reported and the literature reviewed. The typical clinical symptoms include progressive shortness of breath and cough, often associated with fever. Hypoxaemia and tachypnoea are always present and crackles are frequently audible. Chest radiography reveals a diffuse interstitial or mixed interstitial and alveolar infiltrate, with a predilection for the lower lung fields. Pulmonary function tests show a restrictive pattern with diminished diffusion capacity. Lung biopsy reveals cellular interstitial infiltrates, granulomas or a diffuse alveolar damage pattern accompanied by perivascular inflammation. These clinical and pathological findings are not specific to MTX pneumonitis and can be seen with other drug-induced lung toxicities. It is important that all patients receiving methotrexate be educated concerning this potential adverse reaction and instructed to contact their physicians should significant new pulmonary symptoms develop while undergoing therapy. If methotrexate pneumonitis is suspected, methotrexate should be discontinued, supportive measures instituted and careful examination for different causes of respiratory distress conducted.

Aged↗
PubMed2000

Nodular amyloidoma and primary pulmonary lymphoma with amyloid production: a differential diagnostic problem.

Nodular amyloidomas (NA) of the lung are non-neoplastic inflammatory nodules containing eosinophilic amyloid deposits and a lymphoplasmacytic infiltrate. In some instances, the extensive amyloid deposits may obscure an underlying lymphoproliferative disorder. The histologic and immunohistologic features that discriminate these two differential diagnostic possibilities were studied in this series of six cases of NA and five cases of primary low-grade malignant lymphomas of lung with secondary amyloid deposits (ML). Two of lymphoma cases showed histopathologic and immunophenotypic features of B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (B-cell CLL/SLL), and three cases were low-grade B-cell lymphoma derived from mucosa associated lymphoid tissue (MALT lymphoma). Key discriminating morphologic features between NA and ML included lymphatic tracking of the cellular infiltrate (3/5 ML; 1/6 NA), pleural infiltration (3/5 ML; 0/6 NA), sheet-like masses of plasma cells (5/5 ML; 0/6 NA) and reactive follicles (4/5 ML; 1/6 NA). Lesional circumscription, vascular and bronchial destruction, lymphoepithelial lesions, and granulomas were not helpful discriminators. Immunohistochemical features indicating a dominant CD20+, CD79a+ B-cell population (5/5 ML; 0/6 NA), light chain restriction (4/5 ML; 0/6 NA), and aberrant antigen expression of CD20/CD43 (2/5 ML; 0/6 NA) were helpful. Amyloid tumors with a reactive lymphoplasmacytic infiltrate can be separated from low-grade malignant lymphomas utilizing both histologic and immunohistochemical features.

Adult↗
PubMed2000

Pulmonary atypical carcinoid: predictors of survival in 106 cases.

Pulmonary neuroendocrine tumors (NE) include a spectrum of tumors from typical carcinoid (TC) to atypical carcinoid (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell carcinoma (SCLC). Little is known about prognostic predictors for AC because of its rarity. Survival analysis was performed on 106 ACs with clinical follow-up from the AFIP and the Pathology Panel of the International Association for the Study of Lung Cancer (IASLC). The tumors fulfilled the 1999 WHO/IASLC criteria for AC of a NE tumor with a mitotic rate of 2 to 10 per 2 mm(2) of viable tumor or coagulative necrosis. Multiple clinical and histologic features were analyzed by Kaplan-Meier and Cox regression analysis. Of the clinical features, higher stage (P = .003) and a tumor size of 3.5 cm or greater (P = .003) were associated with a worse prognosis. Features that were histologically unfavorable by univariate analysis were mitotic rate (P =.002), pleomorphism (P = .018), and aerogenous spread (P =.007). Histologically favorable features by univariate analysis were the presence of palisading (P = .008), papillary (P = .039), pseudoglandular (P =.026), and rosette (P = .022) patterns. Female gender showed a trend toward a poorer prognosis (P =.085) and was included in the multivariate model. Multivariate analysis stratified for stage showed mitoses (P<.001), a tumor size of 3.5 cm or greater (P =.017), and female gender (P =.012) to be the only negative independent predictors of prognosis and the presence of rosettes (P = .016) to be the only independent positive predictor. We further divided the AC into subgroups of low (2 to 5 mitoses/2 mm(2)) and high (6 to 10 mitoses/2 mm(2)) mitotic rate and compared the survival with TC and with LCNEC. Within the category of AC, the patients with a higher mitotic rate had a significantly worse survival than those with a lower mitotic rate (P<.001) stratified for stage. Five- and 10-year survival rates for AC (61% and 35%, respectively) stratified for stage were significantly worse than for TC and better than that for LCNEC and SCLC. Chemotherapy or radiation therapy was given in 12 of 52 and 14 of 52 cases, respectively, but the data were insufficient to evaluate tumor response. We conclude that AC is an aggressive neuroendocrine neoplasm with survival intermediate between TC and LCNEC and SCLC. Higher mitotic rate, tumor size of 3.5 cm or greater, female gender, and presence of rosettes are the only independent predictors of survival. Surgical resection remains the treatment of choice, and the role of chemotherapy and radiation therapy remains to be proven.

Adult↗
PubMed2000

A critical examination of the immunophenotype of pulmonary sclerosing hemangioma.

The authors studied a series of 21 cases of pulmonary sclerosing hemangioma (SH) to address conflicting and unconfirmed reports of immunohistologic evidence of differentiation that have been made in the literature. They found the lesional cells of SH to be epithelial membrane antigen (EMA) positive (21 of 21 cases), to be keratin positive only infrequently and focally (six of 21), and to be nonreactive for carcinoembryonic antigen, S-100, smooth muscle actin, and CD34. Faint nuclear staining was seen for estrogen receptors, whereas progesterone receptors were expressed strongly in 17 cases. Neuroendocrine markers (chromogranin A, adrenocorticotrophic hormone, human growth hormone, and calcitonin) were negative uniformly on the lesional cells except for one case in which rare chromogranin-positive cells were present and another case in which rare human growth hormone-positive cells were seen. In contrast to the general EMA-positive, keratin-negative phenotype of the lesional cells, the cells lining the papillae or air spaces within the SH were typically positive for both markers. The following other lesions were identified in the cases studied: carcinoid tumorlets (n = 2), a neuroendocrine body (n = 1), and multiple meningothelial-like nodules (n = 1). All were clearly separable from the SH on morphologic grounds. The authors interpreted these to be chance occurrences of unrelated lesions. Recognition of the phenotype of SH as EMA positive, keratin weak to negative, and negative for S-100, smooth muscle actin, and neuroendocrine markers is notable in its differential diagnosis from other lesions. This phenotype does not suggest a precise lineage or type of differentiation for SH.

Adult↗
PubMed2000

Pulmonary and mediastinal glomus tumors--report of five cases including a pulmonary glomangiosarcoma: a clinicopathologic study with literature review.

Pulmonary and mediastinal glomus tumors are rare lesions, with four previously reported primary pulmonary cases and three mediastinal cases. The authors report one mediastinal glomus tumor, a locally infiltrative type, and four pulmonary glomus tumors, including the first case of primary pulmonary glomangiosarcoma. These tumors show a variety of clinical and pathologic differences from the more common cutaneous variety, including later age at presentation, larger size, and more frequent atypical/malignant features. Mediastinal and pulmonary glomus tumors both have an average patient age at presentation of 45 years. However, compared with their pulmonary counterparts, mediastinal glomus tumors are less common, more often symptomatic, and are larger (average size, 5.4 cm). Additionally, mediastinal glomus tumors more often demonstrate malignant or atypical features. Pulmonary glomus tumors average 3.3 cm in greatest dimension, with the majority measuring less than 2.5 cm. The pulmonary glomangiosarcoma presented was large, measuring 9.5 cm, and showed increased mitotic count (9 mitoses/10 high-power fields), necrosis, cytologic atypia, and was associated with disseminated disease. Regardless of clinical symptoms, histologic features, and even metastases, the vast majority of all benign and malignant glomus tumors are indolent and cured surgically, with adjuvant therapy needed only for occasional patients with more advanced disease. The four patients with glomus tumors reported are currently alive and free of disease as of last follow up. The patient with the glomangiosarcoma developed widespread metastases and died of disease 68 weeks after initial therapy.

Adult↗