Aneurysms of the pulmonary arteries.
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Biomedical subjects
Publications and source records attributed to G Nash.
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Recent studies suggest that there is an increased incidence of squamous cell carcinoma of the anus in male homosexuals, but a precursor lesion has not been identified. We retrospectively analyzed in a blind fashion all anal tissue removed surgically during 1984. Twelve (6.7%) of the 180 specimens from men contained lesions with foci of epithelial atypia. Only one (0.85%) of 118 specimens from women harbored similar atypia. Of seven additional file cases exhibiting atypical anal mucosa, six were from men. Of 14 men with atypical anal lesions whose sexual orientation was known, 11 (79%) were homosexuals. In the 20 cases found to have atypical mucosal lesions, three patterns of atypia were identified, with more than one often occurring in the same specimen. Anal intraepithelial neoplasia (dysplasia) was identified in seven cases (35%) and occurred primarily at the anorectal junction and in anal ducts. Atypical condyloma was found in three cases (15%). A third lesion histologically indistinguishable from Bowen's disease or bowenoid papulosis was found in 12 cases (60%). In ten of these the lesion was adjacent to a condyloma. Although the natural history of these lesions of the anal mucosa is presently unknown, it may resemble that of similar lesions in other anatomic locations.
Sixty-four lung tumors were evaluated for the presence of immunoreactive neuron-specific enolase (NSE), bombesin (Bn), and chromogranin (Cg) to assess their value as markers for neuroendocrine cells in the histologic diagnosis of pulmonary neoplasms. Staining was correlated with the presence and density of neurosecretory granules (number of neurosecretory granules per unit cytoplasmic cross-sectional area) as determined by planimetry on electron micrographs. The cytoplasmic density of neurosecretory granules was significantly greater in the carcinoid tumors than in the small cell carcinomas (P less than 0.001). Neuron-specific enolase was localized in all of the neuroendocrine granule-bearing tumors but was also present in 57 per cent of the nonneuroendocrine carcinomas. Bombesin was present in 68 per cent of the neuroendocrine tumors and in less than 1 per cent of the nonneuroendocrine tumors. Staining for Cg appeared to correlate with the density of neuroendocrine granules, with staining in carcinoid tumors but no staining in small cell anaplastic carcinomas. A panel of antibodies may be required for the reliable identification of neuroendocrine lung tumors by immunohistochemical techniques.
Immunohistochemical staining for involucrin, a cytoplasmic protein synthesized during squamous maturation, was assessed in histologic sections from hysterectomy and cone biopsy specimens from patients with cervical neoplasia. In normal and condylomatous squamous epithelium, diffuse cytoplasmic staining was seen in the suprabasal layers, with no staining of the basal cells. Staining was absent in two cases of cervical intraepithelial neoplasia (CIN), grade III, in which the lesions were composed entirely of undifferentiated cells and markedly decreased in cases involving large numbers of basal cells. In 19 of 23 cases (83 per cent) of CIN, however, focal staining for involucrin was seen in large differentiated cells in the more superficial layers, and in two cases of keratinized CIN diffuse suprabasal staining was observed. Similarly, strong staining for involucrin was present in differentiated areas in one case of microinvasive squamous cell carcinoma and in 93 per cent of cases of infiltrating squamous cell carcinoma. These findings suggest that involucrin is a marker for maturation in cervical squamous epithelial neoplasms. Patterns of immunohistochemical staining for involucrin in keratinized dysplasia and differentiated squamous carcinomas should be taken into consideration if loss of involucrin staining is used as a criterion for neoplastic transformation of cervical epithelium, as has been proposed.
Pathomorphological studies were undertaken to investigate the therapeutic effect of the Ca2+-antagonist nifedipine on malignant hypertensive arteriopathy in Dahl salt-sensitive rats. The individual course of disease was followed by comparing pre-treatment biopsies of the mesenteric arteries with post-treatment findings at necropsy. Within seven weeks, continuous therapy with nifedipine resulted in healing of early vascular lesions and in partial repair of the more advanced ones. Under normalization of blood pressure, vascular fibrinoid exacerbations were prevented and existing intramural fibrin insudates were completely or partially removed. Lamellar fibroelastosis of the intima occurred as a characteristic of repair.
The absence of keratin staining in tumor cells from localized fibrous mesotheliomas in both paraffin-embedded and frozen sections with sensitive peroxidase-antiperoxidase and avidin-biotin techniques is described. In addition ot the absence of staining for whole-stratum corneum keratin proteins, sections were negative for keratins of different molecular weights (45, 55, and 63 kilodaltons) that are characteristically present in mesothelial cells. Ultrastructurally, the cells most closely resembled mesenchymal cells of the fibroblastic type. These findings are in accordance with recent theories that relate the derivation of localized fibrous mesotheliomas to nonmesothelial cells, including subpleural connective tissue. Based on differences in immunohistochemical staining, the tumors appear to be unrelated to diffuse malignant mesotheliomas.
Kaposi's sarcoma frequently develops in patients with the acquired immunodeficiency syndrome (AIDS), and in most cases cutaneous lesions herald the disease. Although the lungs are often involved when the neoplasm becomes disseminated, it is rare for the initial diagnosis to be made by lung biopsy. This report describes two patients with AIDS in whom Kaposi's sarcoma was present in lung biopsy specimens and in whom there was no other systemic evidence of the neoplasm. Both patients experienced hemoptysis, and pulmonary hemorrhage accompanied the neoplasm in each case. Only five microscopic foci of tumor were found in a total of 44 sections of lung examined. The focal distribution of the lesions in the pulmonary interstitium and the presence of coexisting lung disease posed problems in the evaluation of the biopsies. Awareness of the appearances of Kaposi's sarcoma in lung tissue is important because the neoplasm will probably be encountered in lung biopsies with increasing frequency as more cases of AIDS are discovered.
The lungs of 17 homosexual males who died of the acquired immune deficiency syndrome were studied to determine the type and extent of pulmonary disease present at autopsy. All patients had two or more pathologic processes, including one or more infections in their lungs. Cytomegalovirus pneumonia was the most common pulmonary infection identified at autopsy (15 patients) but was documented morphologically rarely during life (two patients). Most patients with Pneumocystis pneumonia had recurrent or persistent pneumocystosis. Although some of these individuals had evidence of early interstitial fibrosis, others showed complete resolution of the pulmonary changes. Diffuse alveolar damage was observed in 12 patients, and cytomegalovirus and/or Pneumocystis carinii was a likely etiologic agent in each instance. Mycobacterium avium-intracellulare infection was identified in four patients but was not associated with significant pulmonary alterations. Kaposi's sarcoma was found in the lungs of six patients. Early pulmonary involvement appeared as interstitial infiltrates with progression to nodular tumor masses obliterating the underlying lung. Pulmonary hemorrhage was an important complication of Kaposi's sarcoma involving the lung.
Gastrointestinal cytomegalovirus (CMV) infection usually occurs in immunosuppressed patients and has recently been reported in patients with the acquired immune deficiency syndrome (AIDS). Serological evidence of CMV infection and a variety of traumatic and infectious gastrointestinal disorders are known to occur in nonimmunosuppressed homosexual males. However, the significance of gastrointestinal CMV infection in nonimmunosuppressed homosexual males is not well known. Three unusual cases of gastrointestinal CMV infection in homosexual males are presented. Infection of a Kock pouch in one patient and an anal ulcer in another, occurred as part of a CMV mononucleosis syndrome. In the third patient, CMV was found in an acutely inflamed appendix. Although gastrointestinal CMV infection has been reported frequently in patients with AIDS, our patients showed no evidence of immunosuppression or AIDS 6 wk to 1 year later. Gastrointestinal CMV infection in homosexual males with gastrointestinal disease should not be considered indicative of AIDS.
Profiles of immunohistochemical staining for different molecular weight keratin proteins (45, 46, 55, and 63 kilodalton (kd] were evaluated in basal and squamous cell carcinomas of the skin and surrounding epidermis. Basal cell carcinomas predominantly stained with antisera to low molecular weight keratins (45 and 46 kd). Staining with antisera to higher molecular weight keratins (55 and 63 kd) was focal and restricted to areas of squamous differentiation. Invasive squamous cell carcinomas in addition to staining with antisera to low molecular weight keratins (45 and 46 kd) showed diffuse staining for 55-kd keratin and foci of staining for 63-kd keratin most prominent in keratinized regions of the tumors. In situ squamous cell carcinomas (Bowen's disease) differed from invasive squamous cell carcinoma in showing increased staining for high molecular weight keratin (63 kd). Abnormal keratin profiles were identified adjacent to and overlying basal and squamous cell carcinomas, with antisera to low molecular weight keratins (45 and 46 kd) staining all layers of the epidermis, and decreased intensity of staining for high molecular weight keratin (63 kd). Keratin profiles may help define abnormal squamous maturation in epidermis adjacent to tumors. Immunohistochemical staining for different molecular weight keratin proteins may also be helpful in the differential diagnosis of skin lesions.
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In this immunohistochemical study, antiserums to different molecular weight keratin proteins (45kd, 46kd, 55kd, and 63kd) were utilized to determine the profiles of keratin proteins present in a variety of pulmonary neoplasms. Different histologic types of lung carcinoma exhibited different patterns of keratin staining. Squamous cell carcinomas stained strongly for 45K, 46K, and 55K keratin, with staining for 63K restricted to areas or individual cells with cytoplasmic keratinization. Adenocarcinomas showed variable, generally weak staining for 45K, 46K, and 55K keratin and were uniformly negative for 63K keratin both in frozen and paraffin sections. Mesotheliomas and reactive mesothelial cells, by contrast, stained positively for 63K keratin in addition to keratins of lower molecular weights. Differences in staining for 63K keratin between mesothelioma and adenocarcinoma may have diagnostic application. Moreover, individual cytokeratins may serve as markers of tumor differentiation and provide information as to the origin of neoplastic cells.
Involucrin is a precursor of the cross-linked envelope protein or marginal band present in human stratum corneum. This study uses immunohistochemical techniques for localization of involucrin in histologic sections from 91 lung tumors in order to evaluate the usefulness of involucrin as a tumor marker in lung neoplasms. Although involucrin is absent from bronchial epithelium, it is expressed in cultured tracheal epithelial cell colonies and in bronchial mucosa with squamous metaplasia. Involucrin was present in all 25 cases of squamous and adenosquamous carcinoma. Staining was focal in 12 cases of squamous cell carcinoma and was most marked in the larger neoplastic cells in the center of squamous cell nests. Only two of 20 cases of adenocarcinoma revealed focal staining for involucrin, and these cases may represent adenosquamous variants. Six of 12 cases of large cell undifferentiated carcinoma stained for involucrin, indicating squamous differentiation, and seven cases of malignant mesothelioma were negative. Isolated involucrin-positive cells were present in two of 16 cases of small cell anaplastic carcinoma and one of 11 carcinoid tumors, identifying variants of neuroendocrine tumors with dual differentiation. Patterns of localization of involucrin in paraffin and frozen sections were compared with staining for cytokeratins in parallel sections. Immunohistochemical localization of involucrin comprises a specific marker for squamous differentiation in lung tumors.
Acute pulmonary disease is a major complication of immunodeficiency, and it has become increasingly important with the expanded use of immunosuppressive drugs. When routine clinical evaluation fails to identify a specific etiologic agent, a morphologic diagnosis is pursued by means of one or more invasive procedures. Interpretation of the material obtained by these procedures poses a challenge to pathologists. In this paper, the important histopathologic patterns of pulmonary disease likely to be encountered in this setting are reviewed, with emphasis on differential diagnosis. In addition, various diagnostic techniques are discussed and compared, with regard to interpretation of findings and diagnostic yields.
The histogenesis of adenomatoid tumors has been a source of controversy. Although most investigators favor a mesothelial derivation, recent ultrastructural evidence suggests that some adenomatoid tumors may be vascular neoplasms. This study reports the pattern of staining of seven adenomatoid tumors with antisera to keratin, factor VIII, and carcinoembryonic antigen (CEA), using an immunoperoxidase technique. All the tumors revealed strong cytoplasmic staining for keratin with no staining for factor VIII (an endothelial cell marker) or CEA. An identical staining pattern was evident in normal and reactive mesothelial cells. These findings support a mesothelial rather than an endothelial derivation for the tumors studied.
Many causes for the adult respiratory distress syndrome (ARDS) have been reported, all with common pathologic, pathophysiologic and biochemical end results. The final common pathway may involve changes in lung content of a critical enzyme, superoxide dismutase, or alterations in surfactant metabolism, or both. The early assumption that the disorder is partially due to oxygen toxicity from inspired oxygen concentrations greater than 60 percent is consistent with findings of recent biochemical studies. Although the lung normally maintains its alveoli dry, during ARDS increased permeability of small pulmonary vessels results in primary pulmonary edema, in contrast to edema from increased vascular pressure. These data have been obtained mainly in animals; whether they apply to humans with ARDS is not certain. Tissue oxygenation is improved by increasing end-expiratory pressure in an animal model of ARDS, more effectively during spontaneous breathing than during mechanical ventilation. During spontaneous breathing, adverse ventilatory effects were caused by stimulation of pulmonary reflexes.