Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Impaired fibrinolysis may contribute to development of adult respiratory distress syndrome (ARDS). Pathologic increases in endogenous plasminogen activator inhibitor (PAI-1) may blunt normal fibrinolysis and unmask alternate fibrinolytic mechanisms, such as elastase-induced fibrin degradation. We measured PAI-1 and elastase-induced fibrin(ogen) degradation products in 69 critically ill patients in our medical intensive care unit (MICU) and in nine healthy volunteers. Factor VIII-related antigen protein (VIII:Ag), a reported marker of acute lung injury, and alpha-1-protease inhibitor (alpha-1-PI), an acute phase reactant, were also measured. MICU patients included 24 control patients with no known risk of ARDS, 35 patients with risk factors for ARDS including sepsis, pneumonia, aspiration, and shock, and 12 patients with ARDS including two patients from at-risk groups who developed ARDS. Plasma PAI-1 was determined by chromogenic assay, elastase-induced peptides by a new radioimmunoassay, VIII:Ag by immunoelectrophoresis, and alpha-1-PI by immunodiffusion. When compared to normal volunteers, MICU control patients had elevated PAI-1, VIII:Ag, elastase-induced peptides, and alpha-1-PI. Patients with ARDS had significantly higher PAI-1 and VIII:Ag than did MICU control patients; elastase-induced peptides and alpha-1-PI were not higher. However, at-risk patients who did not develop ARDS also had high PAI-1 or VIII:Ag. Although these data cannot refute the possible role of these compounds in the pathogenesis of ARDS, they demonstrate that PAI-1 and VIII:Ag may be elevated in many critically ill patients but may not be useful markers for the subsequent development of ARDS.
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PMID:Fibrinolysis in critically ill patients. 250 87

A 17-year-old girl was operated for a solitary well-circumscribed pulmonary parenchymal tumor and reoperated ten times for multiple recurrent similar pulmonary tumors during 24 years. Histologic examination revealed the so-called intravascular bronchioloalveolar tumor (IVBAT) in all instances. The patient died from pneumonia superimposed on decreased respiratory function 24 years after the onset of disease. This is the longest survival so far reported in IVBAT. The treatment was surgical in all phases of the disease, and the patient did not receive radiotherapy or cytostatic drug therapy. Mediastinal and pleural tumor nodules were removed 17 years from the first pulmonary operation, and 24 years after the first operation a fibrous tumor was removed from the retroperitoneal space. Immunohistologically, the tumor cells were positive for vimentin-type of intermediate filaments, in line with their mesenchymal nature. Endothelial markers, Factor VIII-related antigen and Ulex europaeus I lectin binding, were not found in convincingly neoplastic cells, and Schwann cell, epithelial cell, muscle cell, and histiocytic markers were absent. Thus, IVBAT appears to be a low-grade malignant mesenchymal neoplasm, composed of poorly differentiated mesenchymal cells, whose exact nature remains undefined with the currently used cell-type markers.
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PMID:Intravascular bronchioloalveolar tumor. 311 50

A 61-year-old women developed progressive neurologic deficits and died with pneumonia and septicemia. An autopsy demonstrated the characteristic intravascular and focal perivascular infiltrate of malignant angioendotheliomatosis (MAE) throughout the body but concentrated in the central nervous system and skin. Ultrastructurally, the neoplastic cells lacked evidence of endothelial differentiation. Immunohistochemical studies showed focal staining for Factor VIII-related antigen, probably on a nonspecific basis, negative staining for Ulex europaeus I lectin (an endothelial cell marker), and intense staining for leukocyte common antigen. The authors' observations provide evidence that at least some examples of MAE are unusual, angiotropic lymphoid neoplasms.
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PMID:Malignant angioendotheliomatosis. An angiotropic lymphoma? 315 8

In search for an index of endothelial injury that would provide an early diagnosis of radiation pneumonitis, we investigated the plasma levels of von Willebrand Factor (Factor VIII Related Antigen, FVIII:RAg) in 14 patients undergoing pulmonary irradiation. This study was based on observations indicating that damage to the endothelium-rich pulmonary parenchyma may produce alterations in the synthesis, storage or release of FVIII:RAg, detectable in plasma. There was no correlation between FVIII:RAg levels and radiation pneumonitis, radiation dose, volume of irradiated lung, tumor burden, or time-interval between exposure and sampling. The heterogeneity of the neoplasms and the inconstant effects of radiation in the tumor vasculature are among several variables that may explain this lack of correlation. The plasma levels of FVIII:RAg cannot be used to diagnose or predict radiation pneumonitis.
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PMID:Von Willebrand factor levels do not predict or diagnose radiation pneumonitis. 348 36

High grade malignant non-Hodgkin's lymphoma (NHL) was the presenting manifestation of the acquired immunodeficiency syndrome (AIDS) in 3/81 reported cases of AIDS in Denmark (by April 2, 1986). Asymptomatic HIV infection, 1 and 5 yr prior to the onset of lymphoma, was documented in 2 cases. 1 patient became infected by Factor VIII treatment, 2 were male homosexuals. 2 patients had an uncommon tumour presentation in the oral cavity, 1 patient presented with an abdominal mass. The histologic subtypes were immunoblastic (2), and small noncleaved cell, Burkitt's (1). Helper/suppressor T-cell ratio was decreased at onset of lymphoma in 2 cases. All 3 patients have died, 4, 6, and 24 months after diagnosis of NHL. Only 1 patient died of NHL, 1 died of an unclassified pneumonia and the third developed progressing supranuclear HIV-associated polyneuropathy without evidence of CNS lymphoma. Thus, high grade malignant B-cell NHL is a regular initial manifestation of AIDS, and may develop after years of asymptomatic HIV infection.
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PMID:Human immunodeficiency virus (HIV) associated non-Hodgkin's lymphomas in Denmark: report of three cases. 365 75

The occurrence during the last 2 years of 29 cases of AIDS in hemophiliacs (21 in USA and 8 in Europe) suggests possible transmission of this disease by blood products. All these patients had received Factor VIII or IX concentrates and developed pneumocystis carinii pneumonia or other opportunistic infections. Kaposi's sarcoma was not observed in any patient. Recent studies have focused on the frequency of AIDS-related complex in hemophiliacs, which may arise as a crucial problem. However this does not justify at the moment any reduction in the substitutive treatment of hemophiliac patients unless new clues to the understanding of these disorders are provided. Therefore, it is mostly important to clearly define, through research programs and precise follow-up of patients, blood products which can be used safely in hemophiliacs.
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PMID:[Acquired immunodeficiency syndrome and related syndromes in hemophiliacs: status throughout the world]. 643 70

(1) Background: The current outbreak of COVID-19 infection is an ongoing challenge and a major threat to public health that requires surveillance, prompt diagnosis, as well as research efforts to understand the viral pathogenesis. Despite this, to date, very few studies have been performed concerning autoptic specimens. Therefore, this study aimed: (i) to reiterate the importance of the autoptic examination, the only method able to precisely define the cause of death; (ii) to provide a complete post-mortem histological and immunohistochemical investigation pattern capable of diagnosing death from COVID-19 infection. (2) Methods: In this paper, the lung examination of two subjects who died from COVID-19 are discussed, comparing the obtained data with those of the control, a newborn who died from pneumonia in the same pandemic period. (3) Results: The results of the present study suggest that COVID-19 infection can cause different forms of acute respiratory distress syndrome (ARDS), due to diffuse alveolar damage and diffuse endothelial damage. Nevertheless, different patterns of cellular and cytokine expression are associated with anti-COVID-19 antibody positivity, compared to the control case. Moreover, in both case studies, it is interesting to note that COVID-19, ACE2 and FVIII positivity was detected in the same fields. (4) Conclusions: COVID-19 infection has been initially classified as exclusively interstitial pneumonia with varying degrees of severity. Subsequently, vascular biomarkers showed that it can also be considered a vascular disease. The data on Factor VIII discussed in this paper, although preliminary and limited in number, seem to suggest that the thrombogenicity of Sars-CoV2 infection might be linked to widespread endothelial damage. In this way, it would be very important to investigate the pro-coagulative substrate both in all subjects who died and in COVID-19 survivors. This is because it may be hypothesized that the different patterns with which the pathology is expressed could depend on different individual susceptibility to infection or a different personal genetic-clinical background. In light of these findings, it would be important to perform more post-mortem investigations in order to clarify all aspects of the vascular hypothesis in the COVID-19 infection.
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PMID:Preliminary Post-Mortem COVID-19 Evidence of Endothelial Injury and Factor VIII Hyperexpression. 3278 26