Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors established an easy fluorescent microscopy method to measure the ratio of CD4 (helper/inducer T lymphocytes) to CD8 (suppressor/cytotoxic T lymphocytes) (CD4/CD8 ratio) in bronchoalveolar lavage fluid (BALF) in patients with diffuse pulmonary diseases and measles pneumonia. The CD4/CD8 ratio determined by this method strongly correlated with the CD4/CD8 ratio obtained by flow cytometry in both peripheral blood lymphocytes and BALF lymphocytes. When the proportion of lymphocytes in BALF nuclear cells is more than 6%, the CD4/CD8 ratio in BALF was measurable. The CD4/CD8 ratio in peripheral blood was not significantly different among hypersensitive pneumonitis (HP), sarcoidosis (SAR), collagen vascular disease (CVD), idiopathic interstitial pneumonitis (IIP), and measles pneumonia (MP). However, the BALF CD4/CD8 ratio was 0.61 +/- 0.37 in HP, 6.83 +/- 2.73 in SAR, 0.77 +/- 0.40 in CVD, 1.49 +/- 0.29 in IIP. These results were consistent with previously published data. The CD4/CD8 ratio in patients with MP was as low as 0.39 +/- 0.34. In patients with summer type HP, this ratio was low in the acute phase, but became within normal range after moving or reconstructing their homes, accompanied with the improvement of subjective symptoms and the disappearance of inflammation. These data indicate that our method is very simple and useful in the diagnosis and the monitoring of diffuse pulmonary diseases.
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PMID:[Establishment of a simple fluorescent microscopy method for measurement of the CD4/CD8 ratio in BALF]. 212 Apr 96

A clinico-pathological study was done to elucidate characteristic features of subacute interstitial pneumonia. The patients were four men and mine women, with a mean age of 60 years. In ten patients, the disease was idiopathic, three had collagen vascular disease, (and one was undergoing gold therapy for rheumatoid arthritis). The time interval between onset of symptoms and open lung biopsy was 80 +/- 40 days. Eleven patients had progressive dyspnea, seven had coughing, and only one complained of fever. Fine crakles were heard in ten patients. Mild increases in CRP were observed in all cases. Mild increases in total serum IgG concentration were observed in five of eight cases. Multiple patchy infiltration or diffuse interstitial shadows, located predominantly in the lower fields of both lungs were the characteristic chest roentgenographic findings. The average %VC was 62.7 +/- 17% and the average PaO2 was 68.3 +/- 10 Torr. Bronchoalveolar lavage was done in nine patients, and the mean total cell count was 16.5 +/- 10.2 x 10(4)/ml. A moderate increase in lymphocytes (30.8 +/- 18.6%) with a low CD4/8 ratio (0.48 +/- 0.57), a mild increase in neutrophils (6.2 +/- 9.1%), and a mild increase in eosinophils (2.3 +/- 3.7%) were observed. Pathologically, interstitial cellulo-fibrous changes associated with alveolar space closure due to organization of exudate were the main features. Patients were given steroid pulse therapy or oral steroids. The results were mild to marked improvements in chest roentgenographic findings and lung function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical features of subacute interstitial pneumonia--clinico-pathological study based on open lung biopsy findings]. 756 95

In a prospective study of 101 patients with HIV infection and a medium CD4 lymphocyte cell count of 350 x 10(6)/l and a retrospective study of the records of 79 AIDS patients, we compared the first ocular symptoms in HIV-infected patients to the CD4 count. In Walter-Reed stages 2-4 (n = 101) we found sicca syndrome in 9.2%, in 52% lens opacities in the cortex and only in less than 1% HIV-related angiopathy of the retina. In Walter Reed stages 5-6 (n = 79), 26% of the AIDS patients developed CMV retinitis, 33% HIV angiopathy of the retina and only 1% retinal toxoplasmosis. The average CD4 lymphocyte cell count was never better than 100 x 10(6). Lens opacities in HIV-infected patients could be an early ophthalmological symptom of HIV infection.
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PMID:[Ophthalmologic manifestations in early and late stages of AIDS]. 781 2

Endothelin-1 is a recently identified cytokine with potent vasoconstrictor activity which is associated with various diseases involving blood vessels. HIV-1 related retinal microangiopathic syndrome is a frequent finding in patients with AIDS or AIDS-related complex, presenting predominantly with retinal cotton-wool spots. We investigated 55 HIV-1 infected patients by ophthalmoscopy and for endothelin-1 immunoreactivity in plasma and an additional 76 HIV-1 infected patients only for endothelin-1 levels. For reference values 13 age-matched healthy subjects were studied. In 18 of 55 patients (33%) investigated ophthalmoscopically we found evidence of microangiopathic syndrome. Overall, the mean endothelin-1 immunoreactivity in plasma of HIV-1 infected patients was significantly elevated as compared to controls (4.28 +/- 3.62 versus 2.72 +/- 0.67 fmol/ml, P < 0.0001). HIV-1 infected patients with retinal microangiopathic syndrome had significantly higher plasma levels of endothelin-1 immunoreactivity (4.59 +/- 1.38 fmol/ml) compared to HIV-1 infected patients without microangiopathic syndrome (3.18 +/- 1.64 fmol/ml, P = 0.003). Correlation analysis revealed that endothelin-1 immunoreactivity in plasma had no significant association with disease progression, CD4 cell count, beta 2-microglobulin, neopterin, or age. Endothelin-1 immunoreactivity in plasma was correlated exclusively with retinal microangiopathic syndrome in one or both eyes (r = 0.45, P = 0.0006) and with the number of cotton-wool spots (r = 0.50, P = 0.0001). In conclusion, HIV-1 related retinal microangiopathic syndrome is associated with elevated plasma levels of endothelin-1. By virtue of its potent vasoconstrictor activity endothelin-1 may be involved in the pathogenesis of HIV-1 related vascular disease.
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PMID:Endothelin-1 immunoreactivity in plasma is elevated in HIV-1 infected patients with retinal microangiopathic syndrome. 804 76

A number of pathological and clinical data suggest that AIDS could be an underestimated cause of cerebro-vascular disease, especially in young individuals. Eight retrospective cases of stroke in AIDS patients are reported. Mean age was 39 years, mean CD4 cells count 57/mm3. Pathogenic mechanism, particularly the role of opportunistic infections remains unclear. Prognosis does not seem constantly pejorative: only one patient died from stroke, six are still alive with a 6 months follow-up, without relapse and with minor or no sequellae. Alcohol or cocaine (crack) abuse was present in half the cases. The role of specific risk factors and consequently adapted prophylaxis is questionned.
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PMID:[Cerebrovascular accidents and AIDS]. 876 7

Several necropsy reports have suggested that cerebral vascular disease (CVD) is more frequent in HIV positive patients than in HIV negative individuals of the same age, although clinical signs are rare. We describe three patients for whom CVD was the clinical manifestation that led to diagnoses of HIV infection. The patients were two men and a woman aged 29, 52 and 66, respectively, with differing risk factors for CVD: smoking (3), blood hypertension (2), endocarditis (1) and free protein S deficiency (1). The risk factors for HIV infection were also different. The CVD diagnoses were confirmed by computed tomography, which revealed lacunar infarction in two cases with favorable outcomes and embolia-like infarction with subarachnoid hemorrhage in the third patient, who died a few days later. CD4 levels varied (50, 130 and 689/mm3). Our observations lead us to the following conclusions: 1) CVD can be a first clinical manifestation of HIV infection and the disease that allows seropositivity to be diagnosed. Although CVD usually presents in advanced stages of HIV infection, it can also occur in seropositive patients who do not meet the criteria for AIDS. 2) The classical risk factors for vascular disease probably play a dominant role in the etiology of CVD in such patients, alongside systemic complications related to the virus; the direct role of HIV remains to be determined. 3) AIDS should be considered and ruled out in patients with CVD who are at risk for HIV infection, even in older patients with vascular risk factors.
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PMID:[Cerebrovascular disease as a form of presentation of HIV infection]. 900 48

In this article, we describe pulmonary hypertension in two men (31 and 43 years of age) with human immunodeficiency virus (HIV) infection who were examined at Mayo Clinic Rochester. Among 88 reported cases (including the two current ones) of HIV- or acquired immunodeficiency syndrome (AIDS)-associated pulmonary hypertension, 61% were male; the age range was 2 to 56 years (mean, 32). Dyspnea was the usual initial symptom. Of the 74 patients in whom pulmonary artery pressure was recorded or calculated by echocardiography, systolic pressures ranged from 49 to 118 mm Hg (mean, 68). Of the 33 cases in which lung tissue was evaluated microscopically, 28 (85%) were of the plexogenic variant of pulmonary arterial hypertension. Of the other five cases examined histologically, three consisted of thrombotic pulmonary arteriopathy (one was due to recurrent thromboembolism, and the other two were due to in situ thrombosis), and two were of pulmonary venoocclusive disease. No correlation existed between either CD4 counts or a history of pulmonary infections and the development of pulmonary hypertension. In 15 of the 88 patients (17%), confounding factors for hypertensive pulmonary vascular disease were present, including coexisting liver disease in 13 and coagulation abnormalities in 2. In 83% of the patients, the development of pulmonary hypertension seems to have been related primarily to the chronic HIV infection. Pulmonary hypertension was more rapidly progressive in patients with HIV or AIDS than in those with primary pulmonary hypertension; the reported time intervals between onset of symptoms and diagnosis were 6 months and 30 months, respectively. The 1-year survival rate for patients with HIV and pulmonary hypertension was 51%, based on the follow-up data compiled from the 63 patients in whom it was described; this compares with a 1-year survival rate of 68% for patients with primary pulmonary hypertension. Death was considered a direct consequence of pulmonary hypertension in 29 (76%) of the 38 fatal cases.
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PMID:Human immunodeficiency virus infection and pulmonary hypertension: two new cases and a review of 86 reported cases. 944 76

Cellular immune processes may trigger the development of graft vascular disease (GVD). CD4 and CD8 cytotoxic T lymphocytes that infiltrate the allograft could play a role in the development of GVD. We studied the presence of in vivo primed or committed CTL (cCTL) and their avidity for donor HLA class I and class II antigens in graft-infiltrating lymphocyte cultures propagated from endomyocardial biopsies derived from patients with and without signs of GVD. The fraction of cCTL with high avidity for HLA class I or class II antigens was estimated by the addition of anti-CD8 or anti-CD4 MoAbs to the cytotoxic phase of the limiting dilution analysis. In the first year after transplantation no difference in the frequency of donor-specific class I cCTL between patients with and without GVD was found. Addition of anti-CD8 MoAb revealed that most cultures predominantly consisted of cCTL with low avidity for donor HLA class I antigens, irrespective of the development of GVD at 1 year after transplantation. However, in patients who did not develop GVD, the frequency of cCTL with donor HLA class II specificity was significantly higher than in patients who did develop GVD. The avidity for donor HLA class II antigens was comparable in both groups. A high frequency of donor-specific cCTL for HLA class II antigens seems to be a protective factor against the development of GVD. These cCTL might be cytotoxic for cells involved in GVD development, e.g. activated endothelium and smooth muscle cells of donor origin.
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PMID:The frequency and avidity of committed cytotoxic T lymphocytes (cCTL) for donor HLA class I and class II antigens and their relation with graft vascular disease. 952 97

To investigate the effect of IL-4 deletion on cardiac allograft survival, vascularized BALB/c cardiac allografts were placed in C57BL/6, 129Sv x C57BL/6 (IL-4 +/+) or 129Sv x C57BL/6 IL-4 knockout mice (IL-4-/-). Untreated recipients rejected allografts in < 15 days while isografts survived indefinitely (> 100 days). Treatment with anti-CD4 (GK1.5) for 4 days at the time of allografting increased mean survival to > 100 days in C57BL/6, 90+/-16 days in 129Sv x C57BL/6 (IL-4 +/+) and 68 +/- 36 days in 129Sv x C57BL/6 (IL-4-/-) recipients. Although there was a trend towards shorter survival times in the IL-4-/- mAb-treated mice, survival in the three recipient groups was not significantly different (P = 0.07). A 30-day course of anti-CD4 did not further prolong BALB/c heart survival. All long-surviving hearts had histological evidence of parenchymal damage and transplant vascular disease. None of these recipients developed antigen-specific tolerance, since both donor and third party skin graft challenges were rejected when challenged at > 60 days post-graft and all primary grafts failed by 120 days. Thus the effects of IL-4 deletion were subtle and were seen only with low doses of immunosuppression in this high responder strain combination.
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PMID:Effect of IL-4 deletion on cardiac allograft survival in the BALB/c to 129Sv x C57BL/6 strain combination. 989 36

The study was designed to compare second heart and skin grafts and in vitro assays as a means of assessing peripheral tolerance in C57BL/6 mice. Vascularized heterotopic BALB/c hearts were placed in C57BL/6 recipients treated with anti-CD4, GK1.5 (1 mg total per 20 g mouse i.p. on days 0, 1, 2, 3). Those mice in which hearts survived for >60 days were challenged with donor and third-party (CBA) skin grafts or with second heart grafts, of donor or third-party origin, attached to the carotid artery and jugular vein. In vitro alloreactivity was assessed by mixed lymphocyte reactions (MLR) and cell mediated lympholysis (CML) using recipient spleen cells. Parenchymal damage, cellular infiltration and vascular disease were assessed from the histology of long-term allografts and isografts. Allografts in untreated recipients were rapidly rejected while isografts survived > 100 days. Primary allografts in anti-CD4 treated recipients also survived > 100 days, as did donor strain secondary heart transplants given at >60 days after the first graft. Third-party hearts were rapidly rejected, as were donor and third-party skin grafts placed on recipients with long-term allografts. These recipients showed low MLR response to both donor and third-party stimulators and donor-specific suppression of CML at 60 days post graft. Long-surviving heart allografts all showed evidence of parenchymal damage and vascular intimal thickening. Thus in the BALB/c to C57BL/6 donor-recipient strain combination, hearts, but not skin grafts, could be used to demonstrate peripheral tolerance, which seemed to be both organ and major histocompatibility complex (MHC) specific. Despite long survival, BALB/c hearts all showed evidence of parenchymal damage and vascular intimal thickening, a sign of chronic rejection.
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PMID:Assessment of peripheral tolerance in anti-CD4 treated C57BL/6 mouse heart transplants recipients. 1037 76


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