Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We recently reported that the gene for chloroplast tRNA(Cys)(GCA) is a pseudogene in the plastid DNA of Epifagus virginiana, a non-photosynthetic parasitic flowering plant in the family Orobanchaceae. Since this is the only tRNA(Cys) gene in the plastid genome, and since Epifagus appears to possess a functional plastid translational apparatus, it seems probable that nuclear-encoded tRNAs are imported into plastids to effect translation. In this study we have surveyed species closely related to Epifagus to establish how widespread the loss of this tRNA gene has been. We find that Conopholis americana, another non-photosynthetic parasite, lacks the gene altogether, but that seven closely-related photosynthetic plants (both parasitic and free-living) maintain an intact chloroplast tRNA(Cys) gene. Thus, the tRNA(Cys) gene appears to have become non-functional at the same time that photosynthetic ability was lost. This may be because the levels of putatively imported tRNAs are sufficient to meet the demands of plastid gene expression under nonphotosynthetic conditions only.
Curr Genet 1991 Dec
PMID:Lack of a functional plastid tRNA(Cys) gene is associated with loss of photosynthesis in a lineage of parasitic plants. 172 64

We compared 5 patients who had biopsy-proven temporal arteritis and erythrocyte sedimentation rates (ESR) less than 50 mm/hour with 25 patients who had temporal arteritis and high ESR and with 10 patients who had negative temporal artery biopsy results and low ESR. Patients with low-ESR temporal arteritis were similar to the other groups, except that they had a higher mean hemoglobin level than the high-ESR group and a significant increase in the percentage of patients (4 of 5) who had a previous diagnosis of polymyalgia rheumatica or had received steroid therapy compared with either of the other groups. The latter finding suggests that even low-dose steroid therapy can lower the ESR in patients with temporal arteritis. We conclude that the ESR is low in only a small percentage of patients with temporal arteritis, and that most of these patients have a history of polymyalgia rheumatica or steroid therapy.
Arthritis Rheum 1991 Dec
PMID:Temporal arteritis with low erythrocyte sedimentation rate: a review of five cases. 174 42

The possible role of the eosinophil and its cytotoxic granule proteins in the vascular lesions seen in temporal arteritis was elucidated. Sixteen sections of biopsy specimens from arteria temporalis showing giant cell arteritis were stained for eosinophil cationic protein (ECP) by polyclonal antibodies and the immunoperoxidase method. Activated eosinophils were identified by monoclonal antibodies linked to alkaline phosphatase. Activated eosinophils and secreted ECP were seen in all layers of the inflamed vessels and were most evident in necrotic lesions and thrombi. Only a small number of granulocytes seen in the adventitia were immunoreactive for cathepsin G, and no extracellular deposits of this neutrophil granule protein were seen. A few immunoreactive eosinophils were found in the adventitia in two of five negative temporal artery biopsy specimens from patients with polymyalgia rheumatica. All eight coronary artery biopsy specimens with atherosclerotic lesions showed no activated eosinophils or secreted ECP. These findings indicate that eosinophils are involved in the vascular lesion in temporal arteritis and suggest that cytotoxic eosinophil granule proteins may contribute to the necrotic lesions and the development of thrombi.
Ann Rheum Dis 1991 Dec
PMID:Deposition of eosinophil cationic protein in vascular lesions in temporal arteritis. 176 67

Polymyalgia rheumatica and temporal arteritis appear to be separate syndromes rather than two manifestations of an underlying giant cell arteritis. Polymyalgia rheumatica is a synovitis that may be persistent or recurrent, while temporal arteritis is almost always a single episode; documented recurrences are rare. The two syndromes frequently occur in the same patient although not necessarily at the same time and they may be separated by a long interval. In some patients with polymyalgia rheumatica, giant cell arteritis is found on biopsy of an asymptomatic temporal artery. The frequency of this concurrence is variable in different populations. It is high in Scandinavia, low in Israel and intermediate between these extremes in other populations that have been studied.
Baillieres Clin Rheumatol 1991 Dec
PMID:Relation of giant cell arteritis to polymyalgia rheumatica. 180 15

The results of investigations on the humoral immunological mechanisms are conflicting in giant cell arteritis (GCA) and have not been able to explain the pathological findings in the inflamed arterial wall. Altogether, immunological studies suggest that a cell-mediated immune reaction, possibly against an autologous antigen, occurs locally in the arteritic lesions of GCA. The excellent effect of treatment with glucocorticosteroids on the inflammation in GCA can also be explained by this model. The glucocorticosteroids inhibit the synthesis of interleukin-1 (IL-1) by the macrophages and suppress the IL-2 production from the T cells (Palacios, 1982). The observed HLA-DR expression in the arterial wall can be accounted for by the sum of macrophages and activated T cells, the macrophages being the most probable antigen-presenting cells. The interdigitating reticulum cells observed in some of the GCA patients may also be involved in antigen presentation. What the antigen(s) may be is, however, still unknown, as are the factors initiating the inflammatory process. It has recently been possible to extract T lymphocytes from the inflamed tissue and to culture these cells in vitro. After culture, it is possible to study the gene for the T-cell receptor, and probably even the antigenic specificity of the T cells. I hope that this approach may lead to a better understanding of the pathogenic mechanisms in GCA.
Baillieres Clin Rheumatol 1991 Dec
PMID:Immunological studies in giant cell arteritis. 180 18

The clinical features of GCA can be classified into: (1) the systemic manifestations of malaise, weight loss, fever, night sweats and depression; (2) the proximal muscle pain and stiffness of polymyalgia rheumatica; (3) arteritic manifestations of pain or tenderness due to local inflammation; and (4) arteritic manifestations of ischaemia due to narrowing or occlusion of vessels. These may occur singly or in any combination and may come and go with the passage of time. Thus GCA can result in many different clinical signs and symptoms. The feared ocular and cerebrovascular complications of the condition can be prevented by the early institution of corticosteroid treatment. Early diagnosis is therefore vital. This is a simple matter when GCA presents in the classical textbook manner, but in atypical cases diagnosis can be exceedingly difficult. The absence of a reliable way of excluding the disease means that diagnosis is often a clinical exercise. A sound knowledge of the many and varied clinical manifestations of GCA is therefore required if the physician is going to prevent the ocular and cerebrovascular complications of GCA by early diagnosis and treatment.
Baillieres Clin Rheumatol 1991 Dec
PMID:Clinical features of giant cell arteritis. 180 19

Giant cell arteritis (GCA) is an ophthalmic emergency because, if undetected or managed inadequately, there is a high risk of developing a painless, permanent blindness in one or both eyes; however, if it is quickly identified and treated urgently and aggressively, blindness is almost entirely preventable. The ocular manifestations of GCA are essentially ischaemic in nature, with blindness as the most dreaded complication. Blindness is usually due to anterior ischaemic optic neuropathy (AION) and occasionally to other causes, e.g. posterior ischaemic optic neuropathy or central retinal or cilioretinal artery occlusion, although extremely rarely it may be cortical in origin. Diplopia and other types of ophthalmoplegias are seen in some cases but are usually transient in nature. Ischaemic lesions of the anterior segment of the eye are also seen in a few cases. Diagnosis of arteritic AION is discussed at length. Finally, management of GCA from the point of view of visual loss is discussed in detail.
Baillieres Clin Rheumatol 1991 Dec
PMID:Ophthalmic features of giant cell arteritis. 180 20

The most useful investigation in supporting the clinical diagnosis of PMR/GCA is elevation of the ESR or viscosity. Acute phase proteins, particularly C-reactive protein, are also elevated but in most cases are not more helpful than the ESR in either diagnosis or follow-up. The definitive investigation is the demonstration of giant cell arteritis histologically, usually from temporal artery biopsy. The classical changes are internal elastic lamina fragmentation and destruction, with marked intimal thickening and an inflammatory infiltrate in the vessel wall with giant cells. Changes of healed arteritis can be distinguished from ageing changes and can therefore confirm the diagnosis. Positive biopsies are found in about 70% of patients with clinical GCA but are unlikely to be helpful in pure PMR. Elevation of alkaline phosphatase of liver origin is seen in one-third to half of patients with both PMR and GCA. Abnormal tracer uptake has been reported in radionuclide scans with a variety of non-specific abnormalities on liver biopsy. Promising developments include measurement of CD8+ lymphocytes and interleukins.
Baillieres Clin Rheumatol 1991 Dec
PMID:Laboratory investigations including liver in polymyalgia rheumatica/giant cell arteritis. 180 22

Corticosteroids control arteritis in GCA and suppress polymyalgic symptoms within days of starting treatment. PMR patients can be treated with approximately 15 mg prednisolone/day, reducing the dose to 7.5-10 mg by 8 weeks. GCA is normally controlled on 40 mg prednisolone/day, although patients with persistent visual symptoms may need 60-80 mg. Slow reduction to about 20 mg by 8 weeks should minimize relapses. For both PMR and GCA a maintenance dose of 7.5 mg after 6-9 months should be enough. Steroid withdrawal is possible within 2 years of starting treatment, although some will need 4 years or more. Relapse should be defined clinically; the ESR is the most useful laboratory parameter. Steroid side-effects can be minimized by using low doses of prednisolone whenever possible and azathioprine may be used as a steroid-sparing agent.
Baillieres Clin Rheumatol 1991 Dec
PMID:Treatment of polymyalgia rheumatica/giant cell arteritis. 180 23

Polymyalgia rheumatica and giant cell arteritis are amongst the most satisfying conditions for clinicians to diagnose and treat because the unpleasant effects and serious consequences of these conditions can be almost entirely prevented by corticosteroid treatment; the fact that the side-effects of this treatment sometimes seem to be more serious than the complications of the disease is an indication of its effectiveness. Unfortunately, there is no objective way of determining the prognosis in the individual, and decisions concerning duration of treatment remain empirical.
Baillieres Clin Rheumatol 1991 Dec
PMID:Prognosis of polymyalgia rheumatica and giant cell arteritis. 180 24


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