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PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. I. Hutchinson-Horton arteritis].

Temporal arteritis (also known as Horton's or giant cell arteritis) is a panarteritis of the large and medium-calibre cranial vessels. An account is given of its epidemiological, clinical and anatomopathological aspects and its involvement of the locomotor apparatus (Horton's rheumatism). Reference is also made to the close relationship between temporal arteritis and pulseless disease. Some workers are of the opinion that they share the same aetiology, and that their clinical expression in different areas is dictated by age and constitutional factors.

5'-Nucleotidase↗
PubMed1995

Non-giant cell arteritis of the temporal artery presenting as the polymyalgia rheumatica-temporal arteritis syndrome.

We describe a heterogeneous group of 4 elderly patients with atypical vasculitis of the temporal artery who presented clinically with the polymyalgia rheumatica-temporal arteritis syndrome. The first had apparently isolated eosinophilic necrotizing vasculitis without peripheral blood eosinophilia, history of asthma, or pulmonary vasculitis (so called limited form of Churg-Strauss syndrome). Temporal artery biopsy in the 2nd patient revealed small vessel necrotizing vasculitis in the fragment of skeletal muscle surrounding a normal temporal artery (i.e., negative for giant cell arteritis, GCA). This patient subsequently developed rheumatoid polysynovitis. The temporal artery biopsies in the remaining 2 patients showed vasa vasorum vasculitis, without GCA, associated with malignancy in Patient 3 and as an unexpected and apparently isolated finding in Patient 4. All 4 patients responded to the standard corticosteroid therapy for giant cell temporal arteritis. Unusual temporal artery biopsies such as these should be interpreted in relation to clinical findings.

Adrenal Cortex Hormones↗
PubMed1983

[Giant cell arteritis: temporal arteritis, rheumatic polymyalgia].

Fourteen patients have been diagnosed for Giant Cell Arteritis by temporal biopsy or clinical criteria in the last five years. Two of them started with atypical symptoms. Polymyalgia Rheumatica was the commonest symptom (71%). Two patients (14%) had an irreversible blindness in eye one. Histologic changes of arteritis were shown by temporal biopsy in 8 cases, one of which had no cranial manifestations. A raised ESR was a constant finding (100%) followed by a alpha-2 globulin increase (93%) and anaemia (57%). One patient had rare complication of this disease: an aortic arch syndrome. The whole group responded well to the treatment.

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PubMed1994

Fatal myocardial infarction resulting from coronary arteritis in a patient with polymyalgia rheumatica and biopsy-proved temporal arteritis. A case report and review of the literature.

Giant cell arteritis is frequently an attendant complication of polymyalgia rheumatica. While involvement of other arterial beds is occasionally identified, this syndrome is most frequently recognized when symptomatic involvement of the temporal arteries occurs. We describe such a patient who despite initial treatment with high-dose intravenous and standard (5-day) orally administered corticosteroid therapy suffered a fatal myocardial infarction, which at autopsy was shown to be a consequence of granulomatous coronary arteritis. The literature is reviewed and the clinical implications of this case are discussed.

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PubMed1981

Giant cell arteritis (temporal arteritis) presenting as fever of undetermined origin.

A retrospective study of the histories of 100 patients with biopsy-proven giant cell arteritis was performed. Fifteen of these patients had "fever of unknown origin" as the initial manifestation of this disease. All 15 had normal leukocyte counts; however, they had significantly lower hemoglobulin and albumin levels (P greater than 0.01) and significantly higher platelet counts, erythrocyte sedimentation rates, and alkaline phosphatase values (P congruent to 0.05) compared to the other 85 patients. In 4 patients, random temporal artery biopsies were performed despite persistently negative results from diagnostic evaluations and in the absence of any symptoms or findings suggestive of arteritis.

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PubMed1996

Takayasu arteritis--five doctors in the history of Takayasu arteritis.

Takayasu arteritis is a chronic vasculitis mainly involving the aorta, its main branches, pulmonary and coronary arteries. Recent international survey has made clear different sex ratio, different involvement and different clinical manifestations among countries. At the same time, ethnic distribution of this morbid condition has focused on the role of genetic factors and the mechanisms inducing vasculitis. In this paper, five doctors who contributed in history to the elucidation of Takayasu arteritis were introduced as an aid in understanding recent studies on this morbid condition.

Eponyms↗
PubMed2003

Cutaneous arteritis presenting with hyperpigmented macules: macular arteritis.

Macular arteritis is a novel form of cutaneous arteritis in which the primary lesion is a hyperpigmented macule. Traditional stigmata of cutaneous vasculitis such as palpable purpura and erythematous nodules are not present. The disease is asymptomatic and appears to follow an indolent course. Systemic involvement has not been observed.

Adolescent↗
PubMed1979

Experimental candida-induced arteritis in mice. Relation to arteritis in the mucocutaneous lymph node syndrome.

An extract of Candida albicans isolated from a patient with typical mucocutaneous lymph node syndrome (MCLS) can produce coronary arteritis in a mouse when injected intraperitoneally. An unusual feature of this arteritis is that it is granulomatous, shows no fibrinoid change and is confined to the coronary arteries. These characteristics are quite similar to those found in patients with MCLS.

Animals↗
PubMed1978

A concept of diffuse actinic arteritis. The role of actinic damage to elastin in 'age change' and arteritis of the temporal artery and in polymyalgia rheumatica.

Actinic damage (actinic elastosis) affecting the internal elastic lamina appears to be the prime cause of 'age change' and arteritis of the temporal artery. Resorption and removal of altered elastin (elastolysis) is an integral part of the pathology of actinic damage. Actinic irradiation is probably responsible for the destruction and disappearance of a vast number of arterioles in elastotic skin. The intimate connection between temporal arteritis and polymyalgia rheumatica prompts the belief that the vascular and other internal malign components of the temporal arteritis/polymyalgia rheumatica syndrome might likewise be due, albeit indirectly, to the same actinic cause. Actinic elastotic damage at the body surface could have this effect by provoking a state of systemic elastolysis. Although ultraviolet (uv) light is often regarded as the sole cause of actinic elastosis, penetrating infrared (heat) irradiation may deserve a large or even a dominant share of the blame.

Adult↗
PubMed1993

Menière's syndrome: an atypical presentation of giant cell arteritis (temporal arteritis).

The authors discuss three patients with biopsy-proven giant cell arteritis (GCA) who experienced significant auditory and vestibular symptoms. Two of the patients who presented with audiovestibular symptomatology died as a direct result of GCA affecting the vertebral arteries. Postmortem findings are reported. This report illustrates the importance of maintaining a high index of suspicion of GCA in elderly patients who present with the acute onset of audio-vestibular symptoms. These symptoms can be a herald of brain stem infarction if giant cell arteritis is the underlying cause. High-dose prednisone and rheumatologic/neurologic consultation is required.

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PubMed1991

[Multi-infarct dementia in giant cell arteritis (temporal arteritis)].

Dementia is an infrequent and little known manifestation of giant cell arteritis or temporal arteritis (GCA-TA). The cases of 2 women with histologically proven GCA-TA are presented in which, together with the most classical symptoms, they presented a brusque mental deterioration on initiation of the disease. One patient developed a severe irreversible dementia which coincided with a rapid reduction in the doses of corticoids; while the other patient demonstrated improvement in cognitive function with steroid treatment and control of the disease. Magnetic resonance studies revealed multiple areas of infarction in both hemispheres in the two patients. The importance of treating multi-infarct dementia is underlined in the context of GCA-TA with high doses of corticoids. It is also emphasized that GCA-TA should be considered in the evaluation of older patients with mental alterations.

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PubMed1978

Giant cell arteritis-a systemic spectrum including temporal arteritis and polymyalgia rheumatica.

Polymyalgia rheumatica and giant cell arteritis are closely associated disorders that may pose serious threats to the elderly. While the etiological factors remain unknown, these clinical entities may represent different expressions of a common disorder. Recent evidence suggests that autoimmunological involvement of the internal elastic lamina of the large and medium-sized arteries might play an importent role in pathogenesis. Genetic and environmental factors may also contribute. Polymyalgia rheumatica and giant cell arteritis have subtle and protean manifestations and formes frustes occur, contributing to delays in diagnosis unless the clinician holds a high index of suspicion while treating the elderly. The sequelae, including generalized disability, blindness, myocardial and cerebrovascular catastrophies can probably be avoided by timely and prudent use of corticosteroids. These are not uncommon disorders are among the most amenable to treatment of the rheumatological diseases. Family physicians must be diligent in their efforts to diagnose these disorders since early generalized and focal signs and symptoms frequently precede the catastrophic events.

Adrenal Cortex Hormones↗
PubMedDate not supplied

A genetic approach to the aetiology of giant cell arteritis: depletion of the CD8+ T-lymphocyte subset in relatives of patients with polymyalgia rheumatica and arteritis temporalis.

OBJECTIVE: To investigate the CD8+ T-cell concentrations in first degree relatives of patients with giant cell arteritis (GCA) in order to evaluate whether the low CD8+ T-cell values found in most patients with GCA are acquired or hereditary. METHODS: Probands were 5 patients with arteritis temporalis (TA) and 15 with polymyalgia rheumatica (PMR). Forty of 60 available relatives participated in the study. They were all interviewed concerning signs of previous illness. A blood sample screening was performed, including IgM-RF and ANA on Hep-2 cells. Age- and sex-matched controls consisted of 29 persons with no history of inflammatory or malignant diseases. Measurements of the T-lymphocyte subsets CD3+, CD4+ and CD8+ were made after Ficoll-Hypaque separation. RESULTS: Healthy relatives disclosed a significantly decreased CD8+ percentage in their peripheral blood compared with controls. The median CD8+% in relatives was 17% (C1 95% 15-20%) and in controls it was 23% (C1 95% 20-28%). Twelve relatives had a decreased concentration of CD8+ T-cells and 10 showed an elevated CD4+/CD8+ ratio. Two relatives had GCA and 3 had rheumatoid arthritis (RA). In one family 3 healthy siblings participated and showed extremely low CD8+ percentages (2.5%, 6.5%, 3.4%) and absolute values (0.042, 0.102, 0.035 x 10(9)/l) CONCLUSION: TA, PMR and RA are frequently (12.5%) found in the first degree relatives of patients with GCA. The finding of extremely low CD8+ T-cell values in completely healthy relatives indicates that the CD8+ T-cell depletion seen in patients with GCA is a hereditary characteristic.

Antibodies, Antinuclear↗
PubMed1996

Female genital tract giant cell arteritis associated with occult temporal arteritis.

Giant cell arteritis (GCA) of the female genital tract has been described as an incidental finding, but associated temporal arteritis (TA) has been rarely reported. We describe a case of female genital tract GCA associated with occult giant cell TA, which in the absence of cranial symptoms was confirmed by a random temporal artery biopsy. The patient remains asymptomatic at 12 month followup after treatment with prednisolone and azathioprine.

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PubMed2001

Phylogenetic characterisation of the G(L) sequences of equine arteritis virus isolated from semen of asymptomatic stallions and fatal cases of equine viral arteritis in Denmark.

The study describes for the first time the phylogenetic relationship between equine arteritis virus (EAV) isolated from asymptomatic virus-shedding stallions and fatal cases of equine viral arteritis (EVA) in an European country. EAV was isolated from three dead foals and an aborted foetus during three different outbreaks of EVA. From these fatalities, the complete open reading frame 5, encoding the EAV G(L) protein, was amplified by reverse transcription-polymerase chain reaction and subjected to nucleotide sequence analysis. Furthermore, DNA sequences were obtained from virus isolated from semen samples of seven virus-shedding, but clinically healthy, Danish stallions. DNA sequence alignment revealed an overall divergence of 0-14 and 0-10% at the nucleotide and amino acid levels, respectively. Phylogenetic analysis including 24 previously published sequences revealed that European as well as North American "types" of EAV were present in the semen of asymptomatic carrier stallions and in fatal cases of EVA. Our results reveal that the presence of EAV-shedding stallions in Denmark represents a potential source of severe EVA.

Amino Acid Sequence↗
PubMed1999

Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis.

An imported carrier stallion (A) from Europe was implicated in causing an extensive outbreak of equine viral arteritis (EVA) on a Warmblood breeding farm in Pennsylvania, USA. Strains of equine arteritis virus (EAV) present in the semen of two carrier stallions (A and G) on the farm were compared to those in tissues of foals born during the outbreak, as well as viruses present in the semen of two other stallions that became persistently infected carriers of EAV following infection during the outbreak. The 2822 bp segment encompassing ORFs 2-7 (nt 9807-12628; which encode the G(S), GP3, GP4, G(L), M and N proteins, respectively) was directly amplified by RT-PCR from semen samples and foal tissues. Nucleotide and phylogenetic analyses confirmed that virus present in the semen of stallion A initiated the outbreak. The genomes of viruses present in most foal tissues (10/11) and serum from an acutely infected mare collected during the outbreak were identical to that of virus present in the lung of the first foal that died of EVA. Virus in the placenta of one foal differed by one nucleotide (99.9% identity) from the predominant outbreak virus. The relative genetic stability of viruses that circulated during the outbreak contrasts markedly with the heterogeneous virus populations variously present in the semen of persistently infected stallions on the farm. These findings are consistent with the hypothesis that the carrier stallion can be a source of genetic diversity of EAV, and that outbreaks of EVA can be initiated by the horizontal aerosol transmission of specific viral variants that occur in the semen of particular carrier stallions.

Amino Acid Sequence↗
PubMed1989

A population-based case-control study of temporal arteritis: evidence for an association between temporal arteritis and degenerative vascular disease?

The first population-based incident case-control study of temporal arteritis (TA) in the US was conducted using the unique data resources of the Rochester Epidemiology Project. During the period 1950-1985, 88 newly diagnosed cases of biopsy-proven TA were identified among residents of Olmsted County, Minnesota. Cases were each matched to four Olmsted County community controls on age, sex and duration of community medical record. Odds ratios (OR) were calculated for marital status, education, Quetelet index, pregnancy, age at menopause, thyroid disease, diabetes, smoking, hypertension, angina, myocardial infarction, peripheral vascular disease, and stroke. Multivariable conditional logistic regression analysis identified statistically significant adjusted OR for smoking (2.3, 95% CI = 1.3-4.1). Elevated ORs which were not statistically significant were noted for angina, myocardial infarction, and peripheral vascular disease. These data suggest that TA and arteriosclerosis may share a common causal pathway. Alternatively, histopathological misclassification of temporal artery biopsies may have resulted in the observed association. Due to the limited power of this population-based study, multicentre collaboration should be encouraged to more precisely define the epidemiology of TA.

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