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

The clinical syndrome of polymyalgia rheumatica is reviewed. The relationship of this disease with temporal arteritis is discussed, and I consider both syndromes have a pathological basis of generalised giant cell arteritis.Seven cases of polymyalgia and four cases of temporal arteritis were recorded during the six-year period (1969-1975) in one general practice.The outlines of management are discussed, with a plea for earlier recognition of the syndromes of polymyalgia rheumatica and temporal arteritis in general practice.
J R Coll Gen Pract 1976 May
PMID:Giant cell arteritis in general practice. 0 44

The nucleotide sequence of the spc determinant of the Staphylococcus aureus transposon Tn554 has been determined. This gene encodes a spectinomycin adenyltransferase, AAD(9), that mediates resistance to spectinomycin but not to streptomycin. The sequence predicts a 260 amino acid protein of molecular weight 28,943. A spectinomycin-sensitive mutant (spc-1) contains a G----A transition resulting in substitution of threonine (ACA) for alanine (GCA) at residue 165. The predicted amino acid sequence is 36% homologous to that of a widely distributed, gram-negative streptomycin/spectinomycin adenyltransferase, AAD(3") (9), specified by the aadA determinant (Holingshead and Vapnek 1985).
Mol Gen Genet 1985
PMID:Nucleotide sequence of a spectinomycin adenyltransferase AAD(9) determinant from Staphylococcus aureus and its relationship to AAD(3") (9). 299 13

The nucleotide sequences of the recessive dnaQ49 and the dominant mutD5 mutator were determined. The dnaQ49 mutator has a single base substitution in the dnaQ gene, thus causing one amino acid change, 96Val (GTG)----Gly (GGG), in the DnaQ protein (epsilon subunit of DNA polymerase III holoenzyme). The mutD5 mutator possesses two base substitutions in the same gene, resulting in two amino acid changes, 73Leu (TTG)----Trp (TGG) and 164Ala (GCA)----Val (GTA), which were designated the mutD52 and mutD51 mutations, respectively. Construction of chimaeric genes carrying one or two of these mutations revealed: either mutD51 or mutD52 alone causes the dominant mutator phenotype when present in a multi-copy plasmid; mutator phenotype when present in a low-copy plasmid; the dominant mutD51 mutator activity is suppressed by the dnaQ49 mutation when both mutations are present in the same gene. Based on these findings, we devised a model for the action of these mutators.
Mol Gen Genet 1986 Oct
PMID:Structure and function of dnaQ and mutD mutators of Escherichia coli. 354 May 31

This five-year study of 108 patients with giant cell arteritis and/or polymyalgia rheumatica drawn from all departments of a district general hospital emphasizes the difficulties of diagnosis. A correct diagnosis was made by the referring doctor in 33 per cent of patients and on initial attendance at hospital in 67 per cent of patients. Symptoms were present for more than three months before referral to hospital in 39 per cent of patients, and the delay before diagnosis at hospital was greater than one month in 20 per cent. Systemic illness (present in 83 per cent of cases), anaemia (33 per cent), elevated alkaline phosphatase (73 per cent) and raised immunoglobulin levels (48 per cent) caused diagnostic problems in 28 patients at primary care level and in 23 patients at hospital.
J R Coll Gen Pract 1981 May
PMID:Polymyalgia rheumatica and giant cell arteritis--a difficult diagnosis. 731 Jul 59

Giant cell arteritis, also known as temporal arteritis, is a vasculitis of unknown etiology that classically involves the wall of the large to medium size. We are reporting a case of a young onset temporal arteritis presenting with gastrointestinal symptoms. The patient was a 48-year-old male who presented with a 2-week history of fever, diffuse abdominal pain, and malaise. He underwent a laparoscopic cholecystectomy after findings of elevated bilirubin and alkaline phosphatase as well as suspicion of porcelain gallbladder on ultrasound (or computed tomography scan). The patient subsequently developed painless, intermittent vision loss and unilateral headaches. A work-up included temporal artery biopsy, which showed marked lymphocytic infiltrate in the arterial wall consistent with temporal arteritis. The presentation of temporal arteritis may be atypical. We are reporting a case of temporal arteritis at a young age presenting mainly with gastrointestinal symptoms.
J Gen Intern Med 2006 Jul
PMID:Temporal arteritis presenting with gastrointestinal symptoms in a middle aged man. 1680 62

Temporal arteritis is a disease of older individuals that manifests with variable signs, symptoms, and pain in the head and jaw. This disease should be considered in the differential diagnosis if the dentist encounters a patient with puzzling complaints that are not explained by oral and physical findings.
Gen Dent
PMID:Temporal arteritis: don't let this disease fool you. 1733 68

Giant cell arteritis predominantly affects cranial arteries and rarely involves other sites. We report a patient who presented with small bowel obstruction because of infarction from mesenteric giant cell arteritis. She had an unusual cause of her obstruction and a rare manifestation of giant cell arteritis. In spite of aggressive therapy with steroids, she died a month later because of multiple complications. We discuss the diagnosis and management of small bowel obstruction and differential diagnosis of vasculitis of the gastrointestinal tract. We were able to find 11 cases of bowel involvement with giant cell arteritis in the English literature. This case report illustrates that giant cell arteritis can be a cause of small bowel obstruction and bowel infarction. In the proper clinical setting, vasculitides need to be considered early in the differential diagnosis when therapy may be most effective.
J Gen Intern Med 2007 Jan
PMID:Giant cell arteritis presenting as small bowel infarction. 1735 55

Polyarteritis nodosa is a rare necrotizing vasculitis that can be progressive and fatal, and its initial presenting symptom may be leg claudication due to peripheral vascular ischemia. To date, there have been fewer than ten case reports of polyarteritis nodosa presenting as peripheral vascular disease. We report a case of a 38-year-old man initially diagnosed to have premature peripheral vascular disease who presented 1 year later with symptoms consistent with giant cell arteritis and subsequently developed bowel ischemia leading to a fatal outcome. Based on the autopsy and the patient's clinical course, the final diagnosis was polyarteritis nodosa. This case illustrates the challenges in diagnosing polyarteritis nodosa and the importance of considering vasculitis in young patients presenting with atypical presentations of diseases such as peripheral vascular disease or giant cell arteritis.
J Gen Intern Med 2008 Sep
PMID:A case of polyarteritis nodosa presenting initially as peripheral vascular disease. 1883 Jul 68

Fever of unknown origin (FUO) presents a diagnostic challenge. Giant cell arteritis (GCA) may present with FUO and this entity should be included in the differential of elderly patients who present with constitutional symptoms. While a temporal artery biopsy is considered the gold standard for the diagnosis of GCA, a subset of patients with large vessel involvement by GCA may have a negative temporal artery biopsy and no cranial symptoms. We present a 79 year-old woman with FUO and negative temporal artery biopsies in whom diagnosis of GCA was delayed. Further imaging with CT-angiogram and positron emission tomography/computed tomography (PET/CT) scan showed diffuse extensive active vasculitis. The above case underscores the value of imaging studies in the evaluation of patients with FUO from occult large vessel vasculitis.
J Gen Intern Med 2009 Apr
PMID:Delayed diagnosis of biopsy-negative giant cell arteritis presenting as fever of unknown origin. 1922 91

The function of the hepatitis E virus (HEV) open reading frame 3 (ORF3) protein remains unclear. To elucidate the role of the ORF3 protein in the virus life cycle, an infectious cDNA clone (pJE03-1760F/wt) that can replicate efficiently in PLC/PRF/5 and A549 cells and release progeny into the culture medium was used to generate a derivative ORF3-deficient (DeltaORF3) mutant whose third in-frame AUG codon of ORF3 was mutated to GCA. The DeltaORF3 mutant in the culture medium of mutant RNA-transfected PLC/PRF/5 cells was able to infect and replicate within PLC/PRF/5 and A549 cells as efficiently as the wild-type pJE03-1760F/wt virus. However, less than 1/100 of the number of progeny was detectable in the culture medium of DeltaORF3 mutant-infected PLC/PRF/5 cells compared with wild-type-infected PLC/PRF/5 cells, and the HEV RNA level in the culture medium of DeltaORF3 mutant-infected A549 cells was below or near the limit of detection. An immunocapture PCR assay revealed that the ORF3 protein is present on the surface of cell-culture-generated wild-type HEV but not on the DeltaORF3 mutant. Wild-type HEV in the culture supernatant peaked at a sucrose density of 1.15-1.16 g ml(-1), in contrast with the DeltaORF3 mutant in culture supernatant, which banded at 1.27-1.28 g ml(-1), similar to HEV in cell lysate and faecal HEV. These results suggest that the ORF3 protein is responsible for virion egress from infected cells and is present on the surface of released HEV particles, which may be associated with lipids.
J Gen Virol 2009 Aug
PMID:ORF3 protein of hepatitis E virus is essential for virion release from infected cells. 1933 79


1 2 Next >>