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Biomedical subjects

A C Keat

Publications and source records attributed to A C Keat.

At least 19 recordsLinked to original sources

Detection of Chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction.

In 1986, Chlamydia trachomatis elementary bodies were found by direct immunofluorescence (DIF) in synovial-fluid cell deposits and synovial-membrane biopsy samples from five of eight patients with sexually acquired reactive arthritis (SARA) but in none of eight controls with other types of arthritis. Cells from the original slides (stored at 4 degrees C) have now been examined by a polymerase chain reaction (PCR) that amplifies DNA for the major outer membrane protein of C trachomatis. Chlamydial DNA was found in samples from four DIF-positive patients, one DIF-negative patient, and one DIF-negative control. Overall, there was 80% concordance for DIF and PCR results. This study supports our previous finding of chlamydiae in joints in reactive arthritis.

Adult

Septic bone, joint and muscle lesions associated with human immunodeficiency virus infection.

Ten episodes of musculoskeletal sepsis have been seen in nine patients with HIV infection. Seven patients had AIDS, circulating CD4-positive lymphocyte counts being less than 0.1 x 10(9)/l in six. Septic arthritis recurred in seven patients, osteomyelitis in three and pyomyositis and bursitis each occurred in one patient. Staphylococcus aureus was isolated from four patients, atypical micro-organisms being found in three. Presentation of musculoskeletal infection in this patient group may be atypical but rapid diagnosis is important as early antimicrobial therapy is often successful.

Adult

Echocardiographic diastolic abnormalities of the left ventricle in inflammatory joint disease.

Echocardiographic early diastolic abnormalities have been shown recently in 50% of men with ankylosing spondylitis. Similar techniques were used to investigate subjects with rheumatoid arthritis and psoriatic arthritis with or without spondylitis. These subjects had no clinical, radiographic, or electrocardiographic evidence of cardiac or respiratory disease. Echocardiographic abnormalities seen resembled those of ankylosing spondylitis in that the interval between minimum left ventricular dimension and mitral valve opening was prolonged in 12 of 22 subjects with rheumatoid arthritis and in seven of 11 subjects with psoriatic arthritis. Isovolumic relaxation time was significantly prolonged in four subjects with rheumatoid arthritis and one with psoriatic arthritis. Unlike ankylosing spondylitis, however, there was consistent reduction in peak rate of left ventricular dimension increase in subjects with rheumatoid arthritis and psoriatic arthritis. In addition, the dimension increase during atrial systole was greater than normal in nine subjects with rheumatoid arthritis and two with psoriatic arthritis. The most likely cause of these abnormalities is increased connective tissue deposition in the myocardium.

Adult

Intra-articular chlamydial antigen and inflammatory arthritis.

Joint material from 133 patients with well-characterized inflammatory arthritis, including individuals likely to have suffered reactive arthritis, was studied. The majority of patients were also examined for the presence of genital tract infection with Chlamydia trachomatis. Fluorescein-conjugated monoclonal antibodies demonstrated the presence of C. trachomatis antigen in synovial fluid cell deposits or synovial sections from inflamed knee joints of seven patients with reactive arthritis. The significance of these findings is discussed, as is the low rate of detection of chlamydial antigen in either the genital tract or the joint from patients in this study. We emphasize the need for further work aimed at identifying the relevant immunogenic chlamydial antigens responsible for the initiation of reactive arthritis.

Adult

The detection of human immunodeficiency virus DNA in dendritic cells from the joints of patients with aseptic arthritis.

Three patients with inflammatory arthritis were found to be seropositive for human immunodeficiency virus (HIV). Two of these individuals developed synovitis following an episode of yersinia bowel infection. We have studied joint material from all three in an attempt to define the role that HIV may be playing in the aetiology or maintenance of arthritis. Cell-associated HIV DNA was detected within joint fluid by in situ hybridization and the phenotypes of infected cells were established using a double-labelling immunocytochemical technique. Viral DNA was detected in dendritic cells (4-25%) isolated from both the peripheral blood and synovial fluid and in occasional lymphocytes from peripheral blood (less than 0.1%). No infected macrophages were seen. Functional studies using the mixed leucocyte reaction showed that the dendritic cells from synovial fluid were poor stimulators of allogenic peripheral blood lymphocytes whilst being effective at stimulating autologous lymphocytes. In addition, synovial fluid lymphocytes responded poorly to normal control dendritic cells. Infection of these cells with HIV could be contributing to this low stimulatory activity of antigen-presenting cells and to the unresponsiveness of lymphocytes.

Adult

Chlamydial DNA is absent from the joints of patients with sexually acquired reactive arthritis.

The polymerase chain reaction was used to detect the presence of a plasmid essential for the growth of Chlamydia trachomatis. As few as 10 copies of the plasmid in the initial reaction mix were detectable using this technique. In contrast, chlamydial DNA was not detectable in the knee joints of nine patients with definite sexually acquired reactive arthritis (SARA) or nine patients with suspected SARA. Five patients with an undifferentiated seronegative lower limb oligoarthropathy, one with Crohn's disease and another with post-enteric reactive arthritis had evidence of intra-articular chlamydial antigens as judged by fluorescein-labelled monoclonal antibody staining of joint material but, again, no chlamydia plasmid DNA was detected. The nature of the immunofluorescent staining seen in some of these samples remains to be elucidated. It could be due to the presence of chlamydial outer membrane protein or lipopolysaccharide antigens in the joints, either free or in immune complexes, or it may be artefactual. Our results indicate that viable C. trachomatis is not present in the joints of the patients in this study even in the presence of chlamydial antigen detected by fluorescence antibody testing.

Arthritis, Infectious

Reiter's cramp.

We report the occurrence of writer's cramp in a 31 year old B27 positive man with a recent past history of Reiter's syndrome. Although aware of the close linguistic relation between the pen and the penis, we have not previously encountered the two diseases in a single patient.

Adult

Gonococcal arthritis caused by auxotype P in a man with HIV infection.

The development of gonococcal arthritis is reported in a man with HIV infection and CDC Stage IVC2 disease. The diagnosis of disseminated Neisseria gonorrhoeae was facilitated by microbiological examination of a joint aspirate. The auxotype identified by culture was moderately resistant to penicillin, a characteristic which is highly unusual for an organism causing disseminated gonococcal infection. This case serves as an example of the role of HIV infection in the modification of host response to common pathogens and the need for clinicians to modify their management of disseminated gonococcal infection especially in immunosuppressed persons.

Adult

Follow-up study of ankylosing spondylitis over a period of 12 years (1977-1989).

A follow-up study was performed on 256 patients with ankylosing spondylitis. HLA-B27-negative Dutch patients very rarely had classical idiopathic ankylosing spondylitis. Most of these patients had psoriasis or inflammatory bowel disease or they were foreigners living in The Netherlands. Many of the B27-negative patients only have sacroiliitis. Psoriasis or inflammatory bowel disease among the HLA-B27-positive with a classical ankylosing spondylitis is rare.

Female

Rheumatological lesions in individuals with human immunodeficiency virus infection.

One hundred and twenty-three patients with human immunodeficiency virus infection have been referred to rheumatologists at our hospitals between October 1985 and April 1989 because of musculoskeletal symptoms. Thirty-four homosexual men presented with acute, peripheral, non-erosive arthritis (mean number of four joints affected) with the knees being involved in 23. Other features developing concurrently with arthritis included psoriasis, keratoderma blenorrhagica, plantar fasciitis, urethritis, conjunctivitis and anterior uveitis. Four of five patients investigated were HLA-B27-positive; none of 15 patients tested had raised titres of rheumatoid or antinuclear factors. Various infections were associated with the onset of arthritis and two patients with a recent history of diarrhoea had serological evidence of yersinia infection. No micro-organisms were identified within the joint except for HIV itself. At the time of onset of arthritis four of these individuals had the acquired immunodeficiency syndrome (AIDS); 11 were not known to be HIV-positive before testing which was performed following referral for arthritis. Six patients have since developed AIDS and four have died. In 15 individuals, including those who progressed to AIDS, joint symptoms have been severe, persistent and poorly responsive to non-steroidal anti-inflammatory drugs. In only five patients has the arthritis been known to resolve. Synovitis has also been seen in two women: in one of these HIV infection was thought to have been acquired through intravenous drug abuse. Other rheumatic lesions included myalgia/myositis, non-inflammatory peripheral arthritis, spinal pain, soft tissue lesions, arthralgia or myalgia of unknown cause and infective lesions including septic arthritis and bony infection due to histoplasmosis and atypical mycobacterial infection. It appears likely that HIV infection is a risk factor for the development of seronegative arthritis and other rheumatic lesions.

Acquired Immunodeficiency Syndrome

Inflammatory joint disease and human immunodeficiency virus infection.

Nine men positive for antibody to human immunodeficiency virus (HIV) who developed peripheral, non-erosive arthritis were followed up. The clinical features were compatible with reactive arthritis but were atypical in several respects: the joint symptoms were generally severe, persistent, and unresponsive to non-steroidal anti-inflammatory drugs. The onset of arthritis was associated with various infections, none of which are known to be associated with the development of reactive arthritis. HLA typing was performed for three patients, all of whom were positive for HLA-B27. HIV was isolated from the synovial fluid of one patient. No patient had AIDS before developing arthritis, but four progressed to having AIDS after a mean of 7.5 months, and two died. Arthritis resolved in only one patient. The possibility of HIV infection should be considered in all patients with conditions suggesting reactive arthritis. Synovitis in patients with severe immunodeficiency has important pathogenetic implications.

Anti-Inflammatory Agents, Non-Steroidal