Are evidence-based guidelines being followed for the monitoring of ocular toxicity of hydroxychloroquine? A nationwide survey of practice amongst consultant rheumatologists and implications for clinical governance.
(33/221)
OBJECTIVE: To determine whether consultant rheumatologists monitor the ocular toxicity of hydroxychloroquine according to standards set by national guidelines. METHOD: An observational cross-sectional questionnaire study of all consultant rheumatologists in the UK was undertaken. The main outcome measure was the proportion of rheumatologists who practise in compliance with nationally set standards. RESULTS: A wide variation in practice was found. Nearly half the respondents did not assess either baseline visual symptoms or visual acuity, and 3% undertook infrequent visual monitoring at intervals of longer than 1 yr. At least a quarter of rheumatologists within the survey routinely referred patients to ophthalmology, either for baseline visual screening or for regular visual monitoring. Such use of ophthalmology services was outside the recommendations of the guidelines and would suggest that these referrals were unnecessary. No differences in monitoring practices were ascertained between respondents from district general and teaching hospitals. CONCLUSION: The present study shows that nationally set guidelines for the monitoring of ocular toxicity of hydroxychloroquine are not consistently followed by rheumatologists with regard to baseline assessment, referral to ophthalmology and frequency of monitoring. Clinical guidelines aim to reduce variations in practice and to promote uniform and consistent best practice. The present study demonstrates a lack of conformity to national guidelines in respect of the monitoring of ocular toxicity of hydroxychloroquine. Clinical governance provides a framework for assuring quality in health care. The implications of this study for clinical governance would include understanding why barriers to the use of guidelines might occur and how they might be overcome, risk management, accounting for the reasonableness of a decision for positive divergence and audit. (+info)
How aggressive should initial therapy for rheumatoid arthritis be? Factors associated with response to 'non-aggressive' DMARD treatment and perspective from a 2-yr open label trial.
(34/221)
OBJECTIVE: To determine what baseline factors might be associated with response to an initial mild treatment regimen in patients with early rheumatoid arthritis (RA). METHODS: Open label 2-yr study of 111 consecutive patients with early RA of duration less than 1 yr. None of the patients had previously received disease-modifying anti-rheumatic drugs (DMARDs). All patients were assigned to receive hydroxychloroquine (HCQ) at enrollment, and could also take non-steroidal anti-inflammatory drugs (NSAIDs) and prednisone. At any point during follow-up, patients not fulfilling the American College of Rheumatology (ACR) 50 criteria for improvement and/or who were taking prednisone > 10 mg/day were considered treatment failures and therapy changed to methotrexate (MTX), 7.5-20 mg/week. Clinical, laboratory and immunogenetic factors potentially predictive of treatment assignment at month 24 were evaluated. RESULTS: After 24 months of follow-up, a majority of patients (56/94) were either still on solo DMARD therapy with HCQ (n = 49) or off DMARD therapy with controlled/quiescent disease (n = 4), and 38 patients were taking MTX (including 11 in combination with other DMARDs). At month 24, all but 9 patients met ACR50 criteria for treatment response. Features present at enrollment which were predictors of MTX therapy at month 24 were high pain score, baseline rheumatoid factor titre > 1:40, higher number of swollen joints, and poor patient global assessment. The presence of HLA-C7xx at enrollment was also predictive of need for MTX therapy. CONCLUSIONS: This study suggests that even milder treatment with HCQ is greatly beneficial in patients with early RA. There continue to be very few consistently reliable predictors of treatment needs in patients with this disease. (+info)
A good response to early DMARD treatment of patients with rheumatoid arthritis in the first year predicts remission during follow up.
(35/221)
OBJECTIVE: To describe the frequency and duration of remission in the Utrecht rheumatoid arthritis cohort of patients followed since diagnosis, and the clinical and treatment characteristics of patients with remission v those without. METHODS: In 1990 the Utrecht rheumatoid arthritis cohort study group started a clinical trial in which patients with recent onset of rheumatoid arthritis (<1 year) were randomised into four treatment groups: hydroxychloroquine (n = 169); intramuscular gold (n = 163); methotrexate (n = 166); and pyramid (n = 64). After two years, rheumatologists were allowed to prescribe any disease modifying antirheumatic drug. Remission was defined as: duration of morning stiffness < or =15 min, mean VAS pain < or =10 mm, Thompson joint score < or =10, and ESR < or =30 mm/h during at least six months. Cox regression analysis was used to determine baseline clinical, demographic, and treatment predictors of remission. RESULTS: Mean follow up duration was 62 months. Thirty six per cent achieved at least one period of remission. Median duration between diagnosis and the first remission period was 15 months for the intramuscular gold group, 18 months for the methotrexate and hydroxychloroquine groups, and 24 months for the pyramid group (NS). Predictors of remission were early response to initial treatment, less pain, rheumatoid factor negativity, and lower joint score at baseline. CONCLUSIONS: After a mean follow up duration of 62 months, only 36% of the patients had fulfilled the remission criteria at least once. A good response to treatment during the first year seems to be independently associated with remission rather than initial treatment alone. (+info)
Rheumatoid arthritis: more aggressive approach improves outlook.
(36/221)
As recently as 10 years ago, many patients with rheumatoid arthritis would receive only a nonsteroidal anti-inflammatory drug and low-dose corticosteroids until damage to their joints was documented. Now, despite risks of toxicity and adverse effects, a disease-modifying antirheumatic drug such as methotrexate is given as early as possible to retard disease progression and help prevent new erosions. Other agents can be added to or used in place of methotrexate, such as a biologic response modifier that regulates the proinflammatory cytokine tumor necrosis factor-alpha. (+info)
Streptococcal toxic shock syndrome and sepsis manifesting in a patient with chronic rheumatoid arthritis.
(37/221)
Streptococcal-toxic-shock syndrome is caused by virulent strains of exotoxin-producing streptococcus, almost always group-A organisms such as Streptococcus pyogenes. It has often been described in the setting of surgical wounds, burns, childbirth, diabetics, elderly, neonates, and immunocompromised hosts, where the portal of entry is the skin. Our patient was on steroids and nonsteroidal anti-inflammatory drugs for chronic rheumatoid arthritis and developed this deadly infection after a fall. (+info)
Cutaneus pseudolymphoma: a case report.
(38/221)
The authors report on a case of pseudolymphoma cutis in a 48-year-old man. The clinical and histopathological characteristics of this benign skin disorder, especially regarding the differential diagnosis with cutaneous B or T cell lymphomas, are reviewed. Finally, the use of hydroxychloroquine sulfate is suggested for the therapy of pseudolymphoma cutis, especially when the causal factor is unknown. (+info)
Kikuchi-Fujimoto disease: hydroxychloroquine as a treatment.
(39/221)
We describe a case of recurrent Kikuchi's disease in a South Asian-American man that was treated successfully with chloroquine and on recurrence with hydroxychloroquine. Each treatment led to a very prompt response. (+info)
Hydroxychloroquine therapy in patients with primary Sjogren's syndrome may improve salivary gland hypofunction by inhibition of glandular cholinesterase.
(40/221)
OBJECTIVE: To determine whether (i) cholinesterase activity is increased in the saliva of patients with primary Sjogren's syndrome (pSS), (ii) increased levels of cholinesterase of lymphocyte origin could interfere with the secretory activity of submandibular acinar cells, and (iii) hydroxychloroquine at therapeutic doses could interfere with cholinesterase activity. METHODS: The Ellman method was used to determine the levels of salivary cholinesterase activity and the K(i) of both chloroquine and hydroxychloroquine for serum cholinesterase. The ability of lymphocyte cholinesterase to inhibit the acetylcholine (ACh)-evoked rise in [Ca(2+)](i) in mouse submandibular acinar cells was determined using fura-2 microfluorimetry. RESULTS: Patients with pSS had significantly higher levels of cholinesterase activity in both their unstimulated (P < 0.05) and stimulated saliva (P < 0.0001) compared with control subjects. Lymphocyte cholinesterase was capable of inhibiting the ACh-evoked rise in [Ca(2+)](i). The in vitro K(i) for hydroxychloroquine inhibition of cholinesterase was 0.38 +/- 1.4 microM. CONCLUSION: These data suggest that increased levels of cholinesterase present in the salivary glands of patients with pSS may contribute to glandular hypofunction and provide evidence that the therapeutic enhancement of salivary secretion in patients with pSS by hydroxychloroquine may be mediated by inhibition of glandular cholinesterase activity, although further in vivo investigation is needed. (+info)