Amyloidosis is a protein conformational disorder in which amyloid fibrils accumulate in the extracellular space and induce organ dysfunction. Recently, two different amyloidogenic proteins, transthyretin (TTR) and apolipoprotein A-I (Apo A-I), were identified in amyloid deposits in knee joints in patients with knee osteoarthritis (OA). However, clinicopathological differences related to those two kinds of amyloid deposits in the knee joint remain to be clarified. Here, we investigated the clinicopathological features related to these knee amyloid deposits associated with knee OA and the biochemical characteristics of the amyloid deposits. We found that all of our patients with knee OA had amyloid deposits in the knee joints, especially in the meniscus, and those deposits were primarily derived from TTR and/or Apo A-I. Some patients with knee OA, however, had unclassified amyloid deposits. One of our interesting observations concerned the different effects of aging on each type of amyloid formed. The frequency of formation of ATTR deposits clearly increased with age, but that of AApo A-I deposits decreased. Furthermore, we found that ∼16% of patients with knee OA developed ATTR/AApo A-I double deposits in the meniscus. Amyloid deposition may therefore be a common histopathological feature associated with knee OA. Also, aging may induce ATTR formation in the knee joint in elderly patients with knee OA, whereas AApo A-I formation may be inversely correlated with age.
Mycobacterium kansasii, an atypical Mycobacterium, may cause serious illness in humans. Wedescribe a M. kansasii infection of the foot joint, which was diagnosed in a 46-year-old womanwith systemic lupus erythematosus. The diagnosis was based on a positive culture from degenerative tissue and histological diagnosis of a synovium. Wereviewed the literature regarding M. kansasii infection of the joint, bone, and periarticular structures focusing on the complication of rheumatic diseases.
SA 96 (N-(2-mercapto-2-methylpropanoyl)-L-cysteine) is a new sulfhydryl compound having a relatively similar chemical structure to Tiopronin and D-penicillamine. An open trial of SA 96 treatment (300 mg/day after meals for 16 weeks) was carried out in 11 patients with definite or classical rheumatoid arthritis and with therapeutic failure of previous gold salts and/or D-penicillamine therapy. Two cases were withdrawn from the trial, because of a side effect (hepatitis) in one patient and an unrelated illness in another. The results in the 9 patients completing the trial demonstrated statistically significant improvement in the clinical and laboratory measurements. A marked abatement of disease activity was noted in 5 of 9 patients who did not benefit from, or suffered a relapse during previous chrysotherapy and in 1 of 5 patients without benefit, or with relapse following previous D-penicillamine treatment. Among 4 patients who had discontinued D-penicillamine because of its intolerable cutaneous side effects, 3 patients completed the trial, with favourable results. The results of this trial seem to indicate that SA 96 is possibly of value as a slow-acting antirheumatic drug in some patients with therapeutic failure of gold salts or D-penicillamine.
A cross-sectional, retrospective computerized analysis of risk factors for anterior atlantoaxial subluxation (AAS) was performed. Logistic regression performed on the clinical variables involved in 145 cases of rheumatoid arthritis (RA) disclosed a high joint score index and a low blood haemoglobin level as significant independent risk factors. This means that the development of anterior AAS is connected with widespread RA. Linear multiple regression analysis showed an association between the extent of anterior AAS in millimetres and the spread of erosions of the dens of axis and negative correlation with the severity of vertical atlantoaxial dislocation (VD). This suggests that whereas the presence of anterior AAS is connected with the severity of the systemic disease, its actual extent is associated with signs of local involvement, other than severe VD. The duration or cumulative dosage of glucocorticoids were not associated with the development or extent of anterior AAS, nor with the severity of vertical dislocation. This suggests that low dose glucocorticoid treatment is not involved with the development of rheumatoid changes in the upper cervical spine. It should be borne in mind, of course, that although no correlation was found, a causal relation cannot be excluded.
We reviewed ten patients with seronegative spondylarthropathy (SNSA), who all fulfilled the European Spondylarthropathy Study Group criteria for spondylarthropathy (SpA); seven patients also met the Amor criteria for SpA. Seronegative spondylarthropathy was not a uniform syndrome but rather a wide spectrum of complex disease with characteristics of sacroiliitis and enthesopathy. The most frequent symptom at diagnosis of SNSA was inflammatory low back pain, followed by asymmetric oligoarthralgia and Achilles tendonitis and/or plantar fasciitis. Systemic complications were revealed as eye and skin involvement. Imaging methods including pelvic radiography, scintigraphy, and computed tomography scanning were useful in detecting spondylarthropathic changes, which were characteristic of SNSA. Human leukocyte antigen (HLA) typing showed various patterns among patients, in which HLA-B27 was positive in three patients with ankylosing spondylitis. HLA-B51, which is a well-known genetic factor associated with Behçet's disease (BD), was positive in two patients who were apparently distinct from BD. Two patients with palmoplantar pustulosis showed symptoms and signs characteristic of SNSA. Although we have few SNSA patients in the present study, we would like to propose that HLA-B51 positive SpA would be considered as a subset of SNSA, and that pustulotic SpA also would be classified as a member of SNSA. This led us to suggest the possibility to change the concept of SNSA proposed by Moll et al. The optimal treatment remains to be defined, but sulfasalazine was effectively used with almost all patients in combination with nonsteroidal anti-inflammatory drugs.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.