Bone In Systemic Lupus Erythematosus Research Articles

Non-corticosteroid risk factors of symptomatic avascular necrosis of bone in systemic lupus erythematosus: A retrospective case-control study

Objective. Avascular necrosis of bone (AVN) is an important complication of systemic lupus erythematosus (SLE). Corticosteroid therapy has been underlined as a main risk factor for osteonecrosis. However, AVN development in patients who have never received corticosteroid and the absence of AVN in the majority of the patients, who received corticosteroid, propose a role for non-corticosteroid risk factors in AVN development.Methods. This case-control study included two subsets: oral corticosteroid (66 AVN and 248 non-AVN patients) and pulse-therapy subset (39 AVN and 312 non-AVN patients) who have attended our Lupus clinic from 1979 to 2009. Patients received similar cumulative dose corticosteroid, equal maximum dose and 1-year maximum dose of corticosteroid. The demographic data (including sex, age of disease onset, age at the diagnosis of AVN), organs involvement, SLE Disease Activity Index (SLEDAI), Systemic Lupus International Collaborating Clinics/American College of Rheumatology-Damage index (SLICC/ACR-DI), number of disease flare ups were compared between two subsets.Results. The mean age of SLE onset was younger (P value = 0.04) in the AVN patients. In oral corticosteroid subset, malar rash (P value < 0.001) and oral ulcer (P value = 0.003) were seen more frequently in non-AVN patients, whereas psychosis (P value = 0.03) was significantly more prevalent AVN subset in oral corticosteroid subset. In corticosteroid pulse subset, no significant difference in clinical features was noted.Conclusion. In oral corticosteroid subset, younger age of disease onset and psychosis were significantly associated with AVN, whereas malar rash and oral ulcer showed negative association AVN.

Avascular necrosis of bone in systemic lupus erythematosus

IntroductionAvascular necrosis (AVN) is a major cause of morbidity in SLE. Several factors have been associated with the development of osteonecrosis in SLE but corticosteroid therapy has been the most consistent. Many factors such as thromboembolism, fat embolism, thrombophilia, hypofibrinolysis, intramedullary haemorrhage, vasculitis and increased bone marrow pressure are related to corticosteroid-induced osteonecrosis. Aim of the workTo determine the prevalence of avascular necrosis (AVN) of bone in patients with systemic lupus erythematosus (SLE) and to study the predictive factors for AVN in patients with SLE and its association with other SLE disease manifestations. Patients and methodsOne hundred consecutive SLE patients, diagnosed according to the updated American College of Rheumatology criteria (ACR), were studied. A full medical history and rheumatologic examination were administered to all patients. Laboratory and serologic tests were also carried out. Systemic disease activity was scored using the systemic lupus erythematosus disease activity index (SLEDAI). Cases of symptomatic AVN were identified by plain X-ray and magnetic resonance imaging (MRI). Comparisons between groups of patients with and without AVN, and associations between groups were analyzed by the t-test, Pearson correlation as well as multiple regression models to study the predictive factors for AVN in patients with SLE. ResultsAVN was detected in 15% (n=15) of SLE patients. Osteonecrosis of one hip joint was highly predictor for the other (p=0.000). Cumulative corticosteroid dose, Gait disturbance, myalgia and hypertension are the clinical predictors of AVN (p=0.000, 0,000, 0.001, 0.000), respectively, in the regression analysis model. Haemoglobin and proteinuria were the laboratory predictive (p=0.000, 0.000), respectively. ConclusionsLupus patients are at high risk for avascular necrosis (AVN), this risk extended to those on high dose corticosteroid of which patient's screening should be considered and closely monitored by sensitive techniques such as MRI.

Avascular Necrosis of Bone in Systemic Lupus Erythematosus

The association between the type of precipitating autoantibodies and occurrence of avascular necrosis of bone (AVN) was examined. We prospectively analyzed clinical and laboratory findings of our 113 patients with SLE. Seven of 113 (6%) patients developed AVN. Anti-Ro (SS-A) and anti-RNP antibodies coexisted in 3 of 7 AVN patients. The same combination of these two antibodies were observed in 1 without AVN. Antibodies to topoisomerase I were detected in 2 other patients with AVN but not in any of the patients without AVN. The coexistence of the former two or the presence of the latter one is rare in SLE. However, these (combination of) antibodies can be useful as a local ischemic marker predicting the development of AVN.

Avascular necrosis of bone in systemic lupus erythematosus: possible role of haemostatic abnormalities.

The pathogenesis of avascular necrosis of bone (ANB) was investigated in 111 patients with systemic lupus erythematosus (SLE) (24 with ANB, 87 without ANB); patients' ages, corticosteroid treatment, clinical and laboratory features associated with SLE, and haemostatic profiles were all taken into account. The mean ages of patients with and without ANB at the time of diagnosis of SLE was 24.1 and 31.2 years respectively. The mean maximal daily dose of prednisolone in the group with ANB was 50.8 mg, which was significantly higher than the dose (41.8 mg) in the group without ANB. Disease features of SLE, such as Raynaud's phenomenon, hyperlipidaemia, nephrotic syndrome, hypertension, and disease activity, were not found to be related to ANB. The percentage of patients who had lupus anticoagulant as well as a shorter activated partial thromboplastin time was greater in those with ANB than in those without. Multiple factors may be involved in the pathogenesis of ANB in SLE, and it is suggested that haemostatic abnormalities, which could be influenced by corticosteroids and young ages, play some part in the development of ANB.

Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus

In this prospective study, 28 (52 percent) of 54 patients with systemic lupus erythematosus (SLE) had ischemic necrosis of bone in 93 sites. All but two of the patients had multiple sites of involvement, with hips, knees, and shoulders affected in decreasing order of frequency. Demographic, clinical, and laboratory features were comparable in patients with and without ischemic necrosis of bone except for cushingoid changes in 24 (86 percent) of the 28 patients with ischemic necrosis of bone versus four (15 percent) of the 26 patients without ischemic necrosis of bone (p <0.0001). The duration of steroid therapy, total cumulative steroid dose, and the mean daily prednisone dose for the first one, three, six, and 12 months of therapy were not significantly different between the two groups. Mean daily prednisone dose for the highest single month as well as the highest consecutive three, six, and 12 months of therapy was significantly higher in patients with ischemic necrosis of bone. The mean daily dose of prednisone for the highest month of therapy was greater than 40 mg per day in 93 percent and greater than 20 mg per day in all patients with ischemic necrosis of bone. In patients with ischemic necrosis of bone, there was a statistically significant correlation between higher mean prednisone dose at all time intervals and increased number of bony sites involved. A lower mean dose of prednisone was required to produce ischemic necrosis of bone in patients with Raynaud's phenomenon.

Aseptic necrosis of bone in systemic lupus erythematosus. Relationship to corticosteroid therapy

The relationship of corticosteroid therapy to the development of aseptic necrosis (AN) in 365 patients with systemic lupus erythematosus (SLE) was investigated. Seventeen patients (4.7%) were identified as having AN. The dosage of corticosteroids ingested during the initial period of therapy in patients with AN was tabulated and compared with that of 25 SLE control patients. There was a substantially greater dose of costicosteroids ingested in the first one, three, and six months of therapy in the patients with AN than in the control SLE group. Severity of disease and duration of therapy were not found to correlate with AN. Total corticosteroid dose was virtually identical in both groups. Thus, high initial corticosteroid dosages in patients with SLE seem to be associated with the development of AN. (<i>Arch Intern Med</i>138:750-754, 1978)

Aseptic Necrosis of Bone in Systemic Lupus Erythematosus

The relationship of corticosteroid therapy to the development of aseptic necrosis (AN) in 365 patients with systemic lupus erythematosus (SLE) was investigated. Seventeen patients (4.7%) were identified as having AN. The dosage of corticosteroids ingested during the initial period of therapy in patients with AN was tabulated and compared with that of 25 SLE control patients. There was a substantially greater dose of costicosteroids ingested in the first one, three, and six months of therapy in the patients with AN than in the control SLE group. Severity of disease and duration of therapy were not found to correlate with AN. Total corticosteroid dose was virtually identical in both groups. Thus, high initial corticosteroid dosages in patients with SLE seem to be associated with the development of AN.

Avascular necrosis of bone in systemic lupus erythematosus

A skeletal radiologic survey was performed on 35 patients with systemic lupus erythematosus (SLE) to determine the prevalence of avascular necrosis of bone. Fourteen patients had avascular necrosis of a total of 31 bones. Eight of nine symptomatic sites were in the femoral head or condyles. The most frequently involved area was the femoral condyle, followed in order of frequency by the femoral head, talus, capitulum of the elbow, metatarsals, and the patella. No difference was found in the age of onset of SLE, the duration of prednisone and azathioprine therapy, or the average annual dose of prednisone between patients with and without bone disease. It appears that the development of avascular necrosis of bone may results from interference with the blood supply to the bone due to corticosteriod-induced vascular changes andlor from the vasculitic component of blood vessel alteration in SLE.