Tenidap in patients with rheumatoid arthritis. A 4-week, placebo-controlled study.

The present double-blind, placebo-controlled study was conducted to compare the safety and efficacy of tenidap in patients with rheumatoid arthritis (RA). Patients with flare of active RA following NSAID withdrawal were randomized to receive either placebo (n = 67) or tenidap (n = 131; 40-200 mg/day). The mean changes from baseline in efficacy and biochemical variables were compared between treatment groups at endpoint (4 weeks). The improvements in four of the five primary efficacy variables were significantly greater in the tenidap group compared with the placebo group (p < 0.01). Tenidap was also associated with an 18% reduction in erythrocyte sedimentation rate (ESR) and a marked, 51%, reduction in serum C-reactive protein (CRP) level, both of which were significantly greater than the changes in the placebo group (p < 0.05). The percentage of patients who discontinued because of side effects was the same in both groups (3%). In conclusion, tenidap 40-200 mg/day was effective and well tolerated in the treatment of patients with RA for 4 weeks.

Takayasu's arteritis.

Takayasu's arteritis is an uncommon condition with a unique constellation of clinical findings that continues to fascinate clinicians and researchers. Advances in the techniques used for classifying lymphocytes, recognizing markers of cellular activity, and detecting the presence of cytokines has produced more evidence that Takayasu's arteritis is a cell-mediated immune condition. The etiology(ies) or triggering mechanism(s) of the disease remains elusive. Alternatives to standard angiography for vascular imaging, such as digital subtraction angiography, duplex ultrasonography, and magnetic resonance imaging, have improved the facility with which the diagnosis and management of Takayasu's arteritis can be safely accomplished. Percutaneous transluminal angioplasty of the aorta and renal arteries is a safe and effective means to dilate symptomatic stenoses. In the short term, this technique provides relief from claudication, hypertension, and ischemia. Long-term follow-up suggests that restenosis at the angioplasty site occurs in a substantial number of patients. Whether this represents a fibrotic healing process or continued inflammation is unclear. Attempts to control the inflammation with anti-inflammatory and immunosuppressive agents continue to be reported. Prednisone plus methotrexate is a promising combination for use in this life-threatening condition of young people.

Remitting, seronegative (A) symmetrical synovitis with pitting edema--two cases of RS3PE syndrome.

The sparing effect of neurological damage on the development and progression of several arthritic conditions has been documented. We describe the first 2 cases of unilateral remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome in individuals with neurologic disorders. Case 1 suffered from birth trauma resulting in paresis of the right upper extremity and developed RS3PE syndrome in the nonaffected extremities. Case 2 developed RS3PE syndrome on the nonparetic side 7 years after a cerebrovascular accident resulting in hemiparesis.

Borrelia burgdorferi in joint fluid in chronic Lyme arthritis.

Although indirect evidence suggests that chronic Lyme arthritis is caused by persistent infection with Borrelia burgdorferi, direct visualization has been lacking. We report the demonstration of B. burgdorferi from synovial fluid aspirated from the right knee of a 31-year-old man with Lyme arthritis for more than 1 year. After 6 days, culture medium inoculated with synovial fluid showed one motile and several nonmotile spirochetes. Direct immunofluorescence staining showed reactivity with anti-B. burgdorferi serum. Spirochetes were not seen in subcultured material. The patient's arthritis improved with high-dose intravenous penicillin. Identification of B. burgdorferi from the joint fluid of a patient with long-standing arthritis supports the concept that the arthritis is due to persistent infection.

Chronic arthropathy in long-term hemodialysis.

Acute arthritis and periarthritis are known to develop in patients undergoing long-term hemodialysis; however, the long-term consequences of hemodialysis on joint structure and function have not been thoroughly evaluated in a cohort of patients. All patients (11) undergoing hemodialysis for 10 or more years were evaluated for symptoms, joint function, and radiographic abnormalities. Eight patients had joint symptoms, excluding those from a septic or traumatic process. Only four patients had acute episodes of arthritis. Nine patients had abnormalities on physical examination, including decreased range of motion, joint effusion, crepitance, or deformity. Nine patients had abnormal findings on radiography, including narrowing, erosions, and calcification. Those with more severe disease were younger and had been receiving dialysis treatments longer. It is concluded that prolonged hemodialysis is associated with a progressive deterioration of joint structure and function with or without acute episodes of synovitis.

Nifedipine-induced fingertip vasodilation in patients with Raynaud's phenomenon.

The effect of nifedipine on fingertip hemodynamics was studied in 10 patients with Raynaud's phenomenon. Fingertip blood flow (FBF) was determined in a 20 degrees C environment by venous occlusion air plethysmography and fingertip vascular resistance (FVR) was calculated from the mean blood pressure and the FBF. Nifedipine, administered as a 10 mg sublingual dose, increased FBF in 8 of the 10 patients. FVR for the 10 patients decreased 40% from 40.7 +/- 10.8 to 24.2 +/- 6.1 U (p less than 0.05). Seven of the 10 patients were followed in a crossover placebo-controlled clinical trial. The frequency and severity of Raynaud's phenomenon was less in all seven patients when taking nifedipine as compared to placebo. Nifedipine-induced fingertip vasodilation may contribute to clinical improvement in some patients with Raynaud's phenomenon.

Preliminary observations on danazol therapy of systemic lupus erythematosus: effects on DNA antibodies, thrombocytopenia and complement.

Seven patients with systemic lupus erythematosus (SLE) were treated with Danazol in a controlled study. Phenomena observed in some patients treated with Danazol were: 1) decrease in immunoglobulins and antibodies to native DNA; 2) increases in serum complement and platelets; and 3) clinical improvement. Ineffective drug trials were associated with increasing disease activity. Drug side effects were minimal. It appears that the drug may have an ameliorative effect on mildly active SLE patients and sometimes a marked effect on thrombocytopenia. Further evaluation of Danazol appears to be warranted for these types of patients but not for treatment of acute or severe forms of the disease.

Nifedipine as a therapeutic modality for Raynaud's phenomenon.

Eight patients with Raynaud's phenomenon were entered into a double-blind crossover study of nifedipine versus placebo, with 7 patients undergoing finger plethysmography before and after sublingual nifedipine administration. While receiving nifedipine, all patients reported decreased frequency and severity of attacks, and 4 of 5 had digital ulcer healing. Total finger blood flow increased 5 of 6 patients after treatment with sublingual nifedipine. This preliminary study indicates that nifedipine may be a useful agent for treatment of digital vasospasm.

Evidence for a silent or null gene in hereditary C2 deficiency.

Three generations of a family with hereditary C2 deficiency were studied, Six members heterozygous for C2 deficiency were identified by serum C2 levels that were approximately 50% of normal C2 values and the identity was supported by HLA analysis. All six members with low C2 levels had only a single electrophoretic variant. Two of four children did not have the variant found in the parent from whom they inherited the partial C2 deficiency. It is inferred that the low levels of C2 result from the inheritance of a silent or null gene, C2D allelic with the structural genes controlling the electrophoretic variants.