Feasibility of a dyadic intervention for management of osteoarthritis: a pilot study with older patients and their spousal caregivers.

This study evaluated a novel intervention for older osteoarthritis (OA) patients and their spousal caregivers that consisted of standard patient education supplemented by information related to effectively managing arthritis as a couple. Twenty-four female OA patients and their husbands were randomly assigned to either an educational intervention that was targeted at both patient and spouse or to a patient education intervention that was targeted at only the patient. Findings revealed that both interventions were evaluated favorably but the couple intervention was better attended than the patient intervention. In addition, patients in the couple intervention experienced greater increased efficacy in managing arthritis pain and other symptoms. The findings of this pilot study point to the utility of a dyadic intervention approach to management of OA in late life.

Arthritis-associated syndromes.

There are a number of diseases characterized by inflammatory arthropathy that, although not as commonly seen as rheumatoid arthritis, often present to the family physician as difficult diagnostic problems. The diagnosis is frequently most difficult during the early course of these diseases. During recent years, new and altered concepts have arisen regarding both diagnostic and therapeutic management of this challenging group of arthropathies. This article presents a review of the more common arthritis-associated syndromes with emphasis on the differential diagnosis and medicinal therapeutics.

Synovial lymphocyte subsets in rheumatoid arthritis and degenerative joint disease.

There is considerable evidence to indicate that the synovitis of rheumatoid arthritis (RA) is immunologically mediated. Recently, it has been postulated that a suppressor-type cell deficiency may play an important role in the pathogenesis of the synovitis. In addition, an immune component may contribute to the synovial alterations in certain examples of degenerative joint disease (osteoarthritis, OA). Using monoclonal antibodies, we evaluated synovial tissue lymphocytes in 12 patients with RA, 2 with juvenile RA, one with adult Still's disease, and 2 patients with OA synovitis in order to delineate the T cell subset patterns. Helper-type cells predominated in 3 patients with RA, while suppressor-type cells were present in equal or greater numbers in 9. The patients with OA showed helper-type cell predominance. Helper-type to suppressor-type cell ratios vary widely in RA synovia which militates against the primacy of the role of a suppressor-type cell deficiency in this disorder. Patients with OA synovitis may display T cell infiltrates comprised mainly of helper-type cells.

Factors predicting development of renal involvement in progressive systemic sclerosis.

Renal involvement or "scleroderma renal crisis" developed in 60 patients with progressive systemic sclerosis evaluated at the University of Pittsburgh during the period from 1972 to 1982. Forty-seven of these patients had progressive systemic sclerosis with diffuse scleroderma, representing 18 percent of persons with progressive systemic sclerosis and diffuse scleroderma evaluated during this time period. Ten additional patients did not have truncal scleroderma but were suspected of having incompletely developed diffuse scleroderma. Only three patients were classified as having progressive systemic sclerosis with the CREST syndrome. Renal crisis was observed early in the course of the illness, a mean of 3.2 years after onset. During May and June, this complication developed in fewer patients than expected. Thirty-six patients who had diffuse scleroderma and renal involvement after their initial Pittsburgh evaluation were compared with 212 who had diffuse scleroderma without renal involvement during follow-up. The patients with renal involvement had a shorter mean disease duration at the time of their first evaluation (2.4 versus 4.2 years, p less than 0.05) and less frequently had digital pitting scars (29 versus 54 percent), but no other significant clinical, laboratory, or serologic differences were noted. Data available for 31 patients with renal involvement during the six months preceding the onset of renal disease were analyzed. Blood pressure, serum creatinine, urine protein and red blood cells, and plasma renin levels were similar in these patients and the 212 patients without renal involvement. More patients with renal involvement had anemia or clinical evidence of cardiac involvement during this period compared with the patients without renal involvement. During the 12-month period prior to renal involvement, seven of 16 (44 percent) patients with such involvement had an impressive increase in skin thickening on physical examination compared with only 23 of 180 (14 percent) patients without renal involvement at any time during their course. Thus, the subset of patients with diffuse scleroderma who show rapid progression of their skin thickening early in the illness with development of anemia, pericardial effusion, or congestive heart failure have a high risk of "scleroderma renal crisis."

Hypertension and renal failure (scleroderma renal crisis) in progressive systemic sclerosis. Review of a 25-year experience with 68 cases.

This paper reports the experiences of our group with 68 patients with progressive systemic sclerosis (PSS) admitted to hospitals of the University of Pittsburgh Health Center between 1955 and 1981 with scleroderma renal crisis (SRC). The onset of SRC was characterized by four features, namely, onset or aggravation, usually abrupt, of arterial hypertension; appearance of Grade III or IV retinopathy; elevations of peripheral renin activity to at least twice the upper limit of normal; and rapid deterioration of renal function within a period of less than one month. Over 90% of our patients in whom these criteria could be determined had at least three of them present with the onset of SRC. Management of these patients during the first 15 years of this period was uniformly ineffective. Before 1971, no patients lived longer than a year; usual survival ranged from 1 to 3 months. With the advent of renal dialysis and the more effective treatment of severe hypertension, along with the utilization of bilateral nephrectomy in selected anuric patients, some improvement in longevity was achieved. However, only in the past few years have we accumulated a group of 11 patients who have survived for longer than one year. The clinical characteristics of the onset and progression of SRC suggest the sudden imposition of severe stress such as cold or an autoimmune insult affecting vulnerable arteries and arterioles. The renal damage becomes self-perpetuating with extremely high renin activity causing further rise in blood pressure and additional renal and systemic vascular damage. Progress in the last few years seems to have been achieved primarily by the advent of pharmacologic agents that specifically block the effect of angiotensin II by inhibiting the angiotensin I converting enzyme. When diagnosis is prompt and the condition is treated as an emergency with these compounds, we and others have found that normal renal function can be restored in a number of patients. The result is a considerably brighter outlook for patients with this previously rapidly fatal complication of progressive systemic sclerosis.

Clinical and serologic study of Sjögren's syndrome in patients with progressive systemic sclerosis.

Fifty-eight patients with progressive systemic sclerosis (PSS) were evaluated clinically and by biopsy of the minor salivary glands of the lips for the presence of Sjögren's syndrome. Clinical findings included dry eyes in 38%, dry mouth in 32%, parotid enlargement in 4%, and an abnormal Schirmer's test in 34%. Histologic changes in lip biopsies included lymphocytic infiltrates characteristic of Sjögren's syndrome in 17 individuals (29%). In 19 (33%) there was periglandular and intraglandular fibrosis (PSS-fibrosis) without significant inflammation, an alteration characteristic of PSS per se. In the remaining 22 patients (38%) with PSS, no abnormality was found. Of those with PSS and Sjögren's syndrome, 53% had serum antibodies to SS-A and/or SS-B, while only 1 patient with a normal biopsy had either of these antibodies. Anti-SS-A and anti-SS-B were not detected in patients with glandular fibrosis alone. The mortality rate of the PSS-fibrosis group was higher due to a variety of severe internal manifestations related to PSS. Antibodies to SS-A and SS-B are useful serologic markers of the presence of Sjögren's syndrome in patients with PSS.