What other clinical problems occur with increased frequency in Rheumatoid Arthritis patients?
Atherosclerosis —Patients with RA develop atherosclerosis 10 years earlier than those without RA but have the same traditional cardiovascular (CV) risk factors. Traditional CV risk factors underestimate risk in patients with RA, which is estimated to be 1.5-fold higher than the general population. In addition to modifying traditional risk factors (hypertension, hyperlipidemia, obesity, and tobacco use), control of RA disease activity is recommended to reduce CV disease risk in patients with RA.
SS —Approximately 20% to 30% of RA patients develop secondary SS with dry eyes and dry mouth. They are frequently ANA-positive but typically do not have anti-SS-A or anti-SS-B antibodies commonly seen in primary SS.
Amyloidosis —RA patients rarely develop amyloid A-associated amyloidosis. This occurs in longstanding, poorly controlled RA and usually presents as nephrotic syndrome.
Osteoporosis —seen in the majority of RA patients and is related to disease activity, immobility, and medications. Insufficiency fractures of the spine, sacrum, and other areas are common in longstanding disease.
Entrapment neuropathy —median nerve (carpal tunnel), posterior tibial nerve (tarsal tunnel), ulnar nerve (cubital tunnel), and posterior interosseous branch of the radial nerve are most commonly involved.
Laryngeal manifestations —cricoarytenoid arthritis can present as pain, dysphagia, hoarseness, and rarely, stridor.
Ossicles of ear —tinnitus and decreased hearing.
Renal and gastrointestinal involvement —rare. Abnormalities are typically attributable to nonsteroidal antiinflammatory drugs (NSAIDs) causing renal insufficiency or gastric ulcers with hemorrhage.
Large granular lymphocyte (LGL) syndrome —a syndrome of neutropenia, splenomegaly, susceptibility to infections, and LGLs bearing CD2, 3, 8, 16, and 57 surface phenotypes in the peripheral blood smear (although a bone marrow biopsy is often required to confirm the diagnosis). These cells have enhanced natural killer and antibody-dependent cell-mediated cytotoxicity activity. It is now recognized that when this syndrome occurs in RA patients, it is a subset of Felty’s syndrome. Approximately a third of Felty’s syndrome patients have significant clonal expansions of these cells on their peripheral smear, and these patients are HLA-DR4-positive, similar to Felty’s syndrome patients without LGL expansion.