Biomedical subjects
Publications and source records attributed to R J Quinet.
Total hip and knee replacements are among the most common orthopedic surgical procedures performed on patients with arthritis. The procedures are highly successful in appropriately selected patients. The authors approach total joint replacement from a medical perspective, emphasizing indications, contraindications, preoperative evaluation, clinical outcome, and potential complications.
The chronic fatigue syndrome (CFS) is a poorly understood condition with nonspecific signs and symptoms, especially debilitating fatigue. Most patients can pinpoint the onset of their illness and usually describe a flu-like state. The search for an etiologic agent has focused on a number of viruses such as Epstein-Barr, enteroviruses, retroviruses, and human herpesvirus-6. Evidence supports persistent viral infection in a small percentage of CFS patients. Immunologic abnormalities do exist in CFS, which indicate the presence of immune activation in CFS patients. Although abnormal muscle biopsies have been found in some patients with CFS, strength and endurance appear normal, but perception of exertion may be abnormal. Patients with chronic fatigue have a high incidence of premorbid and concurrent psychiatric disorders, and on physical examination many often have reproducible tender points similar to fibromyalgic patients. Clinical evaluation should rule out other potential causes of fatigue, but elaborate diagnostic tests are seldom required. Presently, no specific treatment exists for CFS. A cognitive behavioral approach with or without the use of tricyclics has been advocated. Patients should be encouraged to maintain functional status and should not be discouraged from exercise. Several medications have been tried but with no definite clinical benefit.
A seropositive white man had follow-up for 16 years with a diagnosis of palindromic rheumatism. Treatment had included parenteral gold, methotrexate, prednisone, hydroxychloroquine sulfate, and penicillamine before diarrhea led to a biopsy-proven diagnosis of Whipple's disease. Clinical and radiographic criteria for ankylosing spondylitis were met. In addition to classic Whipple's arthropathy, he had the combined but singular findings of pancarpal destruction and cervical apophyseal fusion. HLA typing revealed the B7 antigen. This case illustrates the pitfalls in diagnosis of a chronic polyarthritis that has, as a typical feature, a long latency before manifesting its more specific signs and symptoms (ie, diarrhea, malabsorption, and hyperpigmentation). Care should be taken during evaluation of any disease with atypical and nonspecific features (eg, positive rheumatoid factor in a patient with polyarthritis) and one should continue to reevaluate the original impression while confirmatory evidence is lacking. Moreover, the roentgenographic findings of pancarpal narrowing, apophyseal fusion, and advanced iliofemoral joint disease, in addition to sacroiliitis and syndesmophyte formation, challenge the generally held notion that Whipple's arthropathy is a nondestructive joint disease.
This case illustrates the potential severity of an uncommon and generally benign condition of the knee--the Pellegrini-Stieda syndrome. The regional bone scan clearly showed the etiologic role of the inflamed ligamentous attachment site. Therapy should include joint rest, nonsteroidal anti-inflammatory agents, and possibly ice for symptomatic relief.
Older patients taking NSAIDs or high-dose aspirin should have complete laboratory evaluations of blood count, urinalysis, BUN/creatine, potassium, and serum transaminases several times yearly; more often if the clinical picture warrants. The use of aspirin, NSAIDs, and other medications should be reviewed in detail with the patient, particularly the rationale. The physician should stress the need to take the medications regularly, not "as needed." Physicians should also take time to warn patients against unorthodox medications and "treatments."
Only two definite cases of quinidine-induced systemic lupus erythematosus (SLE) are reported in the English-language literature. We have treated five patients who had an SLE-like syndrome while receiving quinidine. Symptoms, signs, and abnormal laboratory values improved after quinidine therapy was discontinued and prednisone therapy was started. The disease did not return after steroids were withdrawn. These cases indicate that quinidine can indeed cause an SLE-like syndrome.
Granulocyte lysosomal enzymes can potentially participate in cartilage degradation in inflammatory arthritides. However, we have shown that the quantity of several such enzymes in an inflammatory synovial effusion correlates negatively with the degree of radiographic damage of the joint from which the fluid was sampled. In the current work the quantity of the following 5 protease inhibitors was determined immunochemically in the same fluids: alpha 1 antitrypsin, alpha 1-antichymotrypsin, alpha 2-macroglobulin, inter-alpha-trypsin inhibitor, and Cl esterase inhibitor. These inhibitors are generally covariate and correlate positively with the total protein in the fluid as well as the number of granulocytes and the concentration of granulocyte lysosomal enzymes in the fluid. As did the lysosomal enzymes, the protease inhibitors correlate negatively with radiographic destruction. It is likely that lysosomal enzymes in solution in inflammatory synovial effusions are rendered effete by the presence of protease inhibitors.
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The concentrations of several polymorphonuclear neutrophilic lysosomal constituents were quantitated by immunochemical and enzymatic assays in 28 inflammatory and 9 noninflammatory synovial fluids. The quantities of lactoferrin, myeloperoxidase, and enzymatically determined lysozyme were covariate with the neutrophil count. Enzymatic activities measured with synthetic substrates developed for the assay of chymotryptic-like cationic protein (cathepsin G) and elastase, along with immunochemically determined lysozyme, were independent of the neutrophil count. Although the latter assays were developed and standardized with human neutrophilic lysosomal constituents, they measure different activities in inflammatory synovial effusions. No elastase was detected if elastin was used as the substrate. Regardless of the source of the enzymes, there was a negative correlation between their concentration and the degree of radiographic destruction of the joint from which the fluid was obtained. Lysosomal enzymes in solution in synovial fluid are not likely to be primarily involved in cartilage destruction.