Obliterative bronchiolitis in two rheumatoid arthritis patients treated with penicillamine.
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Biomedical subjects
Publications and source records attributed to H B Stein.
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Of the 31 patients who developed polyarthritis following jejunoileal bypass for obesity, 24 had cutaneous vasculitis (urticarial, pustular, and nodular), 11 paresthesias, 10 Raynaud's phenomenon, and 1 pericarditis. Blind loop symptoms (14 of 26 patients), cryoglobulinemia (10 of 28), and immune deposits in biopsied skin lesions (5 of 7) support the theory of a relationship between bowel bacteria and immune complexes. Treating the blind loop with antibiotics and sphincteroplasty to prevent bacterial reflux into the blind loop helped 5 of 10 and 6 of 9 patients, respectively. A comparison is made to other bowel associated arthritides.
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Adverse effects to D-penicillamine were studied prospectively over 3 years in 259 patients with rheumatoid arthritis. Ninety-five percent had had gold therapy previously, yet 70% benefited from D-penicillamine therapy. Of the 275 courses given, 160 (58%) were complicated by at least one reaction, including rashes (44%), dysgeusia (20%), gastrointestinal upset (18%), stomatitis (10%), proteinuria (7%), thrombocytopenia (3%), and leukopenia (2%). Their occurrences peaked in the first 6 months of treatment, except for proteinuria and thrombocytopenia, which peaked in the second 6 months. Reactions were commoner at daily doses above 250 mg; mean daily doses for proteinuria, thrombocytopenia, and leukopenia were higher (approximately 600 mg/d) than for the others (approximately 500 mg/d). Of 114 discontinued courses, 73 (27%) were due to adverse reactions. The remaining reactions were controlled by altering dosages and symptomatic treatment. Only obliterative bronchiolitis (two cases) was irreversible; it resulted in the only death in our series, possibly attributable to penicillamine.
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Forty-four patients with definite or classic rheumatoid arthritis and failure to tolerate or respond to gold therapy were treated with D-penicillamine on a so-called go-slow, go-low regime. Seventeen patients tolerated the drug and had a 3-13 month follow-up assessment; 8 were markedly improved, 6 moderately or slightly improved, and 3 unimproved. Penicillamine had to be discontinued in 9 patients because of toxic side effects.
This study compares the effect of azathioprine with those of gold and chloroquine in early (Class II) rheumatoid arthritis (RA). Thirty-three similar patients with classic or definite RA of less than 5 years duration were randomly entered, 11 into each drug group. Assessment of standard clinical and laboratory measures at 12 and 24 weeks showed significant improvement in all three groups. In general, all three drugs were effective antirheumatic agents with low toxicity. However, because of serious potential toxicity, azathioprine could not be recommended over gold and chloroquine in early RA therapy.
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Review of 34 cases of Felty's syndrome showed this to be a form of 'super' rheumatoid disease because of the severity of joint disease, the prominence of extra-articular features and the remarkable incidence of infection. The response to splenectomy in these 34 patients was shown by a return towards normal of peripheral blood abnormalities and a decrease in bone marrow granulopoiesis. Although some patients remained free of infection after splenectomy, others have continued to have infections despite the return of white blood cell counts to normal levels. Although splenectomy and subsequent increase in white blood cell levels may be beneficial, our experience suggests that other factors are important in the susceptibility to infection of Felty's syndrome patients. Moreover, we think that splenectomy may have been instrumental in the fatal infection of one of our patients.
The effect of ascorbic acid on the serum and urinary uric acid was studied in 14 subjects. Two to 6 h after the ingestion of 4.0 g of ascorbic acid, the fractional clearance of uric acid increased to 202% +/- 41% of the control value. This uricosuria was inhibited by pyrazinamide and by low-dose acetylsalicylic acid, but was not accompanied by an increase of the creatinine clearnace. Ascorbic acid did not diminish protein-bound uric acid. In 3 subjects who ingested 8.0 g of ascorbic acid for 3 to 7 days the serum uric acid decreased by 1.2 to 3.1 mg/dl as a result of a sustained uricosuria. These results suggest that ascorbic acid could invalidate studies involving the measurement of uric acid and obscure the diagnosis of gout in some cases. Theoretically it could precipitate attacks of gouty arthritis or renal calculi in predisposed persons. These observations show a pharmacologic effect of megadoses of a simple vitamin.
A retrospective study comparing 14 patients with juvenile rheumatoid arthritis (JRA) complicated by chronic iridocyclitis (Group I) with an equal number of JRA patients without this complication (Group II) was conducted to determine which factors might aid in the earlier diagnosis of chronic iridocyclitis. Eleven patients in Group I had oligoarticular disease compared to 5 in Group II. Antinuclear antibody was found in 13 patients in Group I compared to only 2 in Group II. Only one of nine patients tested in Group I for the histocompatibility antigen W-27 was positive. The patient with oligoarticular disease and a positive ANA test should be followed closely by the ophthalmologist for the development of chronic iridocyclitis.
A case of gold-induced enterocolitis and a review of the literature are reported. Gold-induced enterocolitis appears to be an uncommon reaction, occurring in middle-aged females who have received low doses of gold preparations. Symptoms may include fever, nausea, vomiting, abdominal cramps, and diarrhea with or without blood. The whole of the gastrointestinal tract may be involved and fatal cases occur. The diagnosis of a primary enteropathic arthropathy may be suggested. Cessation of gold, glucocorticoids and supportive therapy are indicated. The mechanism of the reaction is still unknown.
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Serologic evidence of Yersinia enterocolitica infection was sought by agglutination testing in serum samples from several populations, including Haida Indians, Red Cross blood donors, and Caucasian patients with rheumatoid arthritis, ankylosing spondylitis, and Reiter's syndrome. No evidence was found to indicate that yersinial infection was etiologically related to Haida spondylitis or Reiter's syndrome. Four of 28 patients with acute arthritis were diagnosed from serologic evidence as having Yersinia-related arthritis.
A patient with procainamide lupus erythematosus had a large pericardial effusion. As in other reported cases histology revealed a fibrinous mononuclear pericarditis and the pericardial fluid was a serosanguinous inflammatory exudate with a high LDH level and normal glucose concentration. The ANF and LE cell preparation were positive in the fluid but the C3 complement was normal. The frequency of pericarditis is similar in systemic and drug-induced lupus erythematosus yet low complement levels need not occur. Complement activation may therefore be unnecessary for the development of either type of lupus pericarditis.
During the course of systemic lupus erythematosus in a young female patient the peripheral blood smear incidentally showed the features of hyposplenism. Silent lupus vasculitis with splenic infarction was suspected as the cause of this.