Gonococcal arthritis.

Disseminated gonococcal infection is a preventable communicable disease. It is an important cause of arthritis in sexually active adults. Prompt recognition and treatment of this common disease results in cure and eliminates unnecessary diagnostic procedures and prolonged hospitalization.

Chlamydia-induced reactive arthritis.

Chlamydia trachomatis infection is now recognized as the most prevalent veneral disease in the Western World. The majority of cases of Reiter's syndrome, one type of reactive arthritis, are secondary to sexually transmitted infections. Evidence of urogenital C. trachomatis infection is found in 36% to 61% of cases of Reiter's syndrome. We investigated the prevalence of infection by this organism in a group of patients with spondyloarthropathies. Positive cultures were obtained in 39.4% of patients with Reiter's syndrome, as well as in 22.2% of patients with psoriatic arthritis and in 20% of patients with ankylosing spondylitis. An important percentage of patients also had positive serum antibodies against C. trachomatis (62.1% of patients with Reiter's syndrome), suggesting presence of infection at some point during the course of the disease. Our findings and those from other authors support the use of long-term antibiotic therapy in patients with reactive arthritis, mainly in those in whom positive culture for C. trachomatis has been obtained as well as in their sex partners.

Candida arthritis.

Septic arthritis can be caused by Candida species. Its true incidence is unknown because only a few cases have been reported. Two clinical syndromes have been identified. The first is an isolated monarthritis caused by the direct intra-articular inoculation of fungi that inhabit the skin, by means of an injection, or during surgery. The second is the development of a mono- or polyarthritis as a complication of hematogenously disseminated candidiasis. The optimum treatment of this condition is not yet known, although the combination of medical and surgical treatment seems to be the most convenient therapeutic modality. Amphotericin-B continues to be the drug of choice.

Pneumatosis cystoides intestinalis in systemic lupus erythematosus with intestinal vasculitis: treatment with high dose prednisone.

Pneumatosis cystoides intestinalis (PCI) is an uncommon disorder usually associated with intestinal and pulmonary obstructive diseases, recent abdominal procedures and systemic illnesses. PCI has been reported in patients with systemic lupus erythematosus associated with intestinal vasculitis. We describe herein a patient with a month history of intermittent abdominal pain, diarrhoea, hyporexia, and weight loss who underwent intestinal resection for acute abdomen. Post-operatively she gave a three-month history of arthritis of the right knee, ankles and feet, arthralgia of the wrists, MCPs and shoulders. She also described weakness, weight loss, Raynaud's phenomenon, and a skin rash. Laboratory examination revealed an increased ESR, low haemoglobin and haematocrit, positive rheumatoid factor, a positive ANA with a speckled pattern, as well antibodies to DNA, SS-A and cardiolipin. The abdominal symptomatology especially pain, cramps and bouts of diarrhoea persisted after the surgery and became worse two months later. Abdominal X-ray showed distention of bowel with cyst formation in the wall of the entire colon. A diagnosis of PCI was made radiologically. The intestinal pathology was reviewed and vasculitis was identified. The patient received treatment with high dose prednisone with an excellent response; prednisone was progressively tapered and she has been asymptomatic without abdominal complaints or other symptoms for over a year.

Anticardiolipin antibodies in unselected pregnant women. Relationship to fetal outcome.

Anticardiolipin antibodies (ACLA) have recently been associated with adverse fetal outcome. The prevalence of elevated ACLA has not been studied in unselected pregnant women, however. Twelve hundred unselected pregnant women were screened for IgG ACLA using an assay standardized by the first international workshop on ACLA. Fifteen (1.25%) were positive for IgG ACLA (greater than 3 SD above the mean) but only 0.5% had moderate to high levels of IgG ACLA (greater than 5 SD above the mean). Low levels of IgG ACLA were not associated with increased risk of fetal loss; however, 50% of women with moderate to high levels of antibody had fetal wastage. These findings further support the association of significantly elevated levels of IgG ACLA with fetal loss.

NSAID-masked gout.

The use of NSAIDs masked the diagnosis of gout in nine patients with the chronic polyarticular form of the disease. The escape from detection of chronic polyarticular gout resulted in a needless dependence on NSAIDs, failure to correct the metabolic problem, and in some cases progression of joint destruction. Although acute inflammation was modified, basic pathogenic mechanisms remained unchecked and joint disease continued. The indiscriminate use of NSAIDs may, by promoting misdiagnosis, become a major obstacle to effective control of this, perhaps the most remediable of arthritic disorders.

Seronegative antiphospholipid syndrome associated with plasminogen activator inhibitor.

Antiphospholipid syndrome is characterized by thrombosis, recurrent fetal loss, thrombocytopenia and is associated with the presence of antiphospholipid antibodies, especially anticardiolipin antibodies. We present a patient with the clinical features of antiphospholipid syndrome, namely recurrent venous and arterial thrombosis, recurrent abortions, thrombocytopenia and libido reticularis but with persistently negative serology for any type of antiphospholipid antibody. The possible existence of 'seronegative' antiphospholipid syndrome is proposed. Of additional interest in this patient is the presence of significantly elevated levels of plasminogen activator inhibitor. The role of this inhibitor, if any, in the antiphospholipid syndrome and/or seronegative antiphospholipid syndrome is not known and merits further study.

Pancreatitis leading to thrombotic thrombocytopenic purpura in systemic lupus erythematosus: a case report and review of literature.

Pancreatitis is a well-established but unusual complication of thrombotic thrombocytopenic purpura (TTP). It is also an unusual complication of systemic lupus erythematosus (SLE). However, TTP occurring as a consequence of acute pancreatitis in a patient with SLE has never been reported. We report a 24-year-old African American woman with active systemic lupus (SLE) who developed thrombotic thrombocytopenic purpura (TTP) following an episode of acute pancreatitis. The TTP was manifested by low-grade fever, microangiopathic hemolytic anemia, renal insufficiency, altered mental status, seizures and thrombocytopenia. The patient was initially treated with pulse corticosteroids with inadequate response and subsequently with daily plasmaphresis, leading to full remission. This case represents first report of pancreatitis leading to TTP in a patient with systemic lupus erythematosus.

Ketorolac-precipitated asthma.

Ketorolac is an effective and popular long-lasting analgesic that is especially useful in the emergency department and postoperatively. It is comparable in potency to the opiates but is preferable to them in many instances. Its relative overall safety as compared to the opiate analgesics may generate an unjustified complacent attitude toward its safety in all instances. Ketorolac, however, is an NSAID, and its major toxicities include those of other NSAIDs. Bronchospastic- and anaphylactic-type life-threatening reactions have occurred with its use. The prescribing physician must be aware of this potential complication and should always obtain a patient's complete history, including information regarding aspirin and NSAID intolerance, asthma, rhinitis, and nasal polyps, before administering it. Its use is contraindicated under those circumstances. When ketorolac is administered to asthmatics, it should be done with extreme caution and monitoring, especially when the intramuscular preparation is used. In this way, morbidity, health care costs, and the potential for mortality will be kept at a minimum.

Antinuclear and antiphospholipid antibodies in healthy women with recurrent spontaneous abortion.

PROBLEM: To determine the presence of absence of subclinical autoimmunity in healthy women with first trimester recurrent spontaneous abortion (RSA), the sera of 72 healthy women with a history of three or more consecutive abortions were analyzed for the presence of antibodies to phospholipid and nuclear antigens. METHOD: Lupus anticoagulant was determined, as were antibodies to cardiolipin. An indirect immunofluorescent antinuclear test was performed and specific antinuclear antibodies to double-stranded DNA, ribonucleoprotein, Smith antigen, and Sjogren's syndrome A and B antigens were tested. RESULTS: Nine women (13.2%) had low levels of antinuclear antibodies, none of which were specific. Four women (5.6%) had moderate to high levels of aCL antibodies. CONCLUSION: We conclude that the prevalence of aCLs and antinuclear antibodies in healthy women with first trimester RSA is low. Subclinical autoimmunity is not a common cause of first trimester RSA.

Cyclophosphamide use in a young woman with antiphospholipid antibodies and recurrent cerebrovascular accident.

We have described a 25-year-old woman with recurrent cerebral thrombosis associated with very high levels of antibodies against phospholipids. Antinuclear antibodies and clinical features of a defined connective tissue disease were absent. Treatment with plasmapheresis, prednisone, intravenous cyclophosphamide, and warfarin was accompanied by disappearance from the serum of the lupus anticoagulant and the biologic false-positive test for syphilis; IgG anticardiolipin antibodies persisted, however, and the patient had a second cerebral thrombosis. Clinical improvement ultimately occurred after the dosage of cyclophosphamide was optimized and the level of IgG anticardiolipin antibody decreased to a level lower than any that has been previously associated with thrombotic complications.

Leukopenia in Still's disease.

Two patients, one a 14-year-old girl and the other a 20-year-old man, with typical manifestations of juvenile rheumatoid arthritis had leukopenia and thrombocytopenia, two heretofore unreported findings. The presence of leukopenia should not be used to exclude a diagnosis of Still's disease.

Anti-SSA(Ro) antibody: a connective tissue disease marker.

The characteristics of 100 patients with anti-SSA(Ro) antibody were studied. By accepted criteria 34 patients had systemic lupus erythematosus, 25 had other known connective tissue diseases (CTD) and 9 had no significant evidence of a CTD. Thirty-two patients had an unclassified CTD characterized in most instances by arthritis, dermatitis, and a positive fluorescent antinuclear antibody test. The results support the concept of a continuous spectrum of autoimmune disease in which anti-SSA(Ro) antibody may be a marker and in which a variety of disorders may be found that cannot be classified by accepted criteria.

Association of HLA-DR7 with both antibody to SSA(Ro) and disease susceptibility in blacks with systemic lupus erythematosus.

The relationship between HLA-DR antigens and various specific antinuclear antibodies was studied in 28 unselected black Americans with systemic lupus erythematosus (SLE). Anti-SSA(Ro) occurred with high frequency (61%) but was not associated with specific clinical features of SLE. HLA-DR7 was strongly associated with anti-SSA antibody; it was present in 13/17 patients with anti-SSA (76%) and 1/11 patients without it (9%). HLA-DR7 occurred in 14/28 of all SLE patients (50%) compared with 17% of 137 local controls (p corrected, less than 0.005). This association of HLA-DR7 with both susceptibility to SLE and a high frequency of anti-SSA antibody suggests a genetic link between the presence of anti-SSA antibody and susceptibility to SLE in the population studied.

Anti-SS-A antibody and other antinuclear antibodies in systemic lupus erythematosus.

Randomly selected sera from 88 patients with systemic lupus erythematosus (SLE) were studied for the frequency of antibodies to SS-A, SS-B, RANA, RNP, Sm, Sc-1, and dsDNA. Results were in agreement with previous reports except for an increased incidence of anti-SS-A antibody (33%). Nine of 14 patients with anti-SS-A antibody on whom serial studies were performed had fluctuating titers. Titer changes often correlated with disease activity and dsDNA antibody levels.

Alpha 1-antitrypsin phenotypes, including M subtypes, in pulmonary disease associated with rheumatoid arthritis and systemic sclerosis.

Alpha 1-antitrypsin is a glycoprotein that functions as the major protease inhibitor in human serum. Many genetic variants of alpha 1-antitrypsin can be detected by electrophoretic techniques. We used isoelectric focusing on ultrathin gels to determine the common M subtypes as well as other variants of alpha 1-antitrypsin in 62 white patients with rheumatoid arthritis (RA) and 51 white patients with systemic sclerosis (SSc). We found no increased prevalence of variant phenotypes in either disease group as a whole. In RA, however, the association between pulmonary interstitial fibrosis and alpha 1-antitrypsin variants was striking. Interstitial fibrosis was seen on chest roentgenogram in only 1 of 30 subjects apparently homozygous for M1 (the "wild type" or "normal" phenotype), compared with 13 of 32 patients with variant phenotypes. Seven of 15 patients with M1M2 (the most common variant phenotype) had pulmonary fibrosis. In contrast, there was no apparent association of variant phenotypes with pulmonary involvement in SSc. Our findings suggest a possible role of alpha 1-antitrypsin in the pathogenesis of interstitial fibrosis in patients with RA. The absence of such an association in SSc suggests that pulmonary involvement in these 2 rheumatic diseases may have different pathogeneses.

Digital vasculitis following allergic desensitization treatment.

Systemic necrotizing vasculitis or a polyarteritis nodosa-like clinical presentation, is an unusual complication of immunotherapy (hyposensitization therapy). We describe a patient who developed features of vasculitis several years after beginning hyposensitization treatment for allergic rhinitis. In the 7 months preceding the onset of the vasculitis he experienced 4 episodes of anaphylaxis immediately after receiving desensitization injections. The vasculitis was characterized by the abrupt onset of pain and discoloration of the middle 3 digits of his right hand. Cyanosis and small areas of frank necrosis of these digits were present. Erythrocyte sedimentation rate and C-reactive protein were elevated and total serum complement was decreased. The development of digital vasculitis following hyposensitization is clearly illustrated in this patient.

Immune complexes in synovial fluid and serum from patients with disseminated gonococcal infection: evidence for local immune complex formation within the joint.

Twenty one patients with acute arthritis associated with disseminated gonococcal infection (DGI) were studied. Synovial fluid (SF) from 14 and serum from 15 (matched in eight) were assayed for the presence of immune complexes (IC) by the Raji cell immunofluorescent assay (Raji IFA) and the 125I-Clq polyethylene glycol (PEG) binding assay. Higher levels and frequency of IC were detected in the SF by both IC assays and these were associated with a significant increase in complexes containing IgM over serum (p less than 0.02). Complexes containing IgG were found predominantly in serum and were infrequent in SF (p less than 0.003). These data suggest that the arthritis of DGI may result from primary immune complex formation within the synovial cavity after local antibody synthesis within the synovium in response to gonococcal seeding.