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Background: Local complications (encapsulation, rashes, rupture, and leakage) can occur after placement of silicone gel-containing breast implants (SBI). Whether SBI exposure results in systemic manifestations in some recipients is controversial. We have carried out a blinded study to assess whether there is any difference between SBI recipients and non-exposed controls in the proportions positive for serum antibodies directed against polymeric substances.Methods: We recruited female SBI recipients (including those without symptoms) who presented to a single rheumatology clinic. A physician global assessment was used to classify SBI recipients who did not meet criteria for specific autoimmune diseases according to the severity of local and systemic signs and symptoms. Controls were recruited from among clinic staff and their acquaintances. Results of the antipolymer antibody (APA) assay were compared with those of an assay for antinuclear antibodies (ANA) and with the severity of the signs and symptoms.Findings: Positive APA results were found in one (3%) of 34 SBI recipients with limited symptoms, two (8%) of 26 with mild symptoms, seven (44%) of 16 with moderate symptoms, and 13 (68%) of 19 with advanced symptoms. Four (17%) of 23 healthy non-SBI-exposed controls and two (10%) of 20 non-exposed women with classic autoimmune diseases were positive for APA. Thus, women with moderate or advanced symptoms were significantly more likely than those with limited or mild symptoms, or non-exposed controls to have APA (p < 0.001). The proportion with positive ANA results was higher for women with classic autoimmune diseases 14 (70%) of 20 than for any SBI-exposed subgroup (0-33%).Interpretation: The APA assay can objectively contribute to distinguishing between SBI recipients with limited or mild signs and symptoms. SBI recipients with more severe manifestations, and patients with specific autoimmune diseases. Further studies will be needed to define the signs and symptoms associated with exposure to SBI. [ABSTRACT FROM AUTHOR]

Objective: The aim of the study is to describe a group of patients with a highly destructive and asymptomatic form of psoriatic arthritis, mimicking a Charcot-like joint disease., Methods: We studied 180 patients with psoriatic arthritis and identified 4 patients with arthritis mutilans mimicking a Charcot-like joint disease. Clinical history, physical exam, and immunological testing were performed as well as X-ray of affected joints. Synovial membrane and sural nerve biopsies were performed and diagnosis of psoriasis was confirmed by skin biopsy., Results: Four patients with psoriatic arthritis mutilans according to Moll and Wright classification criteria (1) and Charcot-like joint disease were identified and evaluated. There were 2 males and 2 females, all Caucasians. The mean age +/- SD was 57.8 +/- 14.2 years. Mean arthritis duration +/- SD was 6 +/- 4.6 years and mean cutaneous duration +/- SD was 13 +/- 10.4 years. All patients had polyarthritis and a sudden onset of bilateral, painless, and highly destructive arthropathy involving large, non-weight bearing (elbows) and weight bearing (knees), and also small joint of hands and feet. Synovial membrane biopsy showed findings similar to those found in Charcot joint disease, including ischemic neuropathy., Conclusion: A newly-recognized subset of patients with psoriatic arthritis and Charcot-like joint disease according to clinical, radiographic and histological features is described. The proposed neurovascular theory may explain the pathogenesis of this presentation.

Therapeutic agents from virtually every pharmacological class have been implicated in the development of drug-induced vasculitis. Clinical manifestations range from small vessel hypersensitivity vasculitis and leukocytoclastic vasculitis to clinical syndromes indistinguishable from classical systemic forms of vasculitis such as Wegener's granulomatosis, polyarteritis nodosa and Churg-Strauss syndrome (CSS). The exact pathogenic mechanisms involved remain to be elucidated; but both cell-mediated and humoral immunity appear to play important roles. Affected individuals may present with cutaneous involvement alone or life-threatening systemic involvement, which may result in severe and sometimes fatal illness. Since clinical presentation as well as serological and pathological parameters is identical to idiopathic forms of vasculitis, a high index of suspicion is necessary to accurately and expeditiously diagnose drug-induced vasculitis. Withdrawal of the offending agent alone is often sufficient to induce prompt resolution of clinical manifestations, obviating the need for systemic corticosteroids or more powerful forms of immunosuppression.

Many therapeutic agents, including recently introduced biologic response modifiers, can induce a variety of vasculitic manifestations ranging from small vessel hypersensitivity vasculitis and leukocytoclastic vasculitis to distinct vasculitic syndromes such as Wegener's granulomatosis, polyarteritis nodosa, and Churg Strauss syndrome. The pathogenic mechanisms remain to be defined and appear to be multifactorial, with cell-mediated and humural immune mechanisms playing important roles. Clinical presentation varies in severity from mild to severe and even fatal illness, can be self-limiting, or follows a more chronic protracted course. There are no significant differences in clinical presentation, serologic abnormalities, and pathologic findings with the idiopathic forms of vasculitis. However, it is extremely important to identify the offending drug because the discontinuation of the drug is often followed by a rapid improvement of the underlying vasculitic disorder.

Background: Poststreptococcal reactive arthritis (PSReA) is a recognized inflammatory articular syndrome that follows group A streptococcal infection in persons not fulfilling the Jones criteria for the diagnosis of acute rheumatic fever. Characteristic features include nonmigratory arthritis, lack of response to aspirin or nonsteroidal anti-inflammatory agents, and the presence of extra-articular manifestations, including vasculitis and glomerulonephritis. Whether or not patients with PSReA develop carditis is a point of contention., Methods: We analyzed the clinical features, laboratory findings, response to therapy, and outcome in patients diagnosed with PSReA between 1983 and 1998 and observed through April 2000. All patients were contacted, reexamined, and repeat antistreptolysin, rheumatoid factor, C3 and C4 complement components, and echocardiograms were performed., Results: Seventeen patients (4 men and 13 women) were included. All were of low socioeconomic status. All patients had acute severe arthritis that began shortly after a sore throat episode. Extra-articular involvement including tenosynovitis, vasculitis, and glomerulonephritis was relatively common. More importantly, none exhibited clinical and/or echocardiographic evidence of cardiac involvement. Longterm antibiotic therapy was not given., Conclusion: Cardiac involvement did not occur in this group of patients with PSReA. Prolonged prophylactic antibiotic therapy may not be required for adult patients presenting with PSReA.

A multitude of tests are available for the diagnosis and management of the vasculitides. Most of them are nonspecific but provide useful information that, when appropriately used in conjunction with the patient's history and physical examination can be of great assistance in arriving at a final diagnosis. In addition, information gathered may be of great help in monitoring disease activity and clinical response to therapy, in indicating the presence of specific organ system involvement, in monitoring toxicity of medication used, and in assessing prognosis. Serial measurements of acute phase reactants, complete blood cell count with differential, biochemistry profiles, urinalysis, and C3 and C4 levels should be obtained in all patients. Antineutrophil cytoplasmic antibodies (ANCA) determination provides valuable information and is highly specific for the diagnosis of small-vessel vasculitides, particularly Wegener's granulomatosis and microscopic polyangiitis. ANCA levels can be particularly useful to assess disease activity in these disorders. Hepatitis-B and, more importantly, hepatitis-C testing is extremely useful, particularly in the presence of liver involvement and associated risk factors. Angiographic studies may confirm the diagnosis, particularly if there is laboratory and clinical evidence of specific organ involvement. It should be noted, however, that angiography may be normal even when vasculitis is present, or the findings may be nonspecific. A definite diagnosis is provided by a tissue biopsy. This should be performed whenever there is access to clinically affected tissue.

Infection by human immunodeficiency virus is characterized by a myriad of clinical manifestations affecting almost every organ system in the body. If untreated, it follows an inexorable course, leading to a profound state of immunosuppression and eventually death from opportunistic infection and/or development of lymphoproliferative malignancy and Kaposi's sarcoma. Rheumatic manifestations may develop at any time of the clinical spectrum, but usually are more often seen in late stages. A variety of disorders may be seen, particularly Reiter's syndrome and undifferentiated spondyloarthropathy. Most patients do well with conventional anti-inflammatory therapy, but some will require the use of immunosuppressive-cytotoxic therapy.

Psoriasis and its related arthritis are chronic inflammatory disorders affecting predominantly the skin and synovium. Although their etiology remains to be established, multiple factors seem to play important roles in their pathogenesis. These environmental (eg, infectious agents and trauma), genetic, and immunologic factors are reviewed in this article.

Inflammatory musculoskeletal complaints are relatively common during the course of HIV infection, although they tend to be more frequent during late stages. The clinical spectrum is varied, ranging from arthralgias to distinct rheumatic disorders, such as Reiter's syndrome and psoriatic arthritis. The therapeutic management often poses a challenge, although most patients respond to conventional first- and second-line anti-inflammatory medications.

Methotrexate is an extremely effective drug in the treatment of psoriasis and psoriatic arthritis. In addition, it possesses a very high benefit-to-toxicity ratio compared with other therapies and immunosuppressive agents used in these disorders. Fortunately, most adverse events related to methotrexate are mild, but serious and life-threatening reactions, particularly liver toxicity, may occur. Careful monitoring is essential to prevent most undesirable side effects.

Better understanding of the etiopathogenic mechanisms and increasing recognition of the natural course of the spondyloarthropathies are leading to a more rational therapeutic approach to several of the disorders included within this large group of arthritides. Our traditional therapeutic approach to these conditions is being challenged, and a more aggressive therapeutic regimen is being advocated in a manner not too much different from that advocated for the treatment of rheumatoid arthritis. Combination therapy with either methotrexate and sulfasalazine or methotrexate and cyclosporine is being used more often and earlier, particularly in psoriatic arthritis. An issue, however, that remains unresolved is the proper use of antibiotic therapy.

Three hundred consecutive women with silicone breast implants (SBI), referred to the arthritis clinic with a variety of musculoskeletal complaints, were evaluated for the presence of underlying connective tissue disease. A complete history and physical examination were performed, as well as laboratory testing for C-reactive protein, rheumatoid factor; and autoantibody determination by indirect immunofluorescence and immunodiffusion. The group mean age was 44.4 years (range 25-69), the mean time from initial implant surgery to appearance of symptoms was 6.8 years (range: 6m-19y) and 83.3% of women studied had clinical manifestations highly suggestive of an underlying connective tissue disorder. Fifty-four percent met criteria for fibromyalgia and/or chronic fatigue syndrome, distinct connective tissue diseases was detected in 11%, undifferentiated connective tissue disease or human adjuvant disease was found in 10.6%, and a variety of disorders such as angioneurotic oedema, frozen shoulder, multiple sclerosis-like syndrome were present. Several other miscellaneous conditions including recurrent unexplained low grade fever, hair loss, skin rash, sicca symptoms, Raynaud's phenomenon, carpal tunnel syndrome, memory loss, headaches, chest pain, and shortness of breath were also seen accompanying specific and non-specific conditions. Seventy percent of patients who underwent explanation of the implants reported improvement of their systemic symptomatology. A significant proportion of SBI patients referred for rheumatic evaluation have clinical manifestations highly suggestive of an underlying connective tissue disease. Furthermore, improvement of their symptomatology follows explanation of the implants in over half of the patients.

Antiphospholipid antibodies (aPL) are associated with thrombosis, thrombocytopenia and recurrent fetal loss in humans and in some animal models. Immunization with beta 2 glycoprotein I (beta 2GPI) induced aPL production in normal rabbits and mice. However, the association of these antibodies with disease manifestations remains controversial. To determine whether induction of aPL by beta 2GPI immunization in an autoimmune strain of mice (MRL/++) would result in acceleration of clinical and serological autoimmune disease manifestations, three groups of 8-week-old female mice were studied. One group was immunized with beta 2GPI, and one with ovalbumin (OVA); the third was not immunized. After two booster injections, sera were analysed for the presence of anticardiolipin (aCL) and anti-DNA by ELISA and anti-nuclear antibody (ANA) by immunofluorescence. Mice were studied for thrombocytopenia, proteinuria, fecundity rates, litter sizes and the development of central nervous system dysfunction. Elevated levels of aCL, anti-DNA and ANA were detected in all beta 2GPI-immunized, in three OVA-immunized, and in none of the unimmunized mice. The anti-DNA antibodies were inhibited by CL micelles, suggesting cross-reactivity between aCL and anti-DNA. Platelet counts, fecundity rates and litter size were reduced in beta 2GPI-immunized but not in OVA-immunized or unimmunized mice. None of the mice developed neurological dysfunction or significant proteinuria over a 10-week period post-immunization. These findings suggest that beta 2GPI immunization induces aPL in MRL/++ mice associated with accelerated autoimmune manifestations resembling the antiphospholipid syndrome.

The eosinophilia-myalgia syndrome associated with L-tryptophan-containing products is highlighted by eosinophilia, incapacitating myalgias, and diverse multisystemic manifestations. In addition to involvement of the skin, skeletal muscle, and peripheral nerves, visceral damage has been quite prominent, particularly affecting the lungs, the heart, and the liver. Hepatic involvement has been manifested by altered liver tests but is clinically silent. We report the unique case of a woman with this syndrome who developed abdominal pain, a clinical picture of hepatitis and chronically abnormal liver tests. Histologic examination of the liver disclosed eosinophilic hepatitis with piecemeal necrosis. The occurrence of clinically overt hepatic involvement has not been reported previously. Potential mechanisms of liver damage in eosinophilia-myalgia syndromes are discussed.

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.

The effects of indomethacin on urinary protein excretion, levels of serum albumin and renal function were studied prospectively in six patients with systemic lupus erythematosus (SLE) and refractory nephrotic syndrome due to lupus nephritis. Two had membranoproliferative glomerulonephritis, two had diffuse proliferative glomerulonephritis, and one each had mesangioproliferative and membranous glomerulonephritis. All experienced a considerable reduction in urinary protein excretion and an increase in serum albumin. Indomethacin was discontinued in two patients because of side effects, and proteinuria recurred to pretreatment levels. The decrease of proteinuria continued during long-term treatment in three patients. Indomethacin did not cause a permanent decline in renal function. Our results suggest that therapy with indomethacin may be beneficial for the treatment of refractory nephrotic syndrome in selected SLE patients. However, because of potential side effects the administration of indomethacin should be monitored closely.