Since 1964 to present, there have been more than 33 cases of concomitant rheumatoid arthritis (RA) and gout reported in the literature. The objective of this study is to present a case series of patients with coexistent rheumatoid arthritis and gout and to provide a review of the literature. A retrospective review of a rheumatology patient database at the University of Alberta was performed (2004-2017). Patient charts were reviewed and the 1987 ARA Revised Classification Criteria for RA and 1977 ARA Classification Criteria for gout were applied to each patient. For gout, positive monosodium urate crystals on synovial fluid analysis, synovial/node biopsy, or positive dual-energy CT-gout protocol were used to satisfy the diagnosis of gout if available. Thirteen patients were identified with both RA and gout (nine men and four women). The mean age was 68.6, while the mean age at the onset of first disease was 55.3 and onset of second disease was 64.4. Eight patients were initially diagnosed with RA and subsequently developed gout, while five patients were first diagnosed with gout and subsequently developed RA. Standard radiographs showed findings characteristic of RA and gout in affected joints. In joints affected by both diseases, the gout findings predominated and the RA changes were milder. Rheumatoid arthritis and gout do coexist in the same patient, contrary to popular belief. Understanding that both conditions can occur concomitantly is necessary for clinical awareness, especially in patients with polyarticular disease that is difficult to treat.

To investigate the prevalence of monosodium urate (MSU) crystal deposits, indicative for gout, in a population of rheumatoid arthritis (RA) patients with concomitant hyperuricemia and to analyze the clinical and disease-specific characteristics of RA patients who exhibit MSU crystal deposits.

Overall, 100 consecutive patients with the diagnosis of RA and a serum urate level above 6mg/dl underwent dual energy computed tomography (DECT) of both feet and hands to search for MSU crystals in a prospective study between October 2011 and July 2013. Presence and extent of MSU crystal deposits on DECT was assessed by automated volume measurement. Demographic and disease-specific characteristics were recorded and included into two logistic regression models to test for the factors associated with MSU crystal deposits in RA.

Hyperuricemic RA patients were mostly male (55%), over 60 years of age (63 ± 11 years), had established disease (8.7 ± 10.5 years) and a mean disease activity score 28 (DAS 28) of 3.2. In total, 20 out of 100 patients displayed MSU crystal deposits in DECT. Interestingly, the majority (70%) of the RA patients positive for MSU crystal deposits were seronegative RA patients. Hence, every third seronegative RA patient had MSU crystal deposits. According to logistic regression model analysis, seronegative status correlated positively with presence of urate deposits (p = 0.019).

These data show that a considerable number of RA patients display periarticular MSU crystal deposits. Seronegative patients were shown to be predominantly affected with every third patient being positive for urate deposits.

Studies suggest that serum uric acid (SUA) is significantly associated with cardiovascular disease (CVD) mortality among women and blacks. CVD rates are higher among patients with rheumatoid arthritis (RA) than the normal population. The objective of this study was to determine if there was an association between SUA levels and self-reported RA in a multiethnic female population in the United States.

This cross-sectional study was conducted using data for 7374 women above 20 years of age in the Third National Health and Nutrition Examination Survey. Multiple and logistic regression methods were used to determine an association between SUA levels and self-reported RA.

Women self-reporting RA had significantly higher SUA levels (p < 0.0001) compared to women not self-reporting RA, also when adjusted for age and race (p < 0.0001). In a regression analysis, significant predictors of SUA levels were: self-reporting RA, race/ethnicity, being married, smoking, use of alcohol, high body mass index, high C-Reactive protein, elevated diastolic or systolic blood pressure, and increased glomerular filtration rate. Education and age were removed from the model. The model explained 24.0% of the variability seen in SUA levels (F = 208.62, p < 0.0001) in this multiethnic female population. When the analyses were repeated stratified by race, self-reporting RA was retained in the model as associated with SUA in white and Mexican American, but not in black women.

Despite the limitations imposed by self-reporting of RA on self-administered questionnaires and in-person interviews, practitioners should be aware that women self-reporting RA are at risk of having high SUA levels as well as more traditional CVD risk factors. These women should be offered appropriate preventive interventions related to their increased risk for CVD events.

Uric acid is released from injured cells and can act as an adjuvant signal to the immune system. Uric acid crystals invoke strong inflammatory responses in tissues. Although their biological effects are evident and the associated signaling mechanisms are becoming clear, it remains unexplained as to why uric acid precipitates rapidly in vivo, in sharp contrast to the minimal crystallization in vitro. We report in this study that a group of IgM Abs is able to bind to these crystals, which is interesting in light that B cell-deficient mice do not sense the proinflammatory adjuvant effect of uric acid. The titers of these Abs increase upon immunization with uric acid crystals. We have produced large quantities of such mAbs. The purified IgM Abs can significantly facilitate uric acid precipitation to form the inflammatory crystals in vitro. Infusion of these Abs into B cell-deficient mice significantly increases the basal level of inflammation in these recipients and restores the host's ability to sense uric acid's adjuvanticity. Therefore, we have identified a factor in determining uric acid precipitation and possibly its ability to function as an endogenous adjuvant. This finding suggests a new mechanism of the pathogenesis of gouty arthritis and uric acid-induced immune activation.

Copresent rheumatoid arthritis (RA) and gout is seldom reported. This study summarizes the findings of eight cases of copresent RA and gout and compares them with 31 pure RA cases. Additional reported cases were retrieved from the current literature by Medline search. Patients with copresent RA and gout were older (p = 0.014) and predominantly male (p < 0.01). Synovial fluid, positive for urate crystals, was aspirated most frequently from the knee (five out of eight), followed by the first metatarsophalangeal joint (three out of eight). Serum creatinine and urate levels in the copresent group were significantly higher (p < 0.01, both), and serum hemoglobin was lower (p = 0.04) than those with pure RA. Copresent subjects had much lower percentage of positive rheumatoid factor (RF) tests than patients with pure RA (37.5 vs 80.6%). Only one copresent subject had both RF and anti-cyclic citrullinated peptide antibody. Of copresent subjects, 75% had gouty arthritis before diagnosis of RA, which is consistent with earlier reports. Seven copresent subjects had gout attacks under disease-modifying antirheumatic drug use. This study revealed that polyarthritis negative for RF in a previously gouty patient may be RA and vice versa. This combination occurs more frequently in males. Moreover, anti-CCP antibody examination is not helpful for this diagnosis. Therefore, physicians must obtain synovial fluid for analysis in joints with intense swelling, especially in old RA subjects with renal insufficiency or involvement of lower extremities. Conversely, RA must be considered in gouty patients with polyarticular involvement.

The aim of this study was to investigate the clinical characteristics of patients with coexisting ankylosing spondylitis (AS) and gout. Between July 1987, and October 2004, sixty-five patients with coexisting AS and gout were enrolled. The clinical manifestations of both AS and gout in these patients were studied. Of the 65 patients included in the study, 61 were men and four were women (men-to-women ratio, 15.3:1). Sixty-three subjects were Han Chinese, and two were Atayal Aborigines. Mean ages at onset of AS and gout were 29.3 +/- 15.6 years (range 7-63) and 42.2 +/- 13.2 years (range 20-74), respectively. Fifty-six patients developed gout after (15.5 +/- 11.2 years; range, 1-51 years) onset of AS; nine patients developed gout before (average, 3.4 +/- 2.2 years; range. 1-7 years) onset of AS. Forty-four (67.7%) patients had chronic peripheral arthritis and all 65 (100%) patients had acute peripheral arthritis. Thirty-three (50.8%) cases had heel pain (enthesopathy), including 22 (33.9%) with chronic heel pain, seven (10.8%) with acute heel pain, and four (6.2%) with concurrent acute and chronic heel pain. Sixty-one (93.9%) subjects were HLA-B27 antigen positive. Medical conditions potentially associated with hyperuricemia or gout were urolithiasis (n = 17), hypertension (n = 21), diabetes mellitus (n = 8), hyperlipidemia (n = 34), congestive heart failure (n = 6), coronary heart disease (n = 5), and stroke (n = 3). The following drugs were prescribed: diuretics (n = 7), low-dose aspirin (n = 4), antituberculous drugs (n = 1), and sulphasalazine (n = 34). Six (6.2%) patients had iatrogenic Cushing syndrome with adrenal insufficiency. Patients with coexisting AS and gout are not rare. Distinguishing between peripheral arthritis or enthesopathies of AS and gout is essential, especially when the course of AS arthritis becomes acute or the course of gout becomes chronic.

To analyze the factors which differentiate chronic tophaceous arthritis from rheumatoid arthritis.

We describe two cases of chronic gouty arthritis masquerading as rheumatoid arthritis. The characteristic features of each of these two conditions and the diagnostic approach are discussed in light of relevant literature.

The correct diagnosis was reached by the combination of accurate history taking (family history of gout, alcoholism, previous diuretic therapy and renal stones), guiding clinical features (subcutaneous tophaceous deposits) and specific radiological (assymetrical erosions with sclerotic margins and overlying edges) and laboratory findings (hyperuricemia and hyperuricosuria). It was confirmed by the identification of monosodium urate (MSU) crystals in the synovial and subcutaneous tissues.

Gout and rheumatoid arthritis rarely coexist. Chronic gouty arthritis may mimic rheumatoid arthritis, and vice-versa. Clinical suspicion supplemented by characteristic laboratory, radiological and histologic findings help at reaching an accurate diagnosis.

To investigate any relationship between the nature, size, and numbers of synovial fluid (SF) calcium pyrophosphate dihydrate (CPPD) crystals, and attacks of pseudogout.

Knee SF was aspirated from nine selected patients, first during an attack of pseudogout (acute sample) and again later when the attack had subsided (interval sample). CPPD crystals were extracted, weighed, examined by high resolution transmission electron microscopy (HRTEM), and characterised by size and crystal habit (monoclinic or triclinic). Structural analysis was carried out by x ray powder diffraction (XRD) and the proportions of monoclinic to triclinic CPPD were estimated from densitometric measurements of selected key reflections.

The mean crystal size, by HRTEM, indicated that the crystals in the acute sample were larger than those in the interval sample. The ratio of monoclinic to triclinic CPPD, whether estimated from their morphological appearance by HRTEM, or from XRD, was greater in the acute than in the interval sample in all nine patients. The total amount of extracted mineral varied, but in every patient the concentration of CPPD per ml of fluid, and the total mineral per joint, were greater in the acute sample than in the interval sample.

In this highly selected group of patients, the large numbers of CPPD crystals associated with attacks of pseudogout included a greater proportion of monoclinic crystals, and larger crystals, than those present when inflammation had subsided. A special, phlogistic population of crystals may exist, originating in different joint tissues, or cleared in a different manner, than the more common populations of smaller crystals with a greater proportion of triclinic CPPD, seen in chronic disease.

Polymorphonuclear leukocytes (PMNs) isolated from peripheral blood and synovial fluid of patients with rheumatoid arthritis and from peripheral blood of volunteers were stimulated with 12-phorbol-13-myristate acetate (PMA). No significant differences in luminol-amplified chemiluminescence were found between different patients and control groups. However, two distinct patterns of native chemiluminescence were observed. Type I showed no, or only a small, increase in native chemiluminescence with integral counts over 30 min less than 3 x 10(5) cpm, and the majority of samples from volunteers were of this type. Type II was characterized by a burst of native chemiluminescence starting 8 to 15 min after cell stimulation. It was found in most PMN samples from patients with rheumatoid arthritis. Integral counts over 30 min were always higher than 10(6) cpm and as high as 10(8) cpm in some cases. A strong inhibition of the Type II native chemiluminescence was caused by desferal, catalase, thiourea, and glutathione. However, the luminol-amplified chemiluminescence remained unchanged or was only slightly decreased under the same experimental conditions. Sodium azide strongly inhibited both kinds of luminescence. Hydroxyl radicals, formed in a Fenton reaction, may be important intermediates in the Type II native chemiluminescence.

Urate crystal formation, and subsequent gout, occurs in only a minority of hyperuricaemic subjects indicating that factors other than hyperuricaemia are involved. Biological substances (especially proteins) alter crystal growth in vitro independently of uric acid concentration. Physiological crystal formation, known to be under biological control, is characterised morphologically by uniformity of size and constraint of crystal shape. To determine whether pathological urate crystal formation is influenced by the surrounding biological milieu we examined, using scanning electron microscopy, the morphology of urate crystals formed either in vivo or in vitro. We found morphological evidence of biological control of in vivo urate crystal formation and demonstrated that those characteristics could be induced in vitro by the addition of serum, synovial fluid and certain serum proteins to the growth medium during crystal formation. Urate crystal formation is dependent, not only on the degree of hyperuricaemia, but also on the surrounding biological milieu.

The effect of coating monosodium urate crystals (MSU) with low density lipoprotein (LDL), postulated previously as a major regulator of gouty inflammation, was studied in a neutrophil chemiluminescence (CL) assay and an air pouch model of inflammation induced by MSU. LDL crystalline coating abrogated the neutrophil CL response but, in contrast, had no inhibitory effect on leucocyte accumulation, levels of the prostaglandin (PG) metabolite 6-keto-PGF1 alpha, and exudation of plasma proteins in the in vivo model. This latter observation raises doubts about the postulated physiological role of LDL in terminating the acute gouty attack.