Rheumatoid Arthritis Nodules Research Articles

Computer-Aided Diagnosis of Pulmonary Nodules in Rheumatoid Arthritis.

(1) Background: Rheumatoid arthritis (RA) is considered a systemic inflammatory pathology characterized by symmetric polyarthritis associated with extra-articular manifestations, such as lung disease. The purpose of the present study is to use CAD in the detection of rheumatoid pulmonary nodules. In addition, we aim to identify the characteristics and associations between clinical, laboratory and imaging data in patients with rheumatoid arthritis and lung nodules. (2) Methods: The study included a number of 42 patients diagnosed with rheumatoid arthritis according to the 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) criteria, examined from January 2017 to November 2022 in the Departments of Rheumatology and Radiology and Medical Imaging of the University of Medicine and Pharmacy of Craiova. Medical records were reviewed. A retrospective blinded review of CT for biopsy-proven pulmonary nodules in RA using Veolity LungCAD software was performed (MeVis Medical Solutions AG, Bremen, Germany). Imaging was also reviewed by a senior radiologist. (3) Results: The interobserver agreement proved to be moderate (κ = 0.478) for the overall examined cases. CAD interpretation resulted in false positive results in the case of 12 lung nodules, whereas false negative results were reported in the case of 8 lung nodules. The mean time it took for the detection of lung nodules using CAD was 4.2 min per patient, whereas the detection of lung nodules by the radiologist was 8.1 min per patient. This resulted in a faster interpretation of lung CT scans, almost reducing the detection time by half (p < 0.001). (4) Conclusions: The CAD software is useful in identifying lung nodules, in shortening the interpretation time of the CT examination and also in aiding the radiologist in better assessing all the pulmonary lung nodules. However, the CAD software cannot replace the human eye yet due to the relative high rate of false positive and false negative results.

SYMPTOMATIC PULMONARY AND INTRACRANIAL NODULES IN A PATIENT WITH LONGSTANDING, UNCONTROLLED RHEUMATOID ARTHRITIS

SESSION TITLE: Medical Student/Resident Pulmonary Manifestations of Systemic Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pulmonary manifestations of rheumatoid arthritis (RA) are found in 60-80% of all RA patients and are responsible for 10-20% of RA-related mortality. RA nodules are observed in approximately 20% of RA patients with 20- 32% prevalence pulmonary RA nodules. Rarer intracranial RA nodules have been described in two case studies.1 Here we present a patient who demonstrates significant symptomatic pulmonary nodulosis along with intracranial nodules leading to intractable seizures and ventilator support. CASE PRESENTATION: Our patient was a 67-year-old woman with a 9-year history of RA, recurrent bilateral knee septic arthritis, and three months of focal seizures who presented to the emergency department for breakthrough focal seizures. Prior magnetic resonance imaging (MRI) showed contrast enhancing right temporal and right thalamic nodules up to 4mm consistent with electroencephalogram (EEG) localization of the seizures. Rheumatologically, the patient had RA flares multiple times per month despite maximal doses of hydroxychloroquine, leflunomide, and methrotrexate (MTX). 6 months prior, an outpatient Chest CT ordered for evaluation of dyspnea showed multiple solid and cavitary pulmonary lesions. Endobronchial ultrasound with biopsy of nodules showed necrotizing granulomatous inflammation consistent with RA nodules. During hospitalization, the patient presented with mildly elevated CRP, RF, and anti-CCP, and mildly decreased complement C3 but otherwise normal exam and negative serologic and cerebrospinal fluid tuberculosis, fungal, bacterial, viral, cancer and autoimmune workup. Repeat imaging showed multiple new bilateral pulmonary nodules up to 2.3 cm with stable intracranial nodules despite empiric acyclovir. The patient continued to have seizures in the unit despite maximal doses of intravenous seizure medication, six days later developing, ultimately fatal severe metabolic acidosis, bradycardia, and hypotension. DISCUSSION: This unique case of symptomatic intracranial and pulmonary nodules in the setting of RA does not have much literature accompaniment, but we hope to add our experience to a potential disease etiology. Several case reports, however, do show reduction in pulmonary nodule size with oral steroid courses. There is currently no strong consensus on treatment of RA nodules. While RA nodules are often considered relatively benign, in this patient the EEG and imaging finding suggest that the nodules may have significantly contributed to this patient’s breakthrough seizures. Unfortunately due to this patient’s comorbidities and tenuous medical status, pathologic review of the brain lesions was not obtained. CONCLUSIONS: This report highlights the need to consider RA as a potentially reversible cause when considering unexplained systemic findings, as well as the need for more research into treatment of extraarticular manifestations of RA. Reference #1: Esposito AJ, Chu SG, Madan R, Doyle TJ, Dellaripa PF. Thoracic Manifestations of Rheumatoid Arthritis. Clin Chest Med 2019;40(3):545–560. DISCLOSURES: No relevant relationships by Oleh Hnatiuk, source=Web Response No relevant relationships by adarsh vangala, source=Web Response No relevant relationships by Nicholas Villalobos, source=Web Response

RARE PRESENTATION OF LUNG DISEASE IN RHEUMATOID ARTHRITIS

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Rheumatoid Arthritis (RA) is a common and functionally disabling disease. Over 2 million adults in the United States have RA. Pulmonary complications are common and responsible for 10 to 20% of all mortality. Rheumatoid nodules are the most common pulmonary manifestations of RA and are usually asymptomatic. In rare cases, they progress to cavitary formation and cause severe clinical symptoms. The following case documents a patient with RA who was found to have cavitary lesions in the lungs. CASE PRESENTATION: 59-year-old male with history of RA (diagnosed in 2014) came to the pulmonologist office for follow up. Patient currently takes Methotrexate and Leflunomide but was off these medications due to insurance issues. Patient was having a dry cough, but no other pulmonary symptoms such as hemoptysis or pleuritic chest pain. Patient denied fever, chills, night sweats or weight loss. A review of his labs showed positive ANA, dsDNA, antihistone, rheumatoid factor, anti-CCP antibodies, along with elevated ESR and CRP. ANCA- myeloperoxidase and proteinase 3, as well as TB Quantiferon testing was negative. Patient's most recent pulmonary function tests failed to show any air flow limitation. Patient had a CT chest in May 2018, which showed multiple sub-centimeter pulmonary nodules with some of them having cavitation (Figure 1). A follow up CT chest was done in Feb 2019 which showed interval increase in size and degree of cavitation in the pulmonary nodules (Figure 2). There is no bronchiectasis, ground glass opacities, or honeycombing. Bronchoscopy was done and BAL was negative for viral inclusions and malignant cells. Negative for pneumocystis and other fungi. DISCUSSION: Most patients with RA found to have cavitary pulmonary nodules present with more severe pulmonary findings compared with non-cavitary lesions, and a longer disease duration. Anti-rheumatic drugs, especially Leflunomide, may play a role in the development of this clinical presentation. This patient who was diagnosed with RA was on Leflunomide therapy, however, had a relatively short disease course (5 years) and rapidly progressing cavitary lesions, which is uncommon. CONCLUSIONS: There is insufficient data about cavitary lesions in relatively newly diagnosed RA. There is a need to formulate new studies to gather data on newly diagnosed disease with rapidly progressing lung cavitations. The high frequency of Leflunomide therapy in patients with RA with cavitary pulmonary nodules should also be emphasized. Reference #1: Brown KK. Rheumatoid lung disease. Proc Am Thorac Soc. 2007;4(5):443-8. Reference #2: Kanıtez, N. A., Çelik, S., Öner, S. Y., Ürer, H. N., Bes, C., & Çetinkaya, E. (2017). Cavitary pulmonary nodules in rheumatoid arthritis; case reports and review of the literature. European journal of rheumatology, 5(1), 65-68. DISCLOSURES: No relevant relationships by Upneet Chawla, source=Web Response

Cavitary pulmonary nodules in rheumatoid arthritis; case reports and review of the literature.

Rheumatoid nodules are the most common pulmonary manifestations of rheumatoid arthritis (RA) and are usually asymptomatic. In rare cases, they progress cavitary formation and cause severe clinical symptoms because of disease activity, infectious diseases, and other etiologies. The determination of clinical and histopathological features may be helpful for differential diagnosis in patients with RA with cavitary pulmonary nodules. Herein, we report two female patients with RA with cavitary pulmonary nodules and aim to obtain more detail data by means of reviewing previously reported cases.

Subjective audiological tests and transient evoked otoacoustic emissions in patients with rheumatoid arthritis: analysis of the factors affecting hearing levels

We investigated hearing functions in patients with rheumatoid arthritis (RA) using audiological tests and transient evoked otoacoustic emissions (TEOAEs). The study group consisted of 20 adult patients with RA (7 males, 13 females); 20 adult healthy subjects without RA (7 males, 13 females) were recruited as controls. All patients were evaluated by pure tone audiometry, high frequency audiometry, tympanometry and TEOAEs. There were no statistical differences between the study and control groups with respect to the pure tone and high frequency audiometries. TEOAE results of 1.0-2.0 kHz % and of 1.5 and 3.0 kHz amplitude values were significantly lower, and ipsilateral stapes reflex threshold value at 1.0 kHz was significantly higher in the study group when compared to respective values in the control group. In elderly patients and those with longer disease duration, RA nodules and higher methotrexate cumulative doses, hearing thresholds increased and TEOAE values decreased. In active stage of the disease, hearing thresholds diminished and in higher Brinkman Index values, TEOAE values decreased. Compliance values decreased in patients with higher Ritchie Articular Index, C-reactive protein, erythrocyte sedimentation rate and platelet counts, and longer disease duration. Sensorineural hearing loss is generally observed in patients with RA, and this condition may be detected by TEOAEs in an early period of the disease. Inflammation during the active stage of the disease and the subsequent fibrosis may cause conductive hearing loss of varying degrees. In those patients detected as having initiation of TEOAE decrease, vasodilator treatment and antioxidant drugs may be useful in protecting the inner ear.

Skin Nodules in Rheumatoid Arthritis Due to Infection with Mycobacterium haemophilum

This article does not have an abstract.

Pulmonary Pathology of the Rheumatic Diseases

Thoracic manifestations of the rheumatic diseases (RDs) are a significant cause of morbidity and mortality worldwide. The five RDs most frequently associated with pleuropulmonary disease are (1) rheumatoid arthritis (RA), (2) systemic lupus erythematosus (SLE), (3) progressive systemic sclerosis (PSS), (4) polymyositis/dermatomyositis (PM/DM), and (5) Sjögren syndrome (SS). The clinical presentation is highly variable, ranging from pleuritic pain alone to slowly progressive breathlessness accompanied by cough. On occasion RD may present acutely with overwhelming respiratory failure as the first pulmonary manifestation. In all of the RDs, the pathology is dominated by either or both inflammation and fibrosis, but the anatomical distribution in each varies somewhat. For example, airway-associated lymphoid hyperplasia is a common manifestation of SS, PM/DM preferentially involves the alveolar parenchyma, and pleural inflammation is most commonly seen in RA. Such changes may be detected radiologically as peribronchovascular disease in SS, ground-glass infiltrates in PM/DM, and pleural disease with effusion in RA. Some RDs are more commonly associated with distinctive histopathology, such as rheumatoid nodules in RA, or lymphoid hyperplasia in both RA and SS. Patients with PSS are at particular risk for pulmonary hypertension when the lung is involved. Also, statistically, acute lung injury occurs more commonly in some, such as SLE and PM/DM. The very common use of immunosuppressive agents in the treatment of RD creates additional diagnostic problems related to drug toxicity and infection. Finally, a major confounding factor occurs when preclinical RD presents first as pulmonary disease (particularly PM/DM), an occurrence that may invoke one of the so-called idiopathic interstitial pneumonias. The most common pleuropulmonary pathological manifestations of the five major RDs are presented and discussed with brief radiological correlations.

Pulmonary rheumatoid nodules demonstrating features usually associated with rheumatoid synovial membrane

To describe the unusual immunohistological characteristics of two pulmonary rheumatoid nodules showing ectopic lymphoid follicles and the features normally associated with rheumatoid synovial membrane, and to discuss the implications of this novel observation. Two formalin-fixed wax-embedded pulmonary rheumatoid nodules were processed for immunohistology. The central structure of the pulmonary nodules was typical of that uniformly expected in a rheumatoid nodule with central necrosis surrounded by a palisade of macrophages. However, a feature not previously observed in nodules was the presence of lymphoid aggregates containing B lymphocytes and, in some cases, showing characteristic features of lymphoid follicles. The presence of B lymphocytes and the development of ectopic lymphoid follicles in rheumatoid nodules have not been described previously. It is similar to synovial membrane, and contrasts with the expected structure of subcutaneous nodules where B cells and lymphoid follicles are normally absent. These observations establish that the morphology of rheumatoid nodules can vary in different tissues. They further suggest that the inflammatory process in the nodule and synovial membrane are likely to be similar, and that the characteristics of different tissues may be an important determinant of apparent differences between inflammatory lesions in synovial membrane and extra-articular nodules in rheumatoid arthritis.

Large benign rheumatoid nodules of the trunk in an elderly patient: radiologic appearance mimicking a soft-tissue sarcoma

An 80-year-old woman without any evidence of rheumatoid arthritis presented with two large (maximum diameter: 6 cm and 7 cm), rapidly growing, rubbery nodules on the trunk. Although the clinical and radiological appearance suggested malignancy, the nodules were pathologically identical to rheumatoid nodules in rheumatoid arthritis, and the nodules regressed spontaneously. The final diagnosis was benign rheumatoid nodules. Recognition of this rare clinical entity is important to avoid unnecessary examination and treatment.

A case of multiple pulmonary nodules

Summary A 58-year-old male smoker presented with pyrexia, dyspnoea and cough productive of green sputum. Chest X-ray revealed a left upper lobe infiltrate and three nodules in the left mid and lower zones. This X-ray also revealed evidence of previous atlanto-axial subluxation. Computed tomography and bronchoscopy confirmed rheumatoid lung disease. We discuss the assessment and management of nodules in rheumatoid arthritis.

Cardiovascular death in rheumatoid arthritis: A population‐based study

To determine whether systemic inflammation confers any additional risk for cardiovascular death among patients with rheumatoid arthritis (RA), after adjusting for traditional cardiovascular risk factors and comorbidities. Using the population-based data resources of the Rochester Epidemiology Project, we assembled an incidence cohort of all Rochester, Minnesota residents ages >or=18 years who first fulfilled the American College of Rheumatology 1987 criteria for RA between January 1, 1955 and January 1, 1995. All subjects were followed up longitudinally through their complete (inpatient, outpatient) medical records, beginning at age 18 years and continuing until death, migration, or January 1, 2001. Detailed information on the occurrence of various cardiovascular risk factors (personal history of coronary heart disease [CHD], congestive heart failure, smoking, hypertension, dyslipidemia, body mass index [BMI], diabetes mellitus, menopausal status) as well as indicators of systemic inflammation and RA disease severity (rheumatoid factor [RF] seropositivity, erythrocyte sedimentation rate [ESR], joint swelling, radiographic changes, RA nodules, RA complications, RA treatments, disease duration) and comorbidities were collected on all subjects. Causes of death were ascertained from death certificates and medical records. Cox regression models were used to estimate the independent predictors of cardiovascular death. This inception cohort comprised a total of 603 RA patients whose mean age was 58 years, of whom 73% were women. During a mean followup of 15 years, 354 patients died and cardiovascular disease was the primary cause of death in 176 patients. Personal history of CHD, smoking, hypertension, low BMI, and diabetes mellitus, as well as comorbidities, including peripheral vascular disease, cerebrovascular disease, chronic pulmonary disease, dementia, ulcers, malignancies, renal disease, liver disease, and history of alcoholism, were all significant risk factors for cardiovascular death (P < 0.01 for each). Multivariable Cox regression analyses, controlled for cardiovascular risk factors and comorbidities, revealed that the risk of cardiovascular death was significantly higher among RA patients with at least 3 ESR values of >or=60 mm/hour (hazard ratio [HR] 2.03, 95% confidence interval [95% CI] 1.45-2.83), RA vasculitis (HR 2.41, 95% CI 1.00-5.81), and RA lung disease (HR 2.32, 95% CI 1.11-4.84). These results indicate that markers of systemic inflammation confer a statistically significant additional risk for cardiovascular death among patients with RA, even after controlling for traditional cardiovascular risk factors and comorbidities.

The HLA-DRB1*0401 Allele and the Development of Methotrexate-Induced Accelerated Rheumatoid Nodulosis

The HLA-DRB1*0401 Allele and the Development of Methotrexate-Induced Accelerated Rheumatoid Nodulosis

HRCT of the lung in collagenoses

Collagen vascular diseases, representing systemic soft tissue disorders, may cause a broad spectrum of pathologic changes of the respiratory tract. The type and extent of manifestations can vary considerably among individuals and entities. This survey describes the chest radiographic and, in particular, high-resolution computed tomographic (HRCT) findings of individual lesions of the respiratory tract. It includes fibrosing alveolitis (alveolitis, interstitial pneumonia, pulmonary fibrosis) and bronchial (bronchitis/bronchiolitis, bronchiectasis), pleural and vascular manifestations, as well as lymphadenopathy and abnormalities related to therapy. We present typical patterns of changes in progressive systemic sclerosis (PSS, scleroderma), systemic lupus erythematosus (SLE), mixed connective tissue disease (MCTD, Sharp syndrome), Sjögren syndrome, overlap syndrome and rheumatoid arthritis (RA). Furthermore, we describe findings which are specific for individual entities such as esophageal involvement in PSS, acute pneumonitis and pulmonary hemorrhage in SLE, lymphoproliferative disease in Sjögren syndrome and necrobiotic nodules in RA.

Low dose long-term corticosteroid therapy in rheumatoid arthritis: An analysis of serious adverse events

purpose: The purpose of this study was to better define the toxicity of low dose (less than or equal to 15 mg/d prednisone or equivalent) long-term (greater than 1 year) corticosteroids in the treatment of rheumatoid arthritis (RA). patients and methods: We examined an historical cohort of 112 RA patients on low dose (6.1 ± 3.1 mg/d, mean ± SD) long-term (6.2 ± 4.6 years) prednisone (CS) and compared them to 112 matched RA patients not using prednisone (CO). CS were matched one-to-one with CO for sex (75% women), age (±5 yrs), race (98% white), and duration of disease (±5 yrs). Subjects were determined by review of unselected medical records from three distinct rheumatology practice settings. For CS, charts were abstracted from the date of prednisone start for pre-defined adverse events (AEs). results: Ninety-two (92) AEs were noted in CS versus 31 in CO and included: fracture (CS:21 versus CO:8), serious infections (CS:14 versus CO:4), gastrointestinal (GI) bleed or ulcer (CS:11 versus CO:4), and cataracts (CS:17 versus CO:5). At time of first AE, CS prednisone average dose was 7.0 ± 2.6 mg with a duration of 4.9 ± 3.9 years. Stepwise multiple logistic regression analysis was used to create a model which included all clinically relevant variables and all parameters significantly different at the cohort inception. Prednisone average dose of greater than 10 to less than or equal to 15 mg/d correlated most strongly with the development of an AE (Odds Ratio (OR) = 32.3, 95% Confidence Interval (CI) 4.6, 220). Average prednisone 5 to 10 mg (OR = 4.5, 95% CI 2.1, 9.6), RA nodules (OR = 3.9, 95% CI 1.9, 8.0), and bony erosions (OR = 2.4, 95% CI 1.2, 4.7) also entered the final model. Kaplan Meier survival curves for the development of the first AE showed a dose-response relationship between prednisone and AE occurrence, independent of rheumatoid nodules. Subset analyses utilized a nested case control design for the development of three serious AEs: fractures, serious infections, and GI events. These analyses revealed possible relationships between prednisone use and the development of each specific AE (prednisone use OR: fracture 3.9, 95% CI 0.8, 18.1; infection 8.0, 95% CI 1.0, 64.0; and GI event 3.3, 95% CI 0.9, 12.1). conclusions: Although disease severity is an important confounding factor, low dose long-term prednisone use equal to or greater than 5 mg/d is correlated with the development of specific adverse events in a dose-dependent fashion.

Antikeratin antibodies in serum and synovial fluid show specificity for rheumatoid arthritis in a study of connective tissue diseases.

Tests for antikeratin antibodies (AKA) were performed on 2152 disease-associated and control sera by indirect immunofluorescence (IF) on rat oesophagus substrate. The incidence of AKA was significantly raised in rheumatoid arthritis (37%) in comparison with systemic sclerosis (8%), psoriasis (7%), ankylosing spondylitis (6%), systemic lupus erythematosus (3%), and normal controls (2%). AKA were detected in synovial fluid obtained from patients with rheumatoid arthritis (RA) (48%) but not from patients with other conditions. Further experiments on AKA-positive sera showed reactivity with stratum corneum of rabbit prepuce and lips. A specific rabbit antihuman keratin antiserum was shown, by IF and inhibition studies, to have a different specificity from that of spontaneous human AKA. AKA were associated with the presence of subcutaneous nodules in RA (p = 0.05), but not with Raynaud's phenomenon, Sjögren's syndrome, or HLA-DR4 positivity. Rheumatoid factor (RF) was not associated with AKA either in RA or in RF-positive disease controls.

IgG and IgM rheumatoid factor in active seronegative nodular rheumatoid arthritis and in children with benign rheumatoid nodules.

Rheumatoid nodules in rheumatoid arthritis are usually associated with high levels of IgM rheumatoid factors and aggressive disease. IgM, IgG, and C3 have been identified in tissue sections of rheumatoid nodules, suggesting pathogenetic importance. The role of IgM and IgG rheumatoid factors in sero-negative RA is poorly understood. Seven patients with active seronegative RA and rheumatoid nodules and 10 seronegative children with the syndrome of benign rheumatoid nodules were studied for the presence of IgG and IgM rheumatoid factors by radioimmunoassay and for complement-fixing IgM rheumatoid factor by haemolytic assay. Elevated titres of hidden complement fixing IgM rheumatoid factor were found in 60 % of the patients with benign rheumatoid nodules studied but in none of the patients with active seronegative nodular RA. Serum IgG and IgM rheumatoid factor levels by radioimmunoassay and circulating immune complex levels in both groups were not significantly different from normal controls. These data suggest IgG and IgM rheumatoid factors do not participate in the pathogenesis of active seronegative rheumatoid arthritis with rheumatoid nodules.

Reticulohistiocytoma of the skin.

CUTANEOUS nodules are seen frequently in patients suffering from diseases of the joints. In most instances they occur as nodules of rheumatoid arthritis. Less often they are associated with rheumatic fever or gout. The nodular dermatosis that we are reporting bears a gross resemblance to the cutaneous lesions of the above diseases. Histopathologic examination shows that these nodules are unique, however, in being composed of masses of bizarre multinucleated giant cells. This dermatosis either is rare or has rarely been reported in the past, and the identity of the pathognomonic cells has been variously interpreted in the few cases that have been observed. Allen 1 studied sections from two cases, and he considered the nodules to be reticulohistiocytomas. In Allington's case 2 the diagnoses of gangliioneuroma, histiocytoma, and myoblastoma were considered. Zak 3 reported four cases as reticulohistiocytomas of the skin. In 1932 we prepared and studied sections from multiple lesions of a patient of Dr.

Subcutaneous Nodules of Rheumatoid Arthritis with Lipoid Deposition

Subcutaneous Nodules of Rheumatoid Arthritis with Lipoid Deposition

Rheumatoid Arthritis

Article1 July 1931Rheumatoid ArthritisRUSSELL L. CECIL, M.D.RUSSELL L. CECIL, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-5-1-23 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptRheumatoid arthritis might well be called the step-child of Medicine for the reason that, like some other chronic diseases, it has always received scant attention from both investigators and practitioners. Osler himself is quoted as having remarked that when an arthritic patient walked into his consultation room, he always had a strong inclination to jump out the window. Most of the research work on arthritis has been spasmodic or accidental, and until recent times few practitioners have made a special study of the disease.It is unfortunate that such a common malady should have received this neglect. Within the last...References1 MOONEDWARDS VHSH: Results of Blood Cultures in Rheumatoid Arthritis, J. Infect. Dis., 1917, 21:154. CrossrefGoogle Scholar2 RICHARDS JH: Bacteriologic Studies in Chronic Arthritis and Chorea, J. Bacteriol., 1920, 5:511. CrossrefMedlineGoogle Scholar3 BILLINGSCOLEMANHIBBS FGHWG: Chronic Infectious Arthritis: Statistical Report with End-Results, J. A. M. A., (April 15) 1922, 78:1097. CrossrefGoogle Scholar4 HADJOPOULOSBURBANK LGRA: Preliminary Study Bearing on the Specific Causative Factors of Multiple Infective Arthritis, J. Bone and Joint Surg., (April) 1927, 9:278. Google Scholar5 FORKNERSHANDSPOSTON CEARMA: Synovial Fluid in Chronic Arthritis, Arch. Int. Med., (Nov.) 1928, 42:675. CrossrefGoogle Scholar6 CECILNICHOLLSSTAINSBY RLEEWJ: The Bacteriology of the Blood and Joints in Chronic Infectious Arthritis, Arch. Int. Med., (May) 1929, 43:571. Bacteriology of the Blood and Joints in Rheumatic Fever, J. Exper. Med., (Nov.) 1929, 50:617. CrossrefGoogle Scholar7 CECILNICHOLLSSTAINSBY RLEEWJ: The Etiology of Rheumatoid Arthritis, Amer. J. Med. Sci., (Jan.) 1931, 181:12. CrossrefGoogle Scholar8 DAWSONOLMSTEADBOOTS MHMRH: Studies on Etiology of Rheumatoid Arthritis. II. Agglutination Reactions with Hemolytic Streptococci in Rheumatoid Arthritis, Proc. Soc. for Exper. Biol. and Med., 1931, 28:421. CrossrefGoogle Scholar9 NYEWAXELBAUM RNEA: Streptococci in Infectious Arthritis and Rheumatic Fever, J. Exper. Med. (Dec.) 1930, 52:885. CrossrefMedlineGoogle Scholar10 DAWSONOLMSTEADBOOTS MHMRH: Studies on the Etiology of Rheumatoid Arthritis. I. Bacteriological Investigations on Blood, Synovial Fluid and Subcutaneous Nodules in Rheumatoid Arthritis, Proc. Soc. for Exper. Biol. and Med., 1931, 28:419. CrossrefGoogle Scholar11 MARGOLISDORSEY HMAH: Chronic Arthritis: Bacteriology of Affected Tissues, Arch. Int. Med. (July) 1930, 46:121. CrossrefGoogle Scholar12 GRAYGOWEN JWCH: A Bacteriologic Study of Chronic Infectious Arthritis, J. Med. Soc. of N. J., 1931. Google Scholar13 SWIFTKINSELLA HFRA: Arch. Int. Med., (March) 1917, 19:381. CrossrefGoogle Scholar14 PARK WH: By personal communication. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York City*Presented before the Baltimore Meeting of The American College of Physicians, March 23rd, 1931. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 July 1931Volume 5, Issue 1Page: 23-28KeywordsArthritisRheumatoid arthritis ePublished: 1 December 2008 Issue Published: 1 July 1931 PDF downloadLoading ...

Studies on the Etiology of Rheumatoid Arthritis. II. Agglutination Reactions with Hemolytic Streptococci in Rheumatoid Arthritis.

The present authors reported bacteriological investigations on blood, synovial fluid and subcutaneous nodules in rheumatoid arthritis, which entirely failed to confirm the results of Cecil, Nicholls and Stainsby. Cecil, Nicholls and Stainsby further stated that the sera of patients suffering from rheumatoid arthritis possessed the property of agglutinating their “typical strains” to a remarkably high titre. Through the courtesy of Dr. Cecil several “typical strains” were made available. Specimens of serum were obtained from a large number of patients suffering from rheumatoid arthritis and agglutination tests were done using these strains as agglutinogens. For control purposes a large number of other organisms, obtained from a variety of sources, was similarly employed against the sera of patients with rheumatoid arthritis. The study was further controlled by utilizing a large number of specimens of serum obtained from patients suffering from both related and unrelated diseases. In addition to the “typical strains” of Cecil, Nicholls, and Stainsby, which, in the authors'experience, showed varying degrees of hemolytic properties, cultures of the following organisms were employed in the agglutination tests: (1) Streptococcus hemolyticus, 4 strains; these included strains obtained from scarlet fever, erysipelas and from the throat of a patient with rheumatic fever; (2) Streptococcus viridans, 7 strains; (3) Streptococcus anhemolyticus, 12 strains; (4) green diplococci (exact nature undetermined) 3 strains; (5) Staphylococci, 5 strains. Specimens of sera obtained from 66 patients suffering from typical rheumatoid arthritis were employed during the course of this study. Control sera were obtained from 50 cases of both related and unrelated diseases. These diseases included the following: osteo-arthritis, 18 cases; gonococcal arthritis, 4 cases; spondylitis, 8 cases; intermittent hydrarthrosis, 1 case; subacute rheumatic fever, 6 cases; non-articular rheumatism, 4 cases; other diseases—chronic nephritis, thromboangiitis obliterans, gastric ulcer, lung abscess, pulmonary tuberculosis, pneumonia, sacro-iliac strain, neurosis, tuberculous peritonitis—9 cases.