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ID PMID Title PublicationDate abstract
16082501 Almost all about citrulline in mammals. 2005 Nov Citrulline (Cit, C6H13N3O3), which is a ubiquitous amino acid in mammals, is strongly related to arginine. Citrulline metabolism in mammals is divided into two fields: free citrulline and citrullinated proteins. Free citrulline metabolism involves three key enzymes: NO synthase (NOS) and ornithine carbamoyltransferase (OCT) which produce citrulline, and argininosuccinate synthetase (ASS) that converts it into argininosuccinate. The tissue distribution of these enzymes distinguishes three "orthogonal" metabolic pathways for citrulline. Firstly, in the liver, citrulline is locally synthesized by OCT and metabolized by ASS for urea production. Secondly, in most of the tissues producing NO, citrulline is recycled into arginine via ASS to increase arginine availability for NO production. Thirdly, citrulline is synthesized in the gut from glutamine (with OCT), released into the blood and converted back into arginine in the kidneys (by ASS); in this pathway, circulating citrulline is in fact a masked form of arginine to avoid liver captation. Each of these pathways has related pathologies and, even more interestingly, citrulline could potentially be used to monitor or treat some of these pathologies. Citrulline has long been administered in the treatment of inherited urea cycle disorders, and recent studies suggest that citrulline may be used to control the production of NO. Recently, citrulline was demonstrated as a potentially useful marker of short bowel function in a wide range of pathologies. One of the most promising research directions deals with the administration of citrulline as a more efficient alternative to arginine, especially against underlying splanchnic sequestration of amino acids. Protein citrullination results from post-translational modification of arginine; that occurs mainly in keratinization-related proteins and myelins, and insufficiencies in this citrullination occur in some auto-immune diseases such as rheumatoid arthritis, psoriasis or multiple sclerosis.
16075171 Revision cervical spine surgery using transarticular or pedicle screws under a computer-as 2005 Jul BACKGROUND: The exact insertion of a cervical screw is technically demanding, especially when normal anatomic landmarks have been obscured and are difficult to identify, such as in revision surgery. The purpose of this study was to evaluate the efficacy of an image-guidance system to aid placement of transarticular and pedicular screws for revision cervical spine surgery. METHODS: Ten patients with recurrent myelopathy, including seven with cerebral palsy, two with a giant cell tumor, and one with rheumatoid arthritis, underwent computer-aided reconstruction surgery. The authors used a frameless stereotactic image-guidance system with simultaneous fluoroscopy. Postoperative computed tomography was used to determine the accuracy of the screw placement. RESULTS: There were no neurovascular complications and no correction loss. All patients showed solid bony union. All four C1/2 transarticular screws were exactly placed inside the pedicles. Of 47 pedicular screws, 11 showed a slight breach of the cortex. When a reference arc could not be attached to the relevant vertebra, the rate of cortical perforation of screws was high (5/10; 50%) compared with the rate when a reference arc was attached to the relevant vertebra (6/37; 16%). CONCLUSION: Although more advanced technology is hopeful, a computer-assisted image-guidance system with simultaneous fluoroscopy is useful for aiding revision surgery to achieve rigid fixation and ensure safety.
15976324 Atherosclerosis in patients with autoimmune disorders. 2005 Sep Recent findings indicate that presence of activated immune competent cells and inflammation are typical of atherosclerosis, the main cause of cardiovascular disease (CVD). The risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE), and is also raised in other autoimmune diseases such as rheumatoid arthritis. Autoimmunity-related CVD and atherosclerosis are important clinical problems. They may also shed light on interactions between immune reactions and atherosclerosis development and manifestations, not least in women, who have a much higher risk of autoimmune disease than men. In general, a combination of traditional and nontraditional risk factors, including dyslipidemia (and to a varying degree, hypertension, diabetes, and smoking), inflammation, antiphospholipid antibodies (aPLs), and lipid oxidation, contribute to CVD in autoimmune diseases. Premature atherosclerosis is likely to be a major underlying mechanism, although distinctive features, if any, of autoimmunity-related atherosclerosis compared with "normal" atherosclerosis are not clear. One interesting possibility is that factors such as inflammation, neoepitopes on endothelial cells, or aPLs make atherosclerotic lesions in autoimmune disease more prone to rupture than in "normal" atherosclerosis. Some cases of autoimmunity-related CVD may be more related to thrombosis than atherosclerosis. Whether premature atherosclerosis is a general feature of autoimmune diseases such as SLE or only affects a subgroup of patients whereas others do not have an increased risk remains to be demonstrated. Treatment of patients with autoimmune disease should also include CVD aspects and be focused on traditional risk factors as well as on disease-related factors. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation present in atherosclerotic lesions.
15912958 Possible anti-inflammatory role of COX-2-derived prostaglandins: implications for inflamma 2005 May Inflammation is the response of any tissue to injury or trauma. The inflammatory response forms the basis of several pathological and pathophysiological processes, including wound healing, rheumatoid arthritis and neurodegenerative disorders, including Alzheimer's disease and stroke. The response is mediated by various signaling molecules and enzymatic pathways, among which the cyclooxygenase (COX) pathway is one of the most predominant. COX catalyzes the formation of prostaglandins and thromboxanes from arachidonic acid (AA). In 1971, Sir John Vane demonstrated for the first time that the mechanism of action of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) is via inhibition of COX. Since the discovery of at least two isoforms of COX, inhibition of COX-2 has generally been considered the basis for the anti-inflammatory effects of NSAIDs. However, more recent studies of COX-2 have controversially postulated that the selective inhibition of COX-2 may not be beneficial, but rather can be detrimental. This is based on the observations that, during inflammation, not all AA-derived mediators are exclusively pro-inflammatory. This review will attempt to discuss the confusing and contradictory data relating to selective COX-2 inhibition and inflammation, particularly focusing on anti-inflammatory AA-derived mediators. We will also try to advance the perspective that inflammation is not just a single process, but is rather a dynamic and continuously changing event, not just in terms of time, mediators and cells, but also in the initiating stimuli, whether it be in the periphery or the central nervous system.
15833069 Involvement of ICAM-1 in bone metabolism: a potential target in the treatment of bone dise 2005 Mar Bone diseases such as osteoporosis, osteoarthritis and rheumatoid arthritis (RA) affect a great proportion of individuals, with debilitating consequences in terms of pain and progressive limitation of function. Existing treatment of these pathologies has been unable to alter the natural evolution of the disease and, as such, a clearer understanding of the pathophysiology is necessary in order to generate new treatment alternatives. One therapeutic strategy could involve the targeting of intercellular adhesion molecule-1 (ICAM-1; CD54). In bone, ICAM-1 is expressed at the surface of osteoblasts (Obs) and its counter-receptor, leukocyte function-associated antigen-1 (LFA-1; CD11a), at the surface of osteoclast (Oc) precursors. ICAM-1 blockade between the Ob and the pre-Oc results in an inhibition of Oc recruitment and a modulation of inflammation, which could potentially help in controlling disease activity in bone pathologies. So far, clinical studies on ICAM-1 blockade in bone diseases have been limited to RA. A better understanding of the implication of this adhesion molecule in Ob/Oc interactions and inflammatory mediation in the bone pathological state, however, is needed. As new discoveries on the role of this adhesion molecule are being reported, ICAM-1 could become a potential target for other bone diseases as well.
15832005 Factor structure of the Korean version of illness intrusiveness rating scale: cross-cultur 2005 Apr The Illness Intrusiveness Rating Scale (IIRS) measures illness-induced disruptions to 13 domains of lifestyles, activities, and interests. A stable three-factor structure has been well documented; however, the cross-cultural validity of this scale needs to be tested. This study investigated the factor structure of the Korean version of IIRS in 712 outpatients at a university medical center. A predominant diagnosis of the patients was rheumatoid arthritis (47%). The Center for Epidemiological Studies-Depression Scale (CES-D), and Health Assessment Questionnaire (HAQ) were also administered. Exploratory Principal Component Analysis identified a two-factor structure, "Relationships and Personal Development (RPD)" and "Instrumental", accounting for 57% of the variance. Confirmatory analyses extracted an identical factor structure. However, a goodness-of-the fit test failed to support two-factor solution (chi(2)=138.2, df=43, p<.001). Two factors had high internal consistency (RPD, alpha=.89; Instrumental, alpha=.75) and significantly correlated with scores of HAQ (RPD, r=.53, p<.001; Instrumental, .r=44, p<.001) and CES-D (RPD, .r=55, p<.001; Instrumental, .r=43, p<.001). These findings supported construct validity of the Korean version of IIRS, but did not support cross-cultural equivalence of the factor structure.
15831320 Cervical pain in the athlete: common conditions and treatment. 2005 Mar In summary, it is important for physicians dealing with neck pain in an athletic population to understand the differences between serious and mild cervical injuries. This is best facilitated by a thorough understanding of the signs and symptoms of serious cervical injury, familiarity with the basic anatomy of the neck and its structures, and a working knowledge of common causes of neck pain and mechanisms of injury. All unconscious athletes should be assumed to have a serious cervical injury until proven otherwise, and preventive measures should be taken to ensure the safety of the athlete. This includes airway management with a jaw thrust only, neck stabilization, and preventing helmet removal. In the conscious athlete who has neck pain, serious cervical injury can often be ruled out with an accurate history and physical examination. In all cases of neck pain, it is imperative that the athlete be protected. This may involve removing the athlete from competition, or transporting him or her to the local emergency room. Often, this decision falls on the shoulders of the doctor in the stands. Thus, a basic understanding of the evaluation and management of neck pain in athletes is an asset for all physicians who frequent athletic events or see athletes in the office. The physician responsible for patients who have Down syndrome or rheumatoid arthritis needs to consider the increased incidence of cervical instability in these patients when evaluating for athletic participation or neck pain.
15715192 Idiopathic non-specific interstitial pneumonia: as an "autoimmune interstitial pneumonia". 2005 Feb Recently, we have experienced significant number of patients diagnosed with non-specific interstitial pneumonia (NSIP) by open lung biopsy or video-assisted thoracoscopic surgery. The purpose of this study is to compare clinical and pathological features of idiopathic NSIP and NSIP associated with underlying diseases (mainly autoimmune disorders). Forty-six patients with histologically proven NSIP were retrospectively collected. Twenty-four patients had underlying diseases (12 polymyositis/dermatomyositis, 5 systemic sclerosis, 2 rheumatoid arthritis, 2 Sjogren's syndrome, 1 ulcerative colitis, 1 primary biliary cirrhosis, and 1 multiple myeloma). Twenty-two of the 46 patients had no underlying diseases. It was very difficult to distinguish idiopathic NSIP and NSIP associated with underlying diseases, clinically and radiologically. Pathologically, Lymphocytic pneumonitis was demonstrated in both groups, and it was impossible to distinguish idiopathic NSIP and NSIP associated with underlying diseases. Since generalized symptoms were not observed in patients with idiopathic NSIP, and clinical and pathological features were identical to NSIP with several autoimmune disorders, we postulate new clinical entities of "autoimmune interstitial pneumonia" in cases without underlying diseases.
16377621 The role of human HtrA1 in arthritic disease. 2006 Mar 10 Human HtrA1 belongs to a widely conserved family of serine proteases involved in various aspects of protein quality control and cell fate. Although HtrA1 has been implicated in the pathology of several diseases, its precise biological functions remain to be established. Through identification of potential HtrA1 targets, studies presented herein propose that within the context of arthritis pathology HtrA1 contributes to cartilage degradation. Elevated synovial HtrA1 levels were detected in fluids obtained from rheumatoid and osteoarthritis patients, with synovial fibroblasts identified as a major source of secreted HtrA1. Mass spectrometry analysis of potential HtrA1 substrates within synovial fluids identified fibronectin as a candidate target, and treatment of fibronectin with recombinant HtrA1 led to the generation of fibronectin-degradation products that may be involved in cartilage catabolism. Consistently, treatment of synovial fibroblasts with HtrA1 or HtrA1-generated fibronectin fragments resulted in the specific induction of matrix metalloprotease 1 and matrix metalloprotease 3 expression, suggesting that HtrA1 contributes to the destruction of extracellular matrix through both direct and indirect mechanisms.
15924695 [Analysis of clinical characteristics and risk factors of corneal melting after laser in s 2005 Apr OBJECTIVE: To study the characteristics of corneal melting after laser in situ keratomileusis and to investigate the risk factors for corneal melting. METHODS: Twelve eyes of 11 patients with corneal melting after LASIK were studied. The patients consisted of 6 men and 5 women, ranging in age from 26 to 41 years. Each eye was routinely examined with slit lamp microscope and confocal microscope. All patients were conducted with systemic examination, especially immunologic index such as rheumatoid factor, anti-SSA and anti-SSB antibodies. The patients with systemic diseases were treated for the systemic diseases as well as for the ocular disorders. RESULTS: Corneal melting occurred unilaterally in all cases; 8 in the left eye and 4 in the right eye. The intervals between onset of corneal melting and LASIK ranged from 2 to 5 weeks. Corneal melting tended to begin from the rim of corneal flaps, especially in the inferior and nasal rims. Eight cases (67%) either had corneal epithelium denudation or thinner corneal flaps during operation or had corneal epithelium edema or epithelium implantation post operatively. 6 cases (55%) were combined with systemic diseases, 1 with thyroiditis, 2 with systemic lupus erythematous, 2 with Sjogren syndrome and 1 with rheumatoid arthritis. One patient once had superficial scleritis, one patient was combined with eczema and erythema of the skin; one patient had foreign body beneath the corneal flap; other patients had no accompanying disorders (3 eyes). All of the cases were cured with treatment by cyclosporine A, topical steroids and protective agents for the cornea. The course of corneal melting ranged from 23 days to 45 days (mean 30.3 days). Corneal nebula or macula of different degrees remained. Four cases had astigmatism with sphere changes above 1.0 diopters. The actual corrected visual acuity of 5 eyes was 2 lines lower than the expected corrected visual acuity, 2 eyes 1 line lower, 5 eyes unchanged. CONCLUSION: Corneal melting is a non-infectious corneal disorder and may accompany with systemic diseases. LASIK may be an inductive factor for corneal melting. A thorough inquiry and examination for systemic diseases are of great importance for the prevention of corneal melting. The treatment for corneal melting should be combined with diagnosis and treatment for the accompanying systemic diseases.
16866652 Scleroderma in South Australia: further epidemiological observations supporting a stochast 2006 Aug The aim of this study was to determine the incidence, prevalence, survival and selective demographic characteristics of scleroderma occurring in South Australia over the 10-year period 1993-2002. Analysis of the database of the South Australian Scleroderma Register: a population-based register established in 1993. Patients with scleroderma resident in South Australia (n = 353 at 2002) were ascertained from multiple sources and clinical and demographic data were obtained from mailed questionnaire and from review of computerized hospital databases, case notes or referring letters. Time-space cluster analysis was carried out according to the Knox method. Control data were obtained from the Australian Bureau of Statistics census. The mean prevalence was 21.4 per 10(5) (95% confidence interval 20.2-22.6) and the mean cumulative incidence of 1.5 per 10(5) (95% confidence interval 1.32-1.73) with no significant change in incidence over the study period (P = 0.13). Cumulative survival improved over the study period, with patients with diffuse disease having significantly reduced survival (as compared with limited disease, P < 0.001). The proportion with diffuse disease ( approximately 22%) remained steady. There was a small but significant predisposition in patients with a continental European birthplace (P < 0.001). A family history of scleroderma was noted in 1.6% with lambda1 (familial risk) of 14.3 (95% confidence interval 5.9-34.5). However, a family history of systemic autoimmunity (especially rheumatoid arthritis) was more common (6%). No socioeconomic stratification, temporal clustering nor spatio-temporal clustering was observed either at time of initial symptom or at 10 years before disease onset. Scleroderma occurs relatively infrequently in South Australia with no significant change in incidence observed over the 10-year study period. However, cumulative survival has improved. Identified risk factors include family history of scleroderma (risk approximately 14-fold), female sex (risk approximately 5-fold) and European birthplace (risk approximately 2.5-fold); however, the majority of the disease variance appears unexplained. A stochastic explanation based on genetic instability is favoured to explain this paradox.
15908882 [Variables influencing bleeding during total hip arthroplasty]. 2005 Apr PURPOSE OF THE STUDY: The purpose of this retrospective analysis was to study the parameters having an effect on blood loss during or after total hip arthroplasty. We examined a series of 350 procedures for primary degenerative hip disease with a normal course (n = 100), rapidly destructive degenerative disease (n = 100), and secondary joint degeneration due to atraumatic osteonecrosis of the femoral head (n = 100) or rheumatoid disease (n = 50). MATERIAL AND METHODS: All arthroplasties were performed via the transtrochanteric approach using Charnley-Kerboull implants. The volume of blood loss was calculated by noting compensated blood loss (transfusion during the procedure and shortly thereafter), and estimated non-compensated loss using the Nadler and Mercuriali and Inghilleri formula. We examined the influence of age, gender, obesity, and surgeon experience. Data were analyzed with the Student-Fisher reduced deviation method was used for quantitative and qualitative variables and the coefficient of correlation for quantitative variables. RESULTS: Blood loss, calculated in ml packed red blood cells (hematocrit 100%), was 573 ml for arthroplasties with a normal course, 713 for arthroplasties secondary to osteonecrosis of the femoral head, and 950 ml for rapidly destructive degenerative disease and finally 609 ml for patients with rheumatoid arthritis. Considering 35% as normal for hematocrit, total estimated blood loss was 1,640, 2,040, 2,710, and 1,740 ml respectively in the different groups. Compared with the group of patients who had a normal course, total blood loss was significantly higher when arthroplasty was performed for osteonecrosis and rapidly destructive degenerative disease (p < 0.001). Age, obesity, and duration of the intervention had no effect on blood loss. Female gender and operator experience had a favorable influence in the group of patients who underwent hip surgery for primary degenerative disease. Blood loss occurring during or shortly after total hip arthroplasty was greater in men, when the procedure was performed for osteonecrosis, and most importantly for rapidly destructive diseases. DISCUSSION: In clinical practice, the influence of gender is not significant enough to require specific preoperative transfusion plans. Conversely, certain etiologies of the joint disease impose transfusion in all such patients, using a blood volume which usually exceeds the possibilities of auto-transfusions.
16405885 Oral administration of the NADPH-oxidase inhibitor apocynin partially restores diminished 2006 Feb 15 Apocynin, an inhibitor of NADPH-oxidase, is known to partially reverse the inflammation-mediated cartilage proteoglycan synthesis in chondrocytes. More recently, it was reported that apocynin prevents cyclooxygenase (COX)-2 expression in monocytes. The present study aimed to investigate whether these in vitro features of apocynin could be confirmed in vivo. In a mouse model of zymosan-induced acute arthritis apocynin was administered orally (0, 3.2, 16 and 80 microg/ml in the drinking water) and the effects on cartilage proteoglycan synthesis were monitored. In a mouse model of zymosan-induced inflammation of the ears apocynin was administered orally (14 mg/kg/day by gavage) and the effects on ear swelling and ex vivo produced prostaglandin E2 (PGE2) by lipopolysaccharide (LPS)-stimulated blood cells were measured. In this study, ibuprofen was used as a positive control (50 mg/kg/day by gavage) and animals received vehicle as a negative control. Apocynin dose-dependently reversed the inhibition of proteoglycan synthesis in articular cartilage of the arthritic joint. A statistically significant increase in proteoglycan synthesis was found at a dose of 80 microg/ml apocynin. Apocynin did not affect the proteoglycan synthesis of the control knee joints. Apocynin significantly decreased the zymosan-induced ear swelling at 1, 2 and 4 h (hours) after zymosan injection versus the vehicle treated group at 14 mg/kg/day. The ex vivo production of PGE2 by LPS-stimulated blood cells was significantly decreased after in vivo apocynin treatment. Ibuprofen decreased ear swelling at the same time-points as apocynin and inhibited the ex vivo produced PGE2. In conclusion, the present study confirmed two important features of apocynin in vivo: (1) oral administration of apocynin can partially reverse the inflammation-induced inhibition of cartilage proteoglycan synthesis, and (2) oral administration of apocynin has COX inhibitory effects similar to the non-steroidal anti-inflammatory drug (NSAID) ibuprofen. Therefore, apocynin might be of potential use during the treatment of chronic inflammatory joint diseases like osteoarthritis or rheumatoid arthritis.
15986349 Infliximab, but not etanercept, induces IgM anti-double-stranded DNA autoantibodies as mai 2005 Jul OBJECTIVE: To analyze the clinical and biologic correlates of autoantibody induction during longer-term tumor necrosis factor alpha (TNFalpha) blockade with either the monoclonal antibody infliximab or the soluble receptor etanercept. METHODS: Thirty-four patients with spondylarthropathy (SpA) and 59 patients with rheumatoid arthritis (RA) were treated with infliximab for 2 years. Additionally, 20 patients with SpA were treated with etanercept for 1 year. Sera were blindly analyzed for antinuclear antibodies (ANAs), anti-double-stranded DNA (anti-dsDNA) antibodies, anti-extractable nuclear antigen (anti-ENA) antibodies, and antihistone, anti-nucleosome, and anticardiolipin antibodies (aCL). The anti-dsDNA antibodies were isotyped. RESULTS: High numbers of infliximab-treated patients with SpA or RA had newly induced ANAs (61.8% and 40.7%, respectively) and anti-dsDNA antibodies (70.6% and 49.2%, respectively) after 1 year, but no further increase between year 1 and year 2 was observed. In contrast, induction of ANAs and anti-dsDNA antibodies was observed only occasionally in the etanercept-treated patients with SpA (10% of patients each). Isotyping revealed almost exclusively IgM or IgM/IgA anti-dsDNA antibodies, which disappeared upon interruption of treatment. Neither infliximab nor etanercept induced other lupus-related reactivities such as anti-ENA antibodies, antihistone antibodies, or anti-nucleosome antibodies, and no clinically relevant lupus-like symptoms were observed. Similarly, infliximab but not etanercept selectively increased IgM but not IgG aCL titers. CONCLUSION: The prominent ANA and anti-dsDNA autoantibody response is not a pure class effect of TNFalpha blockers, is largely restricted to short-term IgM responses, and is not associated with other serologic or clinical signs of lupus. Similar findings with aCL suggest that modulation of humoral immunity may be a more general feature of infliximab treatment.
16882896 Reverse total shoulder arthroplasty. Survivorship analysis of eighty replacements followed 2006 Aug BACKGROUND: Reverse total shoulder arthroplasty is currently being used to treat selected patients with disabling shoulder arthropathy. The purposes of this study were to investigate the medium-term results of reverse total shoulder arthroplasty and to analyze the influence of etiology on the result. METHODS: We carried out a multicenter study with a minimum follow-up of five years and determined the survival rate of the prosthesis according to the initial etiology of the shoulder arthropathy. Eighty prostheses were implanted in seventy-seven patients between 1992 and 1998. Sixty-six shoulders had an arthropathy with a massive rotator cuff tear, and fourteen shoulders had a disorder with another etiology (rheumatoid arthritis, trauma, or revision arthropathy). At the time of review, eighteen patients had died and two were lost to follow-up. The remaining fifty-seven patients (sixty shoulders) were examined or interviewed by telephone at a mean follow-up of 69.6 months. Cumulative survival curves were generated with replacement of the prosthesis, glenoid loosening, and a functional Constant score of <30 as the end points. RESULTS: The survival rate with replacement of the prosthesis and glenoid loosening as the end points were 91% and 84%, respectively, at 120 months, with shoulders that had arthropathy with a massive rotator cuff tear demonstrating a significantly better result than those that had a disorder with another etiology (p < 0.05). On the other hand, the survival rate with an absolute Constant score of <30 as an end point was 58% at 120 months, with no significant difference with respect to etiology. Two breaks were observed in the survival curves. The first concerned survival until replacement of the prosthesis and occurred at around three years, reflecting early loosening of the prosthesis. The curve then became stable. A second break started at around six years and reflected progressive deterioration of the functional result. CONCLUSIONS: Our findings indicate that the reverse total prosthesis should be reserved for the treatment of very disabling shoulder arthropathy with a massive rotator cuff rupture, and it should be used exclusively in patients over seventy years old with low functional demands.
15644757 Small effect of genetic factors on neck pain in old age: a study of 2,108 Danish twins 70 2005 Jan 15 STUDY DESIGN: Classic twin study. OBJECTIVES: To determine the heritability of neck pain in persons 70 years of age and older. SUMMARY OF BACKGROUND DATA: Previous studies have shown a moderate effect of genetic factors on back pain in the elderly. Genetic influence on neck pain in old age is unknown. METHODS: Data on the 1-month prevalence of neck pain from twin pairs participating in the population based Longitudinal Study of Aging Danish Twins formed the basis of this analysis. To assess twin similarity, probandwise concordance rates, odds ratios, and tetrachoric correlations were calculated and compared for monozygotic and dizygotic twins. Further, heritability estimates were calculated using bivariate probit estimation. RESULTS: A total of 2,108 twin individuals, including 1,054 complete twin pairs, answered the question related to neck pain at intake into the Longitudinal Study of Aging Danish Twins study. Low and nonsignificant probandwise concordance rates, odds ratios, and tetrachoric correlations were found for both men and women in monozygotic and dizygotic twin pairs, indicating small or negligible genetic effects. Heritability estimates adjusted for age and significant environmental risk factors (rheumatoid arthritis, osteoarthritis, disc prolapse, and coronary heart disease) showed no significant additive genetic, dominant genetic, or common environmental effects. CONCLUSION: Genetic factors do not play an important role in the liability to neck pain in persons 70 years of age or older.
17243572 Primary Sjögren's syndrome associated with non-Hodgkin's lymphoma of salivary gland and c 2006 Dec A rare case of a young nonsmoker woman with Sjigren's syndrome and salivary gland non-Hodgkin's lymphoma, diagnosed one year later, is presented. Three years after treatment of the lymphoma, asymptomatic progression of the Sjögren 's syndrome was observed with pulmonary involvement--predominantly bullous or cystic lung disease. To our knowledge, this is the only report of Sjögren 's syndrome associated with non-Hodgkin's lymphoma in salivary gland, and complicated with multiple lung cysts.
16831678 Sonographic diagnostic criteria for screening Sjögren's syndrome. 2006 Jul OBJECTIVE: The objective of this study is to establish readily applied sonographic diagnostic criteria for Sjögren's syndrome. STUDY DESIGN: Sonographic images of 79 cases of previously suspected Sjögren's syndrome (including 43 actual cases) were analyzed retrospectively for the following characteristic features: (1) multiple hypoechoic areas, (2) multiple hyperechoic lines or spots, (3) multiple hypoechoic areas surrounded with hyperechoic lines or spots, and (4) obscuration of the gland configuration. Logistic regression analysis was used to extract valuable sonographic findings. Sonographic images of 80 prospective patients (of whom 48 proved to have Sjögren's syndrome) were scored prospectively using selected features to verify the usefulness of the established criteria. RESULTS: Three sonographic findings in parotid and submandibular glands were selected by logistic regression analysis and retrospective and prospective patients compared. Experienced observers could differentiate positive cases of Sjögren's syndrome from negative controls to a highly significant degree. Findings correlated very well with sialographic grading. CONCLUSION: Sonography can be substituted for sialography when applying the selected criteria in screening for Sjögren's syndrome.
16510035 Extrahepatic manifestations of hepatitis C virus. 2006 Feb Given the high prevalence of chronic hepatitis C virus (HCV) infection, its clinical sequelae account for a significant proportion of patients presenting to gastroenterologists and hepatologists. Whereas the hepatic manifestations of hepatitis C are well described, including hepatitis, cirrhosis, and the development of hepatocellular carcinoma, the extrahepatic manifestations, though common, are less well appreciated. Although nonspecific, fatigue and arthralgias are very common in those with chronic hepatitis C. Extrahepatic syndromes have been reported in as much as 36% of HCV patients, but the exact prevalence is not known. Patients with these syndromes can be divided into those with a high degree of association and those with a more moderate or mild association with HCV. The most prevalent extrahepatic diseases with the highest degree of association with HCV are the essential mixed cryoglobulins with skin, neurologic, renal, and rheumatologic complications. Non-cryoglobulin diseases with a less definite relationship to HCV include systemic vasculitis, splenic lymphoma, porphyria cutanea tarda, and the sicca syndromes. This article highlights the pathophysiology and clinical manifestations of these disorders.
16284097 Lymphoma and other malignancies in primary Sjögren's syndrome: a cohort study on cancer i 2006 Jun OBJECTIVES: To assess the risk of lymphoproliferative disease or other malignancy (standardised incidence ratios (SIRs)), in patients with primary Sjögren's syndrome according to the American-European Consensus Criteria (AECC), compared with patients with sicca syndrome (non-AECC) and the background population. To identify predictors of malignancy and describe lymphoma types and survival probabilities. METHODS: A linked register study using information from the Malmö Primary SS Register, Swedish Cancer Register, and Cause-of-Death Register for calculation of SIRs was carried out. Detected lymphomas were reclassified according to the WHO classification. Cox regression analysis was used to study the predictive value of clinical, laboratory, and histological findings at the time of diagnosis. RESULTS: 507 patients with a median follow up of 8 years (range 1 month to 19 years) were included. SIRs (95% confidence interval (CI)) for malignancies in total and for non-Hodgkin's lymphomas (NHL) were 1.42 (0.98 to 2.00) and 15.57 (7.77 to 27.85), respectively, in those fulfilling the AECC (n = 286). In non-AECC sicca patients (n = 221) SIR for malignancy of any kind was 0.77 (0.41 to 1.32); no lymphoproliferative neoplasms were detected. Significant predictors of lymphoproliferative disease were purpura/skin vasculitis (hazard ratio (HR) = 4.64, 95% CI 1.13 to 16.45), low complement factor C3 (HR = 6.18, 95% CI 1.57 to 24.22), low C4 (HR = 9.49, 95% CI 1.94 to 46.54), CD4+ T lymphocytopenia (HR = 8.14, 95% CI 2.10 to 31.53), and a low CD4+/CD8+ T cell ratio < or = 0.8 (HR = 10.92, 95% CI 2.80 to 41.83). 7/12 (58%) NHLs were diffuse large B cell lymphomas. CONCLUSION: A 16-fold increased risk for development of NHL was found. CD4+ T lymphocytopenia is an additional strong risk factor for developing lymphoma.