Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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3653877 | Sjögren's syndrome-like illness associated with the acquired immunodeficiency syndrome-re | 1987 Oct | Three cases of Sjögren's syndrome-like illness occurring in patients with the acquired immunodeficiency syndrome (AIDS)-related complex (ARC) are described. All three patients were male. Positive serologic tests for the human immunodeficiency virus (HIV) were documented in two; the third patient was a prison inmate with a history of drug abuse. The lymphoid infiltrate seen in these cases resembled morphologically the features of persistent generalized lymphadenopathy. One patient complained of dry eyes and arthralgias. Autoimmune phenomena including lupus-like anticoagulant, immune thrombocytopenic purpura, and others have been reported in patients with AIDS and ARC. The occurrence of Sjögren's syndrome in ARC provides further evidence for autoimmune phenomena arising in the severely damaged immune system of ARC patients. Atypical Sjögren's syndrome now requires evaluation for ARC. Proposed criteria for identifying these patients are as follows: 1) young age (less than 40 years); 2) male sex (less than 10 per cent of non-ARC patients are male); 3) homosexuality or bisexuality, or other high-risk groups for AIDS; 4) generalized lymphadenopathy (also seen in rheumatoid arthritis); 5) negative test for rheumatoid factor despite generalized lymphadenopathy; 6) salivary gland lymphoid infiltrate showing features of persistent generalized lymphadenopathy. Patients with such features should be studied for HIV antibodies and other evidence of autoimmune phenomena in order to define more precisely the nature of this new Sjögren's-like illness. | |
2692147 | Risks and benefits of long-term treatment with estrogens. | 1989 Dec 16 | The goal of contemporary hormone replacement is to minimize net predictable lifetime risk; success therefore depends upon quantitative assessments of the net quality of life, of net morbidity and of net mortality. Estrogens ameliorate menopausal symptoms, maintain bone integrity, and produce endometrial cancer; these facts and their quantitative aspects can be stimulated. Other links are gradually becoming clear: estrogens increase biliary disease, but prevent heart disease, and, it now seems, stroke. Conventional wisdom to the contrary notwithstanding, a critical review suggests that breast cancer is probably increased in frequency by long-term estrogen use; the increase is modest as a risk factor but because breast cancer is a common disease, it is substantial in absolute terms. The addition of progestin seems attractive as a method of opposing undesirable estrogenic effects on the endometrium. In fact, there is reason for concern about the effect of an added progestin upon the risks from breast cancer, heart disease, and stroke; even the magnitude of the expected reduction in endometrial cancer may not be great when the hormone is administered sequentially. Using a simple deterministic model of post-menopausal life with hormone replacement, we have inserted available estimates of the regimen-specific relative risk for each outcome, and translated each net impact into common denominators of morbidity and mortality. While estrogens probably increase net morbidity, as measured by either the number of hospitalizations to be anticipated or by the more arbitrary measure of expected days of disability, these negative changes are mostly due to gallbladder disease and endometrial cancer, both largely treatable conditions. Largely because of protection against heart disease, estrogen replacement in modest dose is likely to reduce substantially the number of deaths to be expected in women treated through age 75 and even into more advanced age. Hormone replacement which includes systemic progestin supplementation has not been empirically tested; it may be beneficial, but it is at least as likely to be harmful. Either a modest increment in the number of additional breast cancers produced by estrogens, a modest reduction in the number of cardiac events prevented by estrogens, or a simultaneous minor shift in the same direction for each condition, would have the effect of shifting the net reduction in cumulative deaths into an increase in the number of deaths as a result of treatment.(ABSTRACT TRUNCATED AT 400 WORDS) | |
3109019 | Cryoglobulinemia in primary Sjögren's syndrome: a monoclonal process. | 1986 | Patients with primary Sjögren's syndrome have in their sera and urine free light chains or monoclonal immunoglobulins. In addition, they have mixed monoclonal (IgM kappa) cryoglobulinemia, which is associated with extraglandular disease and greater incidence of autoantibodies. In the present study, it is demonstrated by a high resolution agarose gel electrophoresis, combined with immunofixation, that nine patients with primary Sjögren's syndrome have mixed monoclonal (IgM kappa) cryoglobulins, in contrast to those observed in five patients with secondary Sjögren's syndrome (Sjögren's syndrome and rheumatoid arthritis), 13 patients with rheumatoid arthritis and six patients with systemic lupus erythematosus, which were mixed polyclonal. | |
1646720 | The complex between a tissue inhibitor of metalloproteinases (TIMP-2) and 72-kDa progelati | 1991 Jun 15 | Human rheumatoid synovial cells in culture secrete both 72-kDa progelatinase and a complex consisting of 72-kDa progelatinase and a 24-kDa inhibitor of metalloproteinases, TIMP-2. In addition, the culture medium contains TIMP-1, the classical inhibitor of metalloproteinases, with a molecular mass of 30 kDa. TIMP-1 does not form a complex with free 72-kDa progelatinase. Free progelatinase and progelatinase complexed with TIMP-2 can be activated with the organomercury compound p-aminophenylmercury acetate. The activated complex shows less than 10% the enzyme activity of activated free gelatinase. The progelatinase-TIMP-2 complex could be shown to be an inhibitor for other metalloproteinases, such as gelatinase and collagenase secreted by human rheumatoid synovia fibroblasts, as well as for the corresponding enzymes from human neutrophils. | |
3473635 | Preliminary diagnostic criteria for Sjögren's syndrome. | 1986 | Although Sjögren's syndrome (SS) is a very common autoimmune disease there are no uniformally accepted diagnostic criteria. In this study we evaluated various clinical parameters as criteria for this disorder. Fifty-two patients with sicca complaints but no evidence of other autoimmune rheumatic disorders were studied. These patients were further subdivided into definite primary SS (primSS) (n = 19) and possible primary SS (n = 33). The patients of the definite group fulfilled 2/3 of the following criteria: xerophthalmia defined by subjective complaints, Schirmer's test less than or equal to 5 mm/5 min or positive rose-bengal staining on slit lamp examination, xerostomia defined by subjective complaints and parotid flow rate less than or equal to 1 cc/5 mm/gland and, presence or history of parotid gland enlargement. In all patients the histology of labial minor salivary glands showed round cell infiltrates greater than or equal to 2+ (Tarpley's classification). The clinical manifestations of definite primary SS were compared to those of patients with possible primary SS. In addition, 49 patients with rheumatoid arthritis (RA) and suspected secondary SS were evaluated. Eleven patients were initially classified as definite secondary SS in association with RA (lip biopsy greater than or equal to 2+ and 1/2 of the criteria: xerophthalmia and xerostomia) and the remaining 38 as possible secondary SS with RA.(ABSTRACT TRUNCATED AT 250 WORDS) | |
2112243 | Second-line antirheumatic drugs in the elderly with rheumatoid arthritis: a post hoc analy | 1990 | This study assessed the relative efficacy and toxicity of second-line antirheumatic drugs in patients 65 years of age or older compared to younger counterparts. The results of three prospective, double-blind, parallel, randomized, multicenter trials were reanalyzed, stratifying outcomes by intervention and patient age. Efficacy was assessed by categorizing patient responses as follows: important improvement, no meaningful change, or progressive disease. Toxicity was analyzed by comparing withdrawal rates due to adverse effects. The three trials compared the following treatments: (1) D-penicillamine 10-12 mg/day versus azathioprine 1.25-1.5 mg/kg/day; (2) gold sodium thiomalate 50 mg intramuscularly weekly versus auranofin 6 mg/day versus placebo; and (3) pulse oral methotrexate 7.5-15.0 mg weekly versus placebo. At baseline, 103 patients age 65 or older were similar to 485 patients less than 65 years of age, with the exception of disease duration in all studies and erythrocyte sedimentation rate in one study. For patients completing each study, efficacy outcomes based on age were not significantly different. Withdrawal rates due to adverse drug reactions were also not significantly different. | |
3766605 | Benign hypergammaglobulinemic purpura of Waldenström associated with Sjögren's syndrome. | 1986 Oct | Since its first description, fewer than 150 cases of benign hypergammaglobulinemic purpura of Waldeström have been reported. There is a preponderance of females with this disorder, which is characterized by long-standing purpuric vasculitic lesions usually in the lower extremities, increased sedimentation rate, anemia, leukopenia, and hyperglobulinemia with a normal clotting process. Numerous associations have been shown between this and other systemic disorders such as Sjögren's syndrome, systemic lupus erythematosus, a rheumatoid arthritis. A 40-year-old woman is described who had an 18-year history of recurrent purpura and increased IgG levels. Skin biopsy showed acute vasculitis, and immunofluorescent study revealed fibrinogen precipitation and C3 deposition. Serologic evaluation demonstrated the presence of rheumatoid factor and antinuclear antibodies (1:80). Raji assay showed increased circulating immune complexes, and the T cell subsets were normal. The purpura was associated with symptoms and physical findings of Sjögren's syndrome. On the basis of serologic and skin biopsy findings, an autoimmune origin of the disease is postulated. | |
3528611 | Side effects of cyclosporin A treatment in patients with rheumatoid arthritis. | 1986 Jun | Cyclosporin A (CyA) and azathioprine (Aza) were compared with respect to renal side effects in an open controlled, randomized study of patients with rheumatoid arthritis. Twelve patients were treated with CyA (mean dose 7.8 +/- 1.2 mg/kg/day) and 12 with azathioprine for 26 weeks. All patients also received prednisolone 5 mg/day. The patients had normal serum creatinine (less than 120 mumoles/liter) and protein-free urine before the trial. CyA increased serum creatinine in nine out of the 11 patients followed for 26 weeks, the mean increase was approximately 50%. Creatinine clearance was reduced by 31%. Mean arterial pressure (MAP) and serum potassium were significantly increased by CyA. Urinary beta 2-microglobulin excretion was significantly increased by CyA, in five of the patients more than ten times. Urinary kallikrein excretion was reduced by more than 50% and urinary albumin excretion was doubled. All these parameters remained normal and unchanged in the azathioprine group. CyA was withdrawn in seven patients after 26 weeks. Urinary beta 2-microglobulin was still increased by 85% nine months after CyA treatment. The other parameters were gradually normalized after three to nine months except for one patient who developed renal failure. Urinary beta 2-microglobulin excretion was a very sensitive parameter for renal tubular damage in this study. | |
2511228 | Monitoring the acute phase response: comparison of tumour necrosis factor (cachectin) and | 1989 Oct | The relation between the inflammatory cytokine tumour necrosis factor-alpha (TNF or cachectin), which induces acute phase responses, and an established acute phase protein, C-reactive protein, was studied in various infectious and inflammatory diseases in man. All cases with very high serum concentrations of C-reactive protein (150 to 400 mg/l; normal reference value less than 10 mg/l) also had raised serum concentrations of TNF (53 to 705 ng/l; normal reference value less than 40 ng/l). In 19 out of 91 (21%) of the cases, however, a raised TNF concentration without correspondingly raised C-reactive protein concentration was also noted. Conversely, in 23 out of 106 (22%) cases raised C-reactive protein was observed in the absence of a raised TNF concentration. The ratios were high in allograft rejection and low in myocardial infarction and Kawasaki's disease. The highest mean concentration of circulating TNF was found in bacterial infections, graft rejection, and myocardial infarction. It is concluded that although high C-reactive protein concentrations are usually accompanied by raised TNF concentrations, there are pronounced relative variations in the serum concentrations of these proteins in various disease states, suggesting that there may be independent, disease specific regulatory pathways for TNF and C-reactive protein. | |
3095317 | A metalloproteinase from human rheumatoid synovial fibroblasts that digests connective tis | 1986 Oct 25 | Human rheumatoid synovial cells in culture stimulated with the conditioned culture medium of rabbit macrophages secrete three distinct latent metalloproteinases. One of them, a proteinase that digests proteoglycan and other connective tissue matrix components, was purified as two active forms after activation with 4-aminophenylmercuric acetate. The two forms were homogeneous on sodium dodecyl sulfate-gel electrophoresis with Mr = 45,000 and Mr = 28,000, whereas the latent precursor was estimated to have Mr = 51,000 by gel permeation chromatography. Both active enzymes had optimal activity at pH 7.5-7.8 and were inhibited by EDTA and 1,10-phenanthroline but not by inhibitors for cysteine, serine, or aspartic proteinases. Removal of Ca2+ from the enzyme solution resulted in a complete loss of activity that could be fully restored by the addition of 1 mM Ca2+. The activity of the apoenzyme was restored by the addition of 0.5 mM Zn2+, 5 mM Co2+, or 5 mM Mn2+ in the presence of Ca2+ but not by each metal ion alone. The identical digestion patterns of reduced, carboxymethylated protein substrates indicated that both active forms of the enzyme have the same substrate specificity. The enzyme degraded cartilage proteoglycans, type I gelatin, type IV collagen, laminin, and fibronectin, and removed the NH2-terminal propeptides from chick type I procollagen. This enzyme may play a role in the normal turnover of the connective tissue matrix as well as in the joint destruction of chronic synovitis. | |
3040832 | A non-antibacterial chemically-modified tetracycline inhibits mammalian collagenase activi | 1987 Aug | Tetracyclines (including the semi-synthetic analogues, minocycline and doxycycline) are considered useful adjuncts in periodontal therapy because they suppress Gram-negative periodontopathogens. Recently, these antibiotics were found to inhibit mammalian collagenase activity, a property which may also be of therapeutic value. It has been suggested that the anti-collagenase properties of the tetracyclines are independent of their antibiotic efficacy. To advance this hypothesis further, we chemically converted tetracycline hydrochloride to its non-antimicrobial analogue, de-dimethylaminotetracycline. This chemically-modified tetracycline (CMT), although no longer an effective antibiotic, was found to inhibit the in vitro activity of collagenase from partially purified extracts of human rheumatoid synovial tissue and rachitic rat epiphysis. In a preliminary in vivo study, pathologically-excessive collagenase in skin and gingiva was induced by rendering adult male rats diabetic, and the oral administration of CMT to these rats significantly reduced the excessive collagenase activity in both tissues. Moreover, CMT administration did not affect the severe hyperglycemia in these rats but did prevent, at least in part, the diabetes-induced loss of body weight, skin weight, and skin collagen mass; these effects suggest a lack of toxicity in this animal model. A proposed clinical advantage of CMT over conventional tetracyclines, in the treatment of diseases characterized by excessive collagenolytic activity, is the lack of development of antibiotic-resistant micro-organisms during prolonged use. However, the consideration of clinical trials to support this hypothesis must await further laboratory and extensive toxicity tests. | |
1883326 | Link protein as a monitor in situ of endogenous proteolysis in adult human articular carti | 1991 Aug 15 | The link protein components of proteoglycan aggregates in adult human articular cartilage show heterogeneity due to proteolysis. Cleavages near the N-terminus of the intact link proteins, before residues 17, 19 and 24, generate three proteins of slightly diminished size (LP3). Cleavages within the N-terminal disulphide-bonded loop, before residues 66 and 73 of the intact link proteins, generate proteins that yield smaller degradation products upon reduction (LP fragments). In vitro, modified link protein components of a similar size to LP3 can be generated by a variety of proteinases, but of the physiologically relevant enzymes only stromelysin, cathepsin B and cathepsin G have the ability to yield modified link proteins with N-termini identical with those observed in situ. None of the proteolytic agents tested was able to produce LP fragments with N-termini identical with those observed in situ, and the majority of proteinases were not able to cleave within the disulphide-bonded loops. Cathepsin L and hydroxyl radicals can cleave within the N-terminal disulphide-bonded loop, and have the potential of initially opening the loop to allow further proteolytic processing by other agents to generate the native cleavage sites. | |
3266248 | Rheumatoid adherent synovial cells produce B cell differentiation factor activity neutrali | 1988 Nov | B cell differentiation factor (BCDF) activity assayed on SKW6-CL4 cells was found in adherent synovial cell (ASC) conditioned medium. ASC of patients with RA (n = 8) produced significantly larger amounts of BCDF than those of patients with osteoarthritis (n = 5) (219.0 +/- 212.1 vs 25.5 +/- 12.4 units/microgram.DNA, p less than 0.01). ASC clones, established by the limiting dilution technique, also produced this factor. Experiments with several neutralizing antibodies revealed that this BCDF is inhibited by anti-B cell stimulatory factor-2/interleukin 6 antibody (anti-BSF-2/IL-6 ab) up to 90%, but not by antiinterleukin 1, antiinterleukin 2 or antiinterferon-r antibodies. Our data suggest that ASC could participate in the B cell differentiation process in joint space by producing a molecule which has a similar active site to BSF-2/IL-6. | |
2521783 | Clinical, immunohistochemical, and electron-microscopic findings in gold dermatitis. | 1989 Feb | The clinical, immunohistochemical, and electronmicroscopic features of 13 consecutive patients with gold dermatitis were analyzed: 12 developed an eczematous dermatitis and one a lichenoid dermatosis. The patients had received intramuscular sodium aurothiomalate therapy from 1 month to 4 years before the dermatitis broke out. After cessation of gold therapy, the dermatitis persisted for 1-11 months. A relatively sparse perivascular mononuclear cell infiltrate was found in the affected skin in all cases. With immunoperoxidase staining, most of the infiltrating cells were shown to be OKT-4-positive T-helper lymphocytes. A majority of the infiltrating cells were Ia, i.e., HLA class II antigen, positive. Clearly increased numbers of dermal OKT-6-positive Langerhans' cells were also seen. In epidermis, on the contrary, the expression of both OKT-6 and Ia markers on dendritic cells was decreased. However, electron-microscopic examination revealed large numbers of macrophage-like cells and the Langerhans cells were activated, often in apposition to mononuclear cells within the epidermis. No correlation was observed between the immunohistological findings and the amount of gold received, the duration of gold therapy, and the interval between the last gold injection and biopsy, respectively, although peripheral blood eosinophilia was more common during 5-10 months of gold therapy. There were no specific findings in the patients in whom dermatitis lasted several months after discontinuation of the therapy. Our findings support the view that immunological mechanisms operate in the development of gold dermatitis, although the exact mechanisms remain unknown. | |
1932522 | Antibodies to vascular heparan sulfate proteoglycan in patients with systemic lupus erythe | 1991 | Systemic lupus erythematosus (SLE) is an autoimmune disease which involves the basement membranes of blood vessels in multiple organs. An important component of the microvasculature is vascular heparan sulfate proteoglycan (HSPG). In this study, we investigated the presence in SLE and other immune disease sera of autoantibodies to purified vascular HSPG. Our data demonstrate that antibody to HSPG is found primarily in SLE sera, and not in sera from controls or patients with other immune diseases. The titer of antibody to HSPG correlated with complement depletion in SLE sera. Antibody to HSPG was frequently found in high titer in SLE patients with renal and neurologic involvement. These studies indicate that our assay for antibody to vascular HSPG detects a pathologically relevant autoantibody in SLE sera. The implications of our findings for pathogenesis of vascular autoimmunity are discussed, including the relationship of anti-vascular HSPG antibody to anti-DNA and antiphospholipid antibodies. | |
2803314 | Interleukin-1 beta stimulates phospholipase A2 mRNA synthesis in rabbit articular chondroc | 1989 Oct 16 | A cDNA that codes for human rheumatoid synovial fluid phospholipase A2 (PLA2) hybridized with a RNA of the same size (900 base pairs) isolated from rabbit articular chondrocytes (RAC). Treatment of RAC with 100 ng/ml recombinant human interleukin-1 beta (IL-1) for 24 hours caused a 13-fold increase in mRNA for this PLA2. Timecourse studies demonstrated that maximal induction of PLA2 mRNA occurred by 16 hours post addition of IL-1 (100 ng/ml). Augmentation of RAC PLA2 mRNA levels was dose-dependent; half-maximal induction was estimated to require 0.15 ng/ml IL-1. Actinomycin D inhibited IL-1 effects on PLA2 mRNA levels. Coordinate effects of IL-1 on RAC PLA2 activity were observed with respect to time and dose dependence as well as actinomycin D sensitivity. | |
2940851 | [Immunomodulation with apheresis technics]. | 1986 | The use of apheresis therapy (plasmapheresis/plasmafiltration or cytopheresis) was successful in numerous immunological diseases. Autoimmune and immune complex diseases as well as paraproteinemias with hyperviscosity syndrome (M. Waldenström, plasmocytoma) are the main indications. The several modifications of apheresis and its indications are outlined, and possible immune regulatoric effects of apheresis therapy are discussed. Finally this paper refers to beginning changes from unspecific to more selective methods of apheresis (cascade filtration, cryofiltration, immunoadsorption, enzymatic degradation, continuous electrophoresis) and its significance for clinical and experimental immunology. | |
2075353 | [The clinical significance of disorders of humoral immunity in Sjögren's disease and synd | 1990 Oct | Data on 100 patients: 50 with Sjögren's disease (SD) and 50 with Sjögren's syndrome (SS) accompanied by systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic scleroderma (SSD) were analysed. It was characteristic of SD to have hyperproteinemia, hypergammaglobulinemia, high levels of the rheumatoid factor (RF), circulating immune complexes (CIC), and cryoglobulins, anti-Ro and anti-La; SD + RA was characterized by RF, hypercomplementemia; SS + SLE was characterized by various antibodies to nucleic acids (nDNA, DNP (and anti-Sm, antinuclear factor (ANF) of homogenous and peripheral types of glow, hypercomplementemia. The main systemic manifestations of SD (arthritis, vasculitis) and a high activity of the process was associated with the presence of anti-Ro/La, and marked local manifestations of the dry syndrome--with antibodies to nDNA and dDNA. And vice versa in SS + SLE anti-nDNA antibodies correlated with anemia, serositis, nephritis, vasculitis and the presence of anti-Ro/La--with a comparatively mild renal pathology. The presence of high titres of RF in SB correlated with the absence of the adequate therapy, the presence of hypergammaglobulinemic purpura, weakly pronounced local manifestations; but a decrease in the titres of RF and an increase in the titres of ANF; anti-nDNA, anti-DNP in young patients with SD proved to be a prognostically unfavourable factor. The presence of CIC was associated with hypergammaglobulinemic purpura and affection of the eyes, and hypocomplementemia--with affection of the kidneys, joints and salivary glands in patients with SD. | |
2269296 | Matrix metalloproteinase 2 from human rheumatoid synovial fibroblasts. Purification and ac | 1990 Dec 27 | Human rheumatoid synovial cells in culture secrete at least three related metalloproteinases that digest extracellular matrix macromolecules. One of them, termed matrix metalloproteinase 2 (MMP-2), has been purified as an inactive zymogen (proMMP-2). The final product is homogeneous on SDS/PAGE with Mr = 72,000 under reducing conditions. The NH2-terminal sequence of proMMP-2 is Ala-Pro-Ser-Pro-Ile-Ile-Lys-Phe-Pro-Gly-Asp-Val-Ala-Pro-Lys-Thr, which is identical to that of the so-called '72-kDa type IV collagenase/gelatinase'. The zymogen can be rapidly activated by 4-aminophenylmercuric acetate to an active form of MMP-2 with Mr = 67,000, and the new NH2-terminal generated is Tyr-Asn-Phe-Phe-Pro-Arg-Lys-Pro-Lys-Trp-Asp-Lys-Asn-Gln-Ile. However, following 4-aminophenylmercuric acetate activation, MMP-2 is gradually inactivated by autolysis. Nine endopeptidases (trypsin, chymotrypsin, plasmin, plasma kallikrein, thrombin, neutrophil elastase, cathepsin G, matrix metalloproteinase 3, and thermolysin) were tested for their abilities to activate proMMP-2, but none had this ability. This contrasts with the proteolytic activation of proMMP-1 (procollagenase) and proMMP-3 (prostromelysin). The optimal activity of MMP-2 against azocoll is around pH 8.5, but about 50% of activity is retained at pH 6.5. Enzymic activity is inhibited by EDTA, 1,10-phenanthroline or tissue inhibitor of metalloproteinases, but not by inhibitors of serine, cysteine or aspartic proteinases. MMP-2 digests gelatin, fibronectin, laminin, and collagen type V, and to a lesser extent type IV collagen, cartilage proteoglycan and elastin. Comparative studies on digestion of collagen types IV and V by MMP-2 and MMP-3 (stromelysin) indicate that MMP-3 degrades type IV collagen more readily than MMP-2, while MMP-2 digests type V collagen effectively. Biosynthetic studies of MMPs using cultured human rheumatoid synovial fibroblasts indicated that the production of both proMMP-1 and proMMP-3 is negligible but it is greatly enhanced by the treatment with rabbit-macrophage-conditioned medium, whereas the synthesis of proMMP-2 is constitutively expressed by these cells and is not significantly affected by the treatment. This suggests that the physiological and/or pathological role of MMP-2 and its site of action may be different from those of MMP-1 and MMP-3. | |
3487213 | Radiocolloid scintigraphy in Felty's syndrome. | 1986 Jul | The Tc-99m sulfur colloid liver-spleen scintigrams of nine patients with Felty's syndrome (a triad of rheumatoid arthritis, splenomegaly, and neutropenia) were reviewed. The characteristic scintigraphic findings include (1) moderate or severe splenomegaly, (2) the reversal of liver-to-spleen uptake ratio despite normal liver function tests, and (3) virtually no visualization of the bone marrow uptake and no pulmonary radiocolloid sequestration. In a late stage of cirrhosis of the liver, moderate-to-severe splenomegaly with the reversal of liver-to-spleen uptake ratio almost always accompanies abnormal liver function, and sometimes there may be associated pulmonary radiocolloid uptake. It was therefore concluded that in a proper clinical setting, a radiocolloid scintigraph may differentiate between Felty's syndrome and cirrhosis of the liver in a late stage. |