Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 4030709 | The clinical effectiveness and safety of chronic plasmapheresis in patients with primary b | 1985 | Primary biliary cirrhosis (PBC) is a chronic nonsuppurative, destructive cholangitis, whose etiology is unknown. Morbidity arises early from pruritus and later from hypercholesterolemia with xanthoma formation. Therapy is supportive and directed at the complications of cholestasis. Plasmapheresis has been reported to benefit patients with hyperlipidemia and PBC; thus a pilot study of plasmapheresis utilizing the Haemonetics Model 30 with replacement by albumin and saline was conducted. Five patients (four female and one male) with a mean age of 43 (range 29-58) and a mean duration of illness of 9.5 years (range 6-21) with marked jaundice, xanthomas, xanthelasma, hepatomegaly, fatigability, anorexia, and pruritus, as well as mild nausea were studied. Peripheral neuropathy was present in two patients. Two patients had splenomegaly. Two patients had an associated Sjogren syndrome. All patients had high serum bilirubin, alkaline phosphatase, and cholesterol levels and mild elevations in aspartate amino transferase and alanine amino transferase activities. Immune complexes measured in four patients were present. Antimitochondrial antibody titers were significant in all patients. Patients underwent a mean of 63 plasmapheresis procedures over a mean of 112 weeks removing a mean of 94.7 liters of plasma. No serious toxicity was seen. All patients showed a reduction in pruritus, xanthomas, xanthelasmas, and serum cholesterol values. The two patients who had evidence of Sjogren syndrome noted subjective improvement. All patients who had fatigue, anorexia and nausea also noted moderate improvement. There was no change in hepatomegaly or splenomegaly in patients demonstrating such organomegaly. Liver function did not change significantly. Overall, four patients had improvement in their condition and one patient achieved stability.(ABSTRACT TRUNCATED AT 250 WORDS) | |
| 6208886 | Immunohistochemical and ultrastructural demonstration of keratin in epi-myoepithelial isla | 1984 | Immunohistochemistry of salivary gland suggested that keratin is a specific marker of duct-epithelial cells and myosin for myoepithelial cells. Epi-myoepithelial islands found in some autoimmune sialadenitis, such as Sjögren's syndrome, were mainly composed of keratin-positive cells. Keratin filaments, with bundles and desmosome-attachments were invariably found in epithelial cells with electron microscopy. The islands contained no cells with myoepithelial characteristics. The findings show that there is no obvious participation of myoepithelial cells in the growth of the epi-myoepithelial islands. | |
| 6409824 | Salivary IgA in Sjögren patients. | 1983 Apr | Salivary flow-rate, Na, K and IgA were measured in 12 KCS patients for diagnosis of Sjögren's syndrome. 8 had elevated salivary IgA concentrations. The IgA was analysed on anti-IgA plates and on anti-secretory IgA plates. The results indicate that the elevation in salivary IgA in Sjögren patients is due to secretory IgA. | |
| 6256898 | [Chronic hepatopathy and progressive systemic sclerosis. Frequency of association with Gou | 1980 Dec 8 | Six patients with scleroderma (Barnett's type I and II) associated with hepatopathy are reported. Primary biliary cirrhosis was confirmed in four cases and was probably present in one case, while cirrhosis of unknown origin was present in the sixth patient. The outcome was fatal in two cases. Salivary secretions were reduced in all six cases, and a diagnosis of Gougerot-Sjögren's disease was confirmed in four patients. The frequency with which this triple association has been reported suggests that its incidence has been underestimated. | |
| 625681 | The surgical management of recurrent parotitis. | 1978 Mar | Twenty-eight parotidectomies were carried out upon 26 patients with chronic parotitis. The lesion considered is chronic inflammation of the parotid gland associated with such intraglandular defects as sialadenitis secondary to ductal obstruction by calculi, cellular debris, stenosis or infiltrating lesions, that is, Mikulicz's or Sjögren's syndromes and sialoangiectasis, either primary or secondary to obstruction of the duct. Seventeen near total parotidectomies were done without significant complications or a recurrence of symptoms. Eleven superficial parotidectomies were performed in which symptoms recurred on the 12th postoperative day in one patient. No permanent weakness of the facial nerve occurred in any of the 28 parotidectomies. Based upon this experience, near total parotidectomy with removal of the parotid duct can be performed safely and should be the procedure of choice in patients with chronic, relapsing parotid sialadenitis. | |
| 6431590 | Identification and purification of a 55K polypeptide in Sjögren's syndrome A antigen. | 1984 | The Sjögren's syndrome A antigen (SS-A) purified by affinity chromatography from human spleen was shown to contain a major polypeptide with a mol. wt. of 55 000 daltons confirmed as SS-A by its reactivity with different anti-SS-A sera on affinity columns, immunodiffusion and the Western blot. A similar reactive polypeptide was demonstrated in extracts of rabbit liver, brain, spleen, kidney, lung and thymus. | |
| 7291566 | Manifestations of parotid gland enlargement: radiographic, pathologic, and clinical correl | 1981 Nov | Histologic, clinical, and radiographic presentations of the autoimmune salivary gland diseases are reviewed. The punctate and globular sialographic changes observed actually reflect penetration of contrast material through the uniquely diseased glandular ducts and not sialectasis, as was previously thought. "Pseudosialectasis" is suggested as a more accurate term. The progressive cavitary and destructive patterns seen on sialography appear to reflect complications of secondary infection rather than the specific pathology of these diseases. Conditions causing recurrent enlargement of the parotid gland or development of a multinodular gland include chronic sialadenitis, the sialoses, the granulomatous diseases, primary neoplasms, and metastatic tumors. Although they appear similar clinically, many of these diseases can be differentiated sialographically, and such a radiographic approach is presented. | |
| 6945656 | [Parotid calcinosis of the pseudo-tumoral type (author's transl)]. | 1981 | An atypical feature of a further case of salivary calcinosis reported was its exclusively unilateral parotid site. The clinical appearance was that of a pseudo-tumor following a long period of a spontaneously regressive unilateral parotid swelling. The co-existence of a Gougerot-Sjögren syndrome was confirmed clinically by the presence of a xerostomia, and radiologically by suggestive signs after a parotid sialogram. Immunological features were atypical in nature. | |
| 6259049 | The neuropathology of rheumatoid disease. | 1981 Jan | Patients with active rheumatoid disease may develop encephalopathy, myelopathy, peripheral neuropathy, and myopathy through a variety of tissue mechanisms. Brain involvement is usually characterized by the formation of rheumatoid nodules or by the development of vasculitis or its complications, and there is evidence to suggest that the trapping of immune complexes within the choroid plexus may be important in pathogenesis. Structural damage to the spinal cord and lower brain stem, on the other hand, most commonly results from narrowing of the bony canal, leading either to direct compression of neural tissue or to compromise of its vascular supply. The appearance of peripheral neuropathy generally signifies the presence either of inflammatory epineurial arterial disease or entrapment by neighboring anatomical structures. Skeletal muscle dysfunction may be due to vasculitis, myositis, or denervation atrophy. Both systemic and local anatomical factors, therefore, are of importance in determining the manner in which different parts of the nervous system may be affected in rheumatoid disease. | |
| 6448867 | Decreased autologous mixed lymphocyte reaction in Sjögren's syndrome. | 1980 Nov | The autologous mixed lymphocyte reaction (AMLR) measures the response of peripheral blood T cells to antigens present on the surface of non-T cells. The AMLR was studied in 25 patients with Sjögren's syndrome (SS). The AMLR was decreased in 15 of 25 (60%) of patients with SS (5,272 +/- 6,738 cpm vs. 14,396 +/- 10,092 cpm for the normal controls, P < 0.001). The AMLR was decreased in 8 of 15 patients with only glandular disease who were not on any systemic medications. Patients with SS and associated disease had lower responses than patients with SS alone. Two patients with pseudolymphoma had absent response. The decreased AMLR correlated with a decreased response to concanavalin A, suggesting a possible abnormality of a T cell subpopulation. There was no correlation between the decreased AMLR and age, focus score, serum immunoglobulin concentration, the titer of antilymphocyte antibody, or phytohemagglutinin response. In allogeneic MLR, SS non-T cells and macrophages stimulated normal allogeneic T cells less well than normal non-T cells and macrophages, suggesting a possible abnormality in the cells that stimulate in the cells that stimulate in the allogeneic MLR. | |
| 301029 | Decreased lymphocyte reactivity to a suboptimal concentration of phytohemagglutinin in Sjà | 1977 Apr | Significantly decreased lymphocyte reactivity to a suboptimal concentration of phytohemagglutinin (PHA) was found in patients with Sjögren's syndrome (SS), whereas the response to an optimal concentration was generally normal. Kinetic studies were performed on control lymphocytes. Only suboptimal PHA concentrations stimulated tritiated thymidine (3H-TdR) incorporation in proportion to the number of potentially reactive lymphocytes. Kinetic studies of SS patients suggested that their low reactivity was attributable to fewer functionally reactive lymphocytes rather than to a decreased rate of proliferation. | |
| 127954 | Sjogren's syndrome and drug reaction to practalol. | 1975 Sep 24 | A case is reported of a patient who developed exfoliative dermatitis while being treated with practalol for angina pectoris. The patient also had trigeminal neuropathy, renal impairment and keratoconjunctivitis sicca. The antinuclear factor was diffusely positive but other antibodies were negative. At post mortem the patient was found to have acute pancreatitis, and peritonitis. It is postulated that the patient has antecedent Sjogren's syndrome and on introduction of practalol therapy developed a drug reaction with a generalised exfoliative dermatitis and exacerbation of keratoconjunctivitis sicca leading to bilateral corneal ulceration. The association of similar conditions in patients receiving practalol therapy is reviewed. | |
| 6575996 | Quantitation of human salivary acidic proline-rich proteins in oral diseases. | 1983 Sep | Acidic proline-rich proteins (APRP) were quantitated immunochemically in salivary secretions from groups of: caries-resistant (CR) and caries-susceptible (CS) subjects; heavy- and light-calculus-formers; and patients with Sjögren's Syndrome, drug-induced xerostomia, and recurrent parotitis. In all groups except the parotitis patients, there were comparable levels of APRP, about 40-50 mg%, with similar values in parotid and submandibular saliva. In chronic recurrent parotitis, the values were somewhat higher (about 60 mg%). There were no differences in the proportion of APRP-A to C in a subset of CR and CS. Taken as a whole, the data support the view that the secretion of APRP is stable and that caries status and propensity to calculus formation are not associated with abnormal levels of these phosphoproteins. | |
| 6126150 | Necrotizing arteritis and spinal subarachnoid hemorrhage in Sjögren syndrome. | 1982 Jun | A 37-year-old woman with primary Sjögren syndrome developed mixed cryoglobulinemia and systemic vasculitis. Subarachnoid hemorrhage occurred as a result of necrotizing anterior spinal arteritis. Although rarely seen in mixed cryoglobulinemia, central nervous system complications have recently been documented in Sjögren syndrome. The patient's serum contained antibodies to the Ro(SSA) cytoplasmic antigen, and these antibodies were concentrated in the cryoglobulin fraction. Anti-Ro(SSA) antibodies are associated with the occurrence of vasculitis in patients with Sjögren syndrome, which suggests that the spinal arteritis and subarachnoid hemorrhage in this patient may have been directly related to the underlying connective tissue disorder. | |
| 7027873 | Clinical trial of bromhexine in Sjögren's syndrome. | 1981 Aug | Tear secretion and lysozyme tear content were measured in 30 patients with Sjögren's syndrome after treatment with oral bromhexine, 32 mg/day. In 21 patients (70%) there was a marked increase in tear secretion and in lysozyme content. In patients with keratoconjunctivitis sicca (KCS) good results in clarifying the mucoid eye discharge were obtained. A remarkable amelioration of xerostomia was also noted. Six other patients, serving as controls, were given a placebo and bromhexine. The placebo had no influence on the rate of tear secretion, while bromhexine caused it to increase in 70% of the controls. This side effects of bromhexine treatment encountered in the present study were negligible and transient. We consider bromhexine to be the drug of choice in the treatment of Sjögren's syndrome. | |
| 6971105 | Polyclonally triggered B cells in the peripheral blood and bone marrow of normal individua | 1981 Apr | Numbers of B cells spontaneously secreting Ig (IgG, IgA, and IgM) were determined by a plaque-forming cell (PFC) assay simultaneously in the peripheral blood and bone marrow of normal individuals, patients with systemic lupus erythematosus (SLE), and patients with primary Sjögren's syndrome. Normal individuals had 382 (+/- 89) PFC per 10(6) mononuclear cells in peripheral blood. Patients with either active or inactive Sjögren's syndrome had normal numbers of spontaneous Ig-secreting cells in peripheral blood (P greater than 0.2). Conversely, patients with inactive as well as active SLE had markedly increased spontaneous PFC (P less than 0.05 and P less than 0.001, respectively). Patients with active SLE had significantly greater PFC than patients with inactive SLE; 3,984 (+/- 960) versus 1,605 (+/- 527) PFC per 10(6) mononuclear cells (P less than 0.05). The lack of increased numbers of activated B cells in the blood of patients with Sjögren's syndrome was not explained by a preferential sequestration of activated B cells in the bone marrow. However, of particular interest was the finding that the bone marrow served not only as a major source of virgin B cells but as a lymphoid organ of either in situ activation of B cells or sequestration for activated B cells. Normal individuals had approximately a 20-fold relative increase of activated B cells per 10(6) mononuclear cells in the bone marrow compared to peripheral blood, while patients with inactive and active SLE both had a 35-fold relative increase in activated B cells in bone marrow compared to peripheral blood. The potential relevance of circulating activated B cells and their sequestration in lymphoid organs is discussed concerning the discrepancy in this regard between Sjögren's syndrome and SLE, and our understanding of the significance of polyclonal B cell activation in the pathogenesis of these diseases. | |
| 7193689 | Autoantibodies directed against sicca syndrome antigens in the neonatal lupus syndrome. | 1981 Jan | Clinical and serologic studies on three infants who had the neonatal lupus syndrome and studies on their mothers revealed an association with antibodies to sicca syndrome antigens. From initial studies and a 2-year follow-up, there is evidence that indicates transplacental passage of autoantibodies directed against Sjögren's (sicca) syndrome-associated nuclear antigens from asymptomatic mothers to newborns who subsequently developed neonatal lupus. Besides the presence of antinuclear antibodies, the mothers of these infants also showed high rheumatoid factor titers, and two had evidence of mild decreasing tearing on ophthalmologic examination. On follow-up examination 2 to 3 years later, both infants and mothers lacked evidence of active disease, and only the mothers continued to demonstrate the serologic abnormalities seen initially. Based on our findings, we postulate newborns of mothers with serologic or clinical evidence of Sjögren's (sicca) syndrome may be at greater risk for developing neonatal lupus. | |
| 1173298 | [Dermatoglyphic investigations in respect to the genetic basis of autoimmune diseases (aut | 1975 Jan 10 | Dermatoglyphics of patients with systemic lupus erythematosus, scleroderma and Sjögren's syndrome were very different from the striking findings in Hashimoto's thyroiditis established in 1971 (Weninger and coworkers). Hence, it was concluded that the characteristic dermatoglyphic pattern of Hashimoto's thyroiditis is specific for this autoimmune disease, but not the expression of a general genetic predisposition to autoimmunity. | |
| 4027178 | The immune response to pertussis in the 6-day air pouch: a model of chronic synovitis. | 1985 Aug | We have developed a model of prolonged immunological inflammation in the rat which has a structural resemblance to the synovial changes in rheumatoid arthritis. Pertussis vaccine was injected into 6-day-old subcutaneous air pouches in animals previously sensitized with pertussis vaccine. The resulting inflammatory response persisted up to 30 days. Examination of exudates showed a wave of polymorphonuclear leucocytes over a 13-day period followed by a mononuclear cell predominance up to 30 days. Histologically, an early polymorphonuclear cell infiltration was followed by the formation of a lining layer of large eosinophilic mononuclear cells, together with deep collections of lymphocytes and plasma cells. Concentrations of the acute-phase reactant alpha 1-glycoprotein, in both serum and exudate, peaked at 3 days. This suggests that the local production of interleukin I in this type of tissue reaction is more closely related to the acute inflammatory phase than to more chronic interactions between monocyte derived cells and lymphocytes. | |
| 2987010 | Mononuclear cell-mediated modulation of synovial cell metabolism. I. Collagen synthesis. | 1985 May | Human PHA-stimulated mononuclear cells produce a factor which inhibits synovial cell collagen and non-collagen protein synthesis, whereas it enhances hyaluronic acid (HA) production. Indomethacin (10(-4)-10(-6) M), a cyclo-oxygenase inhibitor, suppresses this effect, suggesting that the mechanism is prostaglandin-mediated. The active material, of apparent molecular weight 12 000-20 000, also displays the properties of the mononuclear cell factor (MCF) previously described by others, since its stimulates collagenase and PGE2 release by the cultured synovial cells. Furthermore, it co-purifies with interleukin 1 (IL 1) as shown by lymphocyte-activating factor activity. This strongly suggests that IL 1 could be responsible for some (or all) the effects observed on MCF-exposed synovial cells. From these data, we deduce the possibility that mononuclear cells may participate in limiting synovial collagen deposition in rheumatoid arthritis. |