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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17149952 | Histopathology of gastric and duodenal Strongyloides stercoralis locations in fifteen immu | 2006 Dec | CONTEXT: Strongyloidiasis is a worldwide parasitic infection affecting approximately 75 million people. In Italy, it was more prevalent in the past among rural populations of irrigated areas. OBJECTIVE: To determine the histopathologic alterations of the gastric and duodenal mucosa associated with the presence of Strongyloides stercoralis parasites. DESIGN: Fifteen cases of strongyloidiasis were observed in immunocompromised patients during a recent 6-year period in Italy. S. stercoralis was found histologically in gastric biopsies (10 cases), in a gastrectomy (1 case), and in duodenal biopsies (9 cases). In 5 cases the parasite was present both in gastric and duodenal biopsies. Four patients were affected by lymphoma, 2 by multiple myeloma, 2 by gastric carcinoma, 1 by chronic myeloid leukemia, 1 by sideroblastic anemia, 1 by colorectal adenocarcinoma, 1 by chronic idiopathic myelofibrosis, 1 by chronic gastritis, 1 by gastric ulcers, and 1 by rheumatoid arthritis in corticosteroid therapy. No patient was affected by human immunodeficiency virus infection. Strongyloidiasis was not clinically diagnosed. RESULTS: Histologic examination revealed several sections of S. stercoralis larvae, many eggs, and some adult forms. All the parasites were located in the gastric and/or the duodenal crypts. Eosinophils infiltrating into the lamina propria were found in all cases; their intensity was correlated with the intensity of the infection. CONCLUSIONS: Histologic diagnosis of strongyloidiasis must be taken into consideration when examining both gastric and duodenal biopsies in immunocompromised patients, to avoid the development of an overwhelming infection of the parasite, which is dangerous for the life of the patient. | |
17058987 | [Ghrelin: beyond hunger regulation]. | 2005 Oct | Man ingests food to mitigate hunger (mediated by physiological and biochemical signals), satisfy appetite (subjective sensation) and because of psychosocial reasons. Satiation biomarkers (stop feeding) are gastric distention and hormones (CCK, GLP-1) and satiety biomarkers (induce feeding) are food-induced thermogenesis, body temperature, glycaemia and also hormones (insulin, leptin and ghrelin). Oxidative metabolism/body composition, tryptophan/serotonin and proinflammatory cytokines are also implicated on hunger physiology. At the present time, ghrelin is the only known circulating orexigenic with potential on hunger/body weight regulation. It is a neuropeptide (endogenous ligand for the GH secretagogue) recently isolated from the oxyntic mucosa and synthesized mainly in the stomach. Its blood concentration depends on diet, hyperglucemia and adiposity/leptin. It is secreted 1-2 hours preprandially and its concentration decreases drastically during the postprandium. Ghrelin acts on the lateral hypothalamus and theoretically inhibits proinflammatory cytokine secretion and antagonizes leptin. Ghrelin physiologically increases food intake and stimulates adipogenesis, gastrointestinal motility and gastric acid secretion, and has other hormonal and cardiovascular functions. Ghrelin blood concentration is reduced in massive obesity, non-alcoholic steatohepatitis, polycystic ovary syndrome, acromegaly, hypogonadism, ageing, short bowel syndrome and rheumatoid arthritis; and increased in primary or secondary anorexia, starvation, chronic liver disease and celiac disease. Cerebral and peritoneal ghrelin administration (rats) and systemic administration (rats and healthy volunteers, cancer patients or patients on peritoneal dialysis) promotes food consumption and increases adiposity, of utmost importance in the treatment of patients with anorexia. | |
17045417 | Heme of consumed red meat can act as a catalyst of oxidative damage and could initiate col | 2007 | Dietary epidemiological studies indicate correlations between the consumption of red meat and/or processed meat and cancer of the colon, rectum, stomach, pancreas, bladder, endometrium and ovaries, prostate, breast and lung, heart disease, rheumatoid arthritis, type 2 diabetes and Alzheimer's disease. The correlation of all these major diseases with dietary red meat indicates the presence of factors in red meat that damage biological components. This hypothesis will focus on the biochemistry of heme compounds and their oxidative processes. Raw red meat contains high levels of oxymyoglobin and deoxymyoglobin and oxyhemoglobin and deoxyhemoglobin and cytochromes in muscle and other tissues. Cooked and processed meat contain hemichromes and hemochromes. After being eaten heme proteins are hydrolyzed to amino acids and peptides and the heme group which is coordinated with strong ligands. The iron of heme coordinates to the sulfur, nitrogen or oxygen of amino acids and peptides and other biological components. The coordinated heme groups are absorbed and transported by the blood to every organ and tissue. Free and coordinated heme preferentially catalyze oxidative reactions. Heme catalyzed oxidations can damage lipids, proteins, DNA and other nucleic acids and various components of biological systems. Heme catalysis with hydroperoxide intermediates can initiate further oxidations some of which would result in oxidative chain reactions. Biochemical and tissue free radical damage caused by heme catalyzed oxidations is similar to that resulting from ionizing radiation. Oxidative biochemical damage is widespread in diseases. It is apparent that decreasing the amount of dietary red meat will limit the level of oxidative catalysts in the tissues of the body. Increasing consumption of vegetables and fruits elevates the levels of antioxidative components, for example, selenium, vitamin E, vitamin C, lycopene, cysteine-glutathione and various phytochemicals. These detrimental processes of heme catalysis of oxidative damage hypothesized here are not well recognized. More investigative studies in this field need to be done. | |
17030479 | Stimulative effects of Ulmus davidiana Planch (Ulmaceae) on osteoblastic MC3T3-E1 cells. | 2007 Feb 12 | Ulmus davidiana Planch (Ulmaceae) has long been known to have anti-inflammatory and protective effects on damaged tissue, inflammation and bone among other functions. To treat rheumatoid arthritis (RA), a herbal medicine, Ulmus davidiana Planch (Ulmaceae) extract (UD) is being used in traditional oriental medicine. The effect of UD on the proliferation and osteoblastic differentiation in non-transformed osteoblastic cells (MC3T3-E1) was studied. UD dose-dependently increased DNA synthesis (significant at 5-20 microg/ml). UD increased alkaline phosphatase (ALP) activity and prolyl hydroxylase activity of MC3T3-E1 cells (5-20 microg/ml). Antiestrogen tamoxifen eliminated the stimulation of proliferation and ALP activity of MC3T3-E1, which was induced by UD. UD at concentrations ranged from 30 to 100 microg/ml inhibited prostaglandin E2 production in MC3T3-E1. These results indicate that UD directly stimulates cell proliferation and differentiation of osteoblasts. These results also suggest and UD is effective for bone anti-resorptive action in bone cells. | |
16886705 | Glycoprotein changes in non-insulin dependent diabetic rats: effect of N-benzoyl-D-phenyla | 2006 Mar | The effect of N-benzoyl-D-phenylalanine (NBDP) and metformin on neonatal streptozotocin (nSTZ) induced diabetes has been studied on plasma and tissue glycoproteins. In some pathological conditions, such as cancer, rheumatoid arthritis and diabetes, there is an abnormal glycosylation of acute phase serum proteins. As most serum proteins are produced in the liver, we have examined glycoprotein metabolism in diabetic condition. To induce non-insulin-dependent diabetes mellitus (NIDDM) a single dose of streptozotocin (100 mg/kg body weight) was injected into two day old rats. After 10-12 weeks, rats weighing above 150 g were selected for NIDDM model. In these rat, blood glucose and plasma glycoproteins were significantly increased whereas plasma insulin was significantly decreased. There was a significant decrease in the level of sialic acid and elevated levels of hexose, hexosamine and fucose in tissues. Oral administration of NBDP and metformin to diabetic rats decreased blood glucose and plasma glycoproteins. Plasma insulin and tissue sialic acid were increased whereas tissue concentrations of hexose, hexosamine and fucose were near normal. Our study suggests that NBDP and metformin possess a significant beneficial effect on glycoproteins in addition to their antidiabetic effect. | |
16855151 | Estrogens in pregnancy and systemic lupus erythematosus. | 2006 Jun | Successful pregnancy depends on an adaptation of the maternal immune system that becomes tolerant to fetal antigens of paternal origin. The altered immune regulation induced by pregnancy occurs predominantly at the maternal-fetal interface, but it has also been observed in the maternal circulation. Th1/Th2 shift is one of the most important immunologic changes during gestation. It is due to the progressive increase of estrogens, which reach peak level in the third trimester of pregnancy. At these high levels, estrogens suppress the Th1-mediated responses and stimulate Th2-mediated immunologic responses. For this reason Th1-mediated diseases, such as rheumatoid arthritis, tend to improve, while Th2-mediated diseases, such as systemic lupus erythematosus (SLE) tend to worsen during pregnancy. However, in some recent studies SLE flare-ups were less frequently observed in the third trimester of gestation in comparison to the second trimester and postpartum period. These data are apparently in contrast to the Th2 immune-response polarization expected during pregnancy due to the progressive increase of estrogens. Some further data suggest that in SLE patients estradiol serum levels are surprisingly lower than expected during the third trimester of pregnancy, probably due to a placental compromise. This occurrence could lead to a lower-than-expected increase of IL-6, accounting for the low humoral immune response and the low disease activity observed in the third trimester of pregnancy in such patients. | |
16793296 | Comorbidity of low back pain: representative outcomes of a national health study in the Fe | 2007 May | BACKGROUND: Unlike other biopsychosocial risk factors, the role of comorbidity in low back pain is largely unknown. AIMS: The purpose is (1) to generate prevalence data on back pain in the total adult population and (2) to identify the most common physical comorbidities in subjects with back pain. This paper also (3) analyses the gender-specific and age-specific comorbidity structure. METHODS: The National German Health Survey is the first study to provide the basis for a representative nationwide analysis of back pain prevalence and the associated comorbidities. The net sample comprises a total of 7124 Germans aged 18-79. RESULTS: One in three Germans (34%) experienced back pain during the seven days prior to being interviewed. The one-year prevalence rate is 59%. All the morbidities investigated by us are more common in subjects with back pain than in individuals without back pain. The most common comorbidities associated with back pain are musculoskeletal disorders like rheumatoid arthritis, osteoarthritis and osteoporosis, followed by cardiovascular and cerebrovascular disease. CONCLUSIONS: The present study investigating 31 physical diseases is the most extensive analysis to date on the topic of back pain and comorbidity. This is an attempt to cast light on the tangled relationships involved in developing and coping with back pain. In view of the large percentage of unspecific back pain, we believe it is important for physicians treating back pain to extend their history and diagnostic analysis skills to embrace comorbidities related to the back pain. | |
16621377 | Anti-inflammatory activities of the triterpene acids from the resin of Boswellia carteri. | 2006 Sep 19 | Boswellic acids are the main well-known active components of the resin of Boswellia carteri (Burseraceae) and these are still dealing with the ethnomedicinal use for the treatment of rheumatoid arthritis and other inflammatory diseases. Although several studies have already been reported on the pharmacological properties, especially on the anti-inflammatory activity, of Boswellia carteri resin and boswellic acids, the ethnomedicinal importance of Boswellia carteri and its components, boswellic acids, prompted us to undertake detailed investigation on the constituents of the resin and their anti-inflammatory activity. Fifteen triterpene acids, viz., seven of the beta-boswellic acids (ursane-type) (1-7), two of the alpha-boswellic acids (oleanane-type) (8, 9), two of the lupeolic acids (lupane-type) (10, 11), and four of the tirucallane-type (12-14, 16), along with two cembrane-type diterpenes (17, 18), were isolated and identified from the methanol extract of the resin of Boswellia carteri. Upon evaluation of 17 compounds, 1-14 and 16-18, and compound 15, semi-synthesized from 14 by acetylation, for their inhibitory activity against 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced inflammation (1 microg/ear) in mice, all of the compounds, except for 18, exhibited marked anti-inflammatory activity with a 50% inhibitory dose (ID(50)) of 0.05-0.49 mg/ear. | |
16461800 | Potential contribution of VH gene replacement in immunity and disease. | 2005 Dec | VH replacement occurs through RAG-mediated recombination between a cryptic recombination signal sequence (cRSS) presented in a rearranged VH gene and a 23-bp RSS from an upstream VH gene. VH replacement renews the entire VH coding region and extends the immunoglobulin heavy-chain (IgH) CDR3 regions preferentially with charged amino acids. VH replacement occurs in bone marrow-immature B cells and contributes significantly to the primary B-cell repertoire in humans. However, the biological significance of VH replacement is not clear. Our recent studies revealed elevated frequencies of VH replacement products in different autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, and Sjögren's syndrome. Moreover, elevated frequencies of VH replacement products were also found in patients with human immunodeficiency virus or hepatitis C virus infections. These results provide the first clue that VH replacement contributes to autoimmune disease and antiviral immunity, and they also suggest a potential link between viral infection and autoimmune disease. | |
16369106 | Antimitochondrial antibody negative primary biliary cirrhosis in Japan: utilization of cli | 2006 Jan | BACKGROUND: We examined patients who showed laboratory and histological evidence of primary biliary cirrhosis (PBC) in the absence of antimitochondrial antibody (AMA) to elucidate the characteristics of AMA negative PBC. METHODS: From a total of 5,805 patients with symptomatic PBC, 2,419 cases (41.7%) were selected in the present study, who were diagnosed using the following criterion; chronic non-suppurative destructive cholangitis was histologically observed and laboratory data did not contradict PBC. The information collected from records included sex, age, symptoms, physical findings, and complicated autoimmune diseases. We then evaluated these data according to the positivity of AMA. RESULTS: Of the total subjects, 470 cases (19.4%) were found to be negative for AMA. The proportion of female patients was higher among the AMA negative group than among the AMA positive one. Pruritus was found less frequently among patients with AMA negative PBC than among those with AMA positive PBC. Levels of alkaline phosphatase,gamma-glutamyl transpeptidase, and IgM were significantly lower among patients with AMA negative PBC than among those with AMA positive PBC. Complications such as Sjögren's syndrome, rheumatoid arthritis, and scleroderma, including CREST syndrome, were found with significantly higher frequency among patients with AMA negative PBC than among those with AMA positive PBC. CONCLUSION: Considering serum level of IgM and frequencies of complicated autoimmune diseases, it is possible that Japanese patients with AMA negative PBC are consistent with the disease entity of autoimmune cholangitis reported in western countries. | |
16134730 | Anti-CD20 therapy of treatment-resistant Wegener's granulomatosis: favourable but temporar | 2005 May | Rituximab is a genetically engineered chimeric monoclonal immunoglobulin (Ig)G1 antibody. It binds the CD20 trans-membrane surface antigen expressed by mature B cells but not by antibody secreting plasma cells, and removes the cells by activating complement, inducing cell-mediated lysis, and by apoptosis. Mainly used for the treatment of non-Hodgkin's lymphomas, rituximab has recently been tried with favourable responses in rheumatoid arthritis, systemic lupus erythematosus, and other chronic immunological diseases. Wegener's granulomatosis (WG) is a granulomatous vasculitis with high morbidity and mortality. It is thought that anti-neutrophil cytoplasmatic antibodies (ANCA) with specificity for proteinase 3 (PR3) are possibly involved in the pathogenesis of the disease. Conventional therapy with cyclophosphamide and corticosteroids generally succeeds in inducing remission, but relapses frequently follow. Among the biological agents, tumour necrosis factor-alpha (TNF-alpha) inhibitors have been tried with some success. Based on a case report we recently treated three refractory WG patients with rituximab and achieved almost complete but temporary remission. CD20+ cells disappeared rapidly in peripheral blood, only to rise prior to subsequent disease flares occurring at 34, 63, and 54 weeks, respectively (Figure 1). A new flare occurred in one patient at 86 weeks. At the end of the observation periods (54, 102, and 120 weeks), only one patient had proteinuria. Chest radiographs became normal in two patients, while infiltrates remained unchanged in the third. Granulomatous retro-orbital or sinus masses in two patients seemed unresponsive to therapy. | |
16126980 | Xenobiotic-induced recruitment of autoantigens to nuclear proteasomes suggests a role for | 2005 Jun | The cell nucleus is a prominent target of autoantibodies in systemic autoimmune disorders. Approximately 2% of the population in Europe and North America suffers from systemic rheumatic diseases, such as rheumatoid arthritis, systemic lupus erythematosus (SLE), and scleroderma. The molecular mechanisms of systemic autoimmunity are largely unknown despite its high prevalence. Contributing factors that have been considered include (1) genetic predisposition, (2) influence of hormones, and (3) environmental factors. The latter are mainly correlated with the generation of scleroderma, as xenobiotic-induced subsets of this disease have been observed in individuals exposed to silica (SiO(2)) dusts, organic solvents, heavy metals, and certain drugs. In addition to the epidemiological relevance, animal models of xenobiotic-induced autoimmunity serve as elegant tools for controlled induction of antigen-driven autoimmune responses. Because antigen processing and presentation constitute the basis for every antigen-driven autoimmune response, effects of xenobiotics on degradation of nuclear autoantigens have been characterized to elucidate molecular mechanisms of autoimmunity that target the cell nucleus. By means of a cell-based disease model, it has been shown that xenobiotics such as mercuric chloride, platinum salts, and silica (nano)particles specifically alter structure, function, and proteolysis in the cell nucleus. Signature proteins of the cell nucleus redistribute to aberrant, nucleoplasmic clusters, where they colocalize with proteasomes and are subjected to proteasomal proteolysis. Recruitment of nuclear autoantigens to proteasomal degradation is correlated with autoimmune responses that specifically target these antigens in both animal models of xenobiotic-induced autoimmunity and patients with idiopathic scleroderma. | |
16093827 | Immune cells and cytokines in systemic lupus erythematosus: an update. | 2005 Sep | PURPOSE OF REVIEW: Systemic lupus erythematosus is characterized by overactive B cells that differentiate into autoantibody-forming cells, aberrant T cell function that provides help to B cells, and the production of pro-inflammatory cytokines. This article reviews recent studies unraveling the complex interplay between cytokines and lymphocytes in systemic lupus erythematosus. RECENT FINDINGS: In systemic lupus erythematosus, T cells are characterized by heightened calcium responses early after activation of their surface receptor. Alterations of the T cell receptor/CD3 complex, namely the substitution of the FcepsilsonRgamma for the T cell receptor zeta chain, and increased mitochondrial potentials can account for this 'overexcitable' phenotype. At the same time, this heightened calcium signal leads to a block of the transcription of the IL-2 gene, a pivotal cytokine for the immune response. The end result is increased spontaneous apoptosis and decreased activation-induced cell death of T cells in systemic lupus erythematosus that in turn leads to enhanced help to B cells and potentially decreased regulatory function. The B cells, on the other hand, are shown to be directly activated by immune complexes by way of Toll-like receptors independently of T cells. Finally, recent studies have tried to elucidate the role of cytokines such as interferon-alpha in systemic lupus erythematosus and, following the paradigm of rheumatoid arthritis, to establish targets for treatment. SUMMARY: The increased apoptosis and aberrant T cell activation coupled with nonspecific activation of B cells lead to the production of auto-antigen: auto-antibody complexes that are the hallmark of systemic lupus erythematosus. Future treatments aiming at correcting the intracellular and intercellular signaling abnormalities may prove effective in restoring immune tolerance in systemic lupus erythematosus. | |
16076611 | Severe protein losing enteropathy with intractable diarrhea due to systemic AA amyloidosis | 2005 Mar | This report concerns two patients with severe protein losing enteropathy and refractory diarrhea due to AA amyloidosis who were successfully treated with corticosteroid and octreotide. In these patients, biopsied tissues from the gastrointestinal (GI) tract showed extensive deposition of AA amyloid, which was caused by rheumatoid arthritis in one case and was of unidentified etiology in the other. Both patients manifested severe diarrhea unresponsive to conventional treatment with hypoproteinemia, and protein leakage from the small intestine to the ascending colon was confirmed by 99mTc-diethylene triamine pentaacetic acid human serum albumin (HSA-D) scintigraphy. Soon after starting a long-acting somatostatin analogue, octreotide, with co-administration of oral prednisolone, their general status improved in parallel with a rapid decrease in the volume of watery diarrhea and an increase in serum levels of albumin and IgG. Also on 99mTc-HSA-D scintigraphy protein leakage from the GI tract was apparently decreased in both patients. Combination therapy with a somatostatin analogue and corticosteroid may be effective for protein losing enteropathy with intractable diarrhea ascribable to GI amyloidosis. Because of the lack of specific therapies in this serious clinical situation, the described therapy should actively be considered as a therapeutic option not only in AA amyloidosis, but also in other types of systemic amyloidosis. | |
15953917 | Oral effects of low-dose methotrexate treatment. | 2005 Jul | Methotrexate is used increasingly in low-dose regimes for a variety of conditions, particularly rheumatoid arthritis. While certain adverse effects of low-dose methotrexate have been described in detail, oral complications have received little attention. This article includes a summary of the uses and pharmacology of low-dose methotrexate and the mechanisms that lead to general and oral toxicity. The literature relevant to potential oral adverse effects is discussed and 7 illustrative cases are presented. The oral effects noted range from nonhealing ulcers to lymphoma-like lesions. Dental practitioners should be aware of the possible oral effects of low-dose methotrexate that have so far been largely unrecognized. | |
15943548 | Comprehensive screening of the thiopurine methyltransferase polymorphisms by denaturing hi | 2005 Summer | The drug-metabolizing enzyme thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation of thiopurines such as 6-mercaptopurine, 6-thioguanine, and azathiopurine, which are used as immunosuppressants and in the treatment of acute lymphoblastic leukemia and rheumatoid arthritis. TPMT enzymatic activity is a polymorphic trait, and poor metabolizers may develop life-threatening bone marrow failure. To avoid such adverse effects, the TPMT enzymatic activity in patients' red blood cells (RBCs) is routinely measured prior to thiopurine administration in a limited number of oncology clinics. In the present study, we took advantage of a highly sensitive and specific automated denaturing high-performance liquid chromatography (dHPLC) technique that not only detects known polymorphic alleles, but also identifies previously uncharacterized sequence variants. We developed a dHPLC-based protocol to analyze the entire coding region and validated the protocol to detect all 16 previously described variant alleles. We further analyzed the entire coding region of the TPMT gene in 288 control samples collected worldwide and identified two novel amino acid substitutions Arg163Cys (487C>T) and Arg226Gln (677G>A) within exons 7 and 10, respectively. The clinical application of this comprehensive screening system for examining the entire TPMT gene would help to identify patients at risk for bone marrow failure prior to 6-mercaptopurine therapy. | |
15928530 | Getting back to the future: a grounded theory study of the patient perspective of total kn | 2005 May | PURPOSE: The purpose of this study was to describe the experience of adults with osteoarthritis who had undergone a total knee joint arthroplasty. METHOD: Grounded theory qualitative methodology was applied. SAMPLE: Purposive and theoretical sample of nine participants. FINDINGS: In managing the experience of total knee joint arthroplasty, participants expressed the basic psychosocial process, "Getting back to the future." There were three main categories identified within this process, "enduring," "thinking twice," and "keeping faith." "Enduring" conceptualized the way the participants lived their daily lives. "Thinking twice" captured the participants' processes of adaptation and problem solving. "Keeping faith" was the combination of determination, trust, and optimism that sustained participants as they progressed through the total knee joint arthroplasty experience to rehabilitation. CONCLUSION: The study provides a grounded theory of the participants' perspectives of undergoing total knee joint arthroplasty, making the process more visible for those involved in their care. Prehabilitation, postoperative care, and discharge planning can facilitate the patients' optimism and motivation to self-help. Further research to explore the process from the perspective of patients with rheumatoid arthritis and patients who have complications is recommended. | |
15832845 | Orbital myositis following streptococcal pharyngitis in a pediatric patient. | 2005 Apr | BACKGROUND: Orbital myositis is a relatively rare ocular inflammatory disease. It is currently classified as an idiopathic orbital inflammatory disease, but has been associated with ocular and systemic disorders, including scleritis, rheumatoid arthritis, Crohn's disease, and systemic lupus erythematosis. Orbital myositis has also been associated with infectious disease such as streptococcal pharyngitis, viral upper respiratory infection, and Borrelia burgdorferi infection. CASE REPORT AND DISCUSSION: This report documents treatment and imaging of a 13-year-old boy who had an episode of right-sided orbital myositis following streptococcal pharyngitis with anti-streptolysin-o (ASO) titer elevation to 1,188 IU/ml. Clinically, this patient demonstrated acute onset of marked restriction and mild under-action of the lateral rectus muscle of the right eye. Thickening of the lateral and medial recti was demonstrated on computed tomography. The mild orbital myositis was treated with oral nonsteroidal anti-inflammatory drug therapy. The nonconcomitant strabismus resolved approximately 7 weeks after initial presentation. General orbital inflammatory disease management and the association of upper respiratory tract infection with orbital myositis are discussed. CONCLUSION: Orbital myositis is a distinct clinical entity that can occur after streptococcal upper respiratory infection, consisting of pain on ocular movement, localized swelling, restrictive strabismus, and inflammatory signs of the involved muscle(s). | |
15830278 | A case of necrotizing glomerulonephritis presenting with nephrotic syndrome associated wit | 2005 Mar | We describe a 68-year-old man with necrotizing glomerulonephritis who presented with nephrotic syndrome accompanied by pulmonary cryptococcosis. He developed rheumatoid arthritis in July 1999 and was treated with low-dose prednisolone. He was admitted to our hospital on November 22 following the appearance of bilateral leg edema in October 2000. Laboratory tests at presentation revealed nephrotic syndrome with renal impairment. Renal biopsy specimens revealed necrotizing glomerulonephritis with crescent, but immunofluorescence study showed lack of staining for immunoglobulins or complement components. Chest X-ray and CT showed abnormal shadows in the right upper lung field, and Cryptococcus neoformans was isolated in a transbronchial lung biopsy. After the diagnosis of pulmonary cryptococcosis was made, the patient was treated with 200 mg/day fluconazole. The pulmonary abnormal shadows immediately improved and urinary protein excretion dramatically decreased. A second renal biopsy, performed about 2 months after the first biopsy, showed disappearance of crescent. Electron microscopic examination of the second renal biopsy showed partial effacement of foot processes without electron-dense deposits. Our findings suggest that necrotizing glomerulonephritis with nephrotic syndrome in this patient represented pauci-immune T-cell-mediated injury related to pulmonary cryptococcosis. | |
15804470 | Placental umbilical cord whole blood transfusion: a safe and genuine blood substitute for | 2005 Apr | BACKGROUND: Afterbirth or placenta is normally discarded. But placental cord blood, because of its rich mix of fetal and adult hemoglobin, plasma, and high platelet count has the potential to be a safe alternative to adult blood. STUDY DESIGN: We transfused 413 U (range 50 mL to 146 mL; mean 86 mL+/-7.6 mL SD; median 80 mL; mean packed cell volume 48+/-4.1% SD; mean hemoglobin concentration 16.2 g/dL+/-1.8 g/dL SD) of placental umbilical cord whole blood, after lower uterine cesarean section from consenting mothers, to 129 informed consenting patients, after screening by the institutional ethics committee, from April 1, 1999, until the present. RESULTS: The list of consenting patients included 54 men and 75 women. Patient age varied from 2 years to 86 years. Seventy-three patients (56.58%) suffered from advanced cancer and 56 (43.42%) patients had other diseases like ankylosing spondylitis, lupus erythematosus, rheumatoid arthritis, aplastic anemia, and thalassemia major. We have not encountered a single case of immunologic or nonimmunologic reaction so far. CONCLUSIONS: We suggest that medical institutions could use this gift of nature, which is free from infection, hypoantigenic with altered metabolic profile, filled with growth factor and cytokine-filled plasma, with the potential of higher oxygen-carrying capacity than adult blood, as an emergency source of blood for the management of disaster or crises anywhere in the world. It also may be safely used for the treatment of malignant and nonmalignant disorders. |