Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.
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PMID:Pathophysiologic factors in recurrent acute pancreatitis. 393 40

Systemic lupus erythematosus (SLE) is an autoimmune disorder of indeterminate etiology characterized by a dysfunctional cellular immune response. We have previously identified a metabolic disorder of the adenylate cyclase/cAMP/protein kinase A (AC/cAMP/PKA) pathway characterized by impaired cAMP-inducible, PKA-catalyzed protein phosphorylation in intact T lymphocytes from subjects with severe SLE disease activity. Because this metabolic disorder may contribute to abnormal T cell immune effector functions, we tested the hypothesis that impaired PKA-dependent protein phosphorylation is the result of a PKA isozyme deficiency in SLE T lymphocytes. Compared with healthy and rheumatoid arthritis (RA) controls, subjects with severe SLE activity exhibited reduced PKA-catalyzed phosphorylation of proteins in the T lymphocyte plasma membrane where the type I isozyme of PKA (PKA-I) is predominantly localized. Both silver staining and biosynthetic labeling of membrane-associated proteins with [35S]methionine demonstrated that reduced protein phosphorylation was not due to either an altered distribution of or absence of proteins. Moreover, phosphorylation of SLE membrane-associated proteins with the PKA catalytic (C) subunit showed a similar distribution and extent of phosphorylation compared with membrane proteins from healthy T cells, suggesting that SLE T cell membrane proteins could be phosphorylated. Sequential column chromatography of the type I and type II isozymes of PKA (PKA-I, PKA-II) demonstrated a deficiency of PKA-I isozyme activity. Compared with a ratio of PKA-I to PKA-II activity of 4.2:1 in healthy T cells, the activity ratio in T cells from subjects with severe SLE disease activity was 0.99:1 (P = 0.01, SLE versus healthy controls for PKA-I). The deficient PKA-I activity was associated with a significant increase of free C-subunit activity (P = 0.04, SLE versus healthy controls for C-subunit). T cells from subjects with mild/moderate SLE disease activity also exhibited diminished PKA-I activity, yielding a ratio of PKA-I to PKA-II activity of 2.4:1. By contrast, T cells from RA controls possessed increased PKA-I, PKA-II, and free C-subunit activities compared with healthy controls, resulting in a ratio of PKA-I to PKA-II activity of 3.6:1. We conclude that the reduced PKA-catalyzed protein phosphorylation in the plasma membrane of SLE T cells is the result of deficient PKA-I isozyme activity. This is the first identification of a deficiency of PKA activity in SLE T lymphocytes; the deficiency, resulting in diminished protein phosphorylation, may alter cellular homeostasis, contributing to the cellular immune dysfunctions observed in SLE.
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PMID:Deficient type I protein kinase A isozyme activity in systemic lupus erythematosus T lymphocytes. 804 Feb 83

The hepatitis C virus (HCV) infection is characterized by a variety of extra-hepatic manifestations in many individuals. Among these, diabetes mellitus (DM) can be included, as such a metabolic disorder has been demonstrated to be more frequent in chronic hepatitis C than in liver disease due to other causes. Recently, we have observed that most patients affected with HCV-associated mixed cryoglobulinemia (13 out of 15, 86.7%), that were at baseline normoglycemic, developed DM following corticosteroid treatment (prednisone > 25 mg/daily) for at least three months. Conversely, when we consider a control group including 36 HCV negative patients affected with various immunomediated disorders, i.e., systemic lupus erythematosus, myasthenia gravis, poly/dermatomyositis and chronic inflammatory demyelinating polyneuropathy, that were initially normoglycemic, corticosteroid induced DM (prednisone > 25 mg/daily for at least three months) occurred only in 16.7% of subjects. Moreover, in other two HCV positive patients suffering from myasthenia gravis, prolonged corticosteroid treatment was complicated by DM. These data, that are still unclear from a pathophysiologic viewpoint, seem to indicate corticosteroid induced DM as a further, unusual extra-hepatic manifestation of the HCV infection.
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PMID:[Frequent occurrence of diabetes mellitus after corticosteroid treatment in mixed cryoglobulinemia. An HCV-related complication?]. 982 89

We report a patient with systemic lupus erythematosus complicated by toluene poisoning. She had erythema, alopecia, arthralgia, and various neurological symptoms. Laboratory findings showed leukocytopenia, low levels of complements, and anti-dsDNA antibody. However, normal interleukin-6 level and IgG index of cerebrospinal fluid and brain magnetic resonance imaging and single photon emission computed tomography findings suggested that her neurological symptoms were caused by metabolic disorder but not neuropsychiatric systemic lupus erythematosus. Erythema, alopecia, and arthralgia improved rapidly after administration of prednisolone and tacrolimus, whereas neurological symptoms improved only gradually. Because of a history of exposure to toluene, her neurological symptoms were considered to be due to toluene poisoning. The differentiation of toluene poisoning from neuropsychiatric systemic lupus erythematosus based on symptoms is difficult because both induce various neuropsychiatric disorders. Laboratory findings of cerebrospinal fluid, radiological findings, and medical interview were useful for differentiation of toluene poisoning from neuropsychiatric systemic lupus erythematosus.
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PMID:A patient with systemic lupus erythematosus complicated by neurological symptoms of toluene poisoning. 2395 15

There is a high prevalence of hyperuricemia (HUA) in the chronic kidney disease (CKD) population. However, there's a dearth of research on HUA's prevalence, subtypes, early detection, and treatment strategies of HUA in lupus nephritis (LN) patients. The aim of this study is to address these knowledge gaps. LN patients presenting to the Department of Nephrology at Shanghai Rui Jin Hospital from January 2011 to January 2016 were recruited. The effective sample size was derived using the power analysis. The demographic, clinical and laboratory characteristics of the LN patients with HUA were compared with those of patients without HUA. Two statistical models for analyzing HUA were built and compared using the receiver operating characteristic (ROC) curve analysis. The total prevalence of HUA in the cohort was 40.11%. The subtypes of HUA included urate underexcretion-type, overproduction-type and combined-type, which proportion being 67.7%, 9.7% and 22.6% respectively. The CKD stage was closely associated with the prevalence of HUA in patients with LN. The other significant associated factors were hypertension, triglycerides, serum creatinine, serum albumin, hemoglobin, parathyroid hormone, phosphorus, calcium, etc. The statistical algorithm successfully identified LN patients at risk of HUA. In conclusion, there was a high prevalence of HUA in LN patients at CKD stages 1-3, and renal underexcretion hyperuricemia was the most prevalent subtype. The occurrence of HUA in LN may be related to renal insufficiency, metabolic disorder and lupus itself. Early care coordination programs can employ risk models to improve HUA prevention and target interventions in LN patients.
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PMID:The prevalence, subtypes and associated factors of hyperuricemia in lupus nephritis patients at chronic kidney disease stages 1-3. 2891 57

The objective of this systematic review was to analyze clinical trials carried out for the investigation of the effect of vitamin D supplementation on systemic lupus erythematosus. The research was performed from August to September 2016, without limits regarding year of publication, restriction of gender, age, and ethnicity. For the guiding question, the PICO strategy was employed. To evaluate the quality of the publications the PRISMA protocol and Jadad scale were used. The risk of bias analysis of the clinical trials was performed using the Cochrane collaboration tool. After the process of article selection and removal of duplicates, four articles were identified as eligible. The results of three studies showed a positive effect of supplementation on disease activity reduction and significant improvement in levels of inflammatory markers, fatigue, and endothelial function. Only one study showed no improvement in disease activity after supplementation. Moreover, all studies showed an increase in serum vitamin D levels. The data from this review provide evidence on the benefits of vitamin D supplementation in patients with lupus and vitamin D insufficiency/deficiency. However, it is still necessary to elucidate whether vitamin D acts in the protection against this metabolic disorder, as well as the standardization of the type, dose and time of vitamin D supplementation.
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PMID:Effect of vitamin D supplementation on patients with systemic lupus erythematosus: a systematic review. 2903 17

We present 2 patients with chronic discoid lupus erythematosus (LE) associated with xanthomatized macrophages on light microscopic findings. Skin biopsies revealed hyperkeratotic and atrophic epidermis, vacuolar degeneration of the dermal-epidermal junction, thickened basement membrane, follicular plugging, and perivascular and perifollicular lymphohistiocytic infiltrate. Notably, large collections of lipid-laden histiocytes were observed within the subjacent dermis. The patients denied history of intralesional steroid treatment. The patients did not demonstrate any clinical or laboratory signs of hyperlipidemia, cholestasis, and diabetes mellitus and insipidus. Accumulation of lipid-laden foam cells in cutaneous LE is a rare phenomenon that has been reported in discoid LE and lupus panniculitis, each only once in the literature. It has also been described within lesions of various other dermatoses in patients without lipid, hepatic, or endocrine abnormalities. Its mechanism remains unclear, but it has been hypothesized that intracellular lipids released from degenerating cells contribute to lipidization of mononuclear scavengers. Xanthomatous infiltration in cutaneous LE is an unusual feature, and its presence may not necessarily signify an underlying metabolic disorder.
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PMID:Two Unusual Cases of Discoid Lupus Erythematosus Associated With Xanthomatized Macrophages. 3146 21

An epigenetic change is a heritable genetic alteration that does not involve any nucleotide changes. While the methylation of specific DNA regions such as CpG islands or histone modifications, including acetylation or methylation, have been investigated in detail, the role of small RNAs in epigenetic regulation is largely unknown. Among the many types of small RNAs, tRNA-derived small RNAs (tsRNAs) represent a class of noncoding small RNAs with multiple roles in diverse physiological processes, including neovascularization, sperm maturation, immune modulation, and stress response. Regarding these roles, several pioneering studies have revealed that dysregulated tsRNAs are associated with human diseases, such as systemic lupus, neurological disorder, metabolic disorder, and cancer. Moreover, recent findings suggest that tsRNAs regulate the expression of critical genes linked with these diseases by a variety of mechanisms, including epigenetic regulation. In this review, we will describe different classes of tsRNAs based on their biogenesis and will focus on their role in epigenetic regulation.
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PMID:tRNA-Derived Small RNAs: Novel Epigenetic Regulators. 3299 97