Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The score on the Hamilton Depression Rating Scale (HDRS), the L-tryptophan:competing amino acid (valine + leucine) (L-TRP:CAA) ratio, and the 3-methoxy-4-hydroxyphenylglycol (MHPG) flow in 24-hr urine were recorded in 83 depressed patients undergoing a Dexamethasone Suppression Test (DST). The subjects were diagnostically subdivided according to DSM-III into minor depression (296.82, 300.40, 309.00), major depression without melancholia (296.X2), with melancholia (296.X3), or with psychotic features (296.X4). Minor depression, major depression with melancholia, and major depression with psychotic features can be regarded as distinct biological entities. Major depression without melancholia is a heterogeneous group with reference to the biological markers. By combining these biological data with age in a discriminant function analysis, 81.9% of all depressed patients can be correctly classified into minor or major depression groups. The combined biological markers can also be used to predict the severity of the depression; 42.5% of the variance in the HDRS score is accounted for by multiple regression on the biological figures. Multivariate statistical techniques considerably improve prediction for both subtype and severity of depression.
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PMID:Prediction of subtype and severity of depression by means of dexamethasone suppression test, L-tryptophan: competing amino acid ratio, and MHPG flow. 381 68

Cystatin C, an efficient inhibitor of cysteine proteinases, is present in all investigated human extracellular fluids. Dexamethasone caused a significant and dose-dependent increase in the cystatin C secretion of cultivated HeLa cells up to a maximal increase of 80% at 10(-6) mol l-1 dexamethasone. Increased production of cystatin C was also observed at lower concentrations, suggesting that glucocorticoids might play a physiological role in the production of cystatin C. The effect of dexamethasone on the cystatin C gene expression was also studied in a transient transfection expression system using chimeric plasmid constructs of the cystatin C gene promoter (positions -2 to -1084) coupled to the structural gene for human growth hormone (hGH). In this system, a small, but statistically significant, increase in hGH secretion was also observed upon dexamethasone treatment, suggesting that the glucocorticoid-induced increase in secretion of cystatin C is due to a promoter-mediated increase in transcription of the cystatin C gene.
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PMID:Promoter-mediated, dexamethasone-induced increase in cystatin C production by HeLa cells. 863 86

We report a case of suspected pseudo-elevation of serum creatinine in a patient with rheumatoid arthritis, whose blood sample was obtained from his right cubital vein immediately after the intra-articular injection of 0.67 mg of a pharmaceutical preparation of dexamethasone (Decadron) containing creatinine as a buffer into his right wrist joint to alleviate arthralgia. The 61-year-old male patient, who had been treated for rheumatoid arthritis, was referred to our outpatient clinic by his family doctor because of sudden elevation of his serum creatinine, which hitherto had been normal. Acute kidney injury (AKI) was suspected, but his medical history, physical examinations, and laboratory findings did not support the diagnosis of AKI. The preserved serum sample obtained when the elevation of his serum creatinine was reported was examined and revealed that the serum concentration of cystatin C was normal, but the serum concentration of creatinine measured with high-performance liquid chromatography method was elevated to a degree consistent with the serum creatinine concentration measured with enzymatic method. Accordingly, we predicted the possibility that creatinine contained in Decadron as a buffer was included in the measurement of his intrinsic serum creatinine. To test this hypothesis, the creatinine concentration of serum samples from another patient with known amounts of added Decadron were measured, and the additive effect of the extrinsic creatinine in the measurement of serum creatinine concentration was confirmed. These findings clearly suggest that we should consider the influence of extrinsic creatinine as an inactive ingredient in the measurement of serum creatinine.
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PMID:[Case of suspected pseudo-elevation of serum creatinine immediately after intra-articular injection into a wrist joint of a pharmaceutical preparation of dexamethasone containing creatinine as a buffer]. 2151 7

Background: Several studies have shown that non-renal factors such as corticosteroids may increase plasma cystatin C levels without affecting kidney function. However, the mechanisms underlying this are unclear. We hypothesized that corticosteroids may increase cystatin C levels in the plasma by promoting its production in tissues. In the present study, we aimed to test our hypothesis in rats by investigating the effect of corticosteroids on cystatin C production in tissues and the glomerular filtration rate (GFR), as measured by the gold standard method (i.e., inulin clearance). Results: Dexamethasone treatment was associated with much higher concentrations of cystatin C in all organ tissue homogenates tested. Dexamethasone increased plasma cystatin C levels in rats, without any decrease in renal inulin clearance. The impact of dexamethasone on plasma and organ tissue cystatin C levels was abolished by RU486, indicating the effect was glucocorticoid receptor-mediated. Conclusions: Our study provides direct evidence that corticosteroids may increase cystatin C levels in the plasma by promoting its production, without any decrease in GFR.
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PMID:Corticosteroids significantly increase cystatin C levels in the plasma by promoting cystatin C production in rats. 3135 65