Serum Sialic Acid and the Long-term Complications of Insulin-dependent Diabetes Mellitus

Powrie, Jake; Watts, Gerald F.; Crook, M; Ingham, J.N.; Taub, Nicholas; Shaw, Ken

doi:10.1002/(sici)1096-9136(199603)13:3<238::aid-dia29>3.0.co;2-w

Cited by 14 publications

(10 citation statements)

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“…A relationship between serum or plasma sialic acid levels and microvascular complications has been observed before in small-scale studies for microalbuminuria and clinical proteinuria in type 1 (6,7) and type 2 diabetes (18), and for retinopathy in type 1 (19) and type 2 diabetes (20). An association with neuropathy has not been reported before.…”

Section: Conclusion -mentioning

confidence: 99%

Relationship Between Plasma Sialic Acid Concentration and Microvascular and Macrovascular Complications in Type 1 Diabetes

Pj³

et al. 2001

Diabetes Care

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The APPENDIX section contains a complete list of centers that participated in the EURODIAB IDDM Complications Study.Abbreviations: AER, albumin excretion rate; CHD, coronary heart disease; CV, coefficient of variation. A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Relationship Between Plasma Sialic Acid Concentration and Microvascular and Macrovascular Complications in Type 1 DiabetesThe EURODIAB Complications StudyOBJECTIVE -To test the hypothesis that an increased plasma concentration of sialic acid, a marker of the acute-phase response, is related to the presence of diabetic micro-and macrovascular complications in type 1 diabetes. RESEARCH DESIGN AND METHODS -We investigated the relationship betweenplasma sialic acid concentration and nephropathy, retinopathy, neuropathy, and coronary heart disease (CHD) in a cross-sectional survey of 1,369 people with type 1 diabetes. Subjects were participants in the EURODIAB IDDM Complications Study, which involved 31 centers in 16 European countries.RESULTS -There was a significantly increasing trend of plasma sialic acid with severity of retinopathy (P Ͻ 0.001 in men) and with degree of urinary albumin excretion (P Ͻ 0.001 men, P Ͻ 0.01 women). Plasma sialic acid correlated with increasing plasma creatinine concentration (P Ͻ 0.009 men, P Ͻ 0.0002 women), and men with neuropathy had a higher plasma sialic acid concentration than those without (P Ͻ 0.006). There was no significant correlation between plasma sialic acid and CHD in either sex. Elevated plasma sialic acid concentrations were also associated with several risk factors for diabetic vascular disease: diabetes duration, HbA 1c , plasma triglyceride and cholesterol concentrations, waist-to-hip ratio, hypertension and smoking (in men), and low physical exercise (in women). In multiple logistic regression analysis, plasma sialic acid was independently related to proliferative retinopathy and urinary albumin excretion rate in men.CONCLUSIONS -We conclude that an elevated plasma sialic concentration is strongly related to the presence of microvascular complications in type 1 diabetes, especially retinopathy and nephropathy. Further study of acute-phase response markers and mediators as indicators or predictors of diabetic microvascular complications is therefore justified.

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Section: Conclusion -mentioning

confidence: 99%

Relationship Between Plasma Sialic Acid Concentration and Microvascular and Macrovascular Complications in Type 1 Diabetes

Pj³

et al. 2001

Diabetes Care

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“…Serum SA has been found previously to be associated with retinopathy [91] and nephropathy but not neuropathy in IDDM patients [106]. A recent study [107] suggests that the presence or absence of diabetic retinopathy in NIDDM patients had no impact on the serum SA levels.…”

Section: Diabetesmentioning

confidence: 90%

Occurrence of sialic acids in healthy humans and different disorders

Sillanaukee

Pönniö

Jä̈askëlainen

1999

Eur J Clin Investigation

226

166

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Sialic acid (SA), N-acetylated derivatives of neuraminic acid, play a central role in the biomedical functioning of humans. The normal range of total sialic acid (TSA) level in serum/plasma is 1.58-2.22 mmol L-1, the free form of SA only constituting 0.5-3 mumol L-1 and the lipid-associated (LSA) forms 10-50 mumol L-1. Notably, considerably higher amounts of free SA are found in urine than in serum/plasma (approximately 50% of the total SA). In inherited SA storage diseases such as Salla's disease, SA levels are elevated many times over, and their determination during clinical investigation is well established. Furthermore, a number of reports describe elevated SA levels in various other diseases, tentatively suggesting broader clinical utility for SA markers. Increased SA concentrations have been reported during inflammatory processes, probably resulting from increased levels of richly sialylated acute-phase glycoproteins. A connection between increased SA levels and elevated stroke and cardiovascular mortality risk has also been reported. In addition, SA levels are slightly increased in cancer, positively correlating with the degree of metastasis, as well as in alcohol abuse, diabetes, chronic renal failure and chronic glomerulonephritis. Several different mechanisms are assumed to underlie the elevated SA concentrations in these disorders. The apparent non-specificity of SA to a given disease limits the potential clinical usefulness of SA determination. In addition, some non-pathological factors, such as aging, pregnancy and smoking, may cause changes in SA concentrations. The absolute increases in SA levels are also rather small (save those in inherited SA storage disorders); this further limits the clinical potential of SA as a marker. Tentatively, SA markers might serve as adjuncts, when combined with other markers, in disease screening, disease progression follow-up, and in the monitoring of treatment response. To become clinically useful, however, the existing SA determination assays need to be considerably refined to reduce interferences, to be specific for certain SA forms, and to be more easy to use.

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“…These aggregates are avidly taken up by intimal smooth muscle cells followed by lipid accumulation (8,9). Serum total sialic acid is also elevated in diabetes mellitus and is associated with certain diabetic complications (10)(11)(12). Moreover, sialic acid has been found to be elevated in myocardial infarction (13,14).…”

Section: Introductionmentioning

confidence: 99%

Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction

Gökmen¹,

Kılıçlı²,

Özçeli̇k³

et al. 2000

Clinical Chemistry and Laboratory Medicine

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Although serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levels associated with increased cardiovascular mortality and also with cerebrovascular disease, the reason for the elevation in serum sialic acid content remains obscure. It has been shown that an increased output of serum proteins by the liver due to some type of acute phase reaction may be one of the possible sources of an increased serum sialic acid concentration in patients with myocardial infarction. An increase in the activity of sialidase, which cleaves the terminal sialic acid residues from oligosaccharides, glycoproteins and gangliosides, may also play an important role in the elevation of serum total sialic acid in myocardial infarction. Elevated serum total sialic acid in the blood might result either from the shedding or secreting of sialic acid from the cell membrane surface, or releasing of cellular sialic acid from the cell into the bloodstream due to cell damage after myocardial infarction. The purpose of the present study is to investigate serum total and lipid-bound sialic acid and the enzymes serum lactate dehydrogenase, creatine kinase and aspartate aminotransferase in patients with acute myocardial infarction, at 24 h post-infarction (day 1), 48 h post-infarction (day 2) and 72 h post-infarction (day 3). A possible role of cell damage in the elevation of serum total and lipid-bound sialic acid levels in these patients was also evaluated. In this study, 40 patients with myocardial infarction ranging in age from 42 to 68 years, and 26 healthy volunteers ranging in age from 45 to 71 years were included. Serum total sialic acid determination was carried out by the thiobarbituric acid method of Warren and lipid-bound sialic acfd by the method of Katopodis. Our data shows that a) there is a gradual increase in the levels of serum total sialic acid and lipid-bound sialic acid during the first three days after the acute myocardial infarction and b) the elevation in serum total sialic acid levels correlates with the elevation in lactate dehydrogenase activity only on day 1 following infarction. Therefore, either the shedding or secreting of sialic acid from the cell or cell membrane surface may be partly responsible for an increased serum sialic acid concentration especially on day 1 following myocardial infarction.

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Serum Sialic Acid and the Long-term Complications of Insulin-dependent Diabetes Mellitus

Cited by 14 publications

References 0 publications

Relationship Between Plasma Sialic Acid Concentration and Microvascular and Macrovascular Complications in Type 1 Diabetes

Relationship Between Plasma Sialic Acid Concentration and Microvascular and Macrovascular Complications in Type 1 Diabetes

Occurrence of sialic acids in healthy humans and different disorders

Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction

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