Unexpected high troponin T and I values in a child with hypertrophic cardiomyopathy and acute chest pain:a case report

Background: Elevated troponin T (cTnT) and/or troponin I (cTnI) can be ascribed to multiple causes, mostly resulting from cardiac tissue damage and in lesser numbers resulting from non-cardiac related causes. The presence of macrotroponins is easily overlooked, with potentially negative consequences.Case summary: This case report presents a case study of a 12-year-old child known to have MYH7 gene-associated hypertrophic cardiomyopathy with acute chest pain combined with an unexpected high cTnT and cTnI. A cardiac cause was deemed unlikely after additional investigation, as these showed no abnormalities. After consulting a laboratory specialist, it could be concluded that the high cTnT and cTnI were a result of macrotroponin complexes, a protein complex consisting of circulating protein and endogenous autoantibodies against that protein, resulting in elevated values with misguiding and uncertain clinical significance.Discussion: Awareness of the existence of macrotroponins could have prevented costly diagnostics and prolonged hospital admission with grave psychological impact, especially in children.</p

Unexpected high troponin T and I values in a child with hypertrophic cardiomyopathy and acute chest pain:a case report

Background: Elevated troponin T (cTnT) and/or troponin I (cTnI) can be ascribed to multiple causes, mostly resulting from cardiac tissue damage and in lesser numbers resulting from non-cardiac related causes. The presence of macrotroponins is easily overlooked, with potentially negative consequences.Case summary: This case report presents a case study of a 12-year-old child known to have MYH7 gene-associated hypertrophic cardiomyopathy with acute chest pain combined with an unexpected high cTnT and cTnI. A cardiac cause was deemed unlikely after additional investigation, as these showed no abnormalities. After consulting a laboratory specialist, it could be concluded that the high cTnT and cTnI were a result of macrotroponin complexes, a protein complex consisting of circulating protein and endogenous autoantibodies against that protein, resulting in elevated values with misguiding and uncertain clinical significance.Discussion: Awareness of the existence of macrotroponins could have prevented costly diagnostics and prolonged hospital admission with grave psychological impact, especially in children.</p

Unexpected high troponin T and I values in a child with hypertrophic cardiomyopathy and acute chest pain:a case report

Background: Elevated troponin T (cTnT) and/or troponin I (cTnI) can be ascribed to multiple causes, mostly resulting from cardiac tissue damage and in lesser numbers resulting from non-cardiac related causes. The presence of macrotroponins is easily overlooked, with potentially negative consequences.Case summary: This case report presents a case study of a 12-year-old child known to have MYH7 gene-associated hypertrophic cardiomyopathy with acute chest pain combined with an unexpected high cTnT and cTnI. A cardiac cause was deemed unlikely after additional investigation, as these showed no abnormalities. After consulting a laboratory specialist, it could be concluded that the high cTnT and cTnI were a result of macrotroponin complexes, a protein complex consisting of circulating protein and endogenous autoantibodies against that protein, resulting in elevated values with misguiding and uncertain clinical significance.Discussion: Awareness of the existence of macrotroponins could have prevented costly diagnostics and prolonged hospital admission with grave psychological impact, especially in children.</p

Unexpected high troponin T and I values in a child with hypertrophic cardiomyopathy and acute chest pain:a case report

Background: Elevated troponin T (cTnT) and/or troponin I (cTnI) can be ascribed to multiple causes, mostly resulting from cardiac tissue damage and in lesser numbers resulting from non-cardiac related causes. The presence of macrotroponins is easily overlooked, with potentially negative consequences.Case summary: This case report presents a case study of a 12-year-old child known to have MYH7 gene-associated hypertrophic cardiomyopathy with acute chest pain combined with an unexpected high cTnT and cTnI. A cardiac cause was deemed unlikely after additional investigation, as these showed no abnormalities. After consulting a laboratory specialist, it could be concluded that the high cTnT and cTnI were a result of macrotroponin complexes, a protein complex consisting of circulating protein and endogenous autoantibodies against that protein, resulting in elevated values with misguiding and uncertain clinical significance.Discussion: Awareness of the existence of macrotroponins could have prevented costly diagnostics and prolonged hospital admission with grave psychological impact, especially in children.</p

Unexpected high troponin T and I values in a child with hypertrophic cardiomyopathy and acute chest pain:a case report

Background: Elevated troponin T (cTnT) and/or troponin I (cTnI) can be ascribed to multiple causes, mostly resulting from cardiac tissue damage and in lesser numbers resulting from non-cardiac related causes. The presence of macrotroponins is easily overlooked, with potentially negative consequences.Case summary: This case report presents a case study of a 12-year-old child known to have MYH7 gene-associated hypertrophic cardiomyopathy with acute chest pain combined with an unexpected high cTnT and cTnI. A cardiac cause was deemed unlikely after additional investigation, as these showed no abnormalities. After consulting a laboratory specialist, it could be concluded that the high cTnT and cTnI were a result of macrotroponin complexes, a protein complex consisting of circulating protein and endogenous autoantibodies against that protein, resulting in elevated values with misguiding and uncertain clinical significance.Discussion: Awareness of the existence of macrotroponins could have prevented costly diagnostics and prolonged hospital admission with grave psychological impact, especially in children.</p

Adiposity Blunts the Positive Relationship of Thyrotropin with Proprotein Convertase Subtilisin-Kexin Type 9 Levels in Euthyroid Subjects

BACKGROUND: Effects of thyroid function status on lipoprotein metabolism may extend into the euthyroid range. Low-density lipoprotein (LDL) metabolism is governed by proprotein convertase subtilisin-kexin type 9 (PCSK9), which down-regulates LDL receptor expression, resulting in higher LDL cholesterol (LDL-C). Here, we tested whether plasma PCSK9 correlates with thyroid function in nonobese and obese euthyroid subjects. METHODS: We assessed the extent to which plasma PCSK9 is determined by thyrotropin (TSH) in 74 euthyroid subjects (31 women; TSH between 0.5 and 4.0 mU/L and free thyroxine [FT4] between 11.0 and 19.5 pM) with varying degrees of obesity (body mass index [BMI] ranging from 20.2 to 40.4 kg/m(2)). RESULTS: TSH, FT4, PCSK9, non–high-density lipoprotein cholesterol (non-HDL-C), LDL-C, and apolipoprotein B (apoB) levels were not different between 64 nonobese subjects (BMI<30 kg/m(2)) and 10 obese subjects (BMI≥30 kg/m(2); p>0.20 for each). PCSK9 correlated positively with TSH in nonobese subjects (r=0.285, p=0.023). In contrast, PCSK9 was not associated positively with TSH in obese subjects (r=−0.249, p=0.49). The relationship of PCSK9 with TSH was different between nonobese and obese subjects when taking age, sex, FT4, and the presence of anti-thyroid antibodies into account (multiple linear regression analysis: β=−0.320, p=0.012 for the interaction term between the presence of obesity and TSH on PCSK9), and was also modified by BMI as a continuous trait (β=−0.241, p=0.062 for the interaction term between BMI and TSH on PCSK9). Non-HDL-C, LDL-C, and apoB levels were dependent on PCSK9 in nonobese subjects (p≤0.01 for each), but not in obese subjects (p>0.50), Accordingly, BMI interacted negatively with PCSK9 on non-HDL-C (p=0.028) and apoB (p=0.071). CONCLUSIONS: This study suggests that circulating PCSK9 levels correlate with thyroid function even in the normal range. This relationship appears to be blunted by obesity. Thyroid functional status may influence cholesterol metabolism through the PCSK9 pathway

(Pre)analytical considerations concerning the analysis of synovial calprotectin

Objectives: Several studies have demonstrated that synovial calprotectin is a highly accurate biomarker in diagnosing periprosthetic joint infections (PJI). Assuring reliability is of great importance and coincides with adequate preanalytical handling. This study focuses on potentially interfering factors.Methods: To assess the stability of synovial calprotectin, the effect of time, storage temperature, EDTA, freeze-thaw cycles, viscosity, and blood and lipid contamination was investigated. In the blood and lipid contamination experiments, hemolyzed and non-hemolyzed blood, homogenized adipose tissue, intralipid and chylomicrons were added. The effect of viscosity was investigated using freeze-thaw cycles, enzymatic pretreatment and sonification.Results: No effect on synovial calprotectin levels was observed in synovial samples kept at room temperature compared to samples kept at 4°C for up to seven days of storage. Freeze-thaw cycles did not result in significantly different calprotectin levels, although samples without EDTA resulted in higher recoveries after 1 and 2 freeze-thaw cycles. Blood and lipid contamination did not interfere with accurate synovial calprotectin analysis. Sample pretreatment to reduce sample viscosity by pretreating samples with DNAse and/or hyaluronidase did not influence calprotectin analysis. Sonification, however, resulted in increased calprotectin values.Conclusions: Synovial calprotectin is a stable biomarker and its analysis is not easily influenced by potential interfering factors.</p

(Pre)analytical considerations concerning the analysis of synovial calprotectin

Objectives: Several studies have demonstrated that synovial calprotectin is a highly accurate biomarker in diagnosing periprosthetic joint infections (PJI). Assuring reliability is of great importance and coincides with adequate preanalytical handling. This study focuses on potentially interfering factors.Methods: To assess the stability of synovial calprotectin, the effect of time, storage temperature, EDTA, freeze-thaw cycles, viscosity, and blood and lipid contamination was investigated. In the blood and lipid contamination experiments, hemolyzed and non-hemolyzed blood, homogenized adipose tissue, intralipid and chylomicrons were added. The effect of viscosity was investigated using freeze-thaw cycles, enzymatic pretreatment and sonification.Results: No effect on synovial calprotectin levels was observed in synovial samples kept at room temperature compared to samples kept at 4°C for up to seven days of storage. Freeze-thaw cycles did not result in significantly different calprotectin levels, although samples without EDTA resulted in higher recoveries after 1 and 2 freeze-thaw cycles. Blood and lipid contamination did not interfere with accurate synovial calprotectin analysis. Sample pretreatment to reduce sample viscosity by pretreating samples with DNAse and/or hyaluronidase did not influence calprotectin analysis. Sonification, however, resulted in increased calprotectin values.Conclusions: Synovial calprotectin is a stable biomarker and its analysis is not easily influenced by potential interfering factors.</p

(Pre)analytical considerations concerning the analysis of synovial calprotectin

Objectives: Several studies have demonstrated that synovial calprotectin is a highly accurate biomarker in diagnosing periprosthetic joint infections (PJI). Assuring reliability is of great importance and coincides with adequate preanalytical handling. This study focuses on potentially interfering factors.Methods: To assess the stability of synovial calprotectin, the effect of time, storage temperature, EDTA, freeze-thaw cycles, viscosity, and blood and lipid contamination was investigated. In the blood and lipid contamination experiments, hemolyzed and non-hemolyzed blood, homogenized adipose tissue, intralipid and chylomicrons were added. The effect of viscosity was investigated using freeze-thaw cycles, enzymatic pretreatment and sonification.Results: No effect on synovial calprotectin levels was observed in synovial samples kept at room temperature compared to samples kept at 4°C for up to seven days of storage. Freeze-thaw cycles did not result in significantly different calprotectin levels, although samples without EDTA resulted in higher recoveries after 1 and 2 freeze-thaw cycles. Blood and lipid contamination did not interfere with accurate synovial calprotectin analysis. Sample pretreatment to reduce sample viscosity by pretreating samples with DNAse and/or hyaluronidase did not influence calprotectin analysis. Sonification, however, resulted in increased calprotectin values.Conclusions: Synovial calprotectin is a stable biomarker and its analysis is not easily influenced by potential interfering factors.</p