Hepatitis B surface antigen (HBsAg) is a distinctive serological marker of acute or chronic hepatitis B infection. HBsAg is the first antigen to appear following infection with HBV and is generally detected 1-10 weeks after the onset of clinical symptoms. HBsAg assays are routinely used to diagnose suspected HBV infection and monitor the status of infected individuals to determine whether the infection has resolved or the patient has become a chronic carrier of the virus.

The HCO3- - Arterial marker on Labcorp's Arterial Blood Gas (ABG) Panel measures the concentration of bicarbonate ions (HCO3-) in the arterial blood. Bicarbonate plays a crucial role in maintaining the acid-base balance of the body, functioning as a buffer to regulate the pH of blood. It helps neutralize excess acids or bases, thus stabilizing the body’s pH levels. HCO3- is closely linked with the respiratory system's ability to excrete CO2 and the kidneys' ability to excrete or retain bicarbonate, making it a key indicator of both metabolic and respiratory health.

HCV Antibody RFX to Quant PCR refers to a diagnostic process used in the detection and quantification of the Hepatitis C Virus (HCV). Initially, the test involves the identification of antibodies produced in response to the HCV infection.

The viral load of hepatitis C refers to the amount of virus present in the bloodstream. The quantitative HCV RNA tests measure the amount of hepatitis C virus in the blood. The result will be an exact number, such as "1,215,422 IU/L." Many people refer to the quantitative measurement as the hepatitis C "viral load."

Monitoring the HDL % of Total Cholesterol is a valuable tool in assessing cardiovascular health. A higher HDL percentage indicates a more favorable cholesterol profile and a reduced risk of heart disease. By maintaining a healthy lifestyle through proper diet, regular exercise, and smoking cessation, you can help improve your HDL percentage and support long-term heart health.

This test identifies 5 subclasses of HDL, 1 is identified as the large HDL subclass. Decreased levels of the large HDL subclass are associated with a 1.8-fold increased risk for CVD. Large HDL particles are functionally associated with an antioxidant, paraoxanase, which may help protect the arterial wall.

Reduced mean HDL size is associated with cardiovascular disease. Since HDL-C is primarily carried in the circulation by large, lipid-rich HDL particles, the inverse relationship between HDL size and cardiovascular risk can be secondary to those established for plasma levels of HDL particles, HDL-C, and large HDL.

The epidemiological data suggest that the HDL particle number may represent a more relevant therapeutic target as compared to HDL-C.

Very high mean HDL size can be paradoxically associated with elevated cardiovascular risk as observed in the EPIC-Norfolk study after multiple adjustment; this association resembles those reported between cardiovascular disease and very high levels of HDL-C as observed, for example, in the IDEAL study.

HDLs comprise a family of heterogeneous particles that vary by size, density, composition, and functionality. Two distinct HDL subfractions, large buoyant HDL2 and small dense HDL3, might exert differential effects on atherosclerosis and display a promising role in CAD risk prediction.

HDL-2 is part of the larger HDL cholesterol family, which is responsible for removing excess cholesterol from the body and transporting it to the liver. HDL-2 is formed when HDL particles in the blood interact with enzymes and acquire more cholesterol.

The large HDL2 is superior to small HDL3 in the assessment of of coronary artery disease risk.

HDL3-C subfractions are significantly and inversely associated with arterial stiffness, suggesting that HDL subfractions are likely more important than HDL-C in preventing cardiovascular disease.

Broadly, HDL can be distinguished into two subfractions, by density: HDL2 cholesterol (HDL2-C) and HDL3 cholesterol (HDL3-C). HDL3-C is well approximated by the sum of small and medium HDL particles (HDL-P), whereas HDL2-C correlates strongly with large HDL-P. There is no consensus, however, on the functions of HDL2-C and HDL3-C. Whereas some researchers have confirmed that large HDL-Ps have a protective effect on CHD, others recognized that the small, dense, protein-rich HDL-Ps display more potent atheroprotective properties than large, buoyant cholesterol-rich particles.

High-density lipoprotein cholesterol (HDL-C) or “good” cholesterol is known to decrease the risk of heart attack and stroke by removing “bad” cholesterol from the blood. It is typically assessed through a lipid profile, which measures “good” cholesterol, “bad” cholesterol, and total cholesterol. A healthcare professional may order a lipid profile when an individual is at an increased risk for heart disease or routinely in healthy adults to monitor cardiovascular health.

HDL-C transports cholesterol from the peripheral tissues and vessel walls to the liver for processing and metabolism into bile salts. Unlike LDL-C, HDL-C is often referred to as “good cholesterol” — it is thought that the process of bringing cholesterol from the peripheral tissue to the liver protects against atherosclerosis.

- Decreased HDL-C levels are considered atherogenic.

- Increased HDL-C levels are considered to protect against atherosclerosis.

The ratio of high density lipoprotein cholesterol/triglycerides is a calculated measure.

Optimal: >0.50

Borderline: 0.25–0.50

Increased Risk: <0.25

HDL-P, a measurement of total HDL particle number concentration, may be a better marker of residual risk than chemically measured high-density lipoprotein cholesterol (HDL-C, the so-called “good” cholesterol) or apolipoprotein A-1 (apoA-1, the major protein on HDL), ie, there may be a more consistent inverse association between cardiovascular endpoints and HDL-P compared with HDL-C.

Direct quantification of HDL-P concentration by NMR may be useful to refine cardiovascular risk and to evaluate novel HDL-directed therapies. Further studies are needed to clarify the role of HDL-P in clinical practice.

Helicobacter pylori (H. pylori) infection occurs when H. pylori bacteria infect your stomach. Helicobacter pylori has been evolving with human beings for well over 50,000 years, since they migrated out of Africa. H. pylori colonization has been implicated in a variety of gastroduodenal diseases.