Гипоальбуминемия: причины, симптомы и диагностика

Hypoalbuminemia (or hypoalbuminaemia) is a medical sign in which the level of albumin in the blood is low. This can be due to decreased production in the liver, increased loss in the gastrointestinal tract or kidneys, increased use in the body, or abnormal distribution between body compartments. Patients often present with hypoalbuminemia as a result of another disease process such as malnutrition as a result of severe anorexia nervosa, sepsis, cirrhosis in the liver, nephrotic syndrome in the kidneys, or protein losing enteropathy in the gastrointestinal tract. One of the roles of albumin is being the major driver of oncotic pressure (protein concentration within the blood) in the bloodstream and the body. Thus, hypoalbuminemia leads to abnormal distributions of fluids within the body and its compartments. As a result, associated symptoms include edema in the lower legs, ascites in the abdomen, and effusions around internal organs. Laboratory tests aimed at assessing liver function diagnose hypoalbuminemia. Once identified, it is a poor prognostic indicator for patients with a variety of different diseases. Yet, it is only treated in very specific indications in patients with cirrhosis and nephrotic syndrome. Treatment instead focuses on the underlying cause of the hypoalbuminemia. Albumin is an acute negative phase respondent and not a reliable indicator of nutrition status.

Patients with hypoalbuminemia are more likely to present with it as a sign of an underlying disease process than as a primary disease process. By itself, hypoalbuminemia decreases the total protein concentration in blood plasma, also known as the colloid osmotic pressure, which causes fluid to exit the blood vessels into tissues to equalize the concentrations. This leads to fluid induced swelling of the extremities known as edema, build up of fluid in the abdomen known as ascites, and fluid surrounding internal organs known as effusions. Patients also present with nonspecific findings such as fatigue and excessive weakness. Muehrcke's lines are a strong indicator of hypoalbuminemia. Hypoalbuminemia by itself may present without any symptoms, as the congenital and complete loss of albumin seen in analbuminemia can be asymptomatic. Alternatively, it can present with death in utero prior to birth or as a disease of adults characterized by edema, fatigue, and hyperlipidemia. The reason for this heterogeneity of presentation is not well understood. Hypoalbuminemia associated with the nephrotic syndrome can lead to the development of hyperlipidemia, although this is usually in the absence of atherosclerosis.

Hypoalbuminemia can be caused through a number of different mechanisms, each with the result of decreasing albumin levels. These include: 1) impaired synthesis within the liver, 2) increased utilization by tissue, 3) distributional issues, and 4) increased excretion or loss. Often, the cause is multifactorial as in liver cirrhosis, where reduced hepatic synthesis and increased capillary leakage combine to further decrease albumin levels.

Albumin is considered a negative acute phase reactant, which means that as inflammation and other acute physiologic processes occur, its levels decrease. This is in contrast to acute phase reactants like C reactive protein (CRP), whose levels increase with inflammatory processes. With respect to mechanism, inflammation leads to decreased production of albumin as a result of increased levels of cytokines, specifically IL 1, IL 6, and TNF α. In adults, on the other hand, nephrotic syndrome is commonly a secondary disease process due to a variety of inciting factors. These inciting factors can be diverse, including toxins, drugs, heavy metals, autoantibodies, post infectious antibody complexes, or immune complexes formed after malignancies like multiple myeloma.

Kwashiorkor is a disease of malnutrition characterized by decreased protein intake and amino acid deficiency resulting in hypoalbuminemia and a characteristic physical presentation. This is an extreme example of how malnutrition can result in hypoalbuminemia. Low albumin levels can also indicate chronic malnutrition from protein losing enteropathy. but can also be seen in cardiac disease and systemic lupus erythematosus.

The liver produces albumin and then secretes into the bloodstream, where it is then distributed into tissues across the body. In the liver, the liver synthesizes albumin as pre proalbumin, converts it first into proalbumin and then albumin in hepatocytes, and releases it into the blood. Once released, albumin distributes itself between the intravascular space (40%) in blood vessels, and extravascular spaces (60%) within the body's different tissues. In the blood plasma, albumin makes up 55 to 60% of total plasma protein by mass, with globulins making up a large part of the rest. In hypoalbuminemia, the amount of albumin in the intravascular space or blood plasma is what is being measured, meaning that abnormal distribution within the two compartments may contribute to a relative hypoalbuminemia in the bloodstream with a normal level in the whole body. including periprosthetic joint infection treatment failure, and cirrhosis. In chronic kidney disease, hypoalbuminemia is an indicator of frailty, which is itself associated with complications, mental distress, quality of life impairment, resource utilization, and mortality.

Hypoalbuminemia is commonly found in hospitalized patients, patients in the ICU, and the elderly within the hospital and the community. Amongst elderly patients, prevalence can be as high as 70%, as shown in a study from Southern Brasil.