Hemolysis in the context of "Cross matching"

Erythrocyte fragility refers to the propensity of erythrocytes (red blood cells, RBC) to hemolyse (rupture) under stress. It can be thought of as the degree or proportion of hemolysis that occurs when a sample of red blood cells are subjected to stress (typically physical stress, and most commonly osmotic and/or mechanical stress). Depending on the application as well as the kind of fragility involved, the amount of stress applied and/or the significance of the resultant hemolysis may vary.

When multiple levels of stress are applied to a given population/sample of cells, a fragility profile can be obtained by measuring the relative or absolute extent of hemolysis existing at each such level, in addition to finding one or more single-number indexes (either measured directly or interpolated) associated with particular respective levels of hemolysis and/or corresponding stress. Fragility testing can be useful to assess cells' ability (or lack thereof) to withstand sustained or repeated stress. Moreover, it can be used to assess how fragility itself varies under different or changing environmental or stress conditions, during or prior to the inducement of the hemolysis. Low fragility is often termed "stability," though technically stability refers to cells' resistance to both stress-induced lysis and spontaneous auto-lysis.

Urobilinogen is a colorless by-product of bilirubin reduction. It is formed in the intestines by the bacterial enzyme bilirubin reductase. About half of the urobilinogen formed is reabsorbed and taken up via the portal vein to the liver, enters circulation and is excreted by the kidney.

Increased amounts of bilirubin are formed in hemolysis, which generates increased urobilinogen in the gut. In liver disease (such as hepatitis), the intrahepatic urobilinogen cycle is inhibited also increasing urobilinogen levels. Urobilinogen is converted to the yellow pigmented urobilin apparent in urine.

Neonatal jaundice is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels. Other symptoms may include excess sleepiness or poor feeding. Complications may include seizures, cerebral palsy, or bilirubin encephalopathy.

In most cases, there is no specific underlying physiologic disorder. In other cases it results from red blood cell breakdown, liver disease, infection, hypothyroidism, or metabolic disorders (pathologic). A bilirubin level more than 34 μmol/L (2 mg/dL) may be visible. Concerns, in otherwise healthy babies, occur when levels are greater than 308 μmol/L (18 mg/dL), jaundice is noticed in the first day of life, there is a rapid rise in levels, jaundice lasts more than two weeks, or the baby appears unwell. In those with concerning findings further investigations to determine the underlying cause are recommended.

Glucose-6-phosphate dehydrogenase deficiency (G6PDD), also known as favism, is the most common enzyme deficiency anemia worldwide. It is an inborn error of metabolism that predisposes to red blood cell breakdown. Most of the time, those who are affected have no symptoms. Following a specific trigger, symptoms such as yellowish skin, dark urine, shortness of breath, and feeling tired may develop. Complications can include anemia and newborn jaundice. Some people never have symptoms.

It is an X-linked recessive disorder that results in defective glucose-6-phosphate dehydrogenase enzyme. Glucose-6-phosphate dehydrogenase is an enzyme that protects red blood cells, which carry oxygen from the lungs to tissues throughout the body, from reactive oxygen species. A defect of the enzyme results in the premature breakdown of red blood cells. This destruction of red blood cells is called hemolysis. Red blood cell breakdown may be triggered by infections, certain medication, stress, or foods such as fava beans. Depending on the specific mutation the severity of the condition may vary. Diagnosis is based on symptoms and supported by blood tests and genetic testing.

Folate deficiency, also known as vitamin B₉ deficiency, is a low level of folate and derivatives in the body. This may result in megaloblastic anemia in which red blood cells become abnormally large, and folate deficiency anemia is the term given for this medical condition. Signs of folate deficiency are often subtle. Symptoms may include fatigue, heart palpitations, shortness of breath, feeling faint, open sores on the tongue, loss of appetite, changes in the color of the skin or hair, irritability, and behavioral changes. Temporary reversible infertility may occur. Folate deficiency anemia during pregnancy may give rise to the birth of low weight birth premature infants and infants with neural tube defects.

Not consuming enough folate can lead to folate deficiency within a few months. Otherwise, causes may include increased needs as with pregnancy, and in those with shortened red blood cell lifespan. Folate deficiency can be secondary to vitamin B₁₂ deficiency or a defect in homocysteine methyl transferase that leads to a "folate trap" in which is an inactive metabolite that cannot be recovered. Diagnosis is typically confirmed by blood tests, including a complete blood count, and serum folate levels. Increased homocysteine levels may suggest deficiency state, but it is also affected by other factors. Vitamin B₁₂ deficiency must be ruled out, if left untreated, may cause irreversible neurological damage.

Pre-eclampsia is a multi-system disorder specific to pregnancy, characterized by the new onset of high blood pressure and often a significant amount of protein in the urine (proteinuria) or by the new onset of high blood pressure along with significant end-organ damage, with or without the proteinuria. When it arises, the condition begins after 20 weeks of pregnancy. In severe cases of the disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. Pre-eclampsia increases the risk of undesirable as well as lethal outcomes for both the mother and the fetus including preterm labor. If left untreated, it may result in seizures at which point it is known as eclampsia.

Risk factors for pre-eclampsia include obesity, prior hypertension, older age, and diabetes mellitus. It is also more frequent in a woman's first pregnancy and if she is carrying twins. The underlying mechanisms are complex and involve abnormal formation of blood vessels in the placenta amongst other factors. Most cases are diagnosed before delivery, and may be categorized depending on the gestational week at delivery. Commonly, pre-eclampsia continues into the period after delivery, then known as postpartum pre-eclampsia. Rarely, pre-eclampsia may begin in the period after delivery. While historically both high blood pressure and protein in the urine were required to make the diagnosis, some definitions also include those with hypertension and any associated organ dysfunction. Blood pressure is defined as high when it is greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in a woman after twenty weeks of pregnancy. Pre-eclampsia is routinely screened during prenatal care.