What is high hematocrit. High Hematocrit: Causes, Risks, and Management Strategies
What are the normal hematocrit values for men and women. How does testosterone replacement therapy affect hematocrit levels. Why is high hematocrit a concern for cardiovascular health. What is the relationship between sleep apnea and hematocrit. How can high hematocrit be managed effectively.
Understanding Hematocrit and Its Importance
Hematocrit is a crucial measure of blood composition, representing the percentage of red blood cells in a person’s blood volume. Normal hematocrit values typically range from 42% for women to 47% for men. These cells play a vital role in oxygen transport throughout the body, making hematocrit levels an important indicator of overall health.
A complete blood count (CBC) test provides comprehensive information about blood components, including:
- Red blood cell count
- Hemoglobin levels
- White blood cell count
- Platelet count
Abnormal hematocrit values can signify underlying health issues. High hematocrit, known as polycythemia, indicates an excess of red blood cells. Conversely, low hematocrit, or anemia, suggests a deficiency in red blood cells. Both conditions can have serious health implications if left untreated.
Red Cell Distribution Width (RDW) and Mean Platelet Volume (MPV)
Two additional parameters often examined alongside hematocrit are RDW and MPV:
- RDW measures the variation in red blood cell size, helping diagnose different types of anemia and assess cardiovascular disease severity.
- MPV indicates the average size of platelets, which are crucial for blood clotting and wound healing.
These measurements provide valuable insights into blood cell characteristics and can help identify various health conditions.
The Link Between Obstructive Sleep Apnea Syndrome (OSAS) and Hematocrit
Obstructive Sleep Apnea Syndrome (OSAS) is a sleep disorder characterized by repeated upper airway collapse during sleep. This condition can lead to poor sleep quality, choking sensations, and hypoxia (low oxygen saturation). Recent research has uncovered a fascinating connection between OSAS and hematocrit levels.
OSAS Study: Methodology and Findings
A comprehensive study conducted between January 2011 and June 2014 explored the relationship between OSAS and blood parameters. Here’s an overview of the study:
- 264 patients underwent polysomnographic evaluation
- 116 patients met the study criteria and agreed to participate
- Exclusion criteria: cardiovascular diseases, smoking, diabetes mellitus, lung disease, hypertension
- Patients were divided into groups based on the apnea-hypopnea index (AHI)
- Control group: 62 individuals with AHI less than 5
The study employed polysomnographic methods, including suprasternal microphones to assess airflow during sleep. Blood samples were collected after an 8-hour fasting period.
OSAS Severity and Blood Parameters
The research revealed intriguing correlations between OSAS severity and various blood parameters:
- RDW values increased with OSAS severity
- MPV levels were higher in severe OSAS patients
- Hematocrit levels showed a positive correlation with OSAS severity
These findings suggest that RDW and MPV could serve as potential markers for OSAS severity, while also highlighting the impact of sleep apnea on hematocrit levels.
Testosterone Replacement Therapy (TRT) and Hematocrit Levels
Testosterone Replacement Therapy (TRT) is a common treatment for men with low testosterone levels. However, it can have significant effects on hematocrit levels, potentially leading to health risks if not properly managed.
TRT-Induced Erythrocytosis
One of the most common side effects of TRT is an increase in red blood cell production, known as erythrocytosis. This condition can lead to elevated hematocrit levels, which may increase the risk of cardiovascular events.
Why does TRT cause an increase in red blood cells?
- Testosterone stimulates erythropoietin production in the kidneys
- Erythropoietin promotes red blood cell formation in the bone marrow
- Testosterone also has a direct effect on bone marrow stem cells, enhancing red blood cell production
Monitoring Hematocrit During TRT
Regular monitoring of hematocrit levels is crucial for patients undergoing TRT. The Endocrine Society guidelines recommend:
- Checking hematocrit levels before starting TRT
- Monitoring hematocrit at 3, 6, and 12 months after initiating therapy
- Annual check-ups thereafter
- If hematocrit exceeds 54%, TRT should be discontinued until levels normalize
Managing High Hematocrit in TRT Patients
For patients experiencing high hematocrit levels due to TRT, several management strategies can be employed:
- Dose adjustment: Reducing the testosterone dose may help lower hematocrit levels
- Change in administration method: Switching from intramuscular injections to transdermal gels or patches may result in more stable hormone levels
- Therapeutic phlebotomy: Regular blood donation or medical blood removal can effectively reduce hematocrit
- Lifestyle modifications: Staying hydrated, avoiding smoking, and managing sleep apnea can help control hematocrit levels
The Role of Sleep Apnea in TRT-Induced High Hematocrit
Sleep apnea can exacerbate the effects of TRT on hematocrit levels. Patients with both conditions may require more aggressive management strategies:
- Treating underlying sleep apnea with CPAP therapy
- More frequent monitoring of hematocrit levels
- Adjusting TRT dosage or administration method
- Considering alternative treatments for low testosterone
Cardiovascular Risks Associated with High Hematocrit
Elevated hematocrit levels can significantly increase the risk of cardiovascular events. Understanding these risks is crucial for patients and healthcare providers alike.
Mechanisms of Cardiovascular Risk
How does high hematocrit contribute to cardiovascular problems?
- Increased blood viscosity: Thicker blood can impair circulation and increase the workload on the heart
- Enhanced platelet activation: Higher hematocrit levels may promote blood clot formation
- Endothelial dysfunction: Impaired blood flow can damage the inner lining of blood vessels
- Increased oxidative stress: Excess red blood cells may lead to increased free radical production
Cardiovascular Conditions Associated with High Hematocrit
Patients with persistently high hematocrit levels may be at increased risk for:
- Thromboembolism (blood clots)
- Myocardial infarction (heart attack)
- Stroke
- Venous thrombosis
- Pulmonary embolism
Regular monitoring and proactive management of hematocrit levels are essential for minimizing these risks.
The Impact of Frequent Blood Donations on Iron Levels
While blood donation can be an effective method for managing high hematocrit, frequent donations may lead to iron deficiency. A study of 235 men revealed important insights into this issue.
Study Findings on Frequent Blood Donors
The research highlighted several key points:
- Frequent blood donors were more likely to develop iron deficiency
- Iron stores, measured by ferritin levels, decreased with donation frequency
- Recovery time for iron stores varied among individuals
Balancing Hematocrit Management and Iron Levels
For patients using blood donation to manage high hematocrit, it’s crucial to strike a balance between hematocrit reduction and maintaining adequate iron levels. Strategies may include:
- Monitoring ferritin levels alongside hematocrit
- Adjusting donation frequency based on individual recovery rates
- Considering iron supplementation under medical supervision
- Exploring alternative methods for hematocrit management
Comprehensive Approach to High Hematocrit Management
Effectively managing high hematocrit requires a multifaceted approach, especially for patients with multiple contributing factors such as TRT and sleep apnea.
Personalized Treatment Plans
Healthcare providers should develop individualized management strategies based on:
- Underlying cause of high hematocrit
- Presence of comorbidities (e.g., sleep apnea, cardiovascular disease)
- Patient’s overall health status and risk factors
- Response to initial interventions
Integrative Management Strategies
A comprehensive approach may include:
- Regular monitoring of hematocrit, ferritin, and other relevant blood parameters
- Adjusting TRT dosage or administration method as needed
- Treating underlying conditions such as sleep apnea
- Implementing lifestyle modifications (e.g., hydration, exercise, smoking cessation)
- Therapeutic phlebotomy with careful monitoring of iron status
- Considering alternative treatments for low testosterone in severe cases
By addressing high hematocrit through a comprehensive, personalized approach, patients can minimize health risks while maintaining the benefits of treatments like TRT.
In conclusion, understanding the complexities of hematocrit management, particularly in the context of TRT and sleep apnea, is crucial for optimizing patient care. Regular monitoring, personalized treatment plans, and a holistic approach to health can help patients navigate the challenges of high hematocrit while maintaining overall well-being.
TRT Induced High Red Blood Cells: How to Manage Hematocrit
Table of Contents
- High hematocrit: Why it is important?
- Obstructive sleep apnea syndrome (OSAS), red blood cells and high hematocrit values
- Hematocrit TRT Study Material and Methods
- Study Results
- Conclusions
- Understanding the occurrence of high red blood cells and hematocrit on testosterone replacement therapy
- CHECK YOUR HEMATOCRIT TEST WITH A CBC PANEL
- Testosterone replacement therapy formulations
- TRT-induced high red blood cell volume ( high hematocrit )
- High hematocrit: The effects of different testosterone products
- Conclusions
- Understanding why blood donations shouldn’t be done too frequently
- A study conducted on 235 men concluded that frequent blood donors can develop iron deficiency
- Methods and materials
- Conclusions
- Caution about frequent blood donations:
- Is supplementing with iron a solution for low iron/ ferritin caused by frequent blood donations?
- References:
Since abnormally high hematocrit values can pose serious health problems, this article will analyze the correlation between testosterone therapy and high hematocrit. TRT, sleep apnea and smoking are contributing factors can cause high hematocrit which can increase cardiovascular risks if not properly managed. This article explains the basics of how to manage high hematocrit while using testosterone.
High hematocrit: Why it is important?
The red cells are some of the most important components of a person’s blood. The term hematocrit refers to the percentage of red blood cells in a human’s body. For women, normal hematocrit values should be around 42% and for men, it should be around 47%.
A complete blood count test will show the number of red blood cells in the blood as well as the hemoglobin values, white blood cells, and platelets. When the hematocrit is too high, meaning that there are too many red blood cells, this condition is known as polycythemia. When the hematocrit values are too low, this condition is known as anemia. Abnormal hematocrit values can put one’s life in danger if not treated promptly.
Since abnormally high hematocrit values can pose serious health problems, this article will analyze the correlation between red blood cell count and various medical conditions such as obstructive sleep apnea syndrome, erythrocytosis caused by testosterone replacement therapy and why people should be careful when donating blood more than once a year.
It is important to also know the red cell distribution width (RDW) which is a laboratory measuring system that analyzes the size of red blood cells. Doctors frequently examine the RDW to determine the causes of anemia and to gain more insights about the severity of different cardiovascular diseases.
Platelets are cytoplasm fragments that quickly react when bleeding is detected in the body. They help in the coagulation process to prevent infection and to initiate the healing process. The mean platelet volume (MPV) is a way of measuring the size of the platelets. Both these terms, RDW and MPV, will be used to examine the link between obstructive sleep apnea syndrome and high hematocrit values.
Obstructive sleep apnea syndrome (OSAS), red blood cells and high hematocrit values
OSAS is a sleep disorder that is characterized by a collapse of the upper airway while sleeping. This leads to a low quality sleep, choking sensations, and even hypoxia (low oxygen saturation). A comprehensive study performed between January 2011 and June 2014 shows that high RDW might be a reliable marker when it comes to the severity of OSAS.
Hematocrit TRT Study Material and Methods
264 patients were admitted to the sleep unit to undertake a polysomnographic evaluation and were subsequently diagnosed with OSAS. 116 of these patients met the criteria of the study and agreed to participate. These patients reported frequent unpleasant symptoms such as daytime sleepiness, severe snoring at nighttime, etc.
The exclusion criteria left out patients who had various types of medical conditions that might have interfered with the results of the study. For example, patients who had known cardiovascular diseases, were smokers, had diabetes mellitus, lung disease or hypertension were not included in the study.
The 116 patients who participated in the study were divided into several groups, depending on the apnea-hypopnea index (AHI) which basically indicates the severity of the sleep apnea. There were 3 groups – mild (AHI between 5 and 15), moderate (AHI between 15 and 30) and severe (AHI higher than 30). There was also a control group of 62 individuals who had an apnea-hypopnea index of less than 5.
The study was performed using polysomnographic methods. Researchers have attached suprasternal microphones to assess the airflow of the patients during sleep. Blood samples were also drawn using a 21-gauge needle syringe after a fasting period of 8 hours. The apnea was defined as a stop of airflow for 10 seconds or more during sleep. Hypopnea was defined as a reduction of airflow between 30% and 50% as well as a decrease in capillary oxygen saturation.
Study Results
At the end of the study, researchers have reached the conclusion that patients with severe OSAS have higher RDW, a higher platelet count and MPV. In addition, the hematocrit and RDW are positively correlated with apnea-hypopnea index. This means that the complete blood count is very important for patients diagnosed with OSAS.
It has been established that patients with OSAS undergo a state of systemic inflammation caused by a wide variety of factors. This state of inflammation can lead to a higher secretion of pro-inflammatory cytokines such as interleukin-6 which in turn can create erythrocyte deformability and a higher level of RDW. Other studies have shown that high RDW levels are also associated with a higher-sensitivity CRP level which is a known marker of inflammation.
One of the most important reasons which make this study unique and highly accurate is the simple fact that patients who suffered from serious health conditions such as coronary artery disease, diabetes mellitus, and hypertension didn’t take part in the study. It is a well-known fact that these illnesses can lead to a higher RDW level which could have compromised the results of the study.
Patients who suffer from OSAS also experience hypercoagulability which is caused by high blood viscosity. Blood viscosity is defined as the resistance of blood to exterior forces and is influenced by hematocrit, the behavior of erythrocytes and other factors. It has been established that hematocrit plays an important role in the coagulability of blood and can lead to increased blood clotting.
When there is an increased blood clotting in the body, the natural flow of blood can be negatively affected and multiple cardiovascular issues can appear. Researchers believe that the hypoxemia experienced by patients with OSAS is caused by a release of inflammatory factors that negatively affect the blood and can lead to hypercoagulability.
It has also been found out that the total platelet count in patients with OSAS was higher in comparison with the patients in the control group or those in the mild group. This is real evidence of the correlation between platelet activation and cardiovascular diseases in patients suffering from OSAS.
Conclusions
This comprehensive study has shown evidence that RDW, MPV, and platelet count are increased in patients diagnosed with OSAS. The RDW index is also positively correlated with oxygen desaturation index and AHI.
Since RDW is included in a standard blood count measurement, it can become an inexpensive and simple tool to diagnose the severity of the OSAS in patients of all ages. As a result, patients who suffer from a severe OSAS can be given priority when it comes to treatment, improving their chances of recovery.
Understanding the occurrence of high red blood cells and hematocrit on testosterone replacement therapy
Erythrocytosis is a medical condition that appears when the body is making too many red blood cells. RBCs are responsible for transporting oxygen to organs and tissues. When they are too many, the blood can become too thick and cause cardiovascular complications.
There are 2 types of erythrocytosis – primary and secondary. The primary erythrocytosis is usually caused by bone marrow problems. RBCs are made in the bone marrow and something might trigger an increase in their production. Secondary erythrocytosis is caused by certain diseases or drugs, including testosterone replacement therapy.
TRT is the go-to treatment for people who suffer from hypogonadism – aka androgen deficiency. This type of treatment is increasingly popular especially among people over 40 years of age. It can increase libido, help to maintain muscle mass, improve mood and general wellbeing. However, one of the side effects of TRT is a simple fact that it can cause erythrocytosis.
This medical condition is represented by an increase in hemoglobin (Hb) and hematocrit (Hct). When the Hb is higher than 18.5 g/dL and the Hct is higher than 52% in men, the patient suffers from erythrocytosis.
Since the RBCs count is too high in people with erythrocytosis, the blood viscosity also increases which can lead to various potentially life-threatening medical issues such as venous thromboembolism. This basically means that small blood clots separate from their original source and are transported by blood through veins and capillaries, causing blockages that lead to stroke, myocardial infarction or other complications.
Testosterone replacement therapy formulations
Testosterone replacement therapy is recommended for men who have testosterone levels lower than 300ng/ dL. It is commonly accepted that the T levels decrease by approximately 1% per year after 35 years of age. TRT has been shown to improve the mood of the patients, correct insulin resistance problems, help increase bone density and muscle mass, among other positive benefits.
Getting testosterone into the body can be done in various ways. There are injections, gels, buccal patches, pellets, and others. Some formulations show results much quicker (injections, for example) and each one of them has different effects on patients, depending on the dosage, administration option, etc.
TRT-induced high red blood cell volume ( high hematocrit )
When the testosterone levels increase in the body, the hemoglobin and hematocrit levels also increase. Studies have shown that people who undergo TRT have higher blood viscosity and platelet adhesiveness which can lead to thromboembolic risks.
Although there are not many studies that link TRT-induced erythrocytosis (high red blood cells) with thromboembolism, one small research performed by Krauss et al on a group of 15 men can lead to interesting conclusions. The 15 men received short-acting IM TE (testosterone injection) every 21 days and had their bloodwork and testosterone levels monitored.
The researchers discovered a correlation between transient ischemic attacks and men who had a mean Hct levels higher than 48%. Although the study was performed on a small group of men, it is an important research finding because throws a spotlight on the potential side effects of TRT. Additionally, the FDA also forces companies that make testosterone products to add a warning on the label stating “possible increased risk of heart attacks and strokes in patients taking testosterone”.
High hematocrit: The effects of different testosterone products
Researchers have discovered that various testosterone formulations have different effects when it comes to the occurrence of erythrocytosis in patients who undergo TRT. For example, short-acting injectables such as IM TC and IM TE render an incidence of erythrocytosis higher than 40%. The other formulations have a much lower incidence and are considered safer, although the testosterone is absorbed much slower into the body.
Men who are prescribed and use transdermal gels such as AndroGel 1.62% have an approximately 13% chance of developing erythrocytosis, according to some studies. These types of gels can have a dose of testosterone of 20-100 mg and can be applied to the shoulder area or directly on the skin.
Similarly, crystalline pellets that are implanted under the skin have a T formulation of 75mg per pellet and can lead to a 35% chance of developing erythrocytosis in the long run. Studies define erythrocytosis as a hematocrit level higher than 52%.
Conclusions
Although it is necessary to develop more complex studies to examine the molecular mechanisms when it comes to erythrocytosis induced by TRT, researchers have discovered that there might be a direct correlation between high hemoglobin and hematocrit levels when patients get testosterone replacement therapy.
Furthermore, some studies show that there is also a higher risk for patients who benefit from TRT to develop CV complications as a result of increased blood viscosity. It’s important to also develop other treatment options for hypogonadal men such as aromatase inhibitors, human chorionic gonadotropin, and others.
Lastly, when TRT is absolutely necessary, patients might take into consideration safer T products such as undecanoates which can be taken orally or transdermal gels.
Understanding why blood donations shouldn’t be done too frequently
It is estimated that approximately 70% of the blood supply in the United States comes from repeat donors. Although donating blood is a commendable act, people should be careful when donating several times a year because they can develop iron deficiency. A plethora of men decides to donate blood to also decrease hematocrit levels.
A study conducted on 235 men concluded that frequent blood donors can develop iron deficiency
The group of 235 men was separated into 3 categories – control group with no donations, group 2 with 2 donations per year and group 3 with 3 donations per year. The age of the donors was between 17 and 65 years and their hemoglobin values were higher than 12. 5 g/dl. Donors who took iron supplements before were excluded from this study to avoid interfering with the results.
Methods and materials
The researchers looked at a couple of important values such as hemoglobin and ferritin levels. Ferritin is a type of intracellular protein responsible for transporting and releasing iron throughout the body. Iron deficiency was defined as serum hemoglobin levels below 13 g/dl and serum ferritin levels below 15 μg/l. No participant in the study has donated blood in the previous 8 weeks.
Conclusions
Researchers have found out that the patients in the case groups (2 and 3) had a decreased level of hemoglobin and ferritin in comparison with the patients in the control group. More specifically, men in the group 3 had ferritin mean levels of 26 and a hemoglobin level of 13.8, those in group 2 had ferritin mean levels of 56 and hemoglobin levels of 15.4 while the control group had ferritin mean levels of 108 and hemoglobin levels of 15. 9.
Caution about frequent blood donations:
The study presented evidence that donating blood more than once or twice per year can significantly deplete iron stores and can lead to anemia. Moreover, the medical industry relies on donations of a healthy supply of blood rich in iron, so certain donors (especially those who donate frequently) might not be eligible for repeat donations.
Likewise, measuring the hemoglobin level only might not be a reliable indicator of a person being suitable for blood donation or not. The ferritin levels should also be taken into account to prevent anemia in various donors.
Is supplementing with iron a solution for low iron/ ferritin caused by frequent blood donations?
This is a good question, but the answer might not be that simple. It is a well-known fact that supplementing with iron should be done carefully since too much iron in the bloodstream can cause damage to organs and tissues. Additionally, those patients who have family members with cancer might not be eligible for iron supplementation. Speaking with a doctor before taking iron supplements is the best thing to do.
Buy a low cost testosterone test
References:
Ohlander et al. Sex Med Rev 2018; 6:77-85
Yousef and Alkhiary, J Sleep Disord Ther 2015, 4:2
High hematocrit as a risk factor for venous thrombosis. Cause or innocent bystander?
In the lay press it is frequently stated that long haul air travel causes venous thrombosis through dehydration in the airplane, leading to hyperviscosity of the blood, which in its turn favors thrombosis. The common advice that is given to prevent thrombosis after air travel is, therefore, ‘to drink ample amounts of fluids’ (http://www.britishairways.com/travel/healthmed-cond/public/en_gb#DVT). This concept of thick, slowly flowing blood is apparently intuitively appealing as a cause of thrombosis. It would also fit the classical triad of Virchow, who postulated that thrombosis is due to the occurrence of stasis, to disturbances of the composition of the blood, or to lesions of the vessel wall. 1 High viscosity could be considered to be both a disturbance of the composition of the blood and a cause of stasis. Nevertheless, viscous blood, evidenced by high hematocrit values, has been poorly studied as a risk factor for venous thrombosis in the general population. The study by Braekkan and colleagues in this issue of the Journal is, therefore, a welcome contribution to the scientific literature.2 Their results from the Tromsø study (a large health survey in Tromsø, Norway) show a hazard ratio of 1.25 per 5% rise in hematocrit.2 In a category-based analysis, a hematocrit in the upper 20 percentile was found to be associated with a 1.5-fold increased risk of venous thrombosis. However, the important question that is not answered by this study is whether the relation is causal, or whether it can be explained by the presence of other diseases that cause both a high hematocrit and venous thrombosis.
Venous thrombosis, as the name implies, is caused by intravascular coagulation in veins, leading to often large thrombi and venous obstruction. Thrombi can detach from the primary site and travel to the lungs, resulting in pulmonary embolism. About 10% of pulmonary emboli are immediately fatal, and an additional 5% cause death later in time, despite diagnosis and treatment. At least 10% of patients with symptomatic venous thrombosis develop a severe post-thrombotic syndrome within 5 years.3 The annual incidence of venous thrombosis is about 2 cases per 1000 individuals4,5 and has a steep age dependence.6 Two-thirds of the cases of venous thrombosis are deep vein thromboses of the leg and one-third consists of pulmonary embolism with or without symptomatic deep vein thrombosis.7,8
Venous thrombosis has multiple causes associated with both genetic and environmental risk factors. The most common genetic risk factors for venous thrombosis are the factor V Leiden mutation9 and the prothrombin G20210A mutation,10 both present in several percent of the Caucasian population. Well-known environmental risk factors are age, oral contraceptive use, pregnancy, recent surgery, major trauma, immobilization and malignant diseases. 11
Hematocrit, expressed as % (proportion of red blood cells of the total blood volume), can be calculated from the red blood cell concentration and the mean corpuscular volume. Increased hematocrit levels are caused either by an increase in the number of red blood cells (erythrocytosis) or by dehydration. Erythrocytosis can be caused by diseases affecting the bone marrow (primary erythrocytosis, such as polycythemia vera) or by diseases or an environment affecting oxygen saturation (secondary erythrocytosis). In the latter situation, the bone marrow produces more red blood cells to counterbalance the decrease in oxygen saturation. In healthy subjects, hypobaric hypoxia present at high altitude leads to an increased hematocrit. In subjects living in these conditions, the bone marrow compensates for the decrease in oxygen saturation by increasing the production of red blood cells (through erythropoietin).12 Sports-men and -women take advantage of this phenomenon by training at high altitudes in order to benefit from a greater potential to carry oxygen in the blood when they return to normoxic, normobaric circumstances.
At sea level, erythrocytosis that is not due to an intrinsic problem in the bone marrow (secondary erythrocytosis) is, in most cases, acquired (congenital causes are rare and will not be discussed here). Acquired erythrocytosis can be caused by exogenous erythropoietin use or by pathological erythropoietin production by certain tumors (e.g. parathyroid carcinoma/adenomas, hepatocellular carcinoma, renal cell cancer, pheochromocytoma), but is generally a result of conditions that lead to hypoxia. Obvious examples are smoking and lung disease, but congenital heart disease with right-to-left cardiopulmonary shunts also leads to increased erythropoietin production.13
An increased risk of venous and arterial thrombosis in relation to primary erythrocytosis has been well described. However, the mechanisms are complex and being debated14 and a direct relation between the hematocrit level and the risk of venous thrombosis is not clearly present in these conditions. An old study from 1978 found a striking correlation between hematocrit level and thrombosis in patients with polycythemia vera,15 but this correlation was not confirmed in a recent study in which no such relation could be demonstrated. 16
With respect to the association of venous thrombosis with hematocrit in the general population, data are scarce and inconclusive. Vaya et al. performed a case-control study in 109 patients with a first deep vein thrombosis, without thrombophilia, and 121 healthy controls. They reported that the percentage of cases with a hematocrit above 45% was higher in cases than in controls, i.e. 43% versus 27%. The association was attenuated when several other factors were included in a multivariate model.17 In one other population-based study (the LITE study, a cohort study in subjects above 45 years of age), no relation between high hematocrit levels and risk of venous thrombosis was demonstrated, but the authors used a relatively low cut-off level for the hematocrit (43.5%).18
The strengths of the new study by Braekkan and colleagues are that it is large, prospective, and carried out in a general population with a high response rate, a long follow-up, and well-validated venous thrombotic events. 2 We may, therefore, assume that the link found between high hematocrit and risk of venous thrombosis is real, but again, the important issue is to decide whether or not the relation is causal or explained by other diseases.
Various studies into a causal association have been performed in patients with polycythemia vera, but as several complex mechanisms play a role in this disease, these studies should not be used as a model to extrapolate the relationship between high hematocrit and venous thrombosis in the general population. Otherwise, there are only a few experimental studies that have examined a direct effect of red blood cell mass on thrombotic mechanisms. The hypothesis that platelet activation plays a role has been tested in two in vitro studies by the same group of researchers; both studies suggest that red blood cells amplify platelet reactivity.19,20 A direct relationship between levels of hematocrit and thrombin generation has only been described in vitro, in a small experimental study of blood samples from five participants. Hematocrit was artificially increased in these samples by centrifugation. It is questionable whether such artificially increased hematocrit levels reflect the complicated mechanism of increased levels of hematocrit in vivo.21
Other arguments for a direct causal relation are more circumstantial or hypothetical: low hematocrit is associated with a risk of bleeding, which is corrected by transfusion;22 increased viscosity of the blood may lead to increased exposure of platelets and coagulation factors to endothelium and, therefore, increased interaction and activation.
An alternative explanation for the relation between increased levels of hematocrit and the risk of venous thrombosis would be the presence of conditions or factors that increase in parallel, but independently, both hematocrit levels and the risk of venous thrombosis, such as smoking, lung disease, or heart disease. Considering that 37% of the cases with venous thrombosis in the study by Braekkan and colleagues were smokers at the time of the thrombosis, and that some medical condition was present in 22%, these factors can be expected to have influenced the results. To determine the effect of hematocrit levels independently of these factors, the data need to be adjusted for such confounders. The authors appropriately addressed this issue in their discussion, but they could not overcome the problem since data on medical conditions in the reference group were lacking. With respect to smoking, the authors were probably not able to fully remove the confounding effect, since smoking was rather roughly classified. So, unfortunately, this study does not exclude the possibility that the relationship that was found between high hematocrit levels and venous thrombosis could be explained by the presence of other conditions. This issue should, therefore, be the focus of studies in the future.
If the relationship is found to hold true in further research, more questions and challenges arise. Why is the association more pronounced in men than in women¿ What are the clinical consequences¿ Do we need to screen all patients with venous thrombosis for high hematocrit levels, or should we be aware of an increased risk of venous thrombosis in all subjects in whom we find a high hematocrit¿ And if we do so, what are the possibilities for treatment or prevention¿ Do high levels of hematocrit interact with other risk factors for venous thrombosis and, therefore, increase the risk of venous thrombosis even more¿ Could it indeed explain part of the link between arterial and venous thrombosis, as the authors suggest¿
In conclusion, Brækkan and colleagues have performed an interesting, large-scale study into the relation between high levels of hematocrit and the risk of venous thrombosis. They convincingly demonstrated a dose-response relation between level of hematocrit and risk of venous thrombosis. However, questions remain on the causal interpretation and the clinical consequences of their results.
Footnotes
- Drs Schreijer and Cannegieter are physicians and epidemiologists at the Department of Clinical Epidemiology of the Leiden University Medical Center. Dr Reitsma is a molecular biologist and head of the Einthoven Laboratory for Experimental Vascular Medicine at the same institution. No potential conflicts of interest relevant to this article were reported.
- No potential conflicts of interests relevant to this article were reported.
References
- Virchow RKL. Gessamelte Abhandlungen zur wissenschaftlichen Medizin. Staatsdruckerei: Frankfurt; 1856. Google Scholar
- Brækkan SK, Mathiesen EB, Njølstad I, Wilsgaard T, Hansen JB. Hematocrit and risk of venous thromboembolism in a general population. The Tromsø study. Haematologica. 2010; 95(1):270-5. PubMedhttps://doi.org/10.3324/haematol.2009.008417Google Scholar
- Kearon C. Natural history of venous thromboembolism. Circulation. 2003; 107(23 Suppl 1):I22-I30. PubMedGoogle Scholar
- Naess IA, Christiansen SC, Romundstad P, Cannegieter SC, Rosendaal FR, Hammerstrom J. Incidence and mortality of venous thrombosis: a population-based study. J Thromb Haemost. 2007; 5(4):692-9. PubMedhttps://doi.org/10.1111/j.1538-7836.2007.02450.xGoogle Scholar
- Oger E. Incidence of venous thromboembolism: a community-based study in Western France. EPI-GETBP Study Group. Groupe d’Etude de la Thrombose de Bretagne Occidentale. Thromb Haemost. 2000; 83(5):657-60. PubMedGoogle Scholar
- Rosendaal FR, van HV, Doggen CJ. Venous thrombosis in the elderly. J Thromb Haemost. 2007; 5 (Suppl 1):310-7. PubMedhttps://doi.org/10.1111/j.1538-7836.2007.02489.xGoogle Scholar
- Anderson FA, Wheeler HB, Goldberg RJ, Hosmer DW, Patwardhan NA, Jovanovic B. A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT Study. Arch Intern Med. 1991; 151(5):933-8. PubMedhttps://doi.org/10.1001/archinte.1991.00400050081016Google Scholar
- White RH. The epidemiology of venous thromboembolism. Circulation. 2003; 107(23 Suppl 1):I4-I8. PubMedGoogle Scholar
- Bertina RM, Koeleman BP, Koster T, Rosendaal FR, Dirven RJ, de RH. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature. 1994; 369(6475):64-7. PubMedhttps://doi.org/10.1038/369064a0Google Scholar
- Poort SR, Rosendaal FR, Reitsma PH, Bertina RM. A common genetic variation in the 3′-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood. 1996; 88(10):3698-703. PubMedGoogle Scholar
- Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet. 1999; 353(9159):1167-73. PubMedhttps://doi.org/10.1016/S0140-6736(98)10266-0Google Scholar
- Tannheimer M, Fusch C, Boning D, Thomas A, Engelhardt M, Schmidt R. Changes of hematocrit and hemoglobin concentration in the cold Himalayan environment in dependence on total body fluid. Sleep Breath. 2009. Google Scholar
- McMullin MF. The classification and diagnosis of erythrocytosis. Int J Lab Hematol. 2008; 30(6):447-59. PubMedGoogle Scholar
- Spivak J. Daily aspirin – only half the answer. N Engl J Med. 2004; 350(2):99-101. PubMedhttps://doi.org/10.1056/NEJMp038177Google Scholar
- Pearson TC, Wetherley-Mein G. Vascular occlusive episodes and venous haematocrit in primary proliferative polycythaemia. Lancet. 1978; 2(8102):1219-22. PubMedGoogle Scholar
- Di Nisio M, Barbui T, Di Gennaro L, Borrelli G, Finazzi G, Landolfi R. The haematocrit and platelet target in polycythemia vera. Br J Haematol. 2007; 136(2):249-59. PubMedhttps://doi.org/10.1111/j.1365-2141.2006.06430.xGoogle Scholar
- Vaya A, Mira Y, Martinez M, Villa P, Ferrando F, Estelles A. Biological risk factors for deep vein thrombosis. Clin Hemorheol Microcirc. 2002; 26(1):41-53. PubMedGoogle Scholar
- Tsai AW, Cushman M, Rosamond WD, Heckbert SR, Polak JF, Folsom AR. Cardiovascular risk factors and venous thromboembolism incidence: the longitudinal investigation of thromboembolism etiology. Arch Intern Med. 2002; 162(10):1182-9. PubMedhttps://doi.org/10.1001/archinte.162.10.1182Google Scholar
- Santos MT, Valles J, Marcus AJ, Safier LB, Broekman MJ, Islam N. Enhancement of platelet reactivity and modulation of eicosanoid production by intact erythrocytes. A new approach to platelet activation and recruitment. J Clin Invest. 1991; 87(2):571-80. PubMedhttps://doi.org/10.1172/JCI115032Google Scholar
- Valles J, Santos MT, Aznar J, Marcus AJ, Martinez-Sales V, Portoles M. Erythrocytes metabolically enhance collagen-induced platelet responsiveness via increased thromboxane production, adenosine diphosphate release, and recruitment. Blood. 1991; 78(1):154-62. PubMedGoogle Scholar
- Horne MK, Cullinane AM, Merryman PK, Hoddeson EK. The effect of red blood cells on thrombin generation. Br J Haematol. 2006; 133(4):403-8. PubMedhttps://doi.org/10.1111/j.1365-2141.2006.06047.xGoogle Scholar
- Hellem AJ, Borchgrevink CF, Ames SB. The role of red cells in haemostasis: the relation between haematocrit, bleeding time and platelet adhesiveness. Br J Haematol. 1961; 7:42-50. PubMedhttps://doi.org/10.1111/j.1365-2141.1961.tb00318.xGoogle Scholar
Clinical blood test with leukocyte formula
General (clinical) blood test with the formula is the main laboratory test most often prescribed for any pathological process. A blood test with a formula includes determining the number of all blood cells (erythrocytes, leukocytes, platelets), determining the content of hemoglobin, hematocrit, erythrocyte indicators (MCV, MCH, MCHC).
When is a formula clinical blood test usually ordered?
This study is prescribed, in preparation for hospitalization and planned surgical interventions, with annual medical examinations, repeatedly during pregnancy, in children before any vaccination.
For any disease, a general blood test with a leukocyte formula is a study that provides the necessary information about the current condition of the patient. The presence of anemia and hematological diseases, the severity of inflammation and the response of the body’s immune system, indicators of the allergic process and possible signs of helminthic invasion – this information can be obtained from a clinical blood test with a formula.
What exactly is determined in the process of analysis?
Erythrocytes (RBC, red blood cells, “red blood cells”) – non-nuclear blood cells containing hemoglobin. The shape of erythrocytes in the form of a biconcave disk provides an increase in their surface area and an increase in the possibilities of gas exchange; gives plasticity when passing through the capillaries. The main function of erythrocytes is to transport oxygen from the lungs to tissues and carbon dioxide from tissues to the lungs. Determination of the number of erythrocytes is of the most important diagnostic value in the diagnosis of anemia in combination with the determination of hemoglobin, hematocrit, erythrocyte indices.
Hemoglobin (Hb, HGB, hemoglobin) is the main component of erythrocytes, the structure consists of protein (globin) and iron (heme), the main function is the transport of oxygen and carbon dioxide and their exchange between the lungs and tissues of the body. The level of hemoglobin depends on gender, age, altitude above sea level (inhabitants of high mountains have higher hemoglobin), smoking. Hemoglobin is measured in grams per 1 ml of blood, therefore, when assessing the level of hemoglobin, you need to pay attention to hematocrit. An increase in hematocrit (usually associated with dehydration) can falsely increase the concentration of hemoglobin.
Hematocrit (Ht, Hematocrit) – the percentage of red blood cells in the total blood volume, reflects hemoconcentration. The determination of hematocrit is used to assess the degree of anemia, the calculation of erythrocyte indices. Changes in hematocrit do not always correlate with changes in the total number of red blood cells, so the hematocrit value is difficult to interpret immediately after acute blood loss or blood transfusion.
MCV (Mean Cell volume) – the average volume of an erythrocyte, a calculated indicator. The mean volume of an erythrocyte is used in the differential diagnosis of anemia. According to the MCV value, normocytic anemias are distinguished (MCV 80-100 fl in adults and children from 5 years old), microcytic (MCV less than 80 fl) and macrocytic (more than 100 fl). In the presence of erythrocytes of different shapes (anisocytosis) or a large number of erythrocytes with an altered form, MCV may not be informative enough.
MCH (Mean Cell Hemoglobin) – the average content of hemoglobin in an erythrocyte (in 1 cell). The calculated indicator, according to the clinical value of the MSI, is similar to the color indicator, but is more reliable, and is calculated in absolute units (pg). Used in the differential diagnosis of anemia. Based on the MSI index, normochromic, hypochromic and hyperchromic anemias are distinguished.
MCHC (Mean Cell Hemoglobin Concentration) – the average concentration of hemoglobin in red blood cells. An indicator of the degree of saturation of an erythrocyte with hemoglobin. This is a concentration index that does not depend on cell volume. MCHC is a sensitive indicator reflecting changes in hemoglobin formation; relevant in the diagnosis of iron deficiency anemia, thalassemia, some types of hemoglobinopathies.
Rel. red cell distribution width (RDW, Red cell Distribution Width) – a measure of the difference in red blood cells by volume. In the blood of a healthy person, erythrocytes differ slightly, and the RDW indicator borders within 12-15%. RDW above normal reflects the heterogeneity (heterogeneity) of erythrocytes (degree of anisocytosis). Used in the differential diagnosis and monitoring of anemia treatment.
Platelets (PLT, Platelets) are blood cells involved in clotting. They are non-nuclear cytoplasmic fragments of their predecessors – megakaryocytes formed in the bone marrow. The average lifespan in the bloodstream is 10 days. In a calm state, platelets have a disc-shaped shape, when activated, they become spherical and form special outgrowths – pseudopodia, thanks to which they connect with each other and stick to the vascular wall (the ability to aggregate and adhere), while releasing biologically active substances that contribute to the restoration of the vascular wall when damaged (angiotrophic function). Platelets provide stop bleeding in small vessels (platelet-vascular hemostasis).
Determining the number of platelets is used to assess the risk of developing thrombotic and hemorrhagic complications, in hemorrhagic syndrome, in a comprehensive examination of the blood coagulation system, and for monitoring during chemotherapy. Fluctuations in the level of platelets during the day are possible.
Leukocytes (WBC, White Blood Cell) are immunity cells, their ratio and maturity is determined in the leukocyte formula.
In the normal leukocyte formula, you can see the following populations of cells and their percentage: neutrophils, monocytes, lymphocytes, basophils, eosinophils. Normally, these cells are present in the blood in relatively stable amounts. Their ratio depends on age. In children under 5-6 years of age, lymphocytes predominate in the blood formula, in adults there is a clear predominance of neutrophils.
What do the test results mean?
White blood cells: an increased number of white blood cells (leukocytosis) can be a sign of infection (both bacterial and viral, a marker of current inflammation (including autoimmune or allergic), a sign of a hematological disease.
A decrease in the level of leukocytes (leukopenia) may be associated with a severe infection (up to sepsis), with the toxic effect of medications taken, and with bone marrow damage.
Neutrophils: An increase in the number of neutrophils may be associated with bacterial infection, inflammation, trauma, severe stress or early postoperative period.
A decrease in the number of neutrophils is usually associated with a reaction to drugs, autoimmune diseases, immunodeficiency states, and bone marrow damage.
Lymphocytes: An increase in the number of lymphocytes (lymphocytosis) can be observed in acute viral infections, infections of the herpes group (EBV infection, CMV infection, etc.), in some bacterial infections (whooping cough, tuberculosis intoxication), chronic inflammatory diseases ( such as ulcerative colitis), lymphocytic leukemia.
A decrease in the number of lymphocytes (lymphopenia) is often associated with autoimmune diseases, chronic viral infections (HIV, viral hepatitis), effects on the bone marrow, and taking corticosteroids.
Monocytes: Monocytes may be elevated in long-term chronic infections (tuberculosis, fungal infections), connective tissue diseases and vasculitis, monocytic or myelomonocytic leukemia.
A short-term decrease in the number of monocytes has no diagnostic value. A long-term decrease in the number of monocytes, combined with other pathology in the blood test, may be associated with aplastic anemia or bone marrow damage.
Eosinophils: An increase in the number of eosinophils may be associated with parasitic infestations, asthma, allergies, inflammatory diseases of the gastrointestinal tract.
The absence of eosinophils in the blood formula may be normal and has no clinical significance.
Basophils: An increase in the number of basophils can be observed in rare allergic reactions, chronic inflammatory diseases, renal failure (uremia).
The decrease or absence of basophils has no clinical significance.
Platelets: in addition to true thrombocytopenia (low platelet count), the rare occurrence of EDTA-dependent thrombocytopenia may occur. Currently, to perform a general blood test, blood is taken in test tubes with an anticoagulant – EDTA. In rare cases, the interaction of the patient’s blood with EDTA leads to aggregation (sticking) of platelets among themselves and the inability to accurately calculate their number. In this case, the analyzer is not able to isolate these cells and accurately count them, which can lead to a falsely low number of platelets in the blood. If a low platelet count is detected by the analyzer, the laboratory conducts a microscopy of the blood smear and gives a conclusion about the presence of platelet aggregates in the smear.
Normal test completion time
Usually the result of a clinical blood test with a formula can be obtained within 1-2 days
Is special preparation required for analysis?
Special preparation is not required. You can take the test 3 hours after eating or on an empty stomach. In infants, blood is usually taken before the next feeding.
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Complete blood count 5 diff is a study of the qualitative and quantitative composition of blood elements.
The test material is venous blood.
CBC 5 diff includes:
- determination of the size, number, shape of erythrocytes and their content of hemoglobin;
- determination of the ratio of plasma volume to blood cells;
- determination of the total number of leukocytes;
- calculation of the percentage of different leukocytes: neutrophils, lymphocytes, monocytes, eosinophils and basophils on an automatic analyzer;
- counting and evaluation of the average size of platelets.
The CBC is performed as the first screening test for complaints of “malaise”. The analysis gives an idea of the possible areas where pathological changes occur and helps the clinician determine further examination tactics.
- Indications:
- screening examinations within the framework of preventive, dispensary observation;
- basic examinations during hospitalization in therapeutic and surgical hospitals;
- diagnosis of anemia;
- diagnostics of inflammatory, infectious diseases;
- diagnostics of diseases of the blood system;
- monitoring of ongoing therapy and the course of various diseases.
- Hb (hemoglobin) – hemoglobin;
- Ht – hematocrit;
- total number of erythrocytes in ;
- MCV * — mean erythrocyte volume;
- RDW * – distribution of erythrocytes by volume;
- MCH * — average content of hemoglobin in 1 erythrocyte;
- MCHC * – average concentration of hemoglobin in erythrocytes;
- total platelet count;
- total leukocyte count ;
- leukocyte formula.
- dehydration: with severe diarrhea, vomiting, increased sweating, diabetes, burn disease, peritonitis;
- physiological erythrocytosis: in residents of highlands, pilots, athletes;
- symptomatic erythrocytosis: with insufficiency of the respiratory and cardiovascular systems, polycystic kidney disease; erythremia.
- anemia of various etiologies;
- hyperhydration.
- dehydration: with severe diarrhea, vomiting, increased sweating, diabetes, burn disease, peritonitis;
- physiological erythrocytosis: in residents of highlands, pilots, athletes;
- symptomatic erythrocytosis: with insufficiency of the respiratory and cardiovascular systems, polycystic kidney disease;
- erythremia.
- anemia of various etiologies;
- hyperhydration.
- dehydration: with severe diarrhea, vomiting, increased sweating, diabetes, burn disease, peritonitis;
- physiological erythrocytosis: in residents of highlands, pilots, athletes;
- symptomatic erythrocytosis: with insufficiency of the respiratory and cardiovascular systems, polycystic kidney disease;
- erythremia.
- anemia of various etiologies;
- hyperhydration.
- B 12 – deficiency and folate deficiency anemia;
- aplastic anemia;
- liver disease;
- hypothyroidism;
- autoimmune anemias;
- smoking and drinking.
- iron deficiency anemia;
- anemia of chronic disease;
- thalassemia;
- some types of hemoglobinopathies.
- anemia with heterogeneity in erythrocyte size, including those associated with nutrition; myelodysplastic, megaloblastic and sideroblastic types; anemia accompanying myelophthisis; homozygous thalassemias and some homozygous hemoglobinopathies;
- a significant increase in the number of reticulocytes;
- condition after red cell transfusion;
- interference – cold agglutinins, leukemia, hyperglycemia.
- B 12 – deficiency and folic acid deficiency anemia;
- aplastic anemia;
- liver disease;
- hypothyroidism;
- autoimmune anemias;
- smoking and drinking.
- iron deficiency anemia;
- anemia of chronic disease;
- some types of hemoglobinopathies.
- hereditary microspherocytic anemia.
- iron deficiency anemia;
- anemia of chronic disease;
- some types of hemoglobinopathies.
- physical overexertion;
- inflammatory diseases, acute and chronic;
- hemolytic anemias;
- anemia due to acute or chronic blood loss;
- conditions after surgical interventions;
- condition after splenectomy;
- oncological diseases and hemoblastoses.
- pregnancy;
- B 12 – deficiency and folic acid deficiency anemia;
- aplastic anemia;
- viral and bacterial infections;
- taking drugs that inhibit platelet production;
- congenital thrombocytopenia;
- splenomegaly;
- autoimmune diseases;
- conditions after undergoing massive blood transfusions.
- physiological leukocytosis: emotional and physical stress, exposure to sunlight, cold, eating, pregnancy, menstruation;
- inflammatory processes;
- viral and bacterial infections;
- conditions after surgery;
- intoxication;
- burns and injuries;
- infarcts of internal organs;
- malignant neoplasms;
- hemoblastosis.
- viral and certain chronic infections;
- taking medications: antibiotics, cytostatics, non-steroidal anti-inflammatory drugs, thyreostatics, etc.;
- autoimmune diseases;
- exposure to ionizing radiation;
- wasting and cachexia;
- anemia;
- splenomegaly;
- hemoblastosis.
Preparation
Special preparation is not required. It is recommended to take blood no earlier than 4 hours after the last meal (for children – before the next feeding). If possible, eliminate high emotional and physical stress the day before.
Interpretation of results
When interpreting the analysis, it should be taken into account that in 5% of healthy people, the blood test values deviate from the accepted reference values. Blood counts depend on race and sex, age.
The most important indicators in the general blood test are:
*It should be taken into account that the value is not specific, the indicator should be used to diagnose anemia only in combination with other indicators of the general blood test and biochemical blood tests.
Determination of CBC parameters allows diagnosing conditions such as anemia/polycythemia, thrombocytopenia/thrombocytosis and leukopenia/leukocytosis, which can either be symptoms of a disease or act as independent pathologies.
Hemoglobin (Hb, hemoglobin)
A protein in erythrocytes that contains heme. The main function is the transport of oxygen.
Units of measurement: g/l.
Increased hemoglobin level:
Decreased hemoglobin:
Hematocrit (Ht, hematocrit)
An indicator of the proportion of cells in the majority of red blood cells to the liquid part of the blood.
Units: %
Increase in hematocrit:
Decreased hematocrit:
Erythrocytes
Units: ppm (10 6 /µl).
Alternative units of measurement: 10 12 cells/L.
Conversion factors: 10 12 cells/L = 10 6 cells/µL = million/µL.
Increased erythrocyte concentration:
Decrease in the concentration of erythrocytes:
MCV
Estimated indicator, which is calculated based on the histogram of the distribution by size of erythrocytes. According to MCV, microcytic, normocytic and macrocytic anemias are distinguished. An increase in the indicator indicates the presence of large erythrocytes in the blood, a decrease indicates the presence of small ones.
Units: fl (femtoliter).
Increased MCV values:
Decreased MCV values:
RDW (Red cell Distribution Width)
The calculated value, which is calculated on the basis of the histogram of the distribution of erythrocytes by volume. Reflects the heterogeneity of erythrocyte sizes. An increase in the indicator indicates that small and large red blood cells are present in the blood sample. Decreasing the value indicates the homogeneity of erythrocytes in the sample.
Units: %
Increasing RDW values:
MCH
A calculated indicator that characterizes the average mass of hemoglobin in an erythrocyte. An increase in the indicator is associated with a supersaturation of erythrocytes with hemoglobin, a decrease indicates a deficiency of hemoglobin.
Units: pg (picogram).
MCH increase:
Decreased MCH:
MCHC
A calculated indicator that characterizes the average mass of hemoglobin contained in a unit volume of an erythrocyte.
Units: g/dl.
Alternative units of measurement: g/l.
Conversion factor: g/l x 0.1 ==> g/dl.
Increase in MCHC values:
Decreased MCHC values:
It should be borne in mind that the MCHC value is not specific, the indicator should be used to diagnose anemia only in combination with other indicators of a complete blood count and a biochemical blood test.
Platelets
Units: thousand/µL (10 3 cells/µL).
Alternative units of measurement: 10 9 cells/l.
Conversion factors: 10 9 cells/l = 10 3 cells/µl = thousand/µl.
Increased platelet concentration:
Decreased platelet concentration:
Leukocytes
Cells with nuclei that perform protective functions. Formed in the red bone marrow and organs of the lymphatic system. There are 5 populations: neutrophils, lymphocytes, monocytes, eosinophils or basophils. Functions and lifetime depend on which population the leukocyte belongs to.
Units: thousand/µl (10 3 cells/µl).
Alternative units of measure: 10 9 cells/l.
Conversion factors: 10 9 cells/l = 10 3 cells/µl = thousand/µl.
Increase in the concentration of leukocytes:
Decreased leukocyte count:
Leukocyte formula
Leukocyte formula – the percentage of different types of leukocytes in peripheral blood and counting their number per unit volume.