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Ibs vs epi: Digestive Alphabet Soup: The difference between IBS and EPI

Digestive Alphabet Soup: The difference between IBS and EPI


Digestive issues – it’s a topic that many find “taboo” and uncomfortable to talk about. The truth is, people shouldn’t have to suffer in silence. Digestive difficulties are more common than one thinks and it’s important to know the facts.


So, how do you know when gas and diarrhea is more than just an inconvenience? We’ve put together this digestive “alphabet soup” to help raise awareness of two common digestive issues: IBS and EPI. Educating yourself on the facts, symptoms and causes will not only help you get a better understanding of these disorders, but it should encourage a visit to the gastroenterologist to get these issues resolved.

Irritable Bowel Syndrome (IBS)

Irritable bowel syndrome (IBS) is a fairly common and chronic disorder, but it’s also frequently misunderstood. Symptoms usually include abdominal pain, cramping, bloating, constipation and diarrhea.  Feelings of being unable to completely empty bowels, nausea and gas are also common symptoms. IBS is not the same as inflammatory bowel disease (IBD), which is a more serious condition that causes inflammation in the digestive tract.


According to the National Institute of Health (NIH), an estimated 10-15 percent of Americans are affected by IBS, but only five to seven percent get diagnosed. And surprisingly, it is more common in younger people, rather than those over 45. Women are up to two times more likely than men to develop IBS, perhaps because women’s colons are longer than men’s. The suggested cause of IBS is an imbalance of bacteria in the gut.


Unfortunately, because doctors do not fully understand the causes of IBS, there is no known cure. In some cases, diet and lifestyle changes can help control symptoms, however some individuals require medication other interventions. Three types of IBS are based on different patterns of changes in your bowel movements or abnormal bowel movements. It can be important for your doctor to know which type you have, as some medicines work on for some types of IBS or make other types worse.


Exocrine Pancreatic Insufficiency (EPI)

Exocrine Pancreatic Insufficiency (EPI) is a condition that occurs when the pancreas fails to provide the necessary amount of digestive enzymes to aid in the digestion of food. People with EPI can’t properly digest the nutrients in food such as fats, proteins and carbohydrates. Uncomfortable GI symptoms include bloating, gas, weight loss and oily diarrhea that floats. Other symptoms, like tiredness and loss of muscle, may be present due to a lack of nutrients in the body. The symptoms of EPI are very similar to Crohn’s disease, celiac disease, IBD, ulcerative colitis and small intestinal bacterial overgrowth (SIBO), which can make it very hard to diagnose.


Anything that damages the pancreas and stops or blocks the release of its enzymes can result in EPI. There are many causes of EPI – the two most common are cystic fibrosis and chronic pancreatitis. Other medical conditions that can cause EPI are celiac disease, Crohn’s disease, diabetes, pancreatic cancer and more. Different stool studies can help determine the diagnosis of EPI.


The good news is EPI is a manageable condition. The goal of treatment is to replace the digestive function of the pancreas. EPI symptoms can be treated with diet, vitamin and mineral supplements and pancreatic enzyme replacement therapy (PERT). PERTs are the main treatment for EPI – they help break down the nutrients in food. Eating plenty of fruits and vegetables, having smaller meals more frequently, and abstaining from alcohol and smoking is advised. If you have been diagnosed with EPI, you should work with your doctor to make sure all your dietary needs are being met.


If you’re spending too much time in the bathroom, you’re not alone. If you’re suffering from the symptoms of IBS or EPI, it’s important to work with a board-certified gastroenterologist to diagnose and treat your condition. To learn more, contact the professionals at Northeast Digestive Health Center.


Do You Have Exocrine Pancreatic Insufficiency or Something Else?

People who have exocrine pancreatic insufficiency (EPI), a disease that interferes with the body’s ability to digest fat in food, typically experience a host of symptoms that impact their digestive system, including stomach pain, gas, and bloating.

The problem is that many of these symptoms overlap with those of other gastrointestinal (GI) conditions, making it hard for doctors to correctly diagnose EPI.

“It’s fairly common for physicians to misdiagnose EPI,” says Michelle A. Anderson, MD, an associate professor emerita of medicine in the division of gastroenterology at the University of Michigan Hospital and Health Systems in Ann Arbor who is now in private practice in Scottsdale, Arizona. “A lot of people will come in with nonspecific symptoms. They may say, ‘I have an upset stomach’ or ‘I have bloating.’ The doctor needs to probe to find out what the real issue is.

Even people who are at risk for EPI can go undiagnosed. A study published in April 2020 in the journal Alimentary Pharmacology and Therapeutics found that testing for the condition was “infrequent.” The researchers found that only about 7 percent of people with chronic pancreatitis and 2 percent of people with pancreatic cancer — two at-risk groups — were tested for EPI.

If people with EPI are misdiagnosed or remain undiagnosed, they won’t receive a prescription for pancreatic enzyme replacement therapy (PERT), which is the proper treatment for the condition. Without these enzymes, the body isn’t able to process the fat-soluble vitamins A, D, E, and K, something that can lead to vitamin deficiencies and, eventually, complications such as osteoporosis, vision problems, and even neurological issues.

Conditions That Cause EPI-Like Symptoms

EPI’s symptoms mirror those of many other digestive health problems, including:

  • Irritable bowel syndrome: IBS is marked by abdominal pain, bloating, bouts of diarrhea or constipation, and flatulence. People with IBS will see mucus in their stool, says Dr. Anderson, rather than fat. (Fatty stools, or steatorrhea, are a telltale sign of EPI.) Like those of EPI, IBS symptoms tend to occur after eating, but IBS may also be triggered by stress, infection, and other factors.
  • Crohn’s disease: A type of inflammatory bowel disease (IBD), Crohn’s is marked by chronic inflammation of the GI tract, such as the end of the small intestine. As with EPI, notes Anderson, people who have Crohn’s often experience abdominal pain, diarrhea, steatorrhea, and weight loss. But, she adds, Crohn’s also typically causes bloody stools, fever, and anemia, a decrease in red blood cells that can cause fatigue.
  • Ulcerative colitis: People with either EPI or ulcerative colitis can experience abdominal pain, diarrhea, and weight loss, but Anderson says that ulcerative colitis doesn’t typically cause bloating, flatulence, or steatorrhea, though it can trigger mucus — not fat — in stools. Ulcerative colitis is more similar to Crohn’s, in that it’s an IBD, but with colitis, inflammation is located in the large intestine. The two conditions also share symptoms such as anemia, loss of appetite, and bloody stools, as well as some that affect the skin, eyes, and joints.
  • Celiac disease: Celiac disease, or gluten sensitivity, and EPI arguably have the most symptoms in common, says Anderson. Like those with EPI, people with celiac disease experience abdominal pain, bloating, diarrhea, steatorrhea, and weight loss but may also have anemia, and some — about 10 percent of the people she treats, Anderson says — will feel constipated. Another difference is that the diarrhea caused by celiac disease tends to be more watery. While you may primarily notice symptoms of EPI after eating foods that contain fat, people with celiac disease experience symptoms when eating breads, pastas, cereals, and other foods that contain gluten.
  • Infections: In some instances, bowel problems may be a sign of excess bacteria in your small intestine. Small intestinal bacterial overgrowth (SIBO), when the bacteria in the small intestine grow out of control, shares many of the symptoms of EPI. These symptoms include abdominal pain, nausea, and diarrhea.

How EPI Is Diagnosed

According to Anderson, physicians have historically used stool collection studies during the diagnostic process for EPI. During these tests, designed to assess the ability of the pancreas to produce and secrete fat-digesting enzymes, people who are suspected to have EPI are instructed to consume a high-fat diet — more than 100 grams of fat a day, equal to a stick of butter — for two or three days.

Doctors then measure the amount of fat in the stool: If there is more than 7 grams over a 24-hour period, it’s considered malabsorption and thus signals EPI.

A drawback with this test is that Crohn’s disease and ulcerative colitis may also cause problems with fat absorption, so they would also provide a positive test result — and that doesn’t necessarily mean that something is wrong with the pancreas, says Anderson.

Fecal elastase tests are also used to diagnose EPI. Elastase is one of the enzymes produced by the pancreas to help the body digest fat. Low levels of the enzyme in the stool means the pancreas is not producing sufficient amounts — a condition that results in EPI.

“If elastase levels are low, we know the problem is in the pancreas, and it’s not something else,” Anderson explains.

On the other hand, Anderson notes, if you see blood in your stools, it would indicate that you might have a condition other than EPI. “Bloody stools [indicate] ulcerative colitis, Crohn’s, or maybe even an underlying cancer — not EPI,” she says.

According to a study published in March 2019 in the journal Clinical and Experimental Gastroenterology, other tests for EPI include breath tests, pancreatic function tests, and imaging to check if the ducts in the pancreas are functioning. But because EPI’s symptoms overlap with those of many other GI problems, it’s important for doctors to test for EPI if a patient has any conditions that are linked to EPI, such as pancreatitis or cystic fibrosis, or nutritional deficiencies that don’t seem to have a clear cause.

Anderson emphasizes that people who suspect they have EPI can — and should — influence their doctor’s decision to test for it, simply by using their own judgment.

“I always ask my patients, ‘Do you see fat in the toilet after you go to the bathroom?’ If they look at their stool and see fat globules or an oily sheen, as opposed to thick, yellow mucus or red blood, that’s a pretty specific sign that they have EPI instead of another disease, she says. “It’s not always an easy or comfortable conversation to have, but it can be the key to a timely diagnosis.

Additional reporting by Elizabeth Yun

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Smoking and complications of coronary heart disease (CHD)

September 7, 2021

Ischemic heart disease (CHD) is currently the leading cause of death in developed countries. Recent European statistics have confirmed that CHD is the direct cause of all deaths in 43% of men and 55% of women. In addition, the prevalence of coronary artery disease is growing rapidly in developing countries, and it is expected that this nosology will soon become the leading cause of death there too. Studies conducted in the early 2000s show that cigarette smoking is also a cause of high mortality in developing countries. Cigarette smoking is a major and well-known risk factor that is closely associated with coronary heart disease.

Although cigarette smoking is also a modifiable risk factor for CHD, it is not easy to quit smoking, and a significant proportion of patients with CHD continue to smoke despite all recommendations and warnings. Recent studies show that cigarette smoking leads to multiple negative consequences in the cardiovascular system. Smoking causes endothelial dysfunction, increases the concentration of systemic inflammatory proteins (interleukin 6, C-reactive protein, homocysteine, fibrinogen), changes the lipid profile and increases the risk of atherosclerosis by increasing cholesterol, low-density lipoprotein and triglycerides. In addition, smoking contributes to the progression of atherosclerosis by increasing oxidative stress, lipid peroxidation, mitochondrial damage, increased levels of matrix metalloproteinases, and finally increases platelet activation, triggering the coagulation cascade, which can eventually lead to atherothrombosis.

To confirm / refute the theory of the negative effect of smoking on hemostasis, a study was conducted of platelet aggregation in smoking patients and patients in the control group.

Venous blood samples obtained in preparation for the study were collected at least 12 hours after smoking cessation and at least 2 hours after the “last” intake of aspirin as a COX blocker.

Platelet function tests were performed in the morning, immediately before and 15 minutes after the first cigarette. All participants smoked one cigarette of regular tobacco from the same commercial pack. Platelet function was assessed using a PFA-200 platelet function analyzer (Siemens Healthcare, Marburg, Germany) 2 using collagen and epinephrine (Col/Epi) and collagen and adenosine diphosphate (Col/ADP) cartridges.

The results of the study showed that platelet hyperactivity after aspirin was present in 20% of smokers and 15% of non-smokers.

A significant increase (lengthening) of the aggregation completion time on PFA-200 after smoking one cigarette was found. The trend towards an increase in aggregation time also persisted for patients on aspirin therapy, regardless of the age and gender of the test patients in the main and control groups.

The results once again highlight the importance of smoking cessation in patients with CAD. Antithrombotic therapy in patients with CAD who continue to smoke deserves more careful evaluation, as these people may

there is an increased activity of platelets, which cannot be suppressed by aspirin.

Clinical guidelines do not currently include evaluation of platelet function (platelet aggregation) in patients with CAD receiving aspirin.

Therefore, patients with coronary artery disease should avoid smoking, as increased platelet aggregation can lead to atherothrombotic complications (eg, acute coronary syndrome).

It should be noted that other antithrombotic agents, such as clopidogrel, may have potential indications for CAD patients who continue to smoke, as the latest published data show that clopidogrel does not adversely affect cigarette smoking, but on the contrary, its effectiveness may even increase from due to increased enzymatic activation of the liver. New antithrombotic drugs with different mechanisms of action may also have potential indications for use in smoking patients with CAD.


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Results of the All-Russian scientific-practical conference “Modern nurse in traumatology and orthopedics”.

took place in the city of Kurgan on the basis of the Federal State Budgetary Institution “NMITs TO named after acad. G. A. Ilizarov” Ministry of Health

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Correlation of various indicators of the lipid spectrum with the early development of coronary heart disease in men | Tyurina

According to the “lipid hypothesis”, lipid metabolism disorders are a risk factor for the development of atherosclerosis and coronary heart disease (CHD). Underestimation of the importance of dyslipidemia at the population and individual level subsequently leads to an extremely high level of cardiovascular morbidity and mortality. The early development of coronary artery disease may be associated with various risk factors and, most likely, with a combination of several factors, but the involvement of lipoproteins in the development of atherosclerosis is an indisputable fact. Currently, much attention is paid to the problems of diagnosis and treatment of various forms of dyslipidemia in the world, however, it becomes obvious that the routine determination of such indicators as total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) is not enough. An elevated concentration of lipoprotein(a) (Lp(a)) or hyperlipoproteinemia(a) (hyperLp(a)) is associated with the development of atherothrombogenic atherosclerosis in various vascular beds and a wide range of cardiovascular diseases (CVD) [1-6]. In addition, the need to evaluate the contribution of Lp(a) concentration in the diagnosis of familial hypercholesterolemia is becoming more and more obvious [7]. Elucidation of the significance of various lipid parameters, reflecting various forms of lipid metabolism disorders, in the development of CVD is an important clinical and biological task. The aim of the study was to evaluate the relationship between the early manifestation of coronary artery disease and the initial routine and new indicators of the lipid spectrum.

Material and methods

Longitudinal study with retrospective data collection included 228 men aged 58±9 years, observed at the N.N. acad. E.I. Chazov of the Ministry of Health of Russia, of which the main group consisted of 166 patients with a history of early (up to 55 years) manifestation of coronary artery disease [8]. Inclusion criteria were identified stenosing (≥50%) atherosclerosis of one or more coronary arteries according to primary coronary angiography; verified myocardial ischemia or a history of data on myocardial revascularization or myocardial infarction, documented. The control group consisted of 62 men who did not have coronary artery disease, which was defined as the absence of stenosing atherosclerosis according to coronary angiography or transient myocardial ischemia during exercise testing. The following categories of people were excluded from the study: patients with chronic renal failure (glomerular filtration rate <30 ml / min / 1.73 m2, calculated using the CKD-EPI formula), malignant neoplasms, autoimmune diseases, carriers of human immunodeficiency virus, hepatitis B and C .

The study was carried out in accordance with the principles of the Helsinki Declaration of Human Rights. The study protocol was approved by the Independent Ethical Committee for Clinical Research of the National Medical Research Center for Cardiology of the Ministry of Health of Russia, Protocol No. 251 dated November 25, 2019. Written informed consent was obtained from all patients prior to inclusion in the study.

Blood lipids and Lp(a) levels were measured in all patients by enzyme-linked immunosorbent assay [9]. Retrospectively, for all patients of the IHD group, data were collected on lipid spectrum and Lp(a) concentration at the time of IHD manifestation, in patients of the control group – at the first visit to our clinic. The median follow-up period for patients in the main group was 11.5 years, while in the control group it was 5 years (Fig. 1).

Fig. 1. Study design.
Abbreviations: IHD, coronary heart disease; Lp(a), lipoprotein(a).

LDL-C was calculated according to the Martin-Hopkins formula, the level of corrected LDL-C (LDL-C corr ), taking into account cholesterol, which is part of Lp(a), was calculated according to the Dahlen formula: LDL-C corr = LDL-C — 0.3 × Lp(a)/38.7 [10]. The cholesterol index of all atherogenic classes of lipoproteins, including remnants of lipoproteins (non-HDL cholesterol), was calculated by the formula: non-HDL cholesterol = total cholesterol – HDL cholesterol.

In accordance with the recommendations of the European Society of Cardiology [11], the diagnosis of hypercholesterolemia was made at an initially detected level of total cholesterol >5 mmol/l and/or LDL cholesterol >3.0 mmol/l and/or non-HDL cholesterol >3. 8 mmol/l , hyperLp(a) — at the level of Lp(a) ≥30 mg/dl.

Statistical processing of the results was carried out using the MedCalc 20.106 statistical software package. The Kolmogorov-Smirnov test was used to determine the normality of the distribution. Indicators with a normal distribution were presented as mean values ​​with standard deviations (M ± SD), indicators with a distribution other than normal were presented as a median and values ​​of the 25th and 75th percentiles. When comparing indicators between groups, Student’s t test or nonparametric Mann-Whitney U test were used. Differences were considered statistically significant at p<0.05. Fisher's exact test was used to compare the frequency of data in groups. In multivariate analysis, the method of logistic regression was used, where risk factors were introduced into the model, which demonstrated an association with the development of early coronary artery disease in a one-way correlation analysis. When creating the model, the absence of internal correlations between the estimated parameters was taken into account. For the prognostic assessment of lipid factors measured during initial hospitalization, the risk ratio for the development of coronary artery disease and the confidence interval (CI) were calculated. Analysis of CAD-free survival was performed using Kaplan-Meier curves.


At the time of inclusion in the study, the groups were comparable in terms of age, obesity and family history. In the main group, there were more patients taking statins, suffering from hypertension and type 2 diabetes mellitus, and also smoking (Table 1).

Table 1

General characteristics of the men included in the study

Abbreviation: coronary artery disease, ischemic heart disease.

The initial concentration of atherogenic lipoproteins (Table 2) was significantly higher in patients with early manifestation of coronary artery disease. Significant differences were also observed in the concentration of Lp(a).

Table 2

Lipid spectrum parameters

* – p<0. 001 relative to the control group at each of the two visits.
Abbreviations: Lp(a) – lipoprotein(a), TC – total cholesterol, HDL-C – high-density lipoprotein cholesterol, LDL-C – low-density lipoprotein cholesterol, LDL-C not associated with high density lipoproteins.

On the contrary, at the time of inclusion in the study, the parameters of the lipid spectrum of LDL-C corr and non-HDL-C were higher in the control group than in the CHD group, which is associated with low-intensity lipid-lowering therapy or its absence due to the low cardiovascular risk in this group. categories of patients.

Lipid metabolism disorders, such as hyperLp(a) and hypercholesterolemia, identified by the initial excess of the threshold concentration of Lp(a) and lipid spectrum parameters, were significantly more common in the group of patients with early CAD compared with the control group (Fig. 2).

Fig. 2. Histogram of the distribution of lipid and Lp(a) concentrations, as well as the proportion of patients with elevated Lp(a), LDL-C, LDL-C corr and non-HDL-C in the control group (A, C, E, G) and the group with early CAD (B, D, F, H).
Note: * — p<0.001.
Abbreviations: IHD — coronary heart disease, Lp(a) — lipoprotein(a), LDL-C — low-density lipoprotein cholesterol, LDL-C , Non-HDL cholesterol – cholesterol that is not associated with high-density lipoproteins.

According to the results of ROC-analysis, non-HDL cholesterol, reflecting the concentration of cholesterol of the entire spectrum of atherogenic lipoproteins, had an advantage in assessing the likelihood of early development of coronary artery disease over determining acute cholesterol – the area under the curve (AUC) was 0.68 (95% CI 0.61-0.73) vs 0.63 (95% CI 0.56-0.69), respectively, ∆AUC=0.05, p<0.005. In contrast, LDL-C corr (AUC=0.64 (95% CI 0.58-0.71)) predicted CAD worse than LDL-C (AUC=0.70 (95% CI 0.64-0, 76)), ∆AUC=0.06, p<0.0001, indicating the influence of Lp(a) on the predictive value of LDL-C. Therefore, in further work, only the LDL-C index corr was used, reflecting the content of only low-density lipoproteins in plasma, but not Lp(a).

According to the results of logistic regression analysis, Lp(a) concentration ≥30 mg/dl along with elevated levels of non-HDL-C or LDL-C corr were associated with early development of coronary artery disease, regardless of heredity and smoking in the general cohort of men examined, which indicates independent influence of various forms of dyslipidemia on the early occurrence of coronary artery disease. The proportion of patients with coronary artery disease in subgroups formed depending on LDL cholesterol corr and hyperLp(a) is shown in fig. 3 and also illustrates the independent effect of both elevated Lp(a) and LDL-C corr .

Fig. 3. Proportion of patients with early manifestation of coronary heart disease, depending on the initial concentrations of Lp(a) and LDL-C corr .
Abbreviations: IHD — ischemic heart disease, Lp(a) — lipoprotein(a), LDL-C corr — low-density lipoprotein cholesterol, corrected for the level of cholesterol, which is part of Lp(a).

Earlier development of CAD was observed in patients with isolated hyperLp(a) (Fig. 4).

Fig. 4. Age of IHD manifestation in patients of the main group depending on the concentration of LDL-C corr , non-HDL-C and Lp(a).
Note: Data are presented as median and 95% CI.
Abbreviations: CI — confidence interval, Lp(a) — lipoprotein(a), LDL cholesterol corr. high density lipoproteins.

Analysis of the Kaplan-Meier survival curves in the total cohort of examined patients showed: if we take the risk coefficient at normal levels of Lp(a), non-HDL cholesterol and LDL cholesterol corr as a unit, any form of lipid metabolism disorder was associated with an increased risk of developing early coronary artery disease (Table 3). In addition, patients with isolated elevated Lp(a) levels had CAD manifestation 8 years earlier, 47 vs 55 years.

Table 3

Median CAD-free survival and relative risk of early CAD depending on lipid and Lp(a) concentrations

Abbreviations: CI — confidence interval, CAD — coronary heart disease, Lp(a) — lipoprotein(a), HDL cholesterol — high density lipoprotein cholesterol, LDL cholesterol – low density lipoprotein cholesterol, LDL cholesterol corr – corrected low density lipoprotein cholesterol, nonHDL cholesterol – cholesterol not associated with high density lipoproteins.

At the same time, any violation of lipid metabolism leads to a significant increase in the risk of early coronary artery disease relative to men with normal Lp(a) and LDL-C corr (Fig. 5 A) or non-HDL-C (Fig. 5 B).

Fig. 5 . Kaplan-Meier survival curves in male groups depending on baseline Lp(a) and LDL-C corr (A) or Lp(a) and non-HDL-C (B).
Note: symbols: A – (1) Lp(a) <30 mg/dl, LDL-C corr <3.0 mmol/l; (2) Lp(a) <30 mg/dl, LDL-C corr ≥3.0 mmol/l; (3) Lp(a) ≥30 mg/dl, LDL-C corr <3.0 mmol/l; (4) Lp(a) ≥30 mg/dl, LDL-C corr. ≥3.0 mmol/l. B – (1) Lp(a) <30 mg/dl, non-HDL cholesterol <3.8 mmol/l; (2) Lp(a) <30 mg/dl, non-HDL cholesterol ≥3.8 mmol/l; (3) Lp(a) ≥30 mg/dl, non-HDL cholesterol <3.8 mmol/l; (4) Lp(a) ≥30 mg/dL, non-HDL cholesterol ≥3.8 mmol/L.
Abbreviations: IHD — ischemic heart disease, Lp(a) — lipoprotein(a), LDL-C corr – low-density lipoprotein cholesterol, corrected for the level of cholesterol, which is part of Lp (a), non-HDL cholesterol – cholesterol not associated with high-density lipoproteins.


In our work, as part of a longitudinal study with retrospective data collection, we analyzed the impact of various forms of lipid metabolism disorders, assessed by routine and new indicators of the lipid spectrum and Lp(a) concentration, on the early development of CAD in men.

For a long time, the main focus in the prevention of CVD was aimed at achieving the target level of LDL-C. Accumulating evidence suggests that not only LDL, but also other classes of apoB100-containing lipoproteins such as very low density lipoproteins, intermediate density lipoproteins, chylomicron remnants, and Lp(a) also have an atherogenic potential. As a result of numerous epidemiological studies and randomized clinical trials, convincing evidence has emerged of a continuous and independent causal relationship between elevated levels of Lp(a) and CVD [2]. HyperLp(a) is associated with CV risk both in primary care groups [12] and in patients already receiving statins [13] or PCSK9 inhibitors[14] and reached the target levels of LDL-C. A meta-analysis of data from 29 thousand patients showed that the association between Lp(a) and the development of CVD was stronger with statins than with placebo, which indicates the leading role of Lp(a) in the residual risk of cardiovascular complications [13]. These data are consistent with the results of our study, which showed that in patients with hyperLp(a), elevated levels of non-routine lipid spectrum indicators (LDL-C corr , non-HDL-C) did not significantly increase the risk of early development of coronary artery disease relative to men with normal Lp(a) levels. . Of all blood lipids, the weakest association with the early development of coronary artery disease was associated with total cholesterol, the strongest was non-HDL cholesterol, since this indicator most fully reflects the concentration of cholesterol, which is part of the atherogenic classes of apoB100-containing lipoproteins, and, accordingly, has a greater predictive ability in relation to the onset and development of CVD.

The level of LDL-C that is dealt with in clinical practice is usually calculated using various formulas, so when we talk about the level of “LDL-C”, we are talking about a value that includes not only cholesterol in the composition of the particle LDL, but also cholesterol in Lp(a). This is probably not clinically relevant in individuals with normal Lp(a) levels (<30 mg/dL), but in individuals with hyperLp(a), who account for 20-30% of the population, “LDL-C” may significantly least consist of cholesterol in the composition of Lp(a) [15]. We also showed a significant decrease in the diagnostic value in relation to the early development of coronary artery disease in LDL-C corr , which excluded cholesterol, which is part of the Lp(a) particle, from the LDL-C index compared to LDL-C.

Thus, in cases with an increased Lp(a) content, the use of standard formulas for calculating LDL cholesterol will lead to its overestimated values. Therefore, in such cases, we recommend calculating the LDL cholesterol value corr . The significance of elevated Lp(a) concentration against the background of “normal” levels of routinely measured lipids (isolated hyperLp(a)) as an independent factor in the early development of CAD at the youngest age, clearly shown in our work, confirms the need for measuring Lp(a) in clinical practice.

Study Limitations . Our study has the following limitations: The study was longitudinal but not prospective, so patients were included on a case-to-control basis, which may influence the results obtained. To exclude the influence of gender as a significant risk factor for CHD, as well as differences in the assessment of the age of early manifestation of CHD, only men were included in the study. Because the median age at onset of CAD was 45.8 years, lipid cut-offs were in line with those recommended for “low-risk” patients.


These results are important for setting goals for LDL-C reduction in patients with hyperLp(a) and require further clinical validation. The development and study of drugs that reduce Lp(a) in isolation [16] will confirm the “Lp(a) hypothesis”, suggesting that the reduction of elevated Lp(a) levels, and not LDL-C, has a clinical advantage in patients with hyperLp(a). ).

Relationships and Activities : All authors declare no potential conflicts of interest to disclose in this article.

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