Do you know how many major [CP] are common in the inspection items?

01

First pair: LDH and HBDH

HBDH is part of LDH

Lactate dehydrogenase (LDH) is an important enzyme involved in the glycolysis and gluconeogenesis process to catalyze the redox reaction between lactic acid and pyruvate
.
There are five forms of isoenzymes: LDH1, LDH2, LDH3, LDH4, and LDH5
.
The distribution of LDH isoenzymes has obvious tissue specificity, so it can be used to diagnose diseases
according to its tissue specificity.
LDH1 is the main focus of the heart and kidneys, followed by LDH2; The lungs are dominated by LDH3 and LDH4; The liver is dominated by LDH5, followed by LDH4
.

Hydroxybutyrate dehydrogenase (HBDH) is a general term for LDH1 and LDH2 containing H subunits, which is meaningful for the diagnosis of myocardial diseases, and because the kidneys also exist, it is necessary to pay attention to the possibility
of urinary tumors when HBDH is significantly increased.

In summary, the difference between the two is the sum of isoenzymes 3, 4, and 5, because the liver is dominated by LDH5, followed by LDH4, so when LDH increases, it is necessary to observe whether it is increased due to HBDH increase, such as HBDH increase, priority is given to the possibility of myocardial damage, such as HBDH is not increased or the increase is not obvious, should be combined with ALT value can reflect liver damage
.

Because HBDH is part of LDH, HBDH < LDH, why do HBDH> LDH appear?

After communicating with the engineer, I learned that HBDH is part of LDH in a sense, but due to differences in methodology (substrate, buffer, PH, etc.
), the result of HBDH may be greater than LDH
.
If LDH detection uses the P method, there is no such phenomenon, the LDHP method is the European method, and the substrate is pyruvate
.
The L method is the American system, the substrate is lactic acid, and the LDH detection P method is about 2.
2 times
higher than the L method.

02

Second pair: FDP and DD

DD is a small fragment of FDP

FDP is a general term for various degradation products produced by fibrin and fibrinogen under the action of plasmin, which mainly reflects the overall fibrinolysis level
of the body.

D-dimer (DD) is a specific degradation product of crosslinked fibrin under the action of plasmin, and elevated levels indicate the presence of secondary hyperfibrinolysis (Figure 1).

Figure 1

In summary, DD is a product of fibrin, FDP is a degradation product of fibrin and fibrinogen, and in theory DD should be a part of FDP, and its value should be less than FDP
.

However, in practice, there will be some cases where DD is greater than FDP, why is this?

Because DD detection is easily interfered with by rheumatoid factors, heterophile antibodies and other factors in plasma, in general, FDP and DD are 5 ~ 10 times the relationship, if it exceeds this range, it means that at least one of the two results is unreliable
.
Therefore, it is necessary to judge whether there is an interference problem
in combination with the actual situation.
The combined detection of the two is more meaningful, and the detection of D-dimer and FDP is of great significance
for the diagnosis and treatment of coagulation-fibrinolytic system diseases and the monitoring of thrombolytic therapy.
[1]

03

Third pair: CR and UREA

Serum urea and serum creatinine are two veterans of kidney function

Creatinine (CR) is a metabolite of muscle in the human body, producing 1mgCR per 20g of muscle, endogenous creatinine comes from the metabolism of the body's own muscles, and exogenous creatinine is the product of
metabolization of meat foods in the body.
Generally speaking, the metabolism of the body's own muscles is stable, if the eating habits do not change much, the intake of meat food is also stable, then the production of blood creatinine is relatively constant
.
The kidneys are the main organs excreted by creatinine, creatinine is excreted from the body after glomerular filtration, and the renal tubules basically do not absorb and no longer secrete.

Therefore, glomerular filtration rate is the main influencing factor
of serum creatinine.

Urea nitrogen (UREA) Urea nitrogen is a metabolite of protein, generally producing 0.
3g of urea
per gram of protein metabolism.

A nitrogenous compound in plasma other than protein, which is filtered from the glomerulus and excreted
.
In renal insufficiency decompensation, BUN will be elevated
.
Therefore, it is clinically used as an indicator to
judge the glomerular filtration function.

The two are used to distinguish between renal function tests

Serum creatinine concentration mainly depends on the glomerular filtration function, when the glomerular filtration rate drops to 1/3 of a healthy person, the serum creatinine concentration will increase significantly, and the determination of serum creatinine is more sensitive to the degree of damage to the glomerular filtration rate than urea nitrogen [2], but it is not an early diagnostic indicator
.

Urea is the end product of human protein metabolism, and the concentration of serum urea depends on the catabolic rate of protein, protein intake in food, and the excretion capacity
of the kidneys.
Due to poor accuracy and sensitivity, the determination of urea can only roughly estimate the glomerular filtration rate, and the concentration of urea in the blood is affected by many extrarenal factors, so it is generally not only used to judge the glomerular filtration rate, but also more meaningful
to measure both.

When renal function is normal, the ratio of urea nitrogen to serum creatinine should be 10 ~ 15:1, the increase in the ratio is mostly prerenal factors, and the decrease in the ratio is mostly nephrogenic disease
.
[3] Of course, with the advancement of technology, there are better projects to replace them, such as B2-MG, CYSC, which can respond more sensitively to glomerular filtration
.

04

Fourth pair: ALT and AST

ALT and AST, two transaminases, are the most common laboratory tests
used for liver function.
ALT is mainly distributed in the hepatocyte plasma, and elevated ALT reflects damage
to the hepatocyte membrane.
AST is mainly distributed in hepatocyte plasma and hepatocyte mitochondria, and its elevation suggests hepatocyte damage to organelle levels
.

ALT is an enzyme
that catalyzes the conversion of glutamate into alanine through transamination.
The content of transaminases in the liver is about 100 times the content in the blood, and the concentration of ALT in hepatocytes is 1000~5000 times
higher than that in serum.
Normally, as long as a small amount is released into the blood, the activity of enzymes in the serum can be significantly increased
.
When the permeability of the hepatocyte membrane is altered, ALT overflows from the cells into the circulating bloodstream, and as long as 1% of the hepatocyte necrosis can increase the enzyme activity in the blood by a factor of 1, transaminases, especially ALT, are a sensitive marker of acute hepatocellular damage [4].

Compared with AST (aspartate aminotransferase), ALT is still more sensitive, more specific, and clinically
practical.

In fact, many reasons can cause changes in the permeability of liver cell membranes, such as fatigue, drinking, colds and even emotional factors
.
The increase in transaminases caused by the above reasons generally does not exceed 60, and when the transaminase value is higher than 80, it has diagnostic significance [5].

It should be emphasized that as long as the liver has inflammation, necrosis, poisoning and other damage, ALT will be released from liver cells into the blood, and the elevation of ALT only indicates that the liver may be damaged
.

We often pay attention to the increase of liver enzymes clinically, but it is difficult to judge
the decrease in ALT activity.
Decreased ALT activity is more common in pyridoxal phosphate deficiency, terminal state of liver disease, renal dialysis, renal insufficiency, etc
.

When the two are combined, liver function can be more comprehensively judged, that is, the AST/ALT ratio, when the AST/ALT ratio is <1, it means that the hepatocyte is mildly diseased, and the mitochondria of hepatocytes remain intact, so the ALT released into the blood is mainly ALT present in the plasma of hepatocytes, so the increase in ALT is larger than that of AST, and the ratio of AST/ALT is <1
.

When the AST/ALT ratio is >1, it means that the hepatocytes are severely damaged, the mitochondria of hepatocytes are also severely damaged, AST is released from the mitochondria and cytoplasm, so AST is significantly increased, AST/ALT> 1, or even >2, such as cirrhosis, the ratio can be increased to 1.
44, and the ratio of chronic active hepatitis is often higher than normal
.
Patients with an AST/ALT ratio of 1.
20 ~2.
26 often develop explosive liver failure
.
[6]

05

Fifth pair: CK and CKMB

CKMB is part of CK

Creatine kinase (ck) is a dimer composed of two different subunits of B and M, mainly found in skeletal muscle, myocardium and brain tissue, CK has three isoenzymes CKMM, CKMB, CKBB.

CKMM is mainly found in skeletal muscle, CKBB is mainly found in brain tissue, and CKMB is mainly found in heart muscle
.
In general, CKMM accounts for a large proportion of normal human serum, and there is almost no CKBB or very small amounts
.
In theory, the activity of CKMB should be less than that of CK
.

Clinically, the activity of CKMB is occasionally greater than that of CK, and there are generally the following two reasons:

1.
CKMB> CK
due to elevated CKBB.
CKMB is a dimer form composed of M subunit and B subunit, we use immunosuppression method when detecting CKMB, M subunit is inhibited, and the content of CKBB is negligible, half of the activity of CKMB (or the activity of CK-B is detected), and the result is multiplied by 2 to obtain the activity
of CKMB.

If the patient increases the amount of CKBB released into the peripheral blood due to brain tissue damage or other conditions, then the detection is no longer CK-B in the case of ignoring CKBB, at this time CK-B includes CKMB and CK-B in CKBB, multiplied by 2, there is a possibility that CKMB is greater than CK [7].

2.
CKMB > CK
due to giant CK.
Jumbo CK includes Ju CK1 and Ju CK2; Giant CK1 is a complex of CK isoenzyme (antigen) and autoantibodies, the most common is CK-BB complex with IgG, IgA, and a few are CK-MM complex with IgG, IgA
.
Giant CK2 is an oligomeric mitochondrial CK, also known as CK-mt, which exists on the mitochondrial membrane of cells, and when mitochondria disintegrate, small fragments of the mitochondrial membrane enter the bloodstream, so CK-mt becomes an oligomeric state
.
When CKMB is measured, antibodies can only inhibit the M subunit, not CK-BB and CK-mt, or CK-MM and CK-BB bound to IgG and IgA, and the calculation result is multiplied by 2, which increases the error, resulting in sometimes the measurement result CKMB exceeding CK
.

The two are used together to diagnose myocardial injury, in the diagnosis of early acute myocardial infarction has great clinical significance, in the acute myocardial infarction 4 ~ 6 hours after the occurrence, you can find CK and CKMB elevated, 24 hours to reach the peak, about three days CKMB can return to normal, if not recovered, indicating that myocardial infarction, ischemic necrosis is still developing
.
[8] Of course, the elevation of the two can also be seen in other myocardial injury diseases, such as myocarditis, skeletal muscle injury, and so on
.

06

summary

In the daily inspection work, we need to carefully observe and carefully summarize, to find some very interesting knowledge, such as HBV and HDV, glycated hemoglobin and glycated serum protein, etc.
, only through in-depth learning can we better grasp what we have learned and better serve the clinic
.

References

[1] SatoN ， Takahashi H ， Nikuni K ， et al.
[Persistent discrepancy betweenFDP and D-dimer in a patient with acute leukemia][J].
RinshoKetsueki， 1995， 36(3)：212-7.

[2] Lin Haiying, Liu Qiong, Li Ying, et al
.
Correlation between serum creatinine, blood urea nitrogen and glomerular filtration rate in patients with chronic kidney disease of different ages[J].
Chinese Journal of Nephrology,2007,23(5):1.

[3] Dong Shuqing
.
Detection values of serum creatinine and urea nitrogen and their ratios and renal damage[J].
Chinese Medical Guide,2011,9(36):2.

[4] ZHANG Xiaomin, LU Ruiping, HAI Xiuling, et al.
Analysis of alanine aminotransferase levels and pathological changes in the liver.
Frontiers in Medicine,2019,9(11):32-33.

[5] WANG Huimin,FANG Suhua.
Causes, harms and precautions of elevated alanine aminotransferase.
Chinese Journal of Health and Nutrition,2018,28(18):103.

[6] Aimé
Lo.
Relationship between hepatocyte injury and AST/ALT in hepatitis B patients[J].
Journal of Clinical Laboratory Laboratory:Electronic Edition,2020,9 (3):1.

[7] GorusF ， Claessens V ， Goubert P ， et al.
A sensitive bioluminescentimmunoinhibition test for CK-B subunit activity and a CK-MB specificELISA compared： correlation with agarose electrophoresis andinfluence of CK-isoenzyme profile on results.
[J].
Clinical Chemistry，1988(7)：1474-8.

[8] Zhang Zhang, Ma Wenzhu, Liu Peixuan, et al
.
Dynamic changes of serum and cardiac creatine kinase (CK) and its isoenzyme (CKMB) after acute myocardial infarction[J].
Jiangsu Medicine, 1986(5).