Typical doping has been widely used by athletes

What are peptide hormones?

Erythropoietin (EPO) and its analogues, growth hormone (hGH) and its analogues, exogenous drugs (Qomatropin peptide drugs) and endogenous hormone (the body’s natural generated) difference is small, the characteristics of drug metabolism in human body short time, have no accurate and reliable detection method for a long time, widely abused by athletes, is also a hot research focus in the struggle the anti-doping drugs, EPO and hGH is a peptide hormone.

Erythrotropin and its Analogue (EPO) Marion, “World’s fastest woman”, Sydney Olympic Gold and bronze medalist.
Jones, who used EPO, hGH and THG, became the first person in history to be jailed for doping.
Other athletes and groups have been found to have used EPO: seven-time Tour DE France winner Neil Armstrong of the United States; Russian cyclist Petro; and German triathlete Nina Dobrev.
Clapford, 2000 Olympic Women’s triathlon champion McMahon of Switzerland, 400m world champion Gromi Young of USA (banned for life), Juventus Football Club of Italy (1994-1998), etc.

The Chinese team, Winter Games champion Wang Fei, the National Games men’s 10,000m champion Tian Mengxu, China’s race walker Qin Aihua have all been down by the drug.

EPO is a kind of peptide hormone secreted by human kidney, which can increase the amount of bone marrow to generate red blood cells, improve the content of hemoglobin, and increase the oxygen carrying and supplying capacity of blood. It is a kind of medicine in clinical treatment of renal anemia.

EPO is favored by some sports events and athletes because it can significantly improve aerobic exercise time. It has obvious effects on endurance events such as cycling, triathlon, rowing, long-distance swimming, long-distance running and winter events. It is said that the maximum performance can be improved by 15%.
Another reason why EPO is favored by athletes is that the international EPO detection technology is not qualified, and athletes from various countries can basically use EPO freely. However, after 2000, the international EPO detection technology has been gradually improved, and the situation has changed somewhat.

The EPO has been blamed for the deaths of 24 cyclists over the past two decades, including eight in 2003, including former Tour DE France champion Pantani.
This is because EPO increases the number of red blood cells in the blood, making the blood viscous and slow blood flow, causing hypertension, causing tissue hypoxia, accelerating blood coagulation, and even leading to venous thrombosis, myocardial infarction, pulmonary embolism or cerebral infarction, leading to death.

Growth hormone and its Analogues (hGH) hGH is a peptide hormone formed in the anterior lobe of the pituitary gland and produced most in sleep. Moreover, with the increase of age, the production of hGH decreases gradually.
HGH quickly enters the liver where it is converted into growth vector C, which regulates growth, immunity and metabolism.

HGH can promote growth and development, promote cell division and proliferation of bone, cartilage, muscle and other tissues, increase protein synthesis, and promote bone growth in childhood and adolescence. It is mainly used for the treatment of dwarfism in clinic.
It can also promote anabolism, muscle growth, strengthen the strength of tendons, so that people’s muscles strong, strength increase, to gain competitive advantage, which is why it is used as a stimulant.
Due to its anti-aging effect, hGH is also used in the field of beauty.

There are also huge health risks associated with using such drugs: acromegaly and deformity.
It damages the liver and bones.
There is a high risk of contracting fatal diseases, such as AIDS, and deaths from brain virus infection due to hGH use have been documented.
HGH can inhibit sugar consumption, resulting in hyperglycemia and urine sugar;
It can also reduce insulin sensitivity and cause glucose intolerance. According to foreign reports, 80% of those who overuse hGH suffer from diabetes and need insulin treatment.
Lead to menstrual disorders, decreased sexual desire and impotence.

Many athletes consider hGH to be “safe” because the test is lagging and no hGH positive has been detected so far.
Marion.
Jones, who was heavily fined for using hGH doping, “confessed” rather than was tested.
DavidHowman, director-general of the world anti-doping agency (WADA), has said: “we know people are taking hGH and they haven’t been punished for 20 years.”
Australian customs seized a large amount of hGH injection in the luggage of an Uzbek coach;
The Italian police also found hGH in the baggage of the Tour DE Italy.

Problems with growth hormone secretion, affecting children’s growth

The lack of growth hormone in the human body will affect height growth, especially when the child grows tall, if there is insufficient growth hormone secretion, it will affect the child’s growth, so pay attention to regulating the growth hormone secretion level in the body, then, let us understand Will insufficient growth hormone secretion affect children’s height?

The child is not good for growth hormone secretion problems, affecting the child’s growth
Seventy to eighty percent of human height is caused by genetic factors. Generally speaking, his parents can’t be short in height. However, there is a case where when a child lacks growth hormone, the child’s growth rate becomes slow. Although there is no problem in intelligence, but in terms of height, as the age increases, the growth rate is much slower than that of children of the same age Finally, it leads to short stature.

This dwarf is uniform, has no special face, and has no chromosomal abnormalities (because congenital ovarian dysplasia will lead to a short girl’s stature. This disease chromosome is different from ordinary people. At the same time, there are special physical symptoms, like What is short neck, elbow valgus, low posterior hairline, etc.).

Therefore, the growth hormone deficiency in children has the characteristic features of the disease and the disease that needs to be identified. Therefore, through detailed diagnosis, this disease is not prone to misdiagnosis or missed diagnosis.

Through the introduction, growth hormone deficiency will affect the growth of the child’s height, so you must understand the growth hormone secretion level in the child’s body, if there is a growth hormone secretion problem, it is best to adjust as soon as possible, otherwise it will not only affect the child’s height growth, but also Will adversely affect the child’s life.

Messi: When I was a kid, I had growth hormone disorders ,Hormone therapy every day

Argentine star Messi revealed that he suffered growth hormone confusion when he was young and needed to inject hormones every night.

The Daily Mail said that Messi ’s condition was also called idiopathic short stature, so he injected hormones into his thighs every night. He told TVAmerica: “I inject hormones into my thighs every night, and I started when I was 12 years old. I am not too impressed with this matter.”

“Before I learned to inject myself, my parents started injecting me when I was 8. This is a small needle and it doesn’t hurt. It was an ordinary thing for me at the time.”

Injecting hormones also brought huge expenses. Messi ’s parents spent £ 1,000 a month until his first club Newell old boy offered to pay for him. In 2001, Messi, who was only 13 years old, joined Barcelona. Barcelona paid all the treatment costs for Messi until he completed the injection course in 2002.

“Joining Barcelona is not difficult for me. I quickly adapted, but my family was not. My siblings came home. My father and I stayed alone, and he asked me” What should we do? ” Say I want to stay. “

appearance suddenly became ugly and hands and feet became thicker, which may be related to pituitary tumors!

Recently, I saw several news reports and shared them with you. I hope you can be alert to this situation!

News 1:

The 42-year-old Ms. Liu found herself ugly in the past six months, her nose became wider, her face wider and her feet larger. She thought she was naturally aging, but she didn’t pay much attention to it, but this change became more and more obvious. After going to the hospital for examination, she realized that it was all because of a pituitary tumor in her head.

News 2:

For more than a year, Mr. Lin, 36 years old, felt that his appearance became more and more ugly, with protruding jaws, swollen lips, and rough skin. He used to wear shoes of size 40 and now wear size 45, and his snoring sound increased. A week ago, I learned after the hospital examination that the cause of his series of changes was a pituitary tumor in the brain. At present, the doctor has removed the pituitary tumor from the nasal cavity through minimally invasive surgery. After a period of symptomatic treatment, he may restore his previous appearance.

Attentive friends must have discovered that the face suddenly becomes ugly, the hands and feet become thicker, and the skin is rough … These symptoms are all caused by pituitary tumors! ! ! In fact, some people will have such a situation in life, but because there is no concept of the symptoms and harm of pituitary tumors, the best treatment time is missed. Let’s take a look at one type of pituitary tumor-growth hormone secretory pituitary tumor.

What is growth hormone secretory pituitary tumor?

There are many types of pituitary tumors. We have also talked about some different types of pituitary tumors and symptoms before.

The growth hormone-secreting pituitary tumors we are going to talk about today have a higher incidence, accounting for the third place in all pituitary tumors, second only to non-functional pituitary tumors and prolactin-secreting pituitary tumors.

Growth hormone-secreting pituitary tumors are mainly manifested as acromegaly and gigantism, simple gigantism is rare, and acromegaly is secondary to more than half of adulthood. The two patients in the above news are all manifestations of acromegaly.

Why do growth hormone-secreting pituitary tumors cause people to become ugly and have thick hands and feet?

Growth hormone-secreting pituitary tumors cause excessive growth hormone (GH) production in the body. What is growth hormone? It is a single peptide chain protein hormone secreted by eosinophils in the anterior pituitary gland. It is a growth regulator with a wide range of physiological functions.

Excessive long-term growth hormone secretion will lead to abnormal hypertrophy of body type and internal organs, accompanied by abnormal physiological functions. In adolescence, adolescents may present with gigantism, and in adults, acromegaly.

Patients with distal limb hypertrophy caused by growth hormone-secreting pituitary tumors will not only have enlarged hands, feet, nose, lips, wide head and face, high cheekbones, but also hoarse voices, sleep snoring, etc. Patients also have tongue and throat soft tissues It will then become hypertrophic, especially when sleeping at night, it is easy to cause breathing problems.

In addition, the incidence of malignant tumors such as pituitary tumor compression symptoms, diabetes, hypertension, cardiovascular and cerebrovascular diseases, respiratory diseases, and colon cancer will also increase. These metabolic disorders and complications seriously affect the health and quality of life of patients.

How to judge whether your condition is related to acromegaly?

Generally, I can judge based on some unique signs. If in recent years, your shoe size has become larger, your face has changed, your cheekbones have protruded, your forehead has become wider, your voice has become lower, your fingers have become thicker, and your skin has roughened, you can rule out whether you have acromegaly disease.

And more than 95% of patients with acromegaly are caused by growth hormone-secreting pituitary tumors, so the above symptoms should go to the regular hospital neurosurgery. However, because many patients have no other discomforts in the early stage when acromegaly symptoms appear, many people do not treat it as a disease, which delays treatment. Many patients with acromegaly in China have not been diagnosed and have not received treatment. This is mainly because people do n’t understand the disease, they do n’t pay attention to it after symptoms appear, and some people think that face ugliness is not a disease until serious complications such as vision loss, heart disease, cerebrovascular disease, diabetic breathing It is a pity that systemic diseases only came to the clinic and missed the opportunity for early diagnosis and treatment.

How to treat a pituitary tumor with growth hormone secretion?

The purpose of the treatment of growth hormone secreting pituitary tumor is to reduce the level of growth hormone in the blood to normal and reduce the size of the tumor. After successful treatment, many acromegaly symptoms and functions will be reversed or improved (except for the bone changes that have occurred and fixed). The treatment methods include surgery, medication and radiation therapy.

Most growth hormone-secreting pituitary tumors are preferably surgically removed. At present, the most commonly used and patient-welcome is the minimally invasive surgery through the transsphenoidal approach assisted by neuroendoscopy, just like the patient in News 2 above. This type of surgery does not require craniotomy, and uses neuroendoscopy technology to directly reach the site where we need to operate from the nostril, leaving the other parts of the pituitary intact, more accurate, safer, and less postoperative complications.

Introduction to Neurosurgery

The Affiliated Hospital of Northwest University · The Third Surgery Hospital of Xi’an City features “Minimally invasive surgery for craniocerebral spinal cord trauma and tumors, minimally invasive interventional surgery for cerebral and spinal vascular diseases and comprehensive treatment of functional neurosurgical diseases” “Green channel” for the treatment of acute cerebrovascular disease and craniocerebral trauma. There are 50 beds and 19 ICU in the center. ICU has the most advanced detection, monitoring equipment and life support system in the world. The department has become a comprehensive neurosurgery integrating clinical, scientific research, teaching, functional rehabilitation and encephalopathy prevention.

Interpretation of sex hormone levels

Hormones are special substances that are synthesized and secreted by certain cells in humans and animals and can regulate the physiological activity of the body. The word “hormone” comes from The Greek language and means “rise up” or “stir”.

All chemicals that transmit information through blood circulation or tissue fluid are now called hormones.

Hormone secretion is very small, nanogram (one billionth of a gram) level, but its regulatory effect is very obvious.

Check for sex hormones common sense

Sex hormones (including progesterone, estrogen) should not be used for at least one month prior to the testing of the underlying hormones, otherwise the results are unreliable (except sex hormones that need to be reviewed after treatment).

Check the endocrine is best in the 3rdto5th day after menstruation tide, this period belongs to the early follicles, can reflect the function of the ovary. But for menstruation long-term not tide and also eager to understand the results of the inspection, can be checked at any time, this time is the default for the premenstrual time, the results also refer to the yellow period of the inspection results.

  Determine is the  3rdto5th day of menstruation, check the sex hormone 5 can be, can not check progesterone, progesterone should be checked during the progesterone (21 days after menstruation or 7 days after ovulation);  The data can approximate the period of the menstrual cycle). People with ambipree and amenorrhea, such as urine pregnancy test negative, vaginal B ultra-checked double-sided ovaries without 10 mm follicles,EM thickness of5mm,can also be used as a basic state.

Folly Stimulator(FSH)

It is a glycoprotein hormone secreted by alkaline cells in the pituitary front, whose main function is the maturation of the ovaries and the secretion of estrogen. The concentration of blood FSH is  1.5to10 mIU/mLin the pre-ovulation period, 8to20 mIU/mL,and 2to10mIU/mLin theovulation stage.  Generally 5 to40 mIU/mL as normal.  FSH values are low during estrogen therapy, Sihan’s syndrome, etc.  FSH is highly common in ovarian premature aging, ovarian insensitivity syndrome, primary amenorrhea, etc. If FSH is higher than 40mIU/mL,it is not effective for ovulation drugs such as cromion.

Projumite oxytocin(LH)

It is also a glycogen hormone secreted by alkaline cells in the pituitary front. The main function is to promote ovulation and progesterone production to promote progesterone and estrogen secretion in the progesterone. The concentration of blood LH is 2to15 mIU/mLin the pre-ovulation period, 30to100mIU/mL,and 4to10mIU/mLin theovulation stage.  The normal value during the non-ovulation period is 5to25 mIU/mL. Less than 5mIU/mL suggests under-functionality of gonadotropins, as seen in Sihan’s syndrome.

During the normal menstrual cycle, the early follicle  (menstrual 2 to 3 days)  blood FSHandLH are maintained at low levels, and the lH rises rapidly before ovulation,withLH reaching 3 to 8 times the base value, up to  160IU/L  Even higher, FSH is only about 2 times the base value, rarely30IU/L,afterovulation FSH,LH quickly returns to follicle levels.

Monitoring the FSHandLH levels in the early stages of follicle sits can determine the function of the gonad axis.  FSH is more valuable than LH in determining ovarian potential.

1. Ovarian failure: The underlying FSHs  40IU/L,LH elevated or40IU/L,forhypersexual gonadotropin(Gn),i.e. ovarian failure;  

2. The basic FSH and LH are both low Gn  amenorrhea, indicating hypothalamus or dyslerating of the dyphthain, and the difference between the two is tested with gonadotropin release hormone (GnRH).

3. Ovarian reserve dysfunction (DOR):Basic FSH/LHs2to3.6 hintS DOR(FSH can be in normal model), is an early manifestation of ovarian dysfunction, often prompting patients on overolyofecation(COH) If the response is poor, the COH scheme and the dose of Gn should be adjusted in a timely manner to improve the responsiveness of the ovaries and obtain the ideal pregnancy rate. Because the increase in FSH/LH only reflects the DOR,rather than thereduced ability to conceive, the ideal pregnancy rate can still be obtained once ovulation is obtained.

4. Foundation FSHs12IU/L,next cycle review, continuous 12IU/L prompt DOR.

5. Polycystic ovary syndrome (PCOS): Basal LH / FSH ﹥ 2 to 3, which can be used as the main indicator for the diagnosis of PCOS (basic LH level IU 10IU / L is an increase, or LH maintains normal levels, while basal FSH is relatively Low levels result in increased LH to FSH ratios).

6. Check 2 basic FSHs20IU/L,which can be considered a lateovary period of concealment, indicating that it may be amenorrhea after 1 year.

Progesterone (P)

Under normal circumstances, follicle blood P has been at a low level, less than 3.2nmol/L,after ovulation ovary progesterone, the level rose rapidly, the blood concentration after the mid-LH peak  of the 6thto8th day reached a peak, the first 4 days of menstruation gradually dropped to follicle level. Serum progesterone levels increase dissonant levels with pregnancy, mainly from ovary progesterone during 6 weeks of pregnancy, and are mainly secreted by the placenta in the middle and late stages of pregnancy. Progesterone usually works at the estrogen level, mainly by converting the endometrium into secretion, facilitating the embryo’s bed and preventing uterine contractions, leaving the uterus stationary before delivery. At the same time, progesterone can also promote the development of breast glandular bubbles, for the lactation preparation.  

Throughout the yellow body period, the change in p-content of peripheral blood is parabolic.

1. Judgement of ovulation: Mid-yellow (28  days of menstrual cycle for women on the 21st of menstruation) Ps15.9nmol/L prompts ovulation. When using ovulation-promoting drugs, the effect of ovulation can be observed using blood progesterone levels.

2. Diagnosis of yellow function insufficiency(LPD):the level ofprogesterone in the yellow body is lower than the physiological value, indicating insufficient yellow function, ovulation-type uterine dysfunction bleeding. The blood progesterone value is still higher than the physiological level of the 4to5 days of menstruation tide, indicating incomplete yellow body atrophy.

3. Judgement of in vitro fertilization – Embryo transfer(IVF-ET)prognosis: The P level before ovulation can be estimated for IVF-ET  prognosis. Muscle Note HCG Day P s 3.18nmol/L (1.0ng/mL) should be considered elevated, the planting rate and clinical pregnancy rate are reduced,Ps4.77nmol/L (1.5ng/mL) suggests premature ephenism.   In IVF-ET long-term procedure surgation, muscle injection HCG day, even if there is no increase in LH concentration, if P (ng/mL) x 1000/E2(pg/mL)1,promptfollicles  Premature lintin, and the clinical pregnancy rate of this type of patients decreased significantly.  Premature pheromation is also a manifestation of DOR.  

4. Identification of ectopic pregnancy: Low blood P levels in ectopic pregnancy, blood P47.7nmol/L (15 ng/mL)in multiple  patients.  Only 1.5% of patients were 79.5nmol/L (25 ng/mL). P 90%of normal intrauterine pregnancypersons is78nmol/L. Blood P levels can be used as a reference basis in the differential diagnosis of intrauterine and ectopic pregnancy.

5. Auxiliary diagnostic precursor abortion: within 12 weeks of pregnancy, progesterone levels are low and the risk of early miscarriage is high. Progesterone values may be aborted if there is a downward trend in progesterone.

6. Observe placental function: Progesterone levels in the blood decrease when placental function is reduced during pregnancy. Single serum progesterone level s 15.6nmol/L(5ng/mL),indicated as stillbirth.

Estrogen (E2)

The base value is 25to45pg/mL. During the normal menstrual cycle, the early eofoam E2 is about 183.5pmol/L (50pg/mL),the first peakreaches before ovulation, up to 917.5to1835pmol/L(250to500pg),then gradually declines, reaches the lowest point afterovulation, and then begins to rise again The yellow ums formed a second peak, below the first peak, about  458.8pmol/L(124.80pg),after a periodofmaintenance, when the yellow body shrinks to the level of early follicle period,  i.e. the 3rd day of menstruation should be 91.75- 183.5pmol/mL(25to50pg/mL).

1.Basic E2> 165.2 ~ 293.6pmol / L (45 ~ 80pg / mL), regardless of age and FSH, it indicates that fertility is decreased.

2、When the basic E2 is ≥ 367pmol / L (100pg / mL), the ovarian response is worse. Even if FSH is 15IU / L, there is almost no possibility of pregnancy.

3.Monitoring indicators offollicle maturation and ovarian hyperstimulation syndrome(OHSS)

(1)Follicular stimulation: When superovulation is promoted, when the follicle is ≥ 18 mm and blood E2 reaches 1100pmol / L (300pg / mL), HMG is stopped and HCG10000IU is injected on the same day or 24 to 36 hours after the last HMG injection.

(2)E2﹤3670pmol/L(1000pg/mL),OHSS generally does not occur.

(3)E2﹥9175pmol/L(2500pg/mL),in order to occur high-risk factors of OHSS, timely disabling or reducing the amount of HMG and disabling HCG to support the corpus luteum function can avoid or reduce the occurrence of OHSS.

(4)E2 ﹥ 14800pmol / L (4000pg / mL), nearly 100% of OHSS occurs and can rapidly develop into severe OHSS.

4. Diagnosis of ovulation: no periodic changes in hormones during absence from ovulation, commonly found in non-ovulation-free dysfunction uterine bleeding, polycystic ovary syndrome, and certain postmenopausal bleeding.

5. Diagnosis of female sexual precociousness: clinically mostly prior to the second sexual characteristics of precocious development before the age of 8, blood E2 levels increased275pmol/L as one of the hormone indicators for diagnostic precociousness.

Prolactin (PRL)

PRL is synthesized and secreted by the pitel eosinophilic PRL cells. Double regulation of hormones released by hypothalamus inhibitors (mainly dopamine) and prolactin. The main functions of PRL are to promote breast development and lactation, as well as to promote breast catheterand and gland development prior to childbirth in conjunction with ovarian steroid hormones. The measurement level and biological effects of PRL are not necessarily parallel, such as milk-free in people with high PRL, whereas those with NORMAL PRL may have milk spills.

PRL secretion is unstable, mood, exercise, sexual intercourse, hunger and eating can all affect its secretion status, and with the menstrual cycle there are small fluctuations, with sleep-related rhythm.  After falling asleep, it rises to a 24-hour peak before waking up in the morning, dropping rapidly after waking up, and dropping to mid-day lows from 10 a.m. to 2 p.m. Therefore, according to this rhythmic secretion characteristics, should be 10 to 11 a.m. time and space abdominal blood pumping (quiet and awake state). Generally speaking, normal lactin levels are normal and do not require review, and elevated PRL levels may be caused by the confusion of the above factors.

PrL significant elevated, can be determined by a single examination,PRL elevation at the normal maximum of 3 times below, should be a second examination, not easily diagnosed with hyperlactinemia(HPRL)abuse brominated pavilion treatment.

PRL is 25 ng/mL or above the unit test normal value is HPRL,PRLis50 ng/mL,andapproximately 20% has prolomas.   PRL,100ng/mL,about 50% have prolomas, can be selectively performed for pituitary CT or magnetic  resonance.  PRL,200ng/mL,often microadenomas, must be done pituitary CT or magnetic resonance.  Elevated PRL levels are also seen in precocious sex, reduced primary thyroid function, premature ovary aging, poor yellow function, long-term breastfeeding, neuropsychiatric stimulation (e.g. chloropropyl, birth control pills, large amounts of estrogen, blood equality).  Patients with polycystic ovary syndrome are mildly high prolactinemia, which may be caused by persistent estrogen stimulation.

PRL reduction: hypothermia, lack of simple prolgive delivery, use of anti-PRL  drugs such as brominated pavilions, left-handed doba, VitB6,  etc.

Androgen (T)

Androgens are secreted by the ovary and adrenal cortex. Androgens are divided into testosterone and andene diketones. Premenopausal, serum testosterone is the main indicator of the source of ovary androgens, and the adrenal cortex is the main source of androgens.

The normal range of serum total testosterone is <1.4nmol / L during follicular phase, <2.1nmol / L during ovulation, <1.7nmol / L during luteal phase, and <1.2nmol / L after menopause.

1. Ovarian masculinity tumors: women in the short term to develop excessive symptoms of sex exacerbation and serum androgen softening often prompt sorovarian masculinity tumors.

2. Polycystic Ovary Syndrome: Testosterone levels usually do not exceed 2 times the upper limit of the normal range, male oleones are often elevated, dehydrogenated pyrodone is normal or mildly  elevated. If the level of androgens is raised before treatment, it should be reduced after treatment, so serum androgen level can be used as one of the indexes to evaluate the efficacy.

3. Abnormal lyrogen seroandhormone serotonin in adrenal cortical hyperplasia tumors.

4. Gender malformations: male pseudo-gender malformations and true gender malformations, testosterone levels within the normal value of men;

5. Female hair yaphosis: When serum testosterone levels are measured, multiple hair follicles are sensitive to androgens.

6. The use of androgen preparations or endocrine drugs with androgen effects, such as Dana,  is used to monitor androgen levels during the drug use.

7. Hyperlactinemia: Women have excessive androgen symptoms and signs, but androgen levels in the normal range, serum prolactin levels should be measured.  

It was the other day.White text to attend the first hospital of Peking University in the course of study The content of the teacher’s lecture,Here’s followed byShare it.
Get sex hormone test sheet, to read in the following order
1、FSH(follicle stimulator)
2、LH(Yellow seromer) andFSHProportion
3、T(Testosterone)
4、PRL(泌Lactosine)
5、E2(estradiol)
6、P(Progesterone)
Step 1:FSH
In general, the lowest point is in the yellow body period0.5 IU/LThe highest point is during ovulation< 20IU/L。
Clinical significance: less than1IU/LTips for the hypothalamus-Poor function;20IU/LSuggests ovarian failure.
Predicting Ovarian Reserve Capacity, Cromefen Stimulation Trial: Menstrual Cycle No.5Day, daily oral cromivenin100mg, total5Days, in menstruationCycle No.10Days, testsFSH。 IfFSH>20IU/L, which indicates that the ovary reserve function is reduced.
LH
In general, the highest point is in ovulation and can be higher than20IU/L。
Clinical significance: less than1IU/L, tips for the hypothalamus-To have low function;LH13-25IU/L,FSHNormal, promptPCOSIt makes more sense to increase the early and mid-follicle periods. Urine testingLHpeak, predictable ovulation.
Hanging function test:GnRHExcitement test, method:GnRH100micrograms, one-time intravenous injections, after medication30-90Minutes, measuredLH、FSH。 Results:LHIncrease3Times andFSHUnchanged, good function;LHNo response, then the drooping function is poor;FSH、LHReaction to advance orFSHReaction slowerLHInthes of progress, ovarian function declines.
Step 2:LH & FSHProportion
Mainly used to infer the yellow function, if>2.5, considering polycystic ovaries or yellow ingress;<1, consider ovarian function decline.
Step 3: Testosterone
Women are0.5-3.0nmol/l(20-80ng/dl), the exception is100ng/dl。
about 80% Testosterone andSHBGcombined, the values were total testosterone, free testosterone (FAIIt makes more sense.
Testosterone Source:50% Since the outer week maleeneDiketone (adrenal production) conversion, each25%From the adrenal glands and ovaries.
Clinical implications: Testosterone is less than or equal200ng/dl(6.9nmol/l), possibly forPCOSgreater than200ng/dl(6.9nmol/l), a tumor that secretes androgens.
Sulphate dehydrogenation methadone (normal range)250-300ng/dl,0.7-0.8umol/l) less than or equal to700ng/dl, possibly forPCOSgreater than700ng/dl, adrenal or ovarian tumors.
17-Oxyprogesterone (normal range)<2ng/ml,6.1nmol/l),>4ng/ml 12.1nmol/lThe dexamethasone suppression test is required.
Dexamethasone Suppression Test: Method: The Day Before11PM-12PMOral dexamethasone between1mgDay8AMBlood.
Results: Cortisol>138nmol/L,Tip Cushing syndrome。
Step 4:PRL
During the day, the level of secretion fluctuates (5-27ng/ml),every 24hour, late follicle about14pulses, yellow late about9pulses. Stress (venous punctures) can lead to increased secretion. Time to draw blood: morning9-11point, fasting, quiet.
Diagnosis criteria for hyperlactinemia: twice>30ng/ml or 880mIU/L
MeasuredPRLIncluding small molecules, large molecules.PRL, large moleculePRLNo function.
Some normal womenPRLCan be high, if the menstruation is normal, can be observed, if amenorrhea or menstrual thinning, need to retest.
Step 5: estradiolE2
The most physiologically active estrogen in the body, normal50-500pg/ml, the ovulation period reaches a peak, if below normal, accompanied byFSH、LHReduce and consider hypothalamus amenorrhea.
Estrogen (estradiol) normal bloodConcentration: Early follicle40-60pg/ml
Mid-cycle250-350pg/ml
Yellow mid-body100-200pg/ml
ESTRADIOL PRODUCED BY THE OVARIES60-600ug/d
Step 6: Progesterone
Timing: Pre-menstrual5-8Days. Objective: To determine whether there is ovulation or not.>30nmol/lThat is, prompt for ovulation.
Normal blood concentration of progesterone (progesterone): follicle period<3ng/ml
Yellow mid-bodyGreater than or equal to10ng/ml
Pregnancy,PRelated to placental growth, early pregnancy30-45nmol/l
Mid-pregnancy75-150nmol/l
Late pregnancy150-600nmol/l, related to the birth weight of the newborn and the weight of the placenta.

Tips for the test sheet:
FSH、LHNormal range,E2Lower, hypothalamus amenorrhea.
FSH、LHReduceE2Lower, pituitary amenorrhea, hypothalamus amenorrhea.
FSHIncreaseFSH/LH>1, ovarian function is declining.
LHSignificantly higher,LH/FSH>2.5,PCOS。
PRLElevated, hyperlactinemia.
TElevated, and hyperpositive hormoneemia.
Each is generally normal, uterine amenorrhea.

Growth hormone deficiency

Growth hormone deficiency

The height of the child is two standard deviations lower than the average height of the same area, the same race, the same sex, and the normal age of the same age, or the height is less than the third percentile of the height of the child. The diagnosis is short.

GHD is one of the common reasons for short stature, and short stature can have adverse effects on children’s work, study, marriage, life and psychology.

Pathogenesis

In addition to the dystocia and the removal of intracranial organic lesions, the diagnosis of GHD must rely on two hGH stimulation tests. Those with hGH peaks below 5 ng/ml are complete GHD, while those with 5 ng/ml are between 5-10 ng/ml. For partial GHD.
 

Common causes of growth hormone deficiency

Pituitary dysplasia: forebrain non-cracking malformation, visual-middle dysplasia, cleft palate, hypothalamic dysplasia, growth hormone, growth hormone releasing hormone deficiency
Idiopathic: Unexplained growth hormone deficiency Autosomal recessive inheritance: Type IA: GH1 gene deletion
Type IB: Growth hormone releasing hormone receptor gene deletion Autosomal dominant inheritance: Type II: GH1 and other genetic variants X-linked inheritance: Type III
Transcription factor gene defects: pit1, Prop1, HESX-1, LHX3 gene mutations, etc. Growth hormone receptor deficiency: Laron syndrome
Insulin-like growth factor (IGF-1) deficient brain injury: perinatal injury (dystocia, ischemia, hypoxia, intracranial hemorrhage, etc.) Invasive brain lesions: Tumor, Langrehans cell hyperplasia Other: less than gestational age, Chromosomal abnormalities, skeletal development disorders, chronic systemic diseases
 
Basic medical history and auxiliary examination

• Male, date of birth: 1996 12 31, Hebei February 12, 2009 (12 years old and February), complained of a short
• G1P1, full-term head position without hypoxic asphyxia, birth weight 5-6 kg, length unknown • Breastfeeding 1 year old, edentulous speech is no different from children of the same age and gender
• 1 year old or 2 years old is unknown, 6 years old first class is in the first row • Nearly one year long height 2-3cm
• Diet, no picky eaters, normal exercise capacity but less active exercise • No signs of secondary sexual development such as unvoiced, no beard and morning bleed
• Past history: Corneal transplantation for left eye trauma at 2 years of age, no history of febrile seizures, no history of infectious diseases such as hepatitis B tuberculosis
• Mother 155cm, father 163cm, non-close relatives get married
• Family history: related relatives who are tall and short (male <160, female <150).
 
Physical examination

• Height 130.8cm (-3.1SD); weight 28kg
• The skin is dry, the thyroid is not big, the heart and lungs (-), the liver and spleen (-) are not swollen in the lower limbs. • The pubic hair is 1 phase, the double testicles are 1 ml each, the penis is 3 cm long, and the circumference is 4.5 cm.

Insulin hypoglycemia GH stimulation test (on)

Levo-multi-growth hormone stimulation test (below)

Bone age and saddle area NMR

Bone age: 7-8 years Pituitary NMR: normal pituitary size; pituitary posterior lobe high signal; pituitary stalk centered.
 
Diagnosis and treatment

Diagnosis: partial deficiency of growth hormone (PGHD) short stature
Diagnose based on:
• 1 height <-3SD (children of the same age and same gender), GV=2.5cm/y • 2 bone age (7-8 years old) < CA (12.3 years old)
• 3 growth hormone stimulation tests GHmax = 6.2ng / ml <10ng / ml

Treatment: 3 units of growth hormone per night before bedtime; increase exercise (aerobic exercise), balanced diet, quality sleep; regular follow-up, monitor height, review IGF-1, thyroid function, blood biochemistry.

• Normal thyroid function (-)
• Liver and kidney function (-), fasting blood glucose normal • Blood routine (-), normal hemoglobin
• No facial changes during treatment, no swelling of hands and feet and eyelids, no leg pain and joint pain, no swelling and inflammation of the injection site
• Outpatient visits in July 2012 (15 years and July) (GH treatment for 39 months):
Height 156.5cm, weight 40kg, double testicles about 1ml bone age: 12-13 years old
• Give 8 units of serostim growth hormone and continue treatment.

Effect of growth hormone on ovarian function

Effect of growth hormone on ovarian function

[Abstract] Growth hormone affects ovarian function by directly binding to the growth hormone receptor on the ovary or by the action of insulin-like growth factor. Basic research indicates that auxin can affect the growth of antral follicles and antral follicles, inhibit follicular atresia, promote follicular maturation, increase the number of ovulation, and may affect the production of sex hormones. Based on the above reasons, many scholars have explored the application value of growth hormone in human assisted ovulation induction therapy. It is expected that auxin can improve the effect of ovulation induction therapy, but the current results are controversial. Improving the use of growth hormone may improve outcomes.
[Key words] growth hormone; ovary; follicle; sex hormone; ovulation

Growth hormone is a hormone secreted by the pituitary gland and has a physiological effect of promoting growth and affecting metabolism. With the in-depth study of reproductive physiology, it is found that growth hormone can
 
Act on the ovary, affecting ovarian function, such as: stimulate follicular growth, increase the number of ovulation and the production of sex hormones. Effect of growth hormone on ovarian function
 
1 growth hormone affects ovarian function
It is currently believed that growth hormone affects ovarian function mainly through two ways: 1 Directly combined with growth hormone receptors (GHR) on the ovary to produce biological effects. Studies have found that growth hormone receptors are present in the ovaries of many species, indicating that growth hormone can act directly on the ovaries. Lebedeva et al [1] found high-affinity growth hormone receptors in follicular granulosa cells and follicular cells before ovulation in chickens. Zhao [ 2 ] used reverse transcription 2 PCR (RT2PCR) to detect the presence of growth hormone receptor mRNA on the anterior antral follicle wall, oocyte and cumulus in the mouse ovary. M archal et al [3] confirmed that the expression of gh rm rmone (GH) receptor m RNA was observed in cumulus cells and oocytes of pigs and cattle, and growth was observed during oocyte maturation. Hormones can promote oocyte maturation, suggesting that there are functional GH receptors in cumulus cells and oocytes of these two animals; 2 growth hormone indirectly affects ovarian function through insulin-like growth factor (IGF) system . Growth hormone induces IGF production in the liver, including IGF2I and IGF2II. IGF reaches the ovaries through the blood circulation and binds to target cell receptors. In addition, growth hormone can directly induce follicular granulosa cells and follicular cells to produce IGF, which regulates ovarian function through paracrine and autocrine effects. Experiments have confirmed the expression of IGF mRNA in follicles at various stages of sheep ovary [4].
IGF can act directly on the ovary, and its role is synergistic with the regulation of growth hormone [5].
2The effect of growth hormone on follicular growth
Follicles are the basic functional unit of the ovaries. Follicles not only undergo morphological changes during development, but also have functional development. Gonadotropins and gonadal hormones play a leading role in this process. However, in the absence of follicle stimulating hormone (FSH), the follicles of FSH knockout mice can still develop into the preantral follicle stage, suggesting that there are other factors affecting follicular development, especially in the early stage of follicular development, FSH may not directly effect. Recent studies have shown that growth hormone affects the growth and development of follicles.

  1. 1 stimulate the growth of anterior follicles
    Growth hormone stimulates antral follicle growth and increases the number of small follicles. Ovarian histology of auxin receptor knockout mice (GHR 2KO) found that the number of anterior antral follicles and antral follicles in the ovary was significantly less than that of wild mice due to the lack of auxin. Treatment with IGF2I not only increases the number of primordial follicles but also reduces follicular follicles [6]. The growth hormone receptor knockout mouse model confirmed that the pre-ovulatory part of follicles (PF) decreased in GHR 2KO mice (42. 9 3. 7 vs 28. 83. 5, P < 0.05), presumably due to lack of growth. Hormone action, leading to a decrease in the number of early follicles.
  2. 2 effects on antral follicles
    Growth hormone enhances the response of antral follicles to gonadotropins. In animal studies, it was found that recombinant bovine growth hormone enhances the response of antral follicles to gonadotropins and shortens the time to recruit dominant follicles [8]. Studies in humans have also suggested that growth hormone has a similar effect. Six patients with growth hormone deficiency received gonadotropin (HM G) + GH ovulation therapy, and found that the FSH threshold level that stimulates follicular development was reduced (ie, the amount of HM G was reduced), and single follicular growth was obtained, suggesting growth hormone It seems that the sensitivity of dominant follicles to FSH can be selectively increased. It has been reported that a patient with primary acromegaly who has undergone controlled ovarian hyperstimulation has successfully delivered triplets, suggesting that high growth hormone levels can enhance the sensitivity of the ovaries to FSH [9]. Although these limited data suggest that growth hormone enhances gonococcal follicle response to gonadotropins, good animal models are needed to conduct basic research to provide sufficient evidence to validate and elucidate specific mechanisms of action.
  3. 3 promote oocyte maturation
    Growth hormone promotes oocyte maturation. Experiments in vitro culture of horse cumulus complex (COC) showed that horse growth hormone promoted oocyte maturation, with 29% of cumulus increasing in the growth hormone group and increasing the percentage of oocytes, while 13% of the control group was enlarged. In the cumulus, horse growth hormone not only increased the number of oocytes in dividing metaphase II, but also increased the maturation rate of oocytes (89% vs 78%, P < 0.05) [3]. Growth hormone-assisted superovulation therapy also supports the results of animal experiments. Growth hormone-assisted treatment significantly increased the number of small follicles (V and V I), the rate of maturation of GV oocytes and the rate of fertilization [10]. Kiapekou [11] co-cultured with GH and/or IGF2I during immature oocyte culture, and both drugs promoted follicular maturation.
  4. 4 inhibition of follicular atresia
    Animal experiments suggest that growth hormone inhibits follicular atresia. Detection of growth hormone receptor/growth hormone binding protein knockout (GHR/GHBP2KO) in mice and wild mice ovary, the results showed that the former ovary weight loss, tissue structure is good. Despite the presence of follicles at various stages of development, the number of growing follicles is reduced. Further analysis of the ovarian tissue sections showed that the ratio of the atresia follicle/healthy follicle in the ovary of GHR/GHBP2KO mice was significantly higher than that of the latter. The study of follicular apoptosis in transgenic mice overexpressing bovine growth hormone more directly confirms the role of growth hormone in inhibiting follicular atresia. In the ovary of normal mice, 46% of follicles showed apoptosis, while only 30% of transgenic mice showed a significant decrease in follicular apoptosis rate, thereby reducing follicular atresia. These atresia follicles contain a large number of apoptotic cells, mainly apoptotic granulosa cells. Apoptosis is involved in follicles at all levels, but the degree of apoptosis varies at different stages. No obvious apoptosis was observed in follicles before ovulation in transgenic mice or normal mice, but the phenomenon of follicular atresia in early sinus was obvious. The results of this experiment are consistent with the rule of follicular degeneration in most early sinus stages, and also indicate growth hormone. Follicular apoptosis in the early sinus can not be completely inhibited.
    3 increase the number of ovulation
    Growth hormone not only stimulates follicular growth, but also increases the number of ovulation. Anne et al. studied GHR/GHBP2KO mice and found that the number of ovulation in GHR/GHBP2KO mice was reduced, which in turn caused the number of litters in GHR/GHB P2KO mice to be significantly lower than that in wild mice. In order to clarify the cause, exogenous gonadotropin was used to induce ovulation treatment. The result was an average of 11. 8 2. 3 mice per mouse, while the latter ovulated with an average of 35. 3 2. 3 mice/rat, suggesting GHR / GHBP2KO rats. The ovaries are defective. Ovarian histological analysis of GHR/GHBP2KO rats also confirmed that the number of healthy follicles at various developmental stages in these ovaries was significantly reduced, especially the number of follicles with a diameter of 200 μm was statistically different from that of the control group. The reduction of follicles and the lack of follicles in the terminal stage of GHR/GHBP2KO mouse follicles are responsible for the decrease in the number of ovulations. Studies on follicular apoptosis in transgenic mice have also confirmed that growth hormone can reduce the atresia of follicles at various developmental stages, thereby increasing the likelihood of ovulation.
    4 affect the production of estrogen and progesterone
    Whether the growth hormone affects the secretion of sex hormones is still controversial.
    The growth hormone-containing culture medium cultured granulosa cells and inner follicular cells of porcine follicles in vitro, and the results showed that growth hormone can promote the secretion of estrogen and progesterone; however, when the two cells are co-cultured, whether or not the culture solution is added or not Growth hormone, progesterone production decreased; and the growth hormone secretion decreased more significantly after the addition of growth hormone; but estradiol secretion increased. It was also found that growth hormone enhances the activity of 3β2 hydroxysteroid dehydrogenase (3β2HSD) /Δ5 isomerase. Therefore, growth hormone directly affects the secretion of sex hormones in porcine follicle cells. However, other studies do not support the conclusion that growth hormone affects the activity of related enzymes. In the GHR 2KO mouse model, a decrease in estradiol secretion was observed, but the expression of aromatase and 3β2HSD mRNA was not different from that in normal mice [7]. Another study showed that growth hormone did not affect the expression of P450c17 mRNA and P450 aromatase mRNA in bovine ovary, and therefore did not affect the secretion of sex hormones. Whether the growth hormone affects the ovarian secretion of steroid hormones needs further research.
    5 application of growth hormone in promoting ovulation
    In view of a large number of experiments, nutropin aq growth hormone can stimulate the growth of follicles, the production of ovarian steroid hormones, and enhance the responsiveness of ovaries to FSH. More and more scholars have applied it to the adjuvant treatment of ovulation.
    In animal ovulation induction therapy, growth hormone has a clear auxiliary ovulation induction effect. Gonzalez et al [15] used GH / gonadotropin-releasing hormone agonist (GnRHa) + FSH, FSH and 7 drugs to induce ovulation without any drug, the number of oocytes was 8. 7 0. 9, 6. 8 1. 3 and 4. 5 0. 8 (P < 0.05), the results confirmed that growth hormone increased the number of follicles that responded to FSH, thereby increasing the rate of ovulation. Starbuck et al [16] used recombinant GH combined with artificial insemination to treat cows, and the pregnancy rate was significantly improved (60.3% vs 40.3%, P < 0.05). The pregnancy rate of cows with milk production for more than 100 days increased. Significant (64.3% vs 25.8%). GH has a good auxiliary ovulation effect, which makes it have high application value in the livestock industry.
    In human assisted reproductive therapy, many scholars have also conducted corresponding research. Wang Ying et al [17] reported the use of growth hormone-assisted ovulation therapy in 7 patients with polycystic ovary syndrome (PCO S). The results showed that growth hormone adjuvant therapy reduced HM G dosage, shortened HM G stimulation time, and increased the advantage. The number of follicles. It has been confirmed that growth hormone adjuvant therapy can increase the rate of ovulation. Tesarik et al used GH to assist ovulation treatment in infertile women over 40 years old. The results showed that the number of follicles in the two groups was similar, but the abortion rate of auxin group was lower than that of the control group, and the peak of estrogen, delivery rate and live birth rate were higher than that of the control. group. The results may be related to growth hormone improving follicular developmental potential. From these results, GH has a certain effect in assisting ovulation induction therapy.
    However, other studies have not shown optimistic results. In a large, multicenter, randomized, double-blind study, 96 infertile ovarian-responsive infertile patients received growth hormone-releasing factor-assisted ovulation therapy, and the results showed that growth hormone releasing factor induced a significant increase in endogenous growth hormone. However, the pregnancy rate and abortion rate were similar in the control group (100 patients) who received placebo adjuvant therapy. The pregnancy rates were 8.3% and 8%, respectively, and the abortion rate was 12.5%, 16 %. The results of a meta-analysis of previous growth hormone ovulation therapy by Tarlatzis [19] showed that the efficacy of growth hormone ovulation in the treatment of patients with low ovarian response was not obvious.

From the above data, the efficacy of growth hormone to promote ovulation is still controversial. In summary, the results of animal experiments confirmed the presence of growth hormone receptors on the ovary, growth hormone involved in the regulation of ovarian function, but its specific regulation mechanism is not very clear, especially the mechanism of action on antral follicles. Although transgenic animal models provide information on the effects of growth hormone on morphological changes in the ovary, how these changes are induced requires further investigation. Due to species differences, the conclusions of animal experiments cannot be directly applied to humans; there is still a lack of basic research on the relationship between human growth hormone and ovarian function; in clinical applications, the application value of growth hormone in assisting superovulation therapy is still controversial, but Two distinct conclusions may be related to the selection of different subjects and different experimental methods. According to the results of animal experiments, growth hormone mainly affects the early stage of follicular development–the pre-anterior follicular stage. However, in ovulation induction therapy, growth hormone is generally used in synchrony with gonadotropin in the early follicular phase. Therefore, it is only It acts on the antral follicle stage and is not enough to affect the antral follicles. If you change the timing of the use of growth hormone, prolonging the use of time may improve the efficacy of its ovulation induction therapy. But a large number of random double-blind studies are needed to confirm this idea. In addition, the doses of growth hormone-assisted ovulation therapy provided by the data need to be different. The appropriate therapeutic dose needs to be further explored, and whether the growth hormone-assisted reproductive offspring has adverse effects still needs long-term follow-up evaluation.