Questions. Diabetes mellitus and pregnancy. Which risk is considered low and which is considered high?

Hi all! Girls who were in similar situations, respond! On May 27th I had my first screening. The ultrasound showed everything was normal. They wrote down the phone number just in case, but I didn’t expect that they might call me back, and then a week later I got a call - come for a referral to the Center for Psychological Surveillance, you are at high risk. I don’t remember myself, I arrived in tears, on weak legs, and took all the papers. Risk 1:53. The next day I went for further examination. The ultrasound specialist looked at both the abdomen and vagina for a very long time, turned on the Doppler several times, and everything seemed to be fine, but he didn’t like DOPPLER METRY OF THE TRISCUPID VALVE: REGURGITATION. I entered the new ultrasound data into the program and the screening results from a week ago, the computer showed a diabetes risk of 1:6. I sent him to a geneticist. After looking at the conclusion, she explained to me that this regurgitation could simply be a feature of the fetus, but coupled with an underestimated PAPP-A indicator - 0.232 MoM, this is a marker of chromosomal abnormalities. Everything else is within normal limits. They suggested undergoing a chorionic villus biopsy. I refused for now, the nurse almost fell out of her chair, like the risk is so high and CA cannot be treated, and if she were me, she wouldn’t even think for a minute. I asked a geneticist about the Panorama analysis (a terribly expensive genetic analysis of maternal blood), she told me that of course you can do it, but it excludes only 5 main CAs and several very rare ones, it cannot completely exclude anomalies, and in my case it is recommended invasion. I’ve already read a ton of articles, questions and the like on this topic, and I just don’t understand what they found so terrible in my analyzes? Regurgitation, as it turned out, is physiological at this stage and goes away by 18-20 weeks (if it doesn’t go away, this indicates a risk of heart defects, for many it goes away after childbirth, and some live with it and doesn’t affect anything. Moreover, the husband has prolapse mintral valve, which was inherited from my mother, maybe this is somehow connected). Hormones may not be indicative at all, because... I’ve been taking it since the beginning of pregnancy, I ate 2 hours before the test (it turns out you can’t eat 4 hours before, they didn’t tell me about it), drank coffee, was nervous and worried about the ultrasound and I’m afraid to donate blood, and Lately chronic fatigue, I’m tired with my older child. And all this affects the results. The geneticist didn’t ask anything of the kind, wasn’t interested, they actually have some kind of conveyor belt there, and it was as if they shoved me there for statistics. But they planted a bit of doubt in me, I cried and was not worried about the year ahead. My husband is trying to persuade me to have a biopsy. I am terribly afraid of the consequences, afraid of losing or harming the child, especially if he is healthy. On the one hand, if everything is fine, I will breathe a sigh of relief and send all the doctors away. On the other hand, if everything is bad, what should you do? Will I be able to terminate the pregnancy, allow my child to be dismembered inside me, especially now that it seems to me that I am beginning to feel him. But another option is whether I can raise a child who needs special approach and a lot of attention, when sometimes you want to run away from your completely healthy daughter... Damn, all these thoughts are eating me up. I don’t know what to do... Just in case, I’ll give you the screening data:

Delivery period: 13 weeks

Heart rate 161 beats/min

Ductus venosus PI 1.160

Chorion/placenta low on the anterior wall

Umbilical cord 3 vessels

Fetal anatomy: everything is determined, everything is normal

b-hCG 1.091 MoM

PAPP-A 0.232 MoM

Uterine artery PI 1,240 MoM

Trisomy 21 1:6

Trisomy 18 1:311

Trisomy 13 1:205

Preeclampsia up to 34 weeks 1:529

Preeclampsia up to 37 weeks 1:524

Diabetes is complex disease, which is difficult to treat. When it develops in the body, carbohydrate metabolism is disrupted and insulin synthesis by the pancreas is reduced, as a result of which glucose ceases to be absorbed by cells and settles in the blood in the form of microcrystalline elements. The exact reasons why it begins to develop this disease, scientists have not yet been able to establish. But they identified risk factors for diabetes mellitus that can trigger the onset of this disease in both older and younger people.

A few words about pathology

Before considering the risk factors for developing diabetes, it must be said that this disease has two types, and each of them has its own characteristics. Type 1 diabetes is characterized by systemic changes in the body, in which not only carbohydrate metabolism, but also the functionality of the pancreas. For some reason, its cells stop producing insulin in the required quantity, as a result of which the sugar that enters the body along with food does not undergo breakdown processes and, accordingly, cannot be absorbed by the cells.

Type 2 diabetes mellitus is a disease in which the functionality of the pancreas is preserved, but due to impaired metabolism, the body's cells lose sensitivity to insulin. Against this background, glucose simply stops being transported into cells and settles in the blood.

But no matter what processes occur during diabetes mellitus, the result of this disease is the same - high levels of glucose in the blood, which leads to serious problems with health.

The most common complications of this disease are the following conditions:

• hyperglycemia – an increase in blood sugar levels beyond normal limits (over 7 mmol/l);
• hypoglycemia – a decrease in blood glucose levels beyond normal limits (below 3.3 mmol/l);
• hyperglycemic coma – increased blood sugar levels over 30 mmol/l;
• hypoglycemic coma – a decrease in blood glucose levels below 2.1 mmol/l;
• diabetic foot – decreased sensitivity lower limbs and their deformation;
• – decreased visual acuity;
• thrombophlebitis - the formation of plaques in the walls of blood vessels;
• hypertension - increased blood pressure;
• gangrene – necrosis of tissues of the lower extremities with subsequent development of an abscess;
• stroke and myocardial infarction.

Common complications of diabetes

These are not all the complications that the development of diabetes mellitus poses to a person at any age. And in order to prevent this disease, it is necessary to know exactly what factors can provoke the occurrence of diabetes and what measures include prevention of its development.

Type 1 diabetes mellitus and its risk factors

Type 1 diabetes mellitus (T1DM) is most often diagnosed in children and young people aged 20-30 years. It is believed that the main factors of its development are:

• viral diseases;
• intoxication of the body;
• poor nutrition;
• frequent stress.

In the occurrence of T1DM main role Hereditary predisposition plays a role. If one of the family members suffers from this disease, then the risk of its development in the next generation is approximately 10-20%.

It should be noted that in in this case we're talking about not about established fact, but about predisposition. That is, if a mother or father has T1DM, this does not mean that their children will also be diagnosed with this disease. Predisposition suggests that if a person does not carry out preventive measures and does not correct image om life, then he has a high risk of becoming diabetic within a few years.

When both parents are diagnosed with diabetes at once, the risk of developing the disease in their children increases several times.

However, even in this case, it is necessary to take into account that if both parents suffer from diabetes, then the likelihood of it developing in their child increases significantly. And it is often in such situations that this disease is diagnosed in children as early as school age, although they don't have yet bad habits and lead active image life.

It is believed that diabetes mellitus is most often “transmitted” through the male line. But if only the mother has diabetes, then the risks of giving birth to a baby with this disease are very low (no more than 10%).

Viral diseases

Viral diseases are another reason why T1DM can develop. Particularly dangerous in this case are diseases such as mumps and rubella. Scientists have long proven that these diseases negatively affect the functioning of the pancreas and lead to damage to its cells, thus reducing the level of insulin in the blood.

It should be noted that this applies not only to already born children, but also to those who are still in the womb. Any viral diseases that a pregnant woman suffers can trigger the development of T1DM in her child.

Intoxication of the body

Many people work in factories and businesses that use chemical substances, the action of which negatively affects the functioning of the entire body, including the functionality of the pancreas.

Chemotherapy, which is used to treat various oncological diseases, also have a toxic effect on the body’s cells, so their implementation also increases the likelihood of developing T1DM in humans several times.

Poor nutrition

Poor nutrition is one of the most common causes of T1DM. Daily diet modern man contains great amount fats and carbohydrates, which puts a strong strain on digestive system, including the pancreas. Over time, its cells are damaged and insulin synthesis is disrupted.

Poor nutrition is dangerous not only for the development of obesity, but also for disruption of the pancreas.

It should also be noted that due to poor nutrition, T1DM can also develop in children aged 1-2 years. And the reason for this is the early introduction into the baby’s diet. cow's milk and cereal crops.

Frequent stress

Stress is a trigger various diseases, including T1DM. If a person experiences stress, his body produces a lot of adrenaline, which promotes the rapid processing of sugar in the blood, resulting in hypoglycemia. This condition is temporary, but if it occurs systematically, the risk of developing T1DM increases several times.

Type 2 diabetes mellitus and its risk factors

As mentioned above, type 2 diabetes mellitus (T2DM) develops as a result of decreased sensitivity of cells to insulin. This can also happen for several reasons:

• hereditary predisposition;
• age-related changes in organism;
• obesity;
• gestational diabetes.

Hereditary predisposition

In the development of T2DM, hereditary predisposition plays an even greater role than in T1DM. Statistics show that the risk of developing this disease in offspring in this case is 50% if T2DM was diagnosed only in the mother, and 80% if this disease was diagnosed in both parents at once.

When parents are diagnosed with T2DM, the likelihood of having a sick child is significantly higher than with T1DM

Age-related changes in the body

Doctors consider T2DM a disease of older people, since it is in them that it is most often detected. The reason for this is age-related changes in the body. Unfortunately, with age, under the influence of internal and external factors internal organs“wear out” and their functionality is impaired. In addition, as many people age, hypertension develops, which further increases the risk of developing T2DM.

Important! In view of all this, doctors highly recommend that all people over 50 years of age, regardless of general well-being and gender, regularly take tests to determine blood sugar levels. And if any abnormalities are detected, begin treatment immediately.

Obesity is the main cause of T2DM in both older and younger people. The reason for this is the excess accumulation of fat in the cells of the body, as a result of which they begin to draw energy from it, and sugar becomes unnecessary for them. Therefore, with obesity, cells stop absorbing glucose, and it settles in the blood. And if a person is available overweight body also leads a passive lifestyle, this further increases the likelihood of developing T2DM at any age.

Obesity provokes the appearance of not only T2DM, but also other health problems

Gestational diabetes

Gestational diabetes is also called “pregnant diabetes” by doctors, as it develops during pregnancy. Its occurrence is due hormonal disorders in the body and excessive activity pancreas (she has to work for “two”). Because of increased loads it wears out and stops producing insulin in the required quantities.

After childbirth, this disease goes away, but leaves a serious mark on the child’s health. Due to the fact that the mother's pancreas stops producing insulin in the required amount, the child's pancreas begins to work at an accelerated rate, which leads to damage to its cells. Moreover, with the development gestational diabetes the risk of obesity in the fetus increases, which also increases the risk of developing T2DM.

Prevention

Diabetes mellitus is a disease whose development can be easily prevented. To do this, it is enough to constantly carry out its prevention, which includes the following measures:

• Proper nutrition. Human nutrition should include many vitamins, minerals and proteins. Fats and carbohydrates must also be present in the diet, since without them the body cannot function normally, but in moderation. You should especially beware of easily digestible carbohydrates and trans fats, since they are the main cause of excess body weight and further development SD. As for infants, parents should ensure that the complementary foods introduced are as beneficial as possible for their body. You can find out what you can give your baby and in what month from your pediatrician.
• Active lifestyle. If you neglect sports and lead a passive lifestyle, you can also easily “earn” diabetes. Human activity promotes rapid fat burning and energy consumption, resulting in an increased cell need for glucose. In passive people, metabolism slows down, resulting in an increased risk of developing diabetes.
• Monitor your blood sugar levels regularly. This rule especially applies to those who have hereditary predisposition to this disease, and people who have turned 50 years old. To monitor your blood sugar levels, it is not at all necessary to constantly go to the clinic and get tested. You just need to purchase a glucometer and conduct blood tests yourself at home.

It should be understood that diabetes is a disease that cannot be cured. As it develops, you have to constantly take medications and give insulin injections. Therefore, if you do not want to always be in fear for your health, healthy image life and promptly treat any diseases that arise. This is the only way to prevent the occurrence of diabetes and maintain your health for many years!

Genetics of diabetes mellitus

Prediction of type 1 diabetes in high-risk groups

T.V. Nikonova, I.I. Dedov, J.I.P. Alekseev, M.N. Boldyreva, O.M. Smirnova, I.V. Dubinkin*.

Endocrinological science Center I (director - academician of RAMS I.I. Dedov) RAMS, I *SSC “Institute of Immunology” I (director - academician of RAMS R.M. Khaitov) M3 RF, Moscow. I

Currently, there is an increase in the incidence of type 1 diabetes throughout the world. This is due to a number of factors, including an increase in the life expectancy of patients with diabetes due to improved diagnostic and medical care, increased fertility and worsening environmental situations. The incidence of diabetes can be reduced by preventive measures, predicting and preventing the development of the disease.

Predisposition to type 1 diabetes is genetically determined. The incidence of type 1 diabetes is controlled by a number of genes: the insulin gene on chromosome 11p15.5 (YOM2), genes on the chromosome \\ts (YOM4), 6ts (YOM5). Highest value of the known genetic markers of type 1 diabetes, they have the genes of the HLA region on chromosome 6p 21.3 (SHOM1); up to 40% of the genetic predisposition to type 1 diabetes is associated with them. No other genetic region determines the risk of developing the disease comparable to HLA.

High risk the development of type 1 diabetes is determined by allelic variants of the HLA genes: OYAB1*03,*04; OOA1 *0501 ,*0301, OOB1*0201, *0302 . 95% of patients with type 1 diabetes have OT*3 or 011*4 antigens, and from 55 to 60% have both antigens. The OOB1*0602 allele is rare in type 1 diabetes and is considered protective.

Clinical manifestations of diabetes are preceded by latent period, characterized by the presence of islet markers cellular immunity; these markers are associated with progressive destruction.

Thus, for family members with a history of type 1 diabetes, disease prognosis is especially important.

The purpose of this work was to form groups at high risk of developing type 1 diabetes in the Russian population of Moscow residents based on the study of genetic, immunological and metabolic markers of diabetes using a family approach.

Materials and research methods

We examined 26 families in which one of the parents has type 1 diabetes, of which 5 were “nuclear” families (101 people in total). The number of family members surveyed ranged from 3 to 10 people. There were 13 fathers with type 1 diabetes, and 13 mothers with type 1 diabetes. There were no families in which both parents had type 1 diabetes.

37 descendants of patients with type 1 diabetes without clinical manifestations diseases, of which 16 were female, 21 were male. The age of the examined offspring ranged from 5 to 30 years. The distribution of examined offspring by age is presented in Table. 1.

Table 1

Age of examined children (descendants)

Age (years) Number

In families with diabetic mothers, 17 children (8 girls, 9 boys) were examined, in families with diabetic fathers - 20 children (8 girls, 12 boys).

Autoantibodies to (3-cells (ICA) were determined in two ways: 1) on cryosections of the human pancreas of blood group I (0) in an indirect immunofluorescence reaction; 2) in the immunoenzyme test “ISLETTEST” from “Biomerica”. Insulin autoantibodies (IAA) were determined in enzyme immunoassay test"ISLETTEST" from Biomerica. Determination of antibodies to HDK was carried out using standard sets“Diaplets anti-GAD” from Boehringer Mannheim.

The determination of C-peptide was carried out using standard kits from Sorrin (France).

HLA typing of patients with diabetes and their family members was performed for three genes: DRB1, DQA1 and DQB1 using sequence-specific primers using polymerase chain reaction(PCR).

Isolation of DNA from lymphocytes peripheral blood carried out according to the method of R. Higuchi N. Erlich (1989) with some modifications: 0.5 ml of blood taken with EDTA was mixed in 1.5 ml Eppendorf microcentrifuge tubes with 0.5 ml of lysis solution consisting of 0. 32 M sucrose, 10 mM Tris - HC1 pH 7.5, 5 mM MgC12, 1% Triton X-100, centrifuged for 1 min at 10,000 rpm, the supernatant was removed, and the cell nucleus pellets were washed 2 times with the indicated buffer. Subsequent proteolysis was carried out in 50 μl of a buffer solution containing 50 mM KCI, 10 mM Tris-HC1 pH 8.3, 2.5 mM MgCI2, 0.45% NP-40, 0.45% Tween-20 and 250 μg/ml proteinase K at 37°C for 20 minutes. Proteinase K was inactivated by heating in a solid-state thermostat at 95°C for 5 min. The resulting DNA samples were immediately used for typing or stored at -20°C. The DNA concentration determined by

fluorescence with Hoechst 33258 on a DNA fluorimeter (Hoefer, USA) averaged 50-100 μg/ml. Total time DNA extraction procedure lasted 30-40 minutes.

PCR was carried out in a 10 μl reaction mixture containing 1 μl of DNA sample and the following concentrations of the remaining components: 0.2 mM each dNTP (dATP, dCTP, dTTP and dGTP), 67 mM Tris-HCl pH=8.8, 2.5 mM MgC12 , 50 mM NaCl, 0.1 mg/ml gelatin, 1 mM 2-mercaptoethanol, and 1 unit of thermostable DNA polymerase. To prevent changes in the concentrations of the components of the reaction mixture due to the formation of condensate, the reaction mixture was covered with 20 μl of mineral oil (Sigma, USA).

Amplification was carried out on a multichannel thermal cycler "MS2" (JSC DNA-Technology, Moscow).

Typing of the DRB1 locus was carried out in 2 stages. During the 1st round, genomic DNA was amplified in two different tubes; in the 1st tube a pair of primers was used that amplified all known alleles of the DRB1 gene, in the 2nd tube a pair of primers was used that amplified only alleles included in the groups DR3, DR5, DR6, DR8. In both cases temperature regime amplification (for the “MC2” thermal cycler with active regulation) was as follows: 1) 94°C - 1 min.; 2) 94°С - 20 s (7 cycles), 67°С - 2 s; 92“C - 1 s (28 cycles); 65°C - 2 s.

The resulting products were diluted 10 times and used in the 2nd round at the following temperature conditions: 92°C - 1 s (15 cycles); 64°C - 1 s.

Typing of the DQA1 locus was carried out in 2 stages. At the 1st stage, a pair of primers was used, amplifying all specificities of the DQA1 locus; at the 2nd stage, pairs of primers were used, amplifying the specificities *0101, *0102, *0103, *0201, *0301, *0401, *0501, *0601 .

The first stage was carried out according to the program: 94 “C - 1 minute; 94°C - 20 s (7 cycles), 58"C - 5 s; 92"C - 1 s, 5 s (28 cycles), 56"C - 2 s.

The amplification products of the 1st stage were diluted 10 times and used at the 2nd stage: 93“C - 1 s (12 cycles), 62“C - 2 s.

Typing of the DQB1 locus was also carried out in 2 stages; on the 1st, a pair of primers was used that amplified all the specificities of the DQB1 locus, the temperature regime was as follows: 94°C - 1 min.; 94°C - 20 s. (7 cycles); 67°C - 5 s.; 93°C - 1 s (28 cycles); 65HP - 2 s.

At the 2nd stage, primer pairs were used that amplified specificities: *0201, *0301, *0302, *0303, *0304, *0305, *04, *0501, *0502, *0503, *0601, *0602/ 08; The products of the 1st stage were diluted 10 times and amplification was carried out in the following mode: 93°C - 1 s. (12 cycles); 67°C - 2 s.

Identification of amplification products and their length distribution was carried out in ultraviolet light (310 nm) after electrophoresis for 15 min either in 10% PAAG, 29:1 at a voltage of 500 V, or in 3% agarose gel at a voltage of 300 V (in both cases, run was 3-4 cm) and stained with ethidium bromide. Digest of plasmid pUC19 with Msp I restriction enzyme was used as a length marker.

Results and its discussion

It was found that in 26 families of 26 parents with type 1 diabetes, 23 people (88.5%) are carriers of the HLA genotypes associated with type 1 diabetes DRB1 *03- DQA1 *0501 - DQB1 *0201; DRB1 *04-DQAl *0301-DQB 1*0302 or their combinations (Table 2). In 2 patients, the genotype contains the DQB 1*0201 allele, associated with type 1 diabetes; only 1 patient in this group had the DRB1 *01 /01 genotype, which

Distribution of genotypes among parents with type 1 diabetes

01?B 1 4/4 2 E1?B 1 - -

Total 23 (88.5%) Total 3

0I?B1-POAI-ROI haplotypes found in the examined individuals

oigvi oaii rovi

In population studies, which was not associated with type 1 diabetes, we did not distinguish subtypes of OK B1 *04, although the polymorphism of this locus may affect the risk of developing type 1 diabetes.

When genotyping the direct descendants of patients with type 1 diabetes, it was revealed that out of 37 people, 30 (81%) inherited the genotypes OYAV1*03, 011B1*04 and their combination associated with type 1 diabetes; 3 individuals had alleles associated with type 1 diabetes in their genotype : in 1 - TOA 1*0501, in 2 patients - TOA 1*0201. A total of 4 out of 37 subjects had a neutral genotype in relation to type 1 diabetes.

The distribution of offspring genotypes is shown in Table. 3. A number of studies have noted that fathers with type 1 diabetes are more likely to pass on a genetic predisposition.

susceptibility to diabetes (in particular, HLA-01*4 geno-types) in their children than in their mothers. However, a study in the UK did not confirm a significant effect of parental gender on HLA-dependent predisposition in children. In our work, we also cannot note a similar pattern of transmission of genetic predisposition: 94% of children inherited HLA genotypes associated with type 1 diabetes from sick mothers and 85% from sick fathers.

DM is known to be a multigene, multifactorial disease. As factors external environment, playing the role of a trigger, nutrition is considered - consumption in infancy and early childhood cow's milk proteins. De-

Table 3

Distribution of genotypes among children whose parents have type 1 diabetes

Genotypes associated with type 1 diabetes Number of carriers Genotypes not associated with type 1 diabetes Number of carriers

0!*B 1 4/4 4 01*B 1 1/15 1

Total 30 (81%) Total 7 (19%)

those with newly diagnosed diabetes have elevated levels antibodies to cow's milk protein, p-lactoglobulin and bovine serum albumin compared to healthy siblings, which is regarded as an independent risk factor for the development of diabetes.

In the group of 37 children examined, only 4 were at breastfeeding up to 1 year, 26 people received breast milk up to 1.5-3 months, 4 - up to 6 months, 3 were on formula milk from the first weeks of life. Of the 5 children with positive antibodies to β-cells, 2 were breastfed for up to 6 months, 3 for up to 1.5 - 3 months; then kefir and milk mixtures were obtained. Thus, 89% of the examined children received cow's milk proteins in infancy and early childhood, which can be regarded as a risk factor for the development of diabetes in genetically predisposed individuals.

In the examined families, clinically healthy offspring were assessed for cytoplasmic antibodies, autoantibodies to insulin and HDK. Of the 37 examined, 5 children turned out to be positive for the presence of antibodies to β-cells, while all 5 are carriers of a genetic predisposition to diabetes (Table 4). 3 of them (8%) had antibodies to HDK, 1 - to ACTC, 1 - antibodies to ACTC

Table 4

Genotypes of children positive for antibodies to (3-cells

Genotype Number of antibody positive

and insulin. Thus, 5.4% of children have antibodies to ACTC; 2 children with positive antibodies to HDC are descendants of “nuclear” families. The age of the children at the time of detection of antibodies is indicated in Table. 5. To predict diabetes great importance have ACTC titer levels: the higher the antibody titer, the more likely development of diabetes, the same applies to antibodies to insulin. According to the literature, high levels antibodies to HDK are associated with a slower rate of development of diabetes (10% at 4 years) than low levels(50% at 4 years), possibly because high levels of anti-HDC antibodies indicate “preferential” activation humoral immunity and to a lesser extent on the activation of cell-mediated

Table 5

Age of examined children at the time of detection of antibodies

Age of children examined (years) Number of children positive for antibodies

bathed immunity (type 1 diabetes is mainly caused by cell-mediated destruction of P cells by cytotoxic T lymphocytes). A combination of different antibodies provides the most optimal level of prediction.

Children with low birth weight (less than 2.5 kg) develop diabetes much earlier than children born with normal weight. From the anamnesis data, it is noteworthy that out of 5 children with positive antibodies, 2 were born with a body weight of more than 4 kg, 2 - less than 2.9 kg.

In direct descendants of patients with type 1 diabetes, the basal level of C-peptide was determined; in all of them this indicator was within the normal range (including children with positive antibodies to P-cells); a study of the level of stimulated C-peptide was not carried out.

1. Patients with type 1 diabetes in 88.5% of cases are carriers of the genotypes OYAVROZ, OOA1*0501, BOV1*0201, OYAV1*04, BOA1*0301, EOV1*0302, or their combinations.

2. In children from families where one of the parents has type 1 diabetes, in 89% of cases a genetic predisposition to diabetes is detected (in the presence of one sick parent), while 81% inherit genotypes completely associated with type 1 diabetes, which allows them to be considered group at very high risk of developing diabetes.

3. Among the direct descendants of patients with type 1 diabetes who have genetic predisposition, positive antibodies to GDC were detected in 8% of cases, ACTC - in 5.4% of cases. These children need diagnostic test antibody titers, glycohemoglobin and study of insulin secretion.

*1 iteration

1. Atkinson M.A., McLaren N.K. // N.Engl.J.Med.-l 994 -331. P.l 4281436.

2. Aanstoot H.J., Sigurdsson E., Jaffe M. et al // Diabetologia-1994-37.

3. Baekkeskov S., Aanstoot H.J., Christgan S. et al // Nature-1 990-377.

4. Bain S.C., Rowe B.R., Barnett A.H., Todd J.A. // Diabetes-1994-43(12). P. 1432-1468.

5. B/ng/ey P.J., Christie M.R., Bonifacio E., Bonfanti R., Shattock Mw Fonte M.T., Bottazzo C.F. // Diabetes-1 994-43. P. 1304-1310.

6. Boehn B.O., Manifras B., Seibler J. et al // Diabetes-1991-40. P.1435-1439.

7. Chern M.M., Anderson V.E., Barbosa J. // Diabetes-1982-31. P.l 1 151118.

8. Davies J.L., Kawaguchi Y., Bennett S.T. et al. // Nature-1994-371.

9. Erlich H.A., Rotter J.I., Chang J. et al. // Nature Gen.-1993-3. P.358-364.

10. Hahl J., Simell T., Ilonen J., Knip M., Simmel O. // Diabetologia-1 99841. P.79-85.

11. Harrison L.C., Honeyman M.C., DeAizpurua H.J. et al // Lancet-1993341. P.l 365-1369.

12. Hashimoto L., Habita C., Beresse J.P. et al. // Nature-1994-371. P.161-164.

1 3. Karjalainen J., Martin J.M., Knip M. et al // N.Engl.J.Med.-l 992-327. P.302-303.

14. Khan N., Couper T.T., // Diabetes Care-1994-17. P. 653-656.

15. Landin-OIsson M., Palmer J.P., Lernmark A. et al // Diabetologia-1992-40. P.l068-1 073.

16. Leslie R.D.C., Atkinson M.A., Notkins A.L. // Diabetologia-1999-42. P.3-14.

17. Levy-Marchal C., Dubois F., Neel M., Tichet J., Czernichow P. // Diabetes-1995-44. P.1029-1032.

1 8. Lorenzen T., Pociot F., Hougaard P., Nerup J. // Diabetologia-1994-37. P.321-321.

19. Lorenzen T„ Pociot F., Stilgren L. et al // Diabetologia-1998-41. P.666-673.

20. Nepom G., Erlich H.A. // Ann.Rev.Immunol.-1 991-9. P.493-525.

21. Nerup J., Mandrup-Poulsen T., Molvig J. // Diabetes Metab. Rev.-1987-3. P.779-802.

22. Owerbach D., Gabbay K.H. // Diabetes-1995-44.p.l 32-136.

23. PociotF. U Dan.Med.Bull.-l996-43. P.216-248.

24. Rewers M., Bugawan T.L., Norris J.M., Blair A. et al. // Diabetologia-1996-39. P.807-812.

25. Rei/onen H., Ilonen J., Knip N., Akerblom H. // Diabetes-1 991-40.

26. Saukkonen T., Virtanen S.M., Karppinen M. et al // Diabetologia-1998-41. P.72-78.

27. Schatz D., Krischer J., Horne G. et al. // J. Clin. Invest.-1994-93. P.2403-2407.

28. Spielman R.S., Baker L, Zmijewski C.M. //Ann. Hum. Genet.-1980-44. P. 135-150.

29. Thivolet C., Beaufrere B., Gebuhrer Y., Chatelain P., Orgiazzi J. // Diabetologia-1991-34. P.l86-191.

30. Tillil H., Kobberling J.// Diabetes-1982-36. P.93-99.

31. ToddJ.A. U Proc. Natl. Acad. Sci. USA-1990-377. P.8560-8565.

32. ToddJ.A., Farral M. // Hum.Mol.Gen.-5. P.1443-1448.

33. Tuomilehto J., Zimmet P., Mackay I.R. et al // Lancet-1994-343.

34. Van der Anvera B., Van Waeyenberge C., Schuit F. et al. // Diabetes-1995-44. P.527-530.

35. Walker A., ​​Goodworth A.G. // Diabetes-1980-29. P.1036-1039.

36. Warram J., Krolewski A.S., Gottlieb M., Kahn C.R. // N.Engl.J.Med.-1984-311. P.149-151.

37. Ziegler A.G., Herskowitz R.D., Jackson R.A. et al // Diabetes Care-1990-13. P.762-775.

Oh, girls, I don’t even know where to start. I never thought that I would find myself in such a situation. Two years ago I really wanted to get pregnant, but it didn’t work out. I went through doctors, ultrasounds, hormone tests - in the end they said that I had severe ovarian dysfunction, and there was no talk of pregnancy. I was worried, but not very much. After all, I have three daughters.
For two years I was regularly checked by a gynecologist and had ultrasounds done. The last time was in February 2017. Then they couldn’t even find one of my ovaries, they said that I was almost starting menopause. In March, I was offered a job that I had been waiting for for three years. I was happy - both the salary and the position were good. And in April my period did not come. Well, delay and delay. Moreover, I have a cycle Last year was from 24 to 27 days. On day 29 I couldn’t stand it - I took a test, Two stripes. I couldn’t believe it for a long time, I bought a few more - two strips. Joy and shock (what will I say at work?). I ran to take hCG. He confirmed that she was 4 weeks pregnant. Until 8 weeks I lived in a frenzy. I took the hCG test every week, I was afraid of an ectopic (ultrasound at 5 weeks refuted my worries), I was afraid of a frozen one. At 8 weeks I did another ultrasound, listened to the baby’s heartbeat, everything was normal - I calmed down. And at 12 weeks the first screening. Ultrasound is normal, the blood test came back bad on Thursday, the risk of diabetes is 1:43. On Friday I already saw a geneticist, she insists on a placenta puncture. Made an appointment for July 11th. God, I'm so scared!!! I'm not so much afraid of the procedure as of its result.
In my life, I have never had an abortion, I haven’t had a miscarriage, and what’s more, I haven’t even given birth myself. I just can’t imagine how I can go to IR if everything turns out to be true. I try to control myself, but sometimes it really hits me. I have a feeling that the verdict has already been read out and the ax has already been raised over me.
I didn’t write about the tests. My hCG is 1.158 MoM (37.9 IU), and PAPP is 0.222 MoM (0.837 IU). TVP 1.91 mm, KTR 73.3 mm.
I just ask for prayers and support, I don’t know how to live to see the results. I want to do another ultrasound this week, although everyone says that it is no longer informative at 15 weeks.

RS: Girls, thank you all for your support. I just had another paid ultrasound. The doctor looked at it for a long time and said that according to the ultrasound, she did not see any developmental defects at all, including those that are typical for children with diabetes. I know that ultrasound cannot guarantee 100% absence genetic disorders, but still a little lighter on the soul. I asked about the puncture. The doctor said that the uterus is not in good shape and the cervix is ​​of good length, i.e. there are no contraindications if I still decide to go for a puncture. And yes, I have a boy according to the ultrasound. Now I'll think about the puncture.

Diabetes mellitus is a serious, serious disease. Beach modern society. Every year, there are more and more cases of this disease being detected, and the saddest thing is that it also affects children.

There are two types: diabetes type 1 and type 2. Type 2 diabetes mostly affects older people or those who are overweight. Their main treatment is rational nutrition and little physical activity.

The first type of diabetes is diagnosed in childhood or adolescence, when hormonal development teenager, but maybe later. With such diabetes, the main thing is insulin injections every day, as well as a strict routine and self-restraint.

In type 1 diabetes, the pancreas slowly “depletes itself”, insulin production decreases, glucose enters the blood large quantities and part of it comes out through human urine.

Doctors need to test the blood for glucose and urine to make a diagnosis. The appearance of type 1 diabetes mellitus has certain prerequisites or, more simply put, factors that influence this disease. These factors must be known in order to avoid the disease and possible complications.

Factors contributing to the appearance of type 1 diabetes

• Heredity. If there is a close relative (mother, father, brother, sister), then the baby’s chances of getting sick increase by 3%, and if one of the parents and a sister (or brother) has diabetes, then the risk increases by 30%.
• Obesity. At initial stages obesity, the risk of developing the disease increases three to five times, and with the third or fourth degree, it increases by 10-30 times.
• Vascular atherosclerosis, hypertension. Surgical treatment or surgical intervention will help avoid complications.
• Pancreatitis. At chronic pancreatitis, which lasts for a long time in the body, serious, irreversible changes appear in the tissues of the pancreas, which also affect the insulin apparatus.
• Endocrine diseases of various nature inhibit insulin production and trigger the pathological process.
• Heart diseases. With this pathology, doctors recommend strictly monitoring blood sugar and adjusting to the right lifestyle.
• Bad ecology. Difficult environmental conditions, the spread of viruses (varicella, mumps, rubella) on a weakened body disrupt the immune system system and, in ultimately lead to this disease.
• Place of residence. In Sweden and Finland people get sick much more often than in other countries.
• Race. Latin Americans and representatives of Asian countries have fewer cases than Europeans.
• Diet. Early feeding breast milk, porridge infant, pediatricians call vitamin D deficiency another additional risk factor for the phenomenon.
• Late labor, preeclampsia (complications during pregnancy).
• Antibodies in the blood against islet cells. If, except hereditary factor, these antibodies are present in a person’s blood, then the chances of getting it will be greater.
• Multiple sclerosis, anemia, may be additional factors development of the disease.
• Stress, long-term depression. Blood sugar increases greatly with prolonged severe stress, and At some point the body cannot cope with such a load.
• Vaccinations in childhood can lead to type 1 diabetes.

Video: Risk factors for developing diabetes mellitus

Unfortunately, there is no complete cure for diabetes. The main treatment is insulin therapy. Many traditional healers It is recommended to engage in special gymnastics, which consists of pole vaulting, running, long jumps, and promotes optimal removal of carbohydrates from the body. And of course, it is necessary to establish proper nutrition.

Unfortunately, still obvious reasons appearance was not detected, but if it is detected on early stages and, knowing all the risk factors for its occurrence, in the future, you can avoid complications or even the disease itself.

Sincerely,