It has been proposed that some components of cow's milk,
as bovine serum albumin or betacaseína could trigger
autoimmune response, as posed by epidemiological data
of Finland, by the increased frequency associated with the introduction DM1
early age of dairy products and high consumption
milk during childhood. However, cross-sectional studies have
found an association, although in the case of betacaseína is
showed T cell proliferation in 51% of diabetic patients
versus 3% of normal subjects (27.31). Similarly, early
exposure to cereals may promote the development of antibodies
against islet cells. Prospective cohort studies in newborn
infants at high risk (given first-degree or genotype
HLA) showed increased risk in those exposed at the age of 3
months, compared to those in age between 4 and 6 months (HR 4.0 to 4.3
and 5.4), in association with cereals containing gluten, also related to the risk of celiac disease (27.31). Some studies, however,
demonstrate a protective role by eating omega
3. Preliminary animal studies support this role by decreasing
the inflammatory response associated with the autoimmune destruction of
beta cells (27,28). Similarly, vitamin D supplements
could have a protective role, apparently associated with polymorphisms
for enzymes involved in metabolism that could interact
with HLA alleles mediated response elements vitamin D
promotra in the region of the HLA-DRB1 * 0301
Tuesday, November 13, 2012
Triggering factors of type 1 diabetes
Together with genetic predisposition have tried to identifytriggering factors of the disease. However, associationsraised had not been fully demonstrated by the apparent needmultiple events that differ in each individual or populationand mechanisms that may present with hit-and-run (hit and run)that leave no trace molecular and therefore is difficult to prove causality,including perinatal and virus due to diet.
Studies in European population identified predisposing factorsas maternal age greater than 25 years, preeclampsia, diseaseneonatal respiratory and jaundice (especially associated with incompatibilityAB0). Protective factors were low birth weight and lowsize. However, the associations were weak, and most importantwhen the disease began before 10 years of age.
Since 1926 has been raised regarding enterovirus, by variationsseasonal onset of diabetes and epidemiological studiesas developed after Coxsackievirus infection epidemicB4 (CVB4) in 1971 on the Pribilof Islands (Alaska). However,no difference in the frequency of monitoring in DM1five years between infected and uninfected subjects. In studiesSubsequent isolation has demonstrated the ability of viralb infect and destroy cells in animal models and in human cellsin vitro, but in autopsy studies have not been shown in the formconsistent commitment by Coxsackie, Epstein-Barr, measles or cytomegalovirus (27.31).
However, functional studies have foundincreased T cell responses to protein in children CVB4DM1 after onset of the disease, including increasedIgM values, and INF to HLA molecules, as part of the responseagainst pancreatic islets. It has also been shown that infectionsenterovirus are 2 times more frequent in siblingsof patients who developed diabetes than those without diabetes, andCoxsackie antibody titers were higher inpregnant women whose children developed DM1 (27,28). It has been postulateda theory of molecular mimicry as a cause of autoimmunity,by the similarity between the protein F2C Coxsackie B4 virus and GAD (autoantigenmain DM1) and the role of apparent contributionHLA-DR3 in the susceptibility, however, the gap between the developmentof the disease and the immune activity peak limitsviral titers utility in the study of patients
Studies in European population identified predisposing factorsas maternal age greater than 25 years, preeclampsia, diseaseneonatal respiratory and jaundice (especially associated with incompatibilityAB0). Protective factors were low birth weight and lowsize. However, the associations were weak, and most importantwhen the disease began before 10 years of age.
Since 1926 has been raised regarding enterovirus, by variationsseasonal onset of diabetes and epidemiological studiesas developed after Coxsackievirus infection epidemicB4 (CVB4) in 1971 on the Pribilof Islands (Alaska). However,no difference in the frequency of monitoring in DM1five years between infected and uninfected subjects. In studiesSubsequent isolation has demonstrated the ability of viralb infect and destroy cells in animal models and in human cellsin vitro, but in autopsy studies have not been shown in the formconsistent commitment by Coxsackie, Epstein-Barr, measles or cytomegalovirus (27.31).
However, functional studies have foundincreased T cell responses to protein in children CVB4DM1 after onset of the disease, including increasedIgM values, and INF to HLA molecules, as part of the responseagainst pancreatic islets. It has also been shown that infectionsenterovirus are 2 times more frequent in siblingsof patients who developed diabetes than those without diabetes, andCoxsackie antibody titers were higher inpregnant women whose children developed DM1 (27,28). It has been postulateda theory of molecular mimicry as a cause of autoimmunity,by the similarity between the protein F2C Coxsackie B4 virus and GAD (autoantigenmain DM1) and the role of apparent contributionHLA-DR3 in the susceptibility, however, the gap between the developmentof the disease and the immune activity peak limitsviral titers utility in the study of patients
Genetic factors type 1 diabetes mellitus
Currently it is well known the requirement of a predispositionspecific gene for the development of DM1. However,genetic correlation evidenced in twins is not complete, sincecorresponds to only 50% in monozygotic twins and is less than 10%in dizygotic. Still, in the long term follow, mostidentical twins with DM1 eventually express autoantibodiesanti-islet and progress to diabetes, although these mayappear until 30 years after the first twin developsdiabetes, which implies that the sensitivity persists for life (27).Multiple genetic polymorphisms are involved in the risk ofDM1, resulting from large genetic association studies, includingCoeliac disease-related loci, but most of thesegenes have small effects and multiple variants that do not allowuse as predictors of risk (27). Rarely should DM1defects by mutation of a single gene. When the form is submittedmonogenic usually accompanied by other autoimmune conditionsaltered regulatory pathways. Examples include syndromeIPEX (immune dysregulation, polyendocrinopathy, enteropathy linkedto X) by Foxp3 gene mutation or autoimmune polyendocrine syndrometype 1 (APS-1) by altering the air transcription factorsevere autoimmune conditions leads to inhibition of expression byperipheral molecules (27). It should highlight the role of CCR5 association,by an insertion of 32 base pairs at a chemokine receptor,with loss of function thereof, and in the case of homozygous,a decrease of 2 times the risk of DM1 (27-29). The main genesrisk involved in the complex are those corresponding to the higher ofcompatibility (MHC) and HLA. The region of chromosome 6p21 (calledlocus IDDM1 insulin dependent diabetes mellitus) is critical todevelopment of many autoimmune diseases, and has been determinedtheir single nucleotide polymorphisms increase somodest risk (OR 1.2 to 1.3) (27,28,30). However, this tendency strengthensthe concept that HLA class II molecules are keysusceptibility, including haplotype DRB1 * 1501-DQA1 * 0102 -DQB1 * 0602, found in over 20% of the population, but only in 1% of patients dominant confers protection againstDM1 (27). In the final spectrum are individuals susceptibilityDR3/4-DQ8 with heterozygous haplotype with increased risk.However, only 30-50% of patients presenting, reflectinggenetic complexity at the DM1 engagement (27,28) (Table 1). The ofInsulin is one of the major genes involved in the developmentof DM1. Located on chromosome 11, its mutations favorRecognition of insulin as an autoantigen and contribute tosusceptibility, since the polymorphism in the promoter region of the gene.Such tandem repeats zone presents variable number (VNTRs)conferring increased risk in the case of VNTR type 1 (repetitionshort) or protective effect in type 3 (long repeats) (27). The genePTPN22, recently identified, encodes a protein tyrosine phosphataselymphoid (LYP), whose allelic variants confer risk in otherautoimmune diseases, acting as part of the signal axis,crucial for the activation of autoreactive T cells in the periphery.Similarly, the CTLA-4 is an allele encoding associated protein 4Cytotoxic T lymphocytes, which is essential for proper regulationnegative immune responses, and mutations have also beenother entities involved in autoimmune lupus erythematosus andrheumatoid arthritis (27,28). Finally, it is estimated that 48% aggregationfamily can claim to known loci, and contributes CMHwith 41%. For example, the brothers with the highest risk HLA DR and DQ(DR3/DR4 heterozygotes) that inherit both HLA identical regionsmay be at risk of developing autoimmunity as high as80%, with a similar risk of diabetes, the lifetime risk isincreases sharply for relatives of individuals with DM1,an average of 6% for their offspring, 5% for siblings and 50%in identical twins (dizygotic if the risk is similar to brothersno twins), compared to 0.4% in patients with no family history90% in first-degree relatives with two types of autoantibodiespositive markers
Context type 1 diabetes mellitus
According to CDC statistics, 23.6 million people in North America
(7.8% of the population) have DM. In 2007 it was made
diagnosis of 1.6 million new cases of diabetes in people
20 years or more, reaching a prevalence of DM1 in residents
United States between 0 and 19 years, from 1.7 / 1,000 population (27). incidence
DM1 overall has increased over the past decades to
5.3% annually in the U.S. If current trends continue, it is expected that
duplication of new cases in European children under 5
between 2005 and 2020, and the prevalence of cases in individuals under
15 years will increase by 70%, a phenomenon characteristic left shift toward a younger age, without being entirely elucidated the factors involved in the phenomenon of growth
pathology (27). The process seems to develop in patients genetically
susceptible triggered by one or more environmental agents, with
progression in months or years during which the patient is
euglycemic asymptomatic, reflecting the large number of B cells
must be destroyed in order to present the state of hyperglycemia
(7.8% of the population) have DM. In 2007 it was made
diagnosis of 1.6 million new cases of diabetes in people
20 years or more, reaching a prevalence of DM1 in residents
United States between 0 and 19 years, from 1.7 / 1,000 population (27). incidence
DM1 overall has increased over the past decades to
5.3% annually in the U.S. If current trends continue, it is expected that
duplication of new cases in European children under 5
between 2005 and 2020, and the prevalence of cases in individuals under
15 years will increase by 70%, a phenomenon characteristic left shift toward a younger age, without being entirely elucidated the factors involved in the phenomenon of growth
pathology (27). The process seems to develop in patients genetically
susceptible triggered by one or more environmental agents, with
progression in months or years during which the patient is
euglycemic asymptomatic, reflecting the large number of B cells
must be destroyed in order to present the state of hyperglycemia
Type 1 diabetes mellitus Classification
Diabetes mellitus type 1 (DM1), which account for 5-10% of all
cases of diabetes, is a chronic autoimmune disease that
characterized by destruction of pancreatic B cells, leading to
absolute insulin deficiency, whereby patients require
exogenous insulin developed diabetic ketoacidosis and if it were not
supplies (25,26). In the specific case of the cellular autoimmune destruction
pancreatic are useful for diagnostic determinations
islet cell autoantibodies (ICA) or other autoantibodies
(antibodies to glutamic acid decarboxylase [antiGAD] insulin,
and IA-2 tyrosine phosphatase and IA2β) in serum. A positive
is indicative of immune-mediated diabetes, since they
present in 85 to 90% of patients, corresponding
5-10% of all diabetes cases (25,27). However, some patients
may lack evidence of autoimmunity and have no
known cause of B cell destruction, which is diabetes
idiopathic, which corresponds to a minimum of cases, especially
in patients with African or Asian ancestry (25,27).
In overall, the disease process occurs before age 30
years there prior consideration as juvenile-onset diabetes,
now recognized that although it can occur at any age.
cases of diabetes, is a chronic autoimmune disease that
characterized by destruction of pancreatic B cells, leading to
absolute insulin deficiency, whereby patients require
exogenous insulin developed diabetic ketoacidosis and if it were not
supplies (25,26). In the specific case of the cellular autoimmune destruction
pancreatic are useful for diagnostic determinations
islet cell autoantibodies (ICA) or other autoantibodies
(antibodies to glutamic acid decarboxylase [antiGAD] insulin,
and IA-2 tyrosine phosphatase and IA2β) in serum. A positive
is indicative of immune-mediated diabetes, since they
present in 85 to 90% of patients, corresponding
5-10% of all diabetes cases (25,27). However, some patients
may lack evidence of autoimmunity and have no
known cause of B cell destruction, which is diabetes
idiopathic, which corresponds to a minimum of cases, especially
in patients with African or Asian ancestry (25,27).
In overall, the disease process occurs before age 30
years there prior consideration as juvenile-onset diabetes,
now recognized that although it can occur at any age.
Gestational diabetes treatment
Support adequate scientific studies that support the factthe treatment of gestational diabetes reduces complicationsand perinatal death is relatively recent. The study ACHOIS (130)demonstrated that treatment of gestational diabetes reducedsignificantly (from 4 to 1%) severe perinatal complications(Death, shoulder dystocia, bone fracture and nerve injury), butwith increased neonatal care admissions, and the mother,more induction of labor, but without the necessity of increasing practicecesareans. In secondary outcomes in the newborn wasSignificantly lower birth weight, fewer large babiesfor gestational age, and fewer macrosomic infants inthe treatment group versus the control group. There is less clarityin the treatment effect in cases of gestational diabetes "lesssevere "and in this regard, some lights came with the publication of the studyLandon (131), which showed no difference in the frequency ofstillbirth or perinatal death or significant decreasecertain neonatal complications (hyperbilirubinemia, hypoglycemia,hyperinsulinemia or trauma at birth), but corroborated the findingsACHOIS in the study (130): significant reduction in birth weight, thenumber of macrosomic newborns and large for gestational age,and mother: fewer cesareans, hypertensive disorders,and less weight gain in pregnancy, in the group treatedversus the control group.
Proper treatment of gestational diabetes should haveas strict glycemic control target that leads to the reduction offetal and maternal complications in pregnancy and childbirth, withproper monitoring of weight gain in pregnancy. TheSelf-monitoring of blood glucose basal and postprandial especially figuresis crucial to guide treatment (122). The goalsglycemic capillary blood are: baseline values 90-99 mg / dL, 1 hourpostprandial <140 mg / dL, 2 hours post prandial <120-127 mg / dL (132),Although these figures are not necessarily accepted by allassociations interested in the subject.
Nutritional management is the mainstay of therapy, and at mostcases may be sufficient to achieve adequate metabolic control (132). If possible, all patients should be sent toassessment by a nutritionist (122.132). Although we will not detail theSpecific aspects of the diet should be taken into account that it mustbe individualized according to the culture, eating habits, physical activity,prepregnancy ideal weight, weight gain, etc.., making adjustmentslater needed to achieve compliance with the targets.Moderate physical activity (eg, walking 30 minutesdaily) has shown benefits in terms of reducing the numbersmaternal blood glucose in some studies. Although the impact of thisexercise in neonatal complications is not yet clear, the exerciseregularly during pregnancy is recommended by the ADA (122) and other organizations (132).As for drug therapy, it is important to mention thatalthough in recent years there has been an increase in publicationssupporting the use of oral hypoglycemic specific asglibenclamide and metformin in pregnancy (133.134), yet the weight of theno evidence to recommend its routine use.Insulin is the drug of choice in gestational diabetes, and isindicated when you can not meet and maintain glycemic targetspreviously mentioned nonpharmacologic measures. Duringpregnancy has approved the use of human insulins (NPH and regular)and short-acting analogues (lispro and aspart, but not glulisine). Notapproved the use of long-acting analogues (glargine and detemir). Themust be strictly individualized therapy.
We suggest you insulin at an average dose of 0.7 IU / kg / day. A common strategydosage is divided into two applications (2/3 in the morningand third before dinner), in the morning dose 2/3 will be NPH andThird is short-acting insulin in the evening dose half will NPHand 1/2 will short-acting insulin. This scheme will logicallyindividual settings according to BMI, the levels ofglycemia and lifestyle
Proper treatment of gestational diabetes should haveas strict glycemic control target that leads to the reduction offetal and maternal complications in pregnancy and childbirth, withproper monitoring of weight gain in pregnancy. TheSelf-monitoring of blood glucose basal and postprandial especially figuresis crucial to guide treatment (122). The goalsglycemic capillary blood are: baseline values 90-99 mg / dL, 1 hourpostprandial <140 mg / dL, 2 hours post prandial <120-127 mg / dL (132),Although these figures are not necessarily accepted by allassociations interested in the subject.
Nutritional management is the mainstay of therapy, and at mostcases may be sufficient to achieve adequate metabolic control (132). If possible, all patients should be sent toassessment by a nutritionist (122.132). Although we will not detail theSpecific aspects of the diet should be taken into account that it mustbe individualized according to the culture, eating habits, physical activity,prepregnancy ideal weight, weight gain, etc.., making adjustmentslater needed to achieve compliance with the targets.Moderate physical activity (eg, walking 30 minutesdaily) has shown benefits in terms of reducing the numbersmaternal blood glucose in some studies. Although the impact of thisexercise in neonatal complications is not yet clear, the exerciseregularly during pregnancy is recommended by the ADA (122) and other organizations (132).As for drug therapy, it is important to mention thatalthough in recent years there has been an increase in publicationssupporting the use of oral hypoglycemic specific asglibenclamide and metformin in pregnancy (133.134), yet the weight of theno evidence to recommend its routine use.Insulin is the drug of choice in gestational diabetes, and isindicated when you can not meet and maintain glycemic targetspreviously mentioned nonpharmacologic measures. Duringpregnancy has approved the use of human insulins (NPH and regular)and short-acting analogues (lispro and aspart, but not glulisine). Notapproved the use of long-acting analogues (glargine and detemir). Themust be strictly individualized therapy.
We suggest you insulin at an average dose of 0.7 IU / kg / day. A common strategydosage is divided into two applications (2/3 in the morningand third before dinner), in the morning dose 2/3 will be NPH andThird is short-acting insulin in the evening dose half will NPHand 1/2 will short-acting insulin. This scheme will logicallyindividual settings according to BMI, the levels ofglycemia and lifestyle
Background gestational diabetes
A fundamental fact, which showed the need to rethinkpreviously employed diagnostic criteria, was the publicationStudy HAPO (Hyperglycemia and Adverse Pregnancy Outcomes) (126), a study that sought to clarify the risk of adverse outcomesassociated with varying degrees of maternal glucose intolerance,but in any case intolerance less severe than that seen in diabetesmanifests mellitus, and wherein the relationship was clearly demonstratedcontinuously feeding glucose levels, even below thegestational diabetes diagnostic figures, with the weight increaseat birth and increased C-peptide levels in the cord bloodumbilical, unable to identify a cutoff point that clearly demarcateglucose critical level above which the risk risesfetal and maternal complications.
Derived from this study, and analyze all available evidencethen, the IADPSG launched new criteria proposedfor diagnosis of gestational diabetes, which had more to dowith fetal and maternal complications than with the probability of occurrencepost-pregnancy diabetes mellitus in the mother. These criteriawere received recently, though with some reservations, by theADA (128).
Previously, the ADA (125) recommended a selective screening inwhere should stratify patient risk for developing diabetesgestational at the first prenatal visit. The evaluation wasperformed only women who did not comply with all thefollowing criteria: age less than 25 years, normal weight, no historyfamily of diabetes (first degree), no history ofdisorders of glucose tolerance, no history of outcomesadverse obstetric and different from ethnic-racial groupshigh risk for diabetes (eg, Hispanic). Womenwho met all the criteria listed, were catalogedlow risk, and did not require further evaluation. Womenhigh risk (obesity, personal history of gestational diabetes,glycosuria, family history of diabetes) should be submitted toa test of oral glucose tolerance. If not confirmedgestational diabetes at the time, the test should be repeated betweenweeks 24 and 28 of gestation. Women of average risk (whichdid not meet the criteria for high or low risk) should be submittedto test oral glucose tolerance, between weeks 24 and 28gestation. The evaluation glucose load (100 or 75 g) couldpreceded by a load of 50 g, non-fasting, and measurementwhen glucose, which selected the patients who should receiveload of 100 g or 75.
Derived from this study, and analyze all available evidencethen, the IADPSG launched new criteria proposedfor diagnosis of gestational diabetes, which had more to dowith fetal and maternal complications than with the probability of occurrencepost-pregnancy diabetes mellitus in the mother. These criteriawere received recently, though with some reservations, by theADA (128).
Previously, the ADA (125) recommended a selective screening inwhere should stratify patient risk for developing diabetesgestational at the first prenatal visit. The evaluation wasperformed only women who did not comply with all thefollowing criteria: age less than 25 years, normal weight, no historyfamily of diabetes (first degree), no history ofdisorders of glucose tolerance, no history of outcomesadverse obstetric and different from ethnic-racial groupshigh risk for diabetes (eg, Hispanic). Womenwho met all the criteria listed, were catalogedlow risk, and did not require further evaluation. Womenhigh risk (obesity, personal history of gestational diabetes,glycosuria, family history of diabetes) should be submitted toa test of oral glucose tolerance. If not confirmedgestational diabetes at the time, the test should be repeated betweenweeks 24 and 28 of gestation. Women of average risk (whichdid not meet the criteria for high or low risk) should be submittedto test oral glucose tolerance, between weeks 24 and 28gestation. The evaluation glucose load (100 or 75 g) couldpreceded by a load of 50 g, non-fasting, and measurementwhen glucose, which selected the patients who should receiveload of 100 g or 75.
Gestational diabetes
The definition of gestational diabetes was until recently
one of the few things that did not generate more discussion, understanding
as any degree of glucose intolerance with onset
or first recognition during pregnancy, regardless of the type
requiring treatment, and the persistence of the condition or not
after pregnancy (122). With the new proposal from the International
Association of Diabetes and Pregnancy Study Groups (IADPSG) (127) is set
new terminology differentiates gestational diabetes
itself of overt diabetes (preexisting diabetes
but hitherto unrecognized) concepts we will need
later.
For over 45 years, O'Sullivan and Mahan (123) established
the criteria for the interpretation of oral tolerance test to
glucose in pregnancy for the diagnosis of gestational diabetes, criteria
that with the changes made 28 years ago by Carpenter
and Coustan (124), remained in use until the end of 2010, being
the hitherto accepted by the American Diabetes Association
(ADA) (125). We should note that the establishment of such criteria
based on the risk of developing diabetes after pregnancy, and not
in identifying women at increased risk of outcomes
adverse perinatal.
one of the few things that did not generate more discussion, understanding
as any degree of glucose intolerance with onset
or first recognition during pregnancy, regardless of the type
requiring treatment, and the persistence of the condition or not
after pregnancy (122). With the new proposal from the International
Association of Diabetes and Pregnancy Study Groups (IADPSG) (127) is set
new terminology differentiates gestational diabetes
itself of overt diabetes (preexisting diabetes
but hitherto unrecognized) concepts we will need
later.
For over 45 years, O'Sullivan and Mahan (123) established
the criteria for the interpretation of oral tolerance test to
glucose in pregnancy for the diagnosis of gestational diabetes, criteria
that with the changes made 28 years ago by Carpenter
and Coustan (124), remained in use until the end of 2010, being
the hitherto accepted by the American Diabetes Association
(ADA) (125). We should note that the establishment of such criteria
based on the risk of developing diabetes after pregnancy, and not
in identifying women at increased risk of outcomes
adverse perinatal.
Management objectives of DM during pregnancy
7.1 Detection of diabetic embryopathy: the leading cause of perinatal morbidity and mortality in patients with pregestational DM are fetal congenital malformations with an incidence between 7.5 and 14.9% (7 to 15 times more frequent than in normal pregnancies) . Morphological changes are the most common cardiovascular (transposition of the great arteries, ventricular septal defects and atrial) and neurological (anencephaly, holoprosencephaly and CNS defects closure). (1, 3, 5).The diabetic patient wishes to become pregnant, should receive adequate preconception counseling. Now, the detection of structural abnormalities (hyperglycemia produced by this during the first eight weeks of pregnancy - critical period) includes:
HbA1C measurement of patient 4 - 6 weeks post-conception: levels above 8.5% is associated with a 20-25% chance of developing fetal anomalies versus 2 - 3.5% when the figures are normal HbA1C (3-4). vaginal ultrasound between 8-10 weeks of pregnancy, especially in those patients with abnormal numbers of HbA1C. Some defects are easily diagnosed by this time (anencephaly, holoprosencephaly). maternal serum alpha-fetoprotein screening (MSAFP) at 16 weeks of gestation. Normally this MSAFP is decreased in diabetic patients and often indicate the need for genetic testing by amniocentesis / cordocentesis. tertiary ultrasound between 18-20 weeks of pregnancy to detect fetal abnormalities not visualized on initial echoes. fetal echocardiography between 24 to 28 weeks gestation7.2 Prenatal: top quality, performing them every 15 days until week 24 and then every week, requesting paraclinical the following: (1) Urinalysis and urine culture: UTIs are more common during pregnancy and are the leading cause of decompensation in the diabetic patient. Be requested in the first prenatal visit and then monthly. BUN - creatinine and uric acid: as indicators of renal function minimum, quarterly. Lipid profile: initial at 24 to 26 weeks gestation and at the end of it HbA1C: at 4-6 weeks after conception and then every month to analyze the quality of metabolic control, keeping it below 7.2%. glycemic monitoring and tests of fetal wellbeing (see below) fundoscopy and EKG: in pregestational DM with vascular compromise ultrasound scans: detecting malformations and assess fetal growth7.3 Strict maternal metabolic control: the mainstay of treatment of gestational diabetes: Tight control of blood glucose during pregnancy, and The early detection of risk factors and / or aggravating s metabolic state (1, 19)Metabolic control objectives are:Avoid symptomatic hypoglycemia Keep the following plasma glycemia:Fasting ------> 65 to <105 mg / dl (ideal <95 mg / dl)Preprandial ------> 70 to 100 mg / dl An hour postprandial ------> <140 mg / dl (ideal <130 mg / dl)Two hours postprandial ------> <120 mg / dl negative ketonuria HbA1C and / or fructosamine: normal lowNow, to achieve the goals of metabolic control should formulate a treatment plan that includes diet, exercise, insulin (if needed) and the management of complications. Diet: is the key or mainstay of therapy in women with gestational diabetes. Weight gain is necessary for proper fetal growth and varies between 8 and 12kg, depending on the weight of the patient prior. Remember that the patient must never lose weight during pregnancy, as this leads to fat mobilization, lipolysis and substances that cross the placenta and have pontenciales teratogenic effects (1). The diet should provide an average of 30-35 cal / kg in patients of average weight and 25 cal / kg in obese patients, divided into three meals and three snacks, emphasizing the refreshment of 22:00 to 23:00 hours to avoid maternal hypoglycemia at dawn (glass of milk and cookies) (15,20). Remember that a gram of protein or H of C provide four calories and one gram of fat provides nine calories. It has been found that by limiting the intake of C to H of 35 to 45% of total calories, more suitably controlling postprandial glycemia (9). regulated and proper exercise is beneficial and safe; releases epinephrine, which increases glucose uptake by the cell and increases the sensitivity of the receivers, keeping blood sugar levels stable. They must walk 10 to 20 minutes after each main meal. Insulin: Insulin requirements increase progressively during pregnancy. In the first quarter are frequent severe hypoglycemia and decrease insulin requirements. During the second quarter, a slight increase occurs monthly, on the third quarter nocturnal hypoglycemia may occur and insulin requirements increase by 50 - 100% above the baseline. The oral hypoglycemic agents are contraindicated for pregnant diabetic control, and that cross the placenta and cause fetal hypoglycemia is severe malformations (1, 5).They must take insulin: DM1 and DM2's always to become pregnant Among patients with GDM, the White group A2 modified by Freinkel (fasting glucose between 105 and 129 mg / dl) and group B (fasting glucose> 130 mg / dl), andThose patients with GDM (15-22%), those with a strict regimen of diet and exercise for two weeks, fasting glucose present ≥ 105 mg / dl two hours postprandial blood glucose or ≥ 120 mg / dl on two or more occasions . These patients benefit greatly from insulin, decreasing rates of fetal and neonatal morbidity (macrosomia, birth trauma, etc).The insulin used during pregnancy should be preferably human, which reduces the formation of insulin antibodies, which pass the placenta and contribute to increased fetal insulin and therefore free to fetal macrosomia and neonatal hypoglycemia. It is intended to maintain blood glucose levels below 95, 140 and 120 mg / dl, postprandial one and two hours respectively (3, 9, 13, 23). In 1997, the market appears Lispro insulin, which has the following advantages: a higher absorption rate for 10 should be positioned immediately before meals and less duration of action, which reduces the possibility of postprandial hypoglycemia and the need for between meals; this insulin lispro, may be substituted 1: 1 by regular insulin. In Table 6, (3.24) we can see the action of the various insulins.Preferred schemes of gestational diabetic insulin are: (1, 4)1. According to the glycemic profile before breakfast, start with a small dose of NPH (5-10 each) before breakfast, with a mixture of NPH and regular insulin (15 U of NPH plus 5 or regulate) before breakfast or with a small dose of regular insulin (10 u) before the food causing the postprandial elevation adjusting the dose according to the self-monitoring as follows: posdesayuno If BG is> 140 mg / dl, place or increase crystalline insulin before breakfast. If BG two hours posalmuerzo is> 140 mg / dl, you should increase the NPH before breakfast.
HbA1C measurement of patient 4 - 6 weeks post-conception: levels above 8.5% is associated with a 20-25% chance of developing fetal anomalies versus 2 - 3.5% when the figures are normal HbA1C (3-4). vaginal ultrasound between 8-10 weeks of pregnancy, especially in those patients with abnormal numbers of HbA1C. Some defects are easily diagnosed by this time (anencephaly, holoprosencephaly). maternal serum alpha-fetoprotein screening (MSAFP) at 16 weeks of gestation. Normally this MSAFP is decreased in diabetic patients and often indicate the need for genetic testing by amniocentesis / cordocentesis. tertiary ultrasound between 18-20 weeks of pregnancy to detect fetal abnormalities not visualized on initial echoes. fetal echocardiography between 24 to 28 weeks gestation7.2 Prenatal: top quality, performing them every 15 days until week 24 and then every week, requesting paraclinical the following: (1) Urinalysis and urine culture: UTIs are more common during pregnancy and are the leading cause of decompensation in the diabetic patient. Be requested in the first prenatal visit and then monthly. BUN - creatinine and uric acid: as indicators of renal function minimum, quarterly. Lipid profile: initial at 24 to 26 weeks gestation and at the end of it HbA1C: at 4-6 weeks after conception and then every month to analyze the quality of metabolic control, keeping it below 7.2%. glycemic monitoring and tests of fetal wellbeing (see below) fundoscopy and EKG: in pregestational DM with vascular compromise ultrasound scans: detecting malformations and assess fetal growth7.3 Strict maternal metabolic control: the mainstay of treatment of gestational diabetes: Tight control of blood glucose during pregnancy, and The early detection of risk factors and / or aggravating s metabolic state (1, 19)Metabolic control objectives are:Avoid symptomatic hypoglycemia Keep the following plasma glycemia:Fasting ------> 65 to <105 mg / dl (ideal <95 mg / dl)Preprandial ------> 70 to 100 mg / dl An hour postprandial ------> <140 mg / dl (ideal <130 mg / dl)Two hours postprandial ------> <120 mg / dl negative ketonuria HbA1C and / or fructosamine: normal lowNow, to achieve the goals of metabolic control should formulate a treatment plan that includes diet, exercise, insulin (if needed) and the management of complications. Diet: is the key or mainstay of therapy in women with gestational diabetes. Weight gain is necessary for proper fetal growth and varies between 8 and 12kg, depending on the weight of the patient prior. Remember that the patient must never lose weight during pregnancy, as this leads to fat mobilization, lipolysis and substances that cross the placenta and have pontenciales teratogenic effects (1). The diet should provide an average of 30-35 cal / kg in patients of average weight and 25 cal / kg in obese patients, divided into three meals and three snacks, emphasizing the refreshment of 22:00 to 23:00 hours to avoid maternal hypoglycemia at dawn (glass of milk and cookies) (15,20). Remember that a gram of protein or H of C provide four calories and one gram of fat provides nine calories. It has been found that by limiting the intake of C to H of 35 to 45% of total calories, more suitably controlling postprandial glycemia (9). regulated and proper exercise is beneficial and safe; releases epinephrine, which increases glucose uptake by the cell and increases the sensitivity of the receivers, keeping blood sugar levels stable. They must walk 10 to 20 minutes after each main meal. Insulin: Insulin requirements increase progressively during pregnancy. In the first quarter are frequent severe hypoglycemia and decrease insulin requirements. During the second quarter, a slight increase occurs monthly, on the third quarter nocturnal hypoglycemia may occur and insulin requirements increase by 50 - 100% above the baseline. The oral hypoglycemic agents are contraindicated for pregnant diabetic control, and that cross the placenta and cause fetal hypoglycemia is severe malformations (1, 5).They must take insulin: DM1 and DM2's always to become pregnant Among patients with GDM, the White group A2 modified by Freinkel (fasting glucose between 105 and 129 mg / dl) and group B (fasting glucose> 130 mg / dl), andThose patients with GDM (15-22%), those with a strict regimen of diet and exercise for two weeks, fasting glucose present ≥ 105 mg / dl two hours postprandial blood glucose or ≥ 120 mg / dl on two or more occasions . These patients benefit greatly from insulin, decreasing rates of fetal and neonatal morbidity (macrosomia, birth trauma, etc).The insulin used during pregnancy should be preferably human, which reduces the formation of insulin antibodies, which pass the placenta and contribute to increased fetal insulin and therefore free to fetal macrosomia and neonatal hypoglycemia. It is intended to maintain blood glucose levels below 95, 140 and 120 mg / dl, postprandial one and two hours respectively (3, 9, 13, 23). In 1997, the market appears Lispro insulin, which has the following advantages: a higher absorption rate for 10 should be positioned immediately before meals and less duration of action, which reduces the possibility of postprandial hypoglycemia and the need for between meals; this insulin lispro, may be substituted 1: 1 by regular insulin. In Table 6, (3.24) we can see the action of the various insulins.Preferred schemes of gestational diabetic insulin are: (1, 4)1. According to the glycemic profile before breakfast, start with a small dose of NPH (5-10 each) before breakfast, with a mixture of NPH and regular insulin (15 U of NPH plus 5 or regulate) before breakfast or with a small dose of regular insulin (10 u) before the food causing the postprandial elevation adjusting the dose according to the self-monitoring as follows: posdesayuno If BG is> 140 mg / dl, place or increase crystalline insulin before breakfast. If BG two hours posalmuerzo is> 140 mg / dl, you should increase the NPH before breakfast.
Management of diabetes mellitus during pregnancy
Differences in maternal-fetal prognosis is necessary to distinguish two types of pregnant women with diabetes: (1)6.1 The diabetic woman who is pregnant (pregestational DM). Within this category there are two groups: Patient without chronic vascular complications: here the good metabolic control allows uncomplicated pregnancy curse. Patients with chronic vascular complications: pregnancy accelerates the development microangiopathic renal and retinal level.6.2 Gestational diabetes mellitus: metabolic disorder here has just set in, the risk of a poor metabolic control rests with the fetus. Reports indicate that when GDM is diagnosed and treated intensively, the risk of stillbirth is not larger than the general obstetric population, equally, that the overall incidence and severity of perinatal conditions is lower.Other factors that determine a maternal-fetal poor prognosis, according Pedersen, are: (1) clinical pyelonephritis chemical acidosis or ketoacidosis Preeclampsia-eclampsiaMalpractice (do not follow the treatment plan or consult belatedly)
The management of DM during pregnancy should be performed in a tertiary care level, it is the duty of primary care levels early diagnosis, initial management and timely referral. Such management requires an interdisciplinary approach, as it involves pharmacological aspects, educational, nutritional, social, psychological and family. To significantly reduce fetal and maternal mortality, the team should include: an obstetrician, a physician trained in diabetologist or diabetes, a neonatologist, a nurse educator, a nutritionist and a psychologist or social worker. Similarly, the patient and family should take an active part in the treatment, with the motivation and education fundamentals for integration.
The management of DM during pregnancy should be performed in a tertiary care level, it is the duty of primary care levels early diagnosis, initial management and timely referral. Such management requires an interdisciplinary approach, as it involves pharmacological aspects, educational, nutritional, social, psychological and family. To significantly reduce fetal and maternal mortality, the team should include: an obstetrician, a physician trained in diabetologist or diabetes, a neonatologist, a nurse educator, a nutritionist and a psychologist or social worker. Similarly, the patient and family should take an active part in the treatment, with the motivation and education fundamentals for integration.
Classification criteria for diabetes
Priscilla White describes its prognostic classification based on the age of onset, duration and complications of the disorder. The biggest shortcoming of this classification is not contemplated that the metabolic instability is the main prognostic factor in insulin-dependent diabetic pregnant. In 1985, Freinkel modified White classification, as follows: (1)Classes:A: Gestational diabetesA1: fasting glucose <105 mg / dl (normal)A2: fasting glucose between 105 and 129 mg / dl (intolerant)B: fasting glucose> 130 mg / dlB1: If the diagnosis is the first time (DMG)B2: home after 20 years and under 10 years evolution, persisting between pregnancies (DM2)Classes C-D-F-H-R: correspond to the DM1 and DM2.The classification published by the National Diabetes Data Group (NDDG) (6) and endorsed by the World Health Organization (WHO) (7) in 1980 and 1985 was based on a combination of clinical features, pathogenesis and treatment requirements. She considered two types of patients: those who formed the clinical category and those that were located in a statistical risk category.In 1995, under the sponsorship of the American Diabetes Association (ADA) created an International Committee of Experts, which proposes a number of changes to the previous classification scheme, based on the literature review and in light of the new knowledge (see Table 2). (8).Remember that if you just build on them, about 35 to 50% of gestational diabetes will remain undiagnosed (1, 4).
The summary and recommendations of previous conferences working in gestational diabetes, (13-15) the screening for GDM was recommended in all pregnancies, with the premise that the DMG healthy, is one of the few institutions where with clarity can make preventive medicine. The universal screening is still recommended for women of ethnic groups with relatively high rates of intolerance to H of C during pregnancy and DM later in life. This includes women of ancestorHispanic, African, Native American, South or East Asian, Pacific Islander or Australian indigenous ancestry, particularly when they reside in western countries or in urban atmospheres. Conversely, certain characteristics are at low risk for GDM and from the standpoint of cost-effective screening is not important to these patients. Those with low risk include:Women who are not members of ethnic groups at high risk for developing DM2.
Those who have no previous history of abnormal glucose tolerance or poor obstetric outcomes usually associated with GDM, and Those who have all of the following: age <25 years, normal body weight and no family history of DM.This screening has a sensitivity ranging from 75 to 85% and specificity ranging from 85 to 90% depending on the series studied (1). It consists of administering the first prenatal (before week 20), 50 grams of glucose and determining an hour plasma glucose (pregestational DM rule) is not necessary that the patient is fasting and can be performed at any time day. If the result is normal, said screening is repeated between 24-28 weeks of gestation time in which the maximum occurs diabetogenic effect of pregnancy. A value ≥ 140 mg / dl (or ≥ 135 mg / dl if fasted overnight) requires a full study using a GTT with 100 g (see Table 3) (8).The diagnosis of GDM is made with two or more values above those listed in Table 3, where a single altered value, the test is considered pathological, presenting the risk of complications such as fetal macrosomia and preeclampsia-eclampsia. Now, the ACOG recommends that in populations with a high prevalence of GDM or francs risk factors for it, must be made directly with 100g OGTT without prior screening (12).Moreover, there have been proposals to change the diagnostic scheme scored before. Thus Carpenter and Coustan (16) proposed cutoffs for plasma glucose seem to represent more accurately the original determinations of O'Sullivan and Mahan, in other words, these extrapolations produce lower values for abnormal levels of plasma glucose and increase the number of pregnancies defined as DMG. Furthermore, additional studies have been carried out using 75 g load, as recommended by WHO, with similar results (17). In Table 4, we can observe the values for these OGTT: (9)
Similarly, diagnosis of GDM is made with two or more values than those noted above. Any of these diagnostic tests with 100g 075g is acceptable, but its sensitivity (diagnostic accuracy) and specificity should still be evaluated (9).
At six weeks postpartum, the patient should be subjected to a GTT with 75g, sampling fasting and two hours postprandial, to be reclassified as 1) diabetes, 2) impaired fasting glucose, 3) glucose intolerance or 4) normoglycemia, according to the new criteria for the diagnosis of DM (see Table 5). Are taken six weeks postpartum, since at this time the normalized insulin receptor affinity and density (1). Do not forget that in most cases of DMG, stabilize glucose returns to normal after delivery. Those normoglycemic patients considered at this time, should be evaluated for diabetes at least every year (1, 8-9).
New diagnostic criteria for DM: diagnostic criteria for DM NDDG and recommended by the WHO, (6-7) were also reviewed and amended by the ADA, for evaluation were taken a number of epidemiological studies that linked fasting glucose , two hours postprandial blood glucose and HbA1C levels
The summary and recommendations of previous conferences working in gestational diabetes, (13-15) the screening for GDM was recommended in all pregnancies, with the premise that the DMG healthy, is one of the few institutions where with clarity can make preventive medicine. The universal screening is still recommended for women of ethnic groups with relatively high rates of intolerance to H of C during pregnancy and DM later in life. This includes women of ancestorHispanic, African, Native American, South or East Asian, Pacific Islander or Australian indigenous ancestry, particularly when they reside in western countries or in urban atmospheres. Conversely, certain characteristics are at low risk for GDM and from the standpoint of cost-effective screening is not important to these patients. Those with low risk include:Women who are not members of ethnic groups at high risk for developing DM2.
Those who have no previous history of abnormal glucose tolerance or poor obstetric outcomes usually associated with GDM, and Those who have all of the following: age <25 years, normal body weight and no family history of DM.This screening has a sensitivity ranging from 75 to 85% and specificity ranging from 85 to 90% depending on the series studied (1). It consists of administering the first prenatal (before week 20), 50 grams of glucose and determining an hour plasma glucose (pregestational DM rule) is not necessary that the patient is fasting and can be performed at any time day. If the result is normal, said screening is repeated between 24-28 weeks of gestation time in which the maximum occurs diabetogenic effect of pregnancy. A value ≥ 140 mg / dl (or ≥ 135 mg / dl if fasted overnight) requires a full study using a GTT with 100 g (see Table 3) (8).The diagnosis of GDM is made with two or more values above those listed in Table 3, where a single altered value, the test is considered pathological, presenting the risk of complications such as fetal macrosomia and preeclampsia-eclampsia. Now, the ACOG recommends that in populations with a high prevalence of GDM or francs risk factors for it, must be made directly with 100g OGTT without prior screening (12).Moreover, there have been proposals to change the diagnostic scheme scored before. Thus Carpenter and Coustan (16) proposed cutoffs for plasma glucose seem to represent more accurately the original determinations of O'Sullivan and Mahan, in other words, these extrapolations produce lower values for abnormal levels of plasma glucose and increase the number of pregnancies defined as DMG. Furthermore, additional studies have been carried out using 75 g load, as recommended by WHO, with similar results (17). In Table 4, we can observe the values for these OGTT: (9)
Similarly, diagnosis of GDM is made with two or more values than those noted above. Any of these diagnostic tests with 100g 075g is acceptable, but its sensitivity (diagnostic accuracy) and specificity should still be evaluated (9).
At six weeks postpartum, the patient should be subjected to a GTT with 75g, sampling fasting and two hours postprandial, to be reclassified as 1) diabetes, 2) impaired fasting glucose, 3) glucose intolerance or 4) normoglycemia, according to the new criteria for the diagnosis of DM (see Table 5). Are taken six weeks postpartum, since at this time the normalized insulin receptor affinity and density (1). Do not forget that in most cases of DMG, stabilize glucose returns to normal after delivery. Those normoglycemic patients considered at this time, should be evaluated for diabetes at least every year (1, 8-9).
New diagnostic criteria for DM: diagnostic criteria for DM NDDG and recommended by the WHO, (6-7) were also reviewed and amended by the ADA, for evaluation were taken a number of epidemiological studies that linked fasting glucose , two hours postprandial blood glucose and HbA1C levels
Effects of diabetes mellitus in pregnancy
H intolerance C during pregnancy is asymptomatic in most cases and a significant increase in morbidity maternofetal. The consequences for the fetus are more severe than the maternal. Of these the most important is macrosomia, due to the difficulty of diagnosis and the controversies that exist regarding their management
Effects of pregnancy on diabetes
Pregnancy creates a heavy burden for diabetes. These patients have a tendency to metabolic instability and require frequent monitoring and strict management. Therefore, higher doses are required to achieve insulin metabolic control, no progression of retinopathy and nephropathy and increased risk of death in patients with diabetic cardiomyopathy
Metabolism of carbohydrates (C H) during pregnancy
Pregnancy is diabetogenic, among others, the following factors: (4)
Insulin resistance: the most important factor is the gradual increase in insulin resistance that occurs during pregnancy. This insulin resistance is the result of the hyperglycemic effect of counter-regulatory hormones secreted by the placenta and is overcome by increased insulin secretion, resulting in a concomitant hyperinsulinemia. Similarly, there is increased destruction of insulin by the kidney and placental insulinasas.
Increased lipolysis: Mother uses fat to meet their needs and keep glucose to cover the fetus.
Changes in gluconeogenesis: the fetus uses alanine and other amino acids, depriving the mother of the main substrates for gluconeogenesis. Now, this consumption of glucose and amino acids by the fetus explains the tendency to fasting hypoglycemia during pregnancy (1).
Summarizing, the metabolism of C H during pregnancy is characterized by:
Tendency to hypoglycemia and ketosis in fasting
postprandial hyperglycemia tendency
Hyperinsulinemia and insulin resistance
Insulin resistance: the most important factor is the gradual increase in insulin resistance that occurs during pregnancy. This insulin resistance is the result of the hyperglycemic effect of counter-regulatory hormones secreted by the placenta and is overcome by increased insulin secretion, resulting in a concomitant hyperinsulinemia. Similarly, there is increased destruction of insulin by the kidney and placental insulinasas.
Increased lipolysis: Mother uses fat to meet their needs and keep glucose to cover the fetus.
Changes in gluconeogenesis: the fetus uses alanine and other amino acids, depriving the mother of the main substrates for gluconeogenesis. Now, this consumption of glucose and amino acids by the fetus explains the tendency to fasting hypoglycemia during pregnancy (1).
Summarizing, the metabolism of C H during pregnancy is characterized by:
Tendency to hypoglycemia and ketosis in fasting
postprandial hyperglycemia tendency
Hyperinsulinemia and insulin resistance
Diabetes Mellitus (DM)
Diabetes Mellitus (DM) comprises a group of metabolic disorders which are characterized by high concentrations of plasma glucose as a result of insufficient insulin secretion, totally or partially, and / or by a resistance to the action of it. Chronic hyperglycemia is associated with long-term damage to various organs, especially kidneys, eyes, nerves, heart and blood vessels.DM is considered the most common metabolic entity during pregnancy, occurring in about 5% of pregnancies. 90% of these patients have Gestational Diabetes Mellitus (GDM), or women with a genetic predisposition to diabetes or metabolic unable to adequately compensate diabetogenic effects of pregnancy, while the remaining 10% are women already diagnosed with diabetes before pregnancy (DM1, DM2 and other types) (1).
Modern resources in the management of diabetes (self-glucose monitoring at home, insulin pumps continuous subcutaneous application, multiple types of insulin, ultrasound and fetal biophysical monitoring), have revolutionized the outcome of pregnancies complicated with this relatively common disorder. Before the discovery of insulin by Banting and Best in 1922, the culmination of pregnancy was probably the death of both mother and fetus, with the use of this hormone decreased dramatically the risks to pregnant women and their product.
In 1939, Priscilla White et al (2) report the successful management of 245 diabetic pregnant and found that the incidence of maternal diabetic ketoacidosis had declined dramatically and that frequency of stillbirths was half of that reported in the period preinsulina.The next three decades showed that pregnancy outcome was closely related to the metabolic control during this period, perinatal mortality rates fell from 35 to 10%.In 1970 he introduced the interdisciplinary management of diabetic pregnant, this and the new technologies as monitoring fetal biophysical assessment of fetal growth by ultrasound and analysis of fetal lung maturity in amniotic fluid (LA), markedly reduce morbidity neonatal. However, there are still major problems in the management of the mother and fetus. Although stillbirth rates have declined significantly, they question how costly biophysical testing and high rates of preterm births and caesarean section. Congenital anomalies are still 7-15 times more common in pregnant women with diabetes than pregnant women without the disease and macrosomia and birth trauma occur with a frequency 10 times higher in diabetic fetuses. (1, 3).
Our knowledge of the interrelationship of diet, physical activity, stress, glucose levels and fetal well-being, remains rudimentary and are unable to prevent macrosomia and birth trauma without unacceptably high rates of caesarean section (3)
Modern resources in the management of diabetes (self-glucose monitoring at home, insulin pumps continuous subcutaneous application, multiple types of insulin, ultrasound and fetal biophysical monitoring), have revolutionized the outcome of pregnancies complicated with this relatively common disorder. Before the discovery of insulin by Banting and Best in 1922, the culmination of pregnancy was probably the death of both mother and fetus, with the use of this hormone decreased dramatically the risks to pregnant women and their product.
In 1939, Priscilla White et al (2) report the successful management of 245 diabetic pregnant and found that the incidence of maternal diabetic ketoacidosis had declined dramatically and that frequency of stillbirths was half of that reported in the period preinsulina.The next three decades showed that pregnancy outcome was closely related to the metabolic control during this period, perinatal mortality rates fell from 35 to 10%.In 1970 he introduced the interdisciplinary management of diabetic pregnant, this and the new technologies as monitoring fetal biophysical assessment of fetal growth by ultrasound and analysis of fetal lung maturity in amniotic fluid (LA), markedly reduce morbidity neonatal. However, there are still major problems in the management of the mother and fetus. Although stillbirth rates have declined significantly, they question how costly biophysical testing and high rates of preterm births and caesarean section. Congenital anomalies are still 7-15 times more common in pregnant women with diabetes than pregnant women without the disease and macrosomia and birth trauma occur with a frequency 10 times higher in diabetic fetuses. (1, 3).
Our knowledge of the interrelationship of diet, physical activity, stress, glucose levels and fetal well-being, remains rudimentary and are unable to prevent macrosomia and birth trauma without unacceptably high rates of caesarean section (3)
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