Physiological Reviews 2013;93(1):137-188

is increasingly apparent that not only is a cure for the current worldwide diabetes epidemic required, but also for its major complications, affecting both small and large blood vessels. These complications occur in the majority of individuals with both type 1 and type 2 diabetes. Among the most prevalent microvascular complications are kidney disease, blindness, and amputations, with current therapies only slowing disease progression. Impaired kidney function, exhibited as a reduced glomerular filtration rate, is also a major risk factor for macrovascular complications, such as heart attacks and strokes. There have been a large number of new therapies tested in clinical trials for diabetic complications, with, in general, rather disappointing results. Indeed, it remains to be fully defined as to which pathways in diabetic complications are essentially protective rather than pathological, in terms of their effects on the underlying disease process. Furthermore, seemingly independent pathways are also showing significant interactions with each other to exacerbate pathology. Interestingly, some of these pathways may not only play key roles in complications but also in the development of diabetes per se. This review aims to comprehensively discuss the well validated, as well as putative mechanisms involved in the development of diabetic complications. In addition, new fields of research, which warrant further investigation as potential therapeutic targets of the future, will be highlighted.

Standards of Medical Care in Diabetes 2019 (PDF download)

PUBLICATION DATE: 2011
Multiple laboratory tests are used in the diagnosis and management of patients with diabetes mellitus. The quality of the scientific evidence supporting the use of these assays varies substantially. An expert committee compiled evidence-based recommendations for the use of laboratory analysis in patients with diabetes. A new system was developed to grade the overall quality of the evidence and the strength of the recommendations. In addition to the long-standing criteria based on measurement of venous plasma glucose, diabetes can be diagnosed by demonstrating increased hemoglobin A1c (Hb A1c) concentrations in the blood. Monitoring of glycemic control is performed by the patients measuring their own plasma or blood glucose with meters and by laboratory analysis of Hb A1c. The potential roles of noninvasive glucose monitoring, genetic testing, and measurement of autoantibodies, urine albumin, insulin, proinsulin, C-peptide, and other analytes are addressed.

Chapter 1. Introduction 1
Chapter 2. Glucose 3
Chapter 3. Glucose Meters 9
Chapter 4. Continuous Minimally Invasive Glucose Analysis 15
Chapter 5. Noninvasive Glucose Analysis 17
Chapter 6. Gestational Diabetes Mellitus 19
Chapter 7. Urinary Glucose 21
Chapter 8. Ketone Testing 23
Chapter 9. Hb A1c 25
Chapter 10. Genetic Markers 31
Chapter 11. Autoimmune Markers 35
Chapter 12. Albuminuria (formerly microalbuminuria) 39
Chapter 13. Miscellaneous Potentially Important Analytes 43

GUIDELINES COMMITTEE:
David B. Sacks, M.B., Ch.B., Chair
Mark Arnold, PhD
George L. Bakris, M.D.
David E. Bruns, M.D.
Andrea Rita Horvath, M.D., Ph.D.
Sue M. Kirkman, M.D.
Ake Lernmark, M.D.
Boyd E. Metzger, M.D.
David Nathan, M.D.

Diabetes Care 2015;38(Suppl. 1):S8–S16

CLASSIFICATION
Diabetes can be classified into the following general categories:
1. Type 1 diabetes (due to b-cell destruction, usually leading to absolute insulin deficiency)
2. Type 2 diabetes (due to a progressive insulin secretory defect on the background of insulin resistance)
3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes)
4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drug- or chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)
This section reviews most common forms of diabetes but is not comprehensive.
For additional information, see the American Diabetes Association (ADA) position statement “Diagnosis and Classification of Diabetes Mellitus” (1).

Table 2.1—Criteria for the diagnosis of diabetes
A1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*
OR
FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h.*
OR
2-h PG ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL
(11.1 mmol/L).
*In the absence of unequivocal hyperglycemia, results should be confirmed by repeat testing.

Clinical Chemistry September 2013 vol. 59 no. 9 1310-1321

BACKGROUND: Gestational diabetes mellitus, defined as diabetes diagnosed during pregnancy that is not clearly overt diabetes, is becoming more common as the epidemic of obesity and type 2 diabetes continues. Newly proposed diagnostic criteria will, if adopted universally, further increase the prevalence of this condition. Much controversy surrounds the diagnosis and management of gestational diabetes.

CONTENT: This review provides information regarding various approaches to the diagnosis of gestational diabetes and the recommendations of a number of professional organizations. The implications of gestational diabetes for both the mother and the offspring are described. Approaches to self-monitoring of blood glucose concentrations and treatment with diet, oral medications, and insulin injections are covered. Management of glucose metabolism during labor and the postpartum period are discussed, and an approach to determining the timing of delivery and the mode of delivery is outlined.

SUMMARY: This review provides an overview of current controversies as well as current recommendations for gestational diabetes care.

Journal of Medical Biochemistry. Volume 30, Issue 3, Pages 207–212

Diabetes is a common metabolic disorder. Its microvascular and macrovascular complications contribute to death, disabilities, and reduction in life expectancy in diabetes. It is a costly disease, and affects not only the patient and family, but also the public health, communities and society. It takes an increasing proportion of the national health care expenditure. The prevention of the development of diabetes and its complications is a major concern. Biomarkers have been investigated for understanding the mechanisms of the development and progression of diabetic complications. In this paper, the biomarkers which are recommended in the clinical practice and laboratory medicine guidelines, and which have been investigated for prediction or diagnosis of diabetes complications, have been reviewed. The results of several clinical studies will be summarized.

Türk Aile Hek Derg 2012;16(Suppl):S35-S43

Obezite global epidemik bir problem haline gelmiştir. Benzer şekilde 1990 yıllarından itibaren çocukluk ve adolesan obezite prevalansında da dramatik artışlar yaşanmaktadır. Çocukluk ve adolesan obezitesinin bir dizi sonuçları vardır. Bunlar arasında dislipidemi, hipertansiyon, kardiak sorunlar, endotelial disfonksiyon, karaciğer yağlanması, hiperinsülinemi, insülin direnci, tip 2 diabet, psikolojik sorunlar, pubertal sorunlar ve ekonomik yük sayılabilir. Adolesan tip 2 diabet oluşumunda genetik ve ırka bağlı faktörlere ek olarak en önemli etken obezite varlığıdır. Bu nedenle obezite ve tip 2 diabetin önlenmesinde pediatristlere önemli görevler düşmektedir.

Türk Biyokimya Dergisi [Turkish Journal of Biochemistry – Turk J Biochem] 2006; 31 (2); 51–56.

Diabetes mellitus hastalığının erken ve geç dönem komplikasyonlarının (mikroanjiyopati, nöropati gibi) patogenezinde oksidatif stres önemli bir rol oynamaktadır. Protein glikasyonu ve glikoz oto-oksidasyonu, lipid peroksidasyonuna neden olabilen serbest radikalleri oluşturmaktadır. Oksidatif stresin diğer potansiyel mekanizmaları arasınd a antioksidan savunma sistemlerinin yetersizliği bulunmaktadır. Bu yazıda serbest radikaller ve antioksidan sistem tartışıldı.

American Diabetes Association

Diabetes Care. 2011 January; 34(Supplement_1): S62–S69.

Criteria for the diagnosis of diabetes

A1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*
OR
FPG ≥126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*
OR
2-h plasma glucose ≥200 mg/dl (11.1 mmol/l) during an OGTT. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dl (11.1 mmol/l).
*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing.

Categories of increased risk for diabetes*

FPG 100 mg/dl (5.6 mmol/l) to 125 mg/dl (6.9 mmol/l) [IFG]
2-h PG in the 75-g OGTT 140 mg/dl (7.8 mmol/l) to 199 mg/dl (11.0 mmol/l) [IGT]
A1C 5.7–6.4%
*For all three tests, risk is continuous, extending below the lower limit of the range and becoming disproportionately greater at higher ends of the range.

Screening for and diagnosis of GDM

Perform a 75-g OGTT, with plasma glucose measurement fasting and at 1 and 2 h, at 24-28 of weeks gestation in women not previously diagnosed with overt diabetes.
The OGTT should be performed in the morning after an overnight fast of at least 8 h.
The diagnosis of GDM is made when any of the following plasma glucose values are exceeded
Fasting: ≥92 mg/dl (5.1 mmol/l)
1 h: ≥180 mg/dl (10.0 mmol/l)
2 h: ≥153 mg/dl (8.5 mmol/l)

Cardiovasc Diabetol. 2009 Nov 23;8:61.

Several inflammatory cytokines are involved in vascular inflammation resulting in endothelial dysfunction which is the earliest event in the atherosclerotic process leading to manifest cardiovascular disease. YKL-40 is an inflammatory glycoprotein involved in endothelial dysfunction by promoting chemotaxis, cell attachment and migration, reorganization and tissue remodelling as a response to endothelial damage. YKL-40 protein expression is seen in macrophages and smooth muscle cells in atherosclerotic plaques with the highest expression seen in macrophages in the early lesion of atherosclerosis. Several studies demonstrate, that elevated serum YKL-levels are independently associated with the presence and extent of coronary artery disease and even higher YKL-40 levels are documented in patients with myocardial infarction. Moreover, elevated serum YKL-40 levels have also been found to be associated with all-cause as well as cardiovascular mortality. Finally, YKL-40 levels are elevated both in patients with type 1 and type 2 diabetes, known to be at high risk for the development of cardiovascular diseases, when compared to non-diabetic persons. A positive association between elevated circulating YKL-40 levels and increasing levels of albuminuria have been described in patients with type 1 diabetes indicating a role of YKL-40 in the progressing vascular damage resulting in microvascular disease. This review describes the present knowledge about YKL-40 and discusses its relation to endothelial dysfunction, atherosclerosis, cardiovascular disease and diabetes and look ahead on future perspectives of YKL-40 research.

Clinical Chemistry 54: 1872-1882, 2008.

Background: Although the methodological quality of therapeutic guidelines (GLs) has been criticized, little is known regarding the quality of GLs that make diagnostic recommendations. Therefore, we assessed the methodological quality of GLs providing diagnostic recommendations for managing diabetes mellitus (DM) and explored several reasons for differences in quality across these GLs.

Methods: After systematic searches of published and electronic resources dated between 1999 and 2007, 26 DM GLs, published in English, were selected and scored for methodological quality using the AGREE Instrument. Subgroup analyses were performed based on the source, scope, length, origin, and date and type of publication of GLs. Using a checklist, we collected laboratory-specific items within GLs thought to be important for interpretation of test results.

Results: The 26 diagnostic GLs had significant shortcomings in methodological quality according to the AGREE criteria. GLs from agencies that had clear procedures for GL development, were longer than 50 pages, or were published in electronic databases were of higher quality. Diagnostic GLs contained more preanalytical or analytical information than combined (i.e., diagnostic and therapeutic) recommendations, but the overall quality was not significantly different. The quality of GLs did not show much improvement over the time period investigated.

Conclusions: The methodological shortcomings of diagnostic GLs in DM raise questions regarding the validity of recommendations in these documents that may affect their implementation in practice. Our results suggest the need for standardization of GL terminology and for higher-quality, systematically developed recommendations based on explicit guideline development and reporting standards in laboratory medicine.

Türkiye Endokrinoloji ve Metabolizma Derneği -2009

İçindekiler
1. Glisemik Bozukluklarda Tanı, Sınıflama ve Tedavi
1.1 Tanım
1.2 Tanı ve Sınıflama
1.3 Tip 1 Diabetes Mellitus
1.4 Tip 2 Diabetes Mellitus
1.5 Gestasyonel Diabetes Mellitus
1.6 Tarama Endikasyonları ve Tanı Testleri
2. Diyabetli Hastalarda Standart Bakım İlkeleri
2.1 Anamnez
2.2 Fizik Muayene
2.3 Konsültasyonlar
2.4 Laboratuvar İncelemeleri
2.5 Komplikasyonlar
2.6 Eğitim
3. Diyabetli Hastalarda Hastaneye Yatırılma İlkeleri
3.1 Akut Metabolik Komplikasyonlar
3.2 Kontrolsüz Diyabet
4. Diyabetli Hastalarda Glisemik Kontrol Hedefleri
4.1 Glisemik Hedefler
4.2 Evde Glukoz Takibi
5. Diyabette Tıbbi Beslenme Tedavisi
5.1 Tıbbi Beslenme Tedavisinde Genel İlkeler
5.2 Karbonhidrat Sayımı Tekniği
6. Diyabette Egzersiz ve Fizik Aktivite
6.1 Genel İlkeler
6.2 Egzersiz ile İlişkili Sorunlar
7. Oral Antidiyabetik ve İnsülinomimetik İlaçların Kullanım İlkeleri
7.1 İnsülin Salgılatıcı İlaçlar
7.2 İnsülin Duyarlılaştırıcı İlaçlar
7.3 Alfa-Glukozidaz İnhibitörleri
7.4 İnsülinomimetik İlaçlar
7.5 Monoterapide Kullanılan Oral İlaçlara Yanıt
7.6 Hazır OAD Kombinasyonları
8. İnsülin Tedavisi İlkeleri
8.1 Genel İlkeler
8.2 İnsülin Tedavi Protokolleri
9. Tip 2 Diyabet Tedavisinde Güncel Yaklaşım
9.1 IDF ve ADA/EASD Önerileri
9.2 TEMD Tip 2 Diyabet Tedavi Algoritması
10. Sürekli Cilt-altı Insülin İnfüzyon Tedavisi (SCİİ) İlkeleri
10.1 SCİİ Endikasyonları
10.2 SCİİ Kontrendikasyonları
10.3 SCİİ Tedavisinin Düzenlenmesi
10.4 SCİİ Tedavisinin Komplikasyonları
11. Pankreas ve Adacık Transplantasyon Endikasyonları
12. Diyabetin Akut Komplikasyonları
12.1 Diyabetik Ketoasidoz
12.2 Hiperozmolar Hiperglisemik Durum
12.3 Laktik Asidoz
12.4 Hipoglisemi
13. Diyabetin Kronik Komplikasyonları
13.1 Makrovasküler Hastalık (Hızlanmış Ateroskleroz)
13.2 Mikrovasküler Komplikasyonlar
14. Diyabetik Ayak Ülserleri
15. Diyabet ve Özel Durumlar
15.1 Diyabet ve Cerrahi
15.2 Total Parenteral Nütrisyon Tedavisi
15.3 Diyabet ve Gebelik
15.4 Yoğun Bakım Hastalarında Hiperglisemi Tedavisi
15.5 Steroid Kullanan Hastalarda Hiperglisemi Tedavisi
15.6 Yaşlılarda Diyabet
15.7 Diyabet ve Yolculuk
15.8 Diyabetlide Aşı Uygulamaları
15.9 Diyabet ve Doğal Afet Durumları
15.10 Diyabet ve Dini Görevler
15.11 Özel Koşullarda Yaşayan Kişilerde Diyabet Bakımı
16. Diyabette Hipertansiyon ve Tedavisi
17. Diyabette Dislipidemi ve Tedavisi
18. Diyabeti Önleme
18.1 Tip 1 Diyabeti Önleme
18.2 Tip 2 Diyabeti Önleme
19. Kaynaklar
20. Kısaltmalar
21. Laboratuvar Testlerinin Normal Referans Aralıkları (Standart ve SI Birimleri Tablosu)

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