Type 1 Diabetes Mellitus 

  • Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD   more...
 
Updated: May 24, 2012
 

Background

Type 1 diabetes mellitus (DM) is a multisystem disease with both biochemical and anatomic/structural consequences. It is a chronic disease of carbohydrate, fat, and protein metabolism caused by the lack of insulin, which results from the marked and progressive inability of the pancreas to secrete insulin because of autoimmune destruction of the beta cells. (See Pathophysiology.) (See also Glucose Intolerance.)

Type 1 DM can occur at any age. It is most common in juveniles but can also develop in adults, especially in those in their late 30s and early 40s. (See Epidemiology.)

Unlike people with type 2 DM, those with type 1 DM usually are not obese and usually present initially with diabetic ketoacidosis (DKA). The distinguishing characteristic of a patient with type 1 DM is that if his or her insulin is withdrawn, ketosis and eventually ketoacidosis develop. Therefore, these patients are dependent on exogenous insulin. (See Presentation.)

Treatment of type 1 DM requires lifelong insulin therapy. A multidisciplinary approach by the physician, nurse, and dietitian, with regular specialist consultation, is needed to control glycemia, as well as to limit the development of its devastating complications and manage such complications when they do occur. (See Treatmentand Medication.)

Despite the differences between type 1 and type 2 DM, the costs of the 2 conditions are often combined. In a study that focused on type 1 alone, Tao et al estimated that in the United States, type 1 DM is responsible for $14.4 billion in medical costs and lost income each year.[1]

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Pathophysiology

Type 1 DM is the culmination of lymphocytic infiltration and destruction of insulin-secreting beta cells of the islets of Langerhans in the pancreas. As beta-cell mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels. After 80-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed. Patients need exogenous insulin to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia, and normalize lipid and protein metabolism.

Currently, autoimmunity is considered the major factor in the pathophysiology of type 1 DM. In a genetically susceptible individual, viral infection may stimulate the production of antibodies against a viral protein that trigger an autoimmune response against antigenically similar beta cell molecules.

Approximately 85% of type 1 DM patients have circulating islet cell antibodies, and the majority also have detectable anti-insulin antibodies before receiving insulin therapy. The most commonly found islet cell antibodies are those directed against glutamic acid decarboxylase (GAD), an enzyme found within pancreatic beta cells.

The prevalence of type 1 DM is increased in patients with other autoimmune diseases, such as Graves disease, Hashimoto thyroiditis, and Addison disease. Pilia et al found a higher prevalence of islet cell antibodies (IA2) and anti-GAD antibodies in patients with autoimmune thyroiditis.[2]

A study by Philippe et al used computed tomography (CT) scans, glucagon stimulation test results, and fecal elastase-1 measurements to confirm reduced pancreatic volume in individuals with DM.[3] This finding, which was equally present in both type 1 and type 2 DM, may also explain the associated exocrine dysfunction that occurs in DM.

Polymorphisms of the class II human leukocyte antigen (HLA) genes that encode DR and DQ are the major genetic determinants of type 1 DM. Approximately 95% of patients with type 1 DM have either HLA-DR3 or HLA-DR4. Heterozygotes for those haplotypes are at significantly greater risk for DM than homozygotes. HLA-DQs are also considered specific markers of type 1 DM susceptibility. In contrast, some haplotypes (eg, HLA-DR2) confer strong protection against type 1 DM.[4]

Sensory and autonomic neuropathy

Sensory and autonomic neuropathy in people with diabetes are caused by axonal degeneration and segmental demyelination. Many factors are involved, including the accumulation of sorbitol in peripheral sensory nerves from sustained hyperglycemia. Motor neuropathy and cranial mononeuropathy result from vascular disease in blood vessels supplying nerves.

Angiopathy

Using nailfold video capillaroscopy, Barchetta et al detected a high prevalence of capillary changes in patients with diabetes, particularly those with retinal damage. This reflects a generalized microvessel involvement in both type 1 and type 2 DM.[5]

Microvascular disease causes multiple pathologic complications in people with diabetes. Hyaline arteriosclerosis, a characteristic pattern of wall thickening of small arterioles and capillaries, is widespread and is responsible for ischemic changes in the kidney, retina, brain, and peripheral nerves.

Atherosclerosis of the main renal arteries and their intrarenal branches causes chronic nephron ischemia. It is a significant component of multiple renal lesions in diabetes.

Vitamin D deficiency is an important independent predictor of development of coronary artery calcification in individuals with type 1 DM.[6] Joergensen et al determined that vitamin D deficiency in type 1 diabetes may predict all causes of mortality but not development of microvascular complications.[7]

Nephropathy

In the kidneys, the characteristic wall thickening of small arterioles and capillaries leads to diabetic nephropathy, which is characterized by proteinuria, glomerular hyalinization (Kimmelstiel-Wilson), and chronic renal failure. Exacerbated expression of cytokines such as tumor growth factor beta 1 is part of the pathophysiology of glomerulosclerosis, which begins early in the course of diabetic nephropathy.

Genetic factors influence the development of diabetic nephropathy. Single-nucleotide polymorphisms affecting the factors involved in its pathogenesis appear to influence the risk for diabetic nephropathy in different people with type 1 DM.[8]

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Etiology

Type 1A DM results from autoimmune destruction of the beta cells of the pancreas and involves both genetic predisposition and an environmental component.

Genetic factors

Although the genetic aspect of type 1 DM is complex, with multiple genes involved, there is a high sibling relative risk.[9] Whereas dizygotic twins have a 5-6% concordance rate for type 1 DM,[10] monozygotic twins will share the diagnosis more than 50% of the time by the age of 40 years.[11]

For the child of a parent with type 1 DM, the risk varies according to whether the mother or the father has diabetes. Children whose mother has type 1 DM have a 2-3% risk of developing the disease, whereas those whose father has the disease have a 5-6% risk. When both parents are diabetic, the risk rises to almost 30%. In addition, the risk for children of parents with type 1 DM is slightly higher if onset of the disease occurred before age 11 years and slightly lower if the onset occurred after the parent’s 11th birthday.

The genetic contribution to type 1 DM is also reflected in the significant variance in the frequency of the disease among different ethnic populations. Type 1 DM is most prevalent in European populations, with people from northern Europe more often affected than those from Mediterranean regions.[12] The disease is least prevalent in East Asians.[13]

Genome-wide association studies have identified several loci that are associated with type 1 DM, but few causal relations have been established. The genomic region most strongly associated with other autoimmune diseases, the major histocompatibility complex (MHC), is the location of several susceptibility loci for type 1 DM—in particular, class II HLA DR and DQ haplotypes.[14, 15, 16]

A hierarchy of DR-DQ haplotypes associated with increased risk for type 1 DM has been established. The most susceptible haplotypes are as follows[17] :

  • DRB1*0301 - DQA1*0501 - DQB1*0201 (odds ratio [OR] 3.64)
  • DRB1*0405 - DQA1*0301 - DQB1*0302 (OR 11.37)
  • DRB1*0401 - DQA1*0301 - DQB*0302 (OR 8.39)
  • DRB1*0402 - DQA1*0301 - DQB1*0302 (OR 3.63)
  • DRB1*0404 - DQA1*0301 - DQB1*0302 (OR 1.59)
  • DRB1*0801 - DQB1*0401 - DQB1*0402 (OR 1.25)

Other haplotypes appear to offer protection against type 1 DM. These include the following[17] :

  • DRB1*1501 - DQA1*0102 - DQB1*0602 (OR 0.03)
  • DRB1*1401 - DQA1*0101 - DQB1*0503 (OR 0.02)
  • DRB1*0701 - DQA1*0201 - DQB1*0303 (OR 0.02)

From 90% to 95% of young children with type 1 DM carry HLA-DR3 DQB1*0201, HLA-DR4 DQB1*0302, or both. Carriage of both haplotypes (ie, DR3/4 heterozygotes) confers the highest susceptibility.

These high-risk haplotypes are found primarily in people of European descent; other ethnic groups are less well studied. In African Americans, the DRB1*07:01 - DQA1*03:01 -DQB1*02:01g haplotype is associated with increased risk (OR 3.96), whereas the DRB1*07:01-DQA1*02:01 - DQB1*02:01g haplotype appears to be protective (OR 0.34).[18]

The insulin gene (INS), which encodes for the pre-proinsulin peptide, is adjacent to a variable number of tandem repeats (VNTR) polymorphism at chromosome 11p15.5.[19] Different VNTR alleles may promote either resistance or susceptibility to type 1 DM through their effect on INS transcription in the thymus; for example, protective VNTRs are associated with higher INS expression, which may promote deletion of insulin-specific T cells.[20]

Other genes that have been reported to be involved in the mechanism of type 1 DM include CTLA4 (important in T-cell activation), PTPN22 (produces LYP, a negative regulator of T-cell kinase signaling), and IL2RA (encodes for CD25 which is involved with regulating T-cell function). UBASH3A (also known as STS2), may be involved in the increased risk not only of type 1 DM but also of other autoimmune disease and Down syndrome; it is located on locus chromosome 21q22.3.[21]

In addition, genome-wide association studies have implicated numerous other genes, including the following[22] :

  • SH2B3
  • ERBB3
  • CLEC16A
  • IL18RAP
  • PTPN2
  • CCR5

Environmental factors

Extragenetic factors also may contribute. Potential triggers for immunologically mediated destruction of the beta cells include viruses (eg, enterovirus,[23] mumps, rubella, and coxsackievirus B4), toxic chemicals, exposure to cow’s milk in infancy,[24] and cytotoxins.

Combinations of factors may be involved. Lempainen et al found that signs of an enterovirus infection by 12 months of age were associated with the appearance of type 1 DM–related autoimmunity among children who were exposed to cow's milk before 3 months of age. These results suggest an interaction between the 2 factors and provide a possible explanation for the contradictory findings obtained in studies that examined these factors in isolation.[25]

One meta-analysis found a weak but significant linear increase in the risk of childhood type 1 DM with increasing maternal age.[26] However, little evidence supports any substantial increase in childhood type 1 DM risk after pregnancy complicated by preeclampsia.[27]

A study by Simpson et al found that neither vitamin D intake nor 25-hydroxyvitamin D levels throughout childhood were associated with islet autoimmunity or progression to type 1 DM.[28] This study was based in Denver, Colorado, and has been following children at increased risk of diabetes since 1993.

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Epidemiology

United States statistics

A 2011 report from the US Centers for Disease Control and Prevention (CDC) estimated that approximately 1 million Americans have type 1 DM.[29] The CDC estimated that each year from 2002 to 2005, type 1 DM was newly diagnosed in 15,600 young people. Among children younger than 10 years, the annual rate of new cases was 19.7 per 100,000 population; among those 10 years or older, the rate was 18.6 per 100,000 population.[29]

Type 1 DM is the most common metabolic disease of childhood. About 1 in every 400-600 children and adolescents has type 1 DM. In adults, type 1 DM constitutes approximately 5% of all diagnosed cases of diabetes.[29]

International statistics

Internationally, rates of type 1 DM are increasing. In Europe, the Middle East, and Australia, rates of type 1 DM are increasing by 2-5% per year.[30] The prevalence of type 1 DM is highest in Scandinavia (ie, approximately 20% of the total number of people with DM) and lowest in China and Japan (ie, fewer than 1% of all people with diabetes). Some of these differences may relate to definitional issues and the completeness of reporting.

Age-related demographics

Previously referred to as juvenile-onset diabetes, type 1 DM is typically diagnosed in childhood, adolescence, or early adulthood. Although the onset of type 1 DM often occurs early in life, 50% of patients with new-onset type 1 DM are older than 20 years of age.

Type 1 DM usually starts in children aged 4 years or older, appearing fairly abruptly, with the peak incidence of onset at age 11-13 years (ie, in early adolescence and puberty). There is also a relatively high incidence in people in their late 30s and early 40s, in whom the disease tends to present less aggressively (ie, with early hyperglycemia without ketoacidosis and gradual onset of ketosis). This slower-onset adult form of type 1 DM is referred to as latent autoimmune diabetes of the adult (LADA).[29]

The risk of development of antibodies (anti-islet) in relatives of patients with type 1 DM decreases with increasing age. This finding supports annual screening for antibodies in relatives younger than 10 years and 1 additional screening during adolescence.[31]

Sex- and race-related demographics

Type 1 DM is more common in males than in females. In populations of European origin, the male-to-female ratio is greater than 1.5:1.

Type 1 DM is most common among non-Hispanic whites, followed by African Americans and Hispanic Americans. It is comparatively uncommon among Asians.

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Prognosis

Type 1 DM is associated with a high morbidity and premature mortality. More than 60% of patients with type 1 DM do not develop serious complications over the long term, but many of the rest experience blindness, end-stage renal disease (ESRD), and, in some cases, early death. The risk of ESRD and proliferative retinopathy is twice as high in men as in women when the onset of diabetes occurred before age 15 years.[32]

Patients with type 1 DM who survive the period 10-20 years after disease onset without fulminant complications have a high probability of maintaining reasonably good health. Other factors affecting long-term outcomes are the patient’s education, awareness, motivation, and intelligence level. The 2012 American Diabetes Association (ADA) standard of care emphasizes the importance of long-term, coordinated care management for improved outcomes and suggests structural changes to existing systems of long-term care delivery.[33]

The morbidity and mortality associated with diabetes are related to the short- and long-term complications. Such complications include the following:

  • Hypoglycemia from management errors
  • Increased risk of infections
  • Microvascular complications (eg, retinopathy and nephropathy)
  • Neuropathic complications
  • Macrovascular disease

These complications result in increased risk for ischemic heart disease, cerebral vascular disease, peripheral vascular disease with gangrene of lower limbs, chronic renal disease, reduced visual acuity and blindness, and autonomic and peripheral neuropathy. Diabetes is the major cause of blindness in adults aged 20-74 years, as well as the leading cause of nontraumatic lower-extremity amputation and ESRD.

Although ESRD is one of the most severe complications of type 1 DM, its incidence is relatively low: 2.2% at 20 years after diagnosis and 7.8% at 30 years after diagnosis.[34] A greater risk is that mild diabetic nephropathy in type 1 diabetic persons appears to be associated with an increased likelihood of cardiovascular disease.[35] Moreover, the long-term risk of an impaired glomerular filtration rate (GFR) is lower in persons treated with intense insulin therapy early in the course of disease than in those given conventional therapy.[36]

Although mortality from early-onset type 1 DM (onset age, 0-14 y) has declined, the same may not be true for late-onset type 1 DM (onset age, 15-29 y). One study suggest that women tend to fare worse in both cohorts and that alcohol and drug use account for more than one third of deaths.[37]

Control of blood glucose, hemoglobin A1c (HbA1c), lipids, blood pressure, and weight significantly affects prognosis. Patients with diabetes face a lifelong challenge to achieve and maintain blood glucose levels as close to the normal range as possible. With appropriate glycemic control, the risk of both microvascular and neuropathic complications is decreased markedly. In addition, aggressive treatment of hypertension and hyperlipidemia decreases the risk of macrovascular complications.

The benefits of glycemic control and control of comorbidities must be weighed against the risk of hypoglycemia and the short-term costs of providing high-quality preventive care. However, studies have shown cost savings due to a reduction in acute diabetes-related complications within 1-3 years of starting effective preventive care.

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Patient Education

Education is a vital aspect of diabetes management. Patients with new-onset type 1 DM require extensive education if they are to manage their disease safely and effectively and to minimize long-term complications. Such education is best coordinated by the patient’s long-term care providers.

At every encounter, the clinician should educate the patient—and, in the case of children, the parents—about the disease process, management, goals, and long-term complications. In particular, clinicians should do the following:

  • Make patients aware of the signs and symptoms of hypoglycemia and knowledgeable about ways to manage it
  • Help patients understand and acknowledge the course of diabetes (eg, by teaching patients that they have a chronic condition that requires lifestyle modification and that they are likely to have chronic complications if they do not take control of their disease)
  • Reassure patients about the prognosis in properly managed type 1 DM

ADA guidelines urge that attention be paid to older adolescent patients who may be leaving their home and their current health care providers. At the transition between pediatric and adult health care, older teens can become detached from the health care system, putting their medical care and their glycemic control at risk.[33] The guidelines identify the National Diabetes Education Program (NDEP) as a source of materials that can help smooth the transition to adult health care.

Education about an appropriate treatment plan and encouragement to follow the plan are especially important in patients with diabetes. Physicians must ensure that the care for each patient with diabetes includes all necessary laboratory tests, examinations (eg, foot and neurologic examinations), and referrals to specialists (eg, an ophthalmologist or podiatrist).

A dietitian should provide specific diet control education to the patient and family. A nurse should educate the patient about self–insulin injection and performing fingerstick tests for blood glucose level monitoring.

For patient education information, see the Diabetes Center, as well as Diabetes.

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Contributor Information and Disclosures
Author

Romesh Khardori, MD, PhD, FACP  Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, and Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy ofSciences,and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Aneela Naureen Hussain, MD, FAAFM Assistant Professor, Department of Family Medicine, State University of New York Downstate Medical Center; Consulting Staff, Department of Family Medicine, University Hospital of Brooklyn

Aneela Naureen Hussain, MD, FAAFM is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, American Medical Women's Association, Medical Society of the State of New York, and Society of Teachers of Family Medicine

Disclosure: Nothing to disclose.

Anne L Peters, MD, CDE Director of Clinical Diabetes Programs, Professor, Department of Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, Los Angeles County/University of Southern California Medical Center

Anne L Peters, MD, CDE is a member of the following medical societies: American College of Physicians and American Diabetes Association

Disclosure: Amylin Honoraria Speaking and teaching; AstraZeneca Consulting fee Consulting; Lilly Consulting fee Consulting; Takeda Consulting fee Consulting; Bristol Myers Squibb Honoraria Speaking and teaching; NovoNordisk Consulting fee Consulting; Medtronic Minimed Consulting fee Consulting; Dexcom Honoraria Speaking and teaching; Roche Honoraria Speaking and teaching

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Miriam T Vincent, MD, PhD Professor and Chair, Department of Family Practice, State University of New York Downstate Medical Center

Miriam T Vincent, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Family Physicians, American Association for the Advancement of Science, Medical Society of the State of New York, North American Primary Care Research Group, Sigma Xi, and Society of Teachers of Family Medicine

Disclosure: Joslin Diabetes Group, Harvard Honoraria Speaking and teaching

Scott R Votey, MD Director of Emergency Medicine Residency, Ronald Reagan UCLA Medical Center; Professor of Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine

Scott R Votey, MD is a member of the following medical societies: Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group

Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, andInternational Society for Clinical Densitometry

Disclosure: Nothing to disclose.

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