Other Types of Diabetes Mellitus (Diabetes Sourcebook Excerpt)
Edited by Sandra J. Judd
Copyright 2011 Omnigraphics, Inc.
Excerpted with permission of the publisher
Chapter 8 – Other Types of Diabetes Mellitus
A number of other types of diabetes exist. A person may exhibit characteristics of more than one type. For example, in latent autoimmune diabetes in adults (LADA), also called type 1.5 diabetes or double diabetes, people show sings of both type 1 and type 2 diabetes.
Other types of diabetes include those caused by the following:
- Genetic defects of the beta cells – the part of the pancreas that makes insulin – such as maturity-onset diabetes of the young (MODY) or neonatal diabetes mellitus (NDM)
- Genetic defects in insulin action, resulting in the body’s inability to control blood glucose levels, as seen in leprechaunism and the Rabson-Mendenhall syndrome
- Diseases of the pancreas or conditions that damage the pancreas, such as pancreatitis and cystic fibrosis
- Excess amounts of certain hormones resulting form some medical conditions – such as cortisol from Cushing syndrome – that work against the action of insulin
- Medications that reduce insulin action, such as glucocorticoids, or chemicals that destroy beta cells
- Infections, such as congenital rubella and cytomegalovirus
- Rare immune-mediated disorders, such as stiff-man syndrome, an autoimmune disease of the central nervous system
- Genetic syndromes associated with diabetes, such as Down syndrome and Prader-Willi syndrome
Latent Autoimmune Diabetes in Adults (LADA)
People who have LADA show signs of both type 1 and type 2 diabetes. Diagnosis usually occurs after age thirty. Researchers estimate that as many as 10 percent of people diagnosed with type 2 diabetes have LADA. Some experts believe that LADA is a slowly developing kind of type 1 diabetes because patients have antibodies against the insulin-producing beta cells of the pancreas.
Many people with LADA still produce their own insulin when first diagnosed, like those with type 2 diabetes. In the early stages of the disease, people with LADA do not require insulin injections. Instead, they control their blood glucose levels with meal planning, physical activity, and oral diabetes medications. However, several years after diagnosis, people with LADA must take insulin to control blood glucose levels. As LADA progresses, the beta cells of the pancreas may no longer make insulin because the body’s immune system has attacked and destroyed them, as in type 1 diabetes.
Diabetes Caused by Genetic Defects of the Beta Cell
Genetic defects of the beta cell cause several forms of diabetes. For example, monogenic forms of diabetes result from mutations, or changes, in a single gene. In most cases of monogenic diabetes, the gene mutation is inherited. In the remaining cases, the gene mutation develops spontaneously. Most mutations in monogenic diabetes reduce the body’s ability to produce insulin. Genetic testing can diagnose most forms of monogenic diabetes.
NDM and MODY are the two main forms of monogenic diabetes. NDM is a form of diabetes that occurs in the first six months of life. Infants with NDM do not produce enough insulin, leading to an increase in blood glucose. NDM can be mistaken for the much more common type 1 diabetes, but type 1 diabetes usually occurs after the first six months of life.
MODY usually first occurs during adolescence or early adulthood. However, MODY sometimes remains undiagnosed until later in life. A number of different gene mutations have been shown to cause MODY, all of which limit the pancreas’s ability to produce insulin. This process leads to the high blood glucose levels characteristic of diabetes.
Diabetes Caused by Genetic Defects in Insulin Action
A number of types of diabetes result from genetic defects in insulin action. Changes to the insulin receptor may cause mild hyperglycemia – high blood glucose – or severe diabetes. Symptoms may include acanthosis nigricans, a skin condition characterized by darkened skin patches, and, in women, enlarged and cystic ovaries plus virilization and the development of masculine characteristics such as excess facial hair. Two syndromes in children, leprechaunism and the Rabson-Mendenhall syndromes, cause extreme insulin resistance.
Diabetes Caused by Diseases of the Pancreas
Injuries to the pancreas from trauma or disease can cause diabetes. This category includes pancreatitis, infection, and cancer of the pancreas. Cystic fibrosis and hemochromatosis can also damage the pancreas enough to cause diabetes.
Diabetes Caused by Endocrinopathies
Excess amounts of certain hormones that work against the action of insulin can cause diabetes. These hormones and their related conditions include growth hormone in acromegaly, cortisol in Cushing syndrome, glucagon in glucagonoma, and epinephrine in pheochromacytoma.
Diabetes Caused by Medications or Chemicals
A number of medications and chemicals can interfere with insulin secretion, leading to diabetes in people with insulin resistance. These medications and chemicals include pentamidine, nicotinic acid, glucocorticoids, thyroid hormone, phenytoin (Dilantin), and Vacor, a rat poison.
Diabetes Caused by Infections
Several infections are associated with the occurrence of diabetes, including congenital rubella, coxsackievirus B, cytomegalovirus, adenovirus, and mumps.
Rare Immune-Mediated Types of Diabetes
Some immune-mediated disorders are associated with diabetes. About one-third of people with stiff-man syndrome develop diabetes. In other autoimmune disease, such as systemic lupus erythematosus, patients may have anti-insulin receptor antibodies that cause diabetes by interfering with the binding of insulin to body tissues.
Other Genetic Syndromes Sometimes Associated with Diabetes
Many genetic syndromes are associated with diabetes. These conditions include Down syndrome, Klinefelter syndrome, Huntington chorea, porphyria, Prader-Willi syndrome, and diabetes insipius.
Excerpted from “Diabetes Overview,” National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, NIH Publication No. 09-3873, November 2008.
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