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Diabetes means "flowing through" and mellitus means "sweet as honey" (Hanas, R, 2005, p.12). Diabetes mellitus is a chronic metabolic disease that the pancreas cannot produce enough insulin or the body cannot effectively use the insulin to lower blood glucose (World Health Organization, 2009). It is also a heterogeneous and polygenic disorder of metabolism of carbohydrate, fat, and protein associated with a relative or absolute insufficiency of insulin secretion and with varying degrees of insulin resistance. Heterogeneity implies that there are differences among various groups of patients in terms of etiology and pathogenesis (genetic, environmental, and immune factors), in natural history, and in response to treatment (Rifkin & Porte, 1990, p.346). So diabetes is not a single disease but a syndrome. One of the risk factors for diabetes is being older. Other risk factors for diabetes include being overweight or obesity, physical inactivity, certain drugs or disease that affect the functioning of the pancreas and family history (Hong Kong Special Administrative Region, 2010). The risk factors of diabetes have additive effects, such that the presence of more risk factors is associated with increased chances of having diabetes (Ko et al., 2000) .
Common symptoms of diabetes include frequency, thirst, fatigue, weight loss, blurred vision and poor wound healing. Diabetes can often be asymptomatic and people affected may remain unaware of the condition until complications develop (Hong Kong Special Administrative Region, 2010). Diabetes can also lead to various adverse consequences, including retinopathy, neuropathy, limb amputation, kidney failure, and heart disease (World Health Organization, 2009). These complications, in particular retinopathy and amputation, affect activities of daily living.
Type of diabetes mellitus
According to the World Health Organization (WHO), there are three common types of diabetes: Type 1, Type 2 and gestational diabetes (World Health Organization, 2009).
Type 1 diabetes mellitus, formerly known as insulin dependent diabetes mellitus (IDDM), usually develops in childhood and adolescence. For this type of diabetes, patients require lifelong insulin injections for survival. It occurs in approximately 10% of all diabetes in the world (World Health Organization, 2010). Genetic factors are very importance in the patients with type 1 diabetes. It can be expressed by the associated increased or decreased frequency of certain histocompatibility locus antigens (HLA) on chromosome number 6 (World Health Organization, 2010). It is likely that in type 1 diabetes, there are one or more immune response genes in linkage disequilibrium with HLA antigens that may increase susceptibility to beta cell damage together with environmental factors (Chuang, Tsai, Juang, Tsai, & Tai, 2000). Genes in the Class II region of the HLA system are associated with type 1 diabetes, not only HLA-DR3 and HLA-DR4 but also HLA-DQ genes. Besides, type 1 diabetes is partly due to non-genetic factor such as environmental factor, and it is thought that both viruses (e.g. coxsackievirus and cytomegalovirus) and toxins (N-nitrose derivatives) contribute to the environmental factor (Atkinson and Eisenbarth, 2001). The combination of genetic and non-genetic factors results in destruction of the insulin secreting beta cells of the pancreas. Those are important indexes in the pathogenesis of type 1 diabetes. The clinical onset of type 1 diabetes mellitus is characterized by both cellular and humoral immune changes. These changes include increased numbers of activated T-lymphocytes expressing the HLA-DR antigen on their cell surface and alterations both the number and function of T-lymphocytes and natural killer cells as well as the production of islet cell antibodies (ICA) and insulin autoantibodies (IAA). In summary, the immune response during the pre-diabetic period involves both cellular and humoral changes probably initiated by an environmental factor and maintained by specific islet cell antigens. This response persists until diagnosis has been made to be diabetes state (Leslie, Lazaus, & Vergani, 1989).
Type 2 diabetes mellitus, formerly known as non-insulin dependent diabetes mellitus (NIDDM), usually appears in adulthood and is due to obesity, lack of exercise and unhealthy diet. This is the commonest type of diabetes, and representing in approximately 90% of diabetic cases worldwide (World Health Organization, 2010). The aetiology of this type of diabetes also has a genetic basis that is commonly expressed by a more frequent familial pattern of occurrence than is seen in type 1 diabetes. The pathogenesis of type 2 diabetes is inadequate insulin secretion form the beta cells in the pancreas and insulin resistance. Environmental factors superimposed on genetic susceptibility are involved in the evolution of type 2 diabetes as well (Stumvoll, Goldstein, & Haeften, 2005). Patients with type 2 diabetes may have an excessive body weight. Obesity resulting in beta cell dysfunction and insulin resistance is an important factor in the pathogenesis of type 2 diabetes (Warren, 2004). In contrary to type 1 diabetes, HLA antigen associations have not been found in most populations with type 2 diabetes. Evidence of cell-mediated immunity and the presence of ICA and IAA characteristic of type 1 diabetes have not been found in type 2 diabetes. Type 2 diabetes has a strong genetic basis of monogenic, e.g. MODY (maturity-onset diabetes of the young, and multi-factorial forms, e.g. TCF7L2 (encoding transcription factor 7-like 2) (Owen & McCarthy, 2007). While the environmental factors involved in the aetiology of type 2 diabetes are thought to be related to diet and obesity (Taylor, 1989). The interaction of gene and environment indicate that increasing environmental pressure may induce susceptibility of the related genes (Reimann et al., 2009).
Gestational diabetes mellitus (GDM) usually develops in pregnant women who have never had diabetes before but who have high blood glucose levels during pregnancy. GDM occurs approximately 7% of pregnancy, which accounts for more than 200,000 cases per year (American Diabetes Association, 2004). Insulin resistance and impaired beta cell function are factors leading to GDM. Pregnancy is at risk of developing diabetes because of impaired insulin sensitivity, particular in second trimester. Placental hormones and cytokines like tissue necrosis factor alpha are thought to be the pathogenesis of insulin resistance. In GDM, beta cell function is deteriorated due to autoimmune response, so in turn decrease the secretion of insulin in the pancreas. Thus, insulin resistance together with impaired secretion during pregnancy results in GDM (Singh & Rastogi, 2008).
Medical complications of diabetes
Diabetes can cause other health-related complications that affect the blood vessels, heart, brain, legs and feet, eyes, kidneys, and nerves (American Diabetes Association, 2009, p.97). These complications are caused by untreated higher blood glucose level and high HbA1c values over time. HbA1c is a fractionated glycohaemoglobin (Motta, Bennati, Cardillo, Ferlito, & Malaguarnera, 2010). It can be used to measure the percentage of the haemoglobin in the red blood cells that has glucose bound to it. So, HbA1c reflects an average of the blood glucose levels (American Diabetes Association, 2003). When plasma glucose level becomes high, glucose may bind to different proteins in the blood, forming Advanced Glycation End products (AGE) that can in turn bind to receptors on the cell wall. Therefore, this can cause damage to the function of cells in blood vessel walls, in retina and smooth muscle cells in inner organs, etc (Bloomgarden, 1996). Because high blood glucose can damage the blood vessels, they will become weak, narrow, or blocked, and then form atherosclerosis. Finally, less blood flows through the blood vessels and the organs will get damaged (American Diabetes Association, 2009, p.98). Thus, diabetes complications are mainly due to vascular impairment, this can be divided into two categories, macrovascular diseases and microvascular diseases (Gossain & Aldasouqi, 2010).
For macrovascular diseases, examples are heart disease and peripheral vascular disease. Developing of atherosclerosis is the main cause, this may lead to stoke, myocardial infarction, coronary heart disease and congestive heart failure (Heydari, Radi, Razmjou, & Amiri, 2010).
On the other hand, for microvascular disease, examples include diabetic retinopathy, nephropathy, neuropathy and diabetic foot (Heydari et al., 2010).
Diabetic retinopathy is caused when high blood glucose levels damage capillaries in the retina. There are two forms of retinopathy. In non-proliferative retinopathy, small blood vessels in the retina bulge and form pouches, called microaneurysms. This causes the retina to swell and lead to blur, distort, reduce, or darken the sight. However, in proliferative retinopathy, the capillaries are so damaged, in response many new, very small blood vessels grow and branch out to other parts of the eye. The new blood vessels are fragile, and may bleed and cause vitreous haemorrhage. Also, broken blood vessels may cause scar tissue to form on the retina and finally lead to detached retina and blind (American Diabetes Association, 2009, p.102-104) (World Health Organization, 2005).
Nephropathy is another serious complication of diabetes. People with diabetes, the blood vessels may become damaged and cause microalbuminuria. At this time, blood vessels in the kidney becoming sclerotic and hypertension may also result (Lodewick, 1998, p.224). Abnormal level of albumin can be detected in urine, when albuminuria â‰¥ 30mg/24h or â‰¥ 20Âµg/min, it is diagnosed as nephropathy (Fares, Kanaan, & Azar, 2010)
Neuropathy is very common in people with type 2 diabetes. It can affect any of the peripheral nerves. Chronic hyperglycaemia and insulin deficiency are important factors in the causation of diabetic neuropathy. It is the lesions involving peripheral nerve axons (Rifkin & Porte, 1990, p.714). For instance, distal symmetric polyneuropathy is nerve damage to the feet and legs and sometimes the hands. It is the most common form of neuropathy. People with this type of neuropathy may have numbness, prickling sensations, muscle weakness, etc (Edwards, Vincent, Cheng, & Feldman, 2008).
Diabetic foot is another common complication of diabetes. In recent theory, most diabetic foot complications occur because of neuropathy not ischemia (Kosinski & Joseph, 2007). Neuropathy is the major predisposing factor of skin break-down and ulcers formation. When ulcers are formed, it can provide a route of entry for bacteria into the deeper tissue of the foot. Diabetic foot problems result from painless trauma and ulceration. Moreover, alter immune function in diabetes together with the vascular insufficiency that prevents adequate delivery of oxygen, nutrients, and antibiotic to the infected area. Then, it can make it easier for wounds in the legs to become infected, also make it difficult for wounds in these areas to heal (Cuttica & Philbin, 2010). In serious cases of ischemia, poor circulation can starve leg and foot tissue of oxygen. Sometimes, this can cause tissues in the legs and feet to die. This is called gangrene. If dead tissues in the legs and feet become infected with bacteria, the lesions can lead to microthrombi formation and further ischemia occurs. The end result of gangrene is amputation of all or part of a foot or leg (American Diabetes Association, 2009, p.100).
Emergency or acute metabolic complications, include diabetic ketoacidosis (DKA), hyperosmolar coma, hypoglycaemia. DKA is a major cause of death in type 1 diabetic patients. It develops as a consequence of a deficiency of insulin. Ketone body production usually parallels with glucose production. Ketoacidosis is primarily due to the overproduction of ketoacids by the liver. The increase in ketoacid production causes loss of bicarbonate and other body buffer, with the subsequent development of metabolic acidosis (Rifkin & Porte, 1990, p.591). Hypoglycaemia coma is characterized by severe hyperglycaemia, hyperosmolarity, and dehydration in the absence of significant ketoacidosis results as coma associated with severe total body fluid depletion and renal functional impairment. For hypoglycaemia, insulin excess is a well recognized risk factor in patients with type 1 diabetes during insulin therapy. Hypoglycaemia is defined as blood glucose less than 50 mg/dl (Rifkin & Porte, 1990, p.526).
Other complications include dental gum disease, infections of skin, bladder and others; increased risk of depression, anxiety, and eating disorders. Complications during pregnancy, includes increased risk of miscarriage, preeclampsia, premature labor, macrosomia (Eisenstat, Nathan, & Barlow, 2007, p.78).
Diagnostic criteria and classification
Confirmation of chronic hyperglycaemia is required for the diagnosis of diabetes mellitus. The state of glycaemia can be divided into three categories: diabetic state, borderline state (i.e. impaired glucose tolerance and impaired fasting glucose), and normal state (Kuzuya et al., 2002). According to the WHO and International Diabetes Federation (IDF), they define diabetes as fasting plasma glucose (FPG) level is â‰¥ 7.0 mmol/l (126 mg/dl) and/or 2-hour plasma glucose (2hPG) level is â‰¥ 11.1 mmol/l (200 mg/dl). Impaired glucose tolerance (IGT) is defined as FPG level is < 7.0 mmol/l (126 mg/dl) and 2hPG level is between 7.8 to 11.0 mmol/l (140 to 200 mg/dl). Impaired fasting glucose (IFG) is defined as FPG level of 6.1 to 6.9 mmol/l (110 mg/dl to 125 mg/dl) and 2hPG level is < 7.8 mmol/l (140 mg/dl). Normal state is defined when FPG is < 6.1 mmol/l (110 mg/dl) and 2hPG < 7.8 mmol/l (140 mg/dl) (World Health Organization and International Diabetes Federation, 2006). Fasting plasma glucose means glucose level in the morning before breakfast after more than 10 hours of fasting, while 2-hour plasma glucose measurement is based on oral glucose tolerance test (OGTT) with 75g oral glucose load (Puavilai, Chanprasertyotin, & Sriphrapradaeng, 1999). IGT and IFG are often termed as pre-diabetes, which imply a higher risk of developing diabetes (Abujbara & Ajlouni, 2009). While gestational diabetes mellitus can be defined as FPG â‰¥ 5.5 mmol/l (100 mg/dl) and 2hPG â‰¥ 8.3 mmol/l (150 mg/dl) (Kuzuya et al., 2002).
However, in order to confirm the diagnosis of diabetes mellitus, some procedures should be followed. Firstly, we must confirm of persistent hyperglycaemia, i.e. the result of FPG or 2hPG should be performed on two separate days. Secondly, diabetes can be diagnosed by a single plasma glucose result plus other condition happens at the same time such as typical symptoms of diabetes, e.g. thirst, polydipsia, polyuria, and weight loss; or HbA1c â‰¥ 6.5%; or in the present of diabetic retinopathy (Kuzuya et al., 2002).
Laboratory tests for monitoring of diabetes mellitus and its complications
Measurement of glycosylated haemoglobin (HbA1c):
HbA1c can be used as an indicator for the control of blood glucose (Manley, 2003). Measurement of HbA1c is a test that indicates how well diabetes is controlled over a two to three-month period. It varies not only according to the level of glycaemia but also to the turnover rate of haemoglobin (Kuzuya et al., 2002). It has been used to monitor and assist diabetes control. HbA1c is a substance that is formed when sugar in the blood binds to the haemoglobin from red blood cells. Blood sugars bind with haemoglobin, forming glycohaemoglobin and a fraction of this is called the HbA1c. Consequently, blood sugar concentration determines HbA1c concentration and indicates what the blood sugar has been averaging over a two to three-month period (Lind, Odén, Fahlén, & Eliasson, 2008). No fasting is necessary for the HbA1c test, and the blood sample can be taken at any time of day. 4-6 % is normal; however â‰¥ 6.5% of HbA1c level can be used as one of the criteria in diagnosis of diabetes (Gomez-Perez et al., 2010).
Measurement of albumin creatinine ratio in urine:
Microalbuminuria is the earliest manifestation of nephropathy and an indicator of increased cardiovascular risk in diabetic patients. The National Kidney Foundation recommends that type 2 diabetes below the age of 70 and type 1 diabetics over the age of 12 should be screened annually for microalbuminuria. In addition, microalbumin may be done in newly diagnosed type 2 diabetes (National Kidney Foundation, 2009). According to the American Diabetes Association, annual testing should begin 5 years after the diagnosis of type 1 diabetes. Microalbuminuria is said to be present if urinary albumin-to-creatinine ratio is greater than 2.5 mg/mmol in male and 3.5 mg/mmol in female (American Diabetes Association, 2009).
Oral glucose tolerance test (OGTT) and Fasting plasma glucose:
OGTT and fasting plasma glucose can be used to diagnosis of diabetes mellitus, impaired glucose tolerance (IGT) and gestational diabetes mellitus. The test procedures of OGTT is: fasting blood for glucose is collected before starting the test, then 75g anhydrous glucose in 250-300 ml water is administrated orally in 5 minutes, after that, a second blood sample for glucose at 2 hours is collected after the glucose load (The expert committee on the diagnosis and classification of diabetes mellitus, 2003).
Other biochemical tests:
Lipid profile (total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides) can be tested every year in order to monitor complication of heart and artery diseases in diabetic patients. Urinalysis (protein, glucose and ketone bodies) is help to monitor kidney complications and ketoacidosis (Lodewick, 1998).
Management of diabetic foot infections:
Most diabetic foot infections are due to polymicrobial with Staphylococcus and Streptococcus in common (Kosinski & Joseph, 2007). Although the initial antibiotic therapy should be empiric in the management of diabetic foot infections, resistance strains are emerged frequently, such as MRSA (Abdulrazak, Bitar, Al-Shamali, & Mobasher, 2005). So, in order to provide a more suitable treatment to the diabetic patients, bacterial culture together with susceptibility test on the given antibiotics should be tested as a guild of definitive therapy (Zgonis, Jolly, Buren, & Blume, 2003). When the infection of diabetic foot proceeds further into bone tissue, it may cause osteomyelitis, and at that time, bone should be sent to microbiology laboratory for cultures and Gram stain (Kosinski & Joseph, 2007). Moreover, laboratory tests for suspected infection of diabetic foot include complete blood picture, erythrocyte sedimentation rate, and C-reactive protein. As patients with diabetic foot infections require a multi-disciplinary approach in the management of the disease, appropriate use of different laboratory tests can allow for early diagnosis and treatment, it can improve patient outcomes (Cuttica & Philbin, 2010).
Diabetes becomes a heavy burden on the health care system and the population. Apart from the direct costs of care and the indirect costs of mortality, there will be a very high cost of disability and reduced quality of life. The increasing number of population, especially older people will increase the number of cases of diabetes. It is estimated that the global prevalence of diabetes from the year of 2000 to 2030 is 2.8% to 4.4% respectively. The total number of diabetic patients will be raised from 171 million in 2000 to 366 million in 2030 (Wild, Gojka, Green, Sicree, & King, 2004). Such a huge increase of diabetes cases in the future, we as health care professional, should make every effort to diagnosis as well as control and monitored for the diabetes mellitus and its complications. The importance of diagnosing diabetes is to allow early detection and treatment, in order to prevent complications. However, prevention is better than cure. Adoption of a healthy lifestyle should start at a young age.