Differentials
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Diabetes Mellitus Type 2Published by: Domus Medica | SSMGLast published: 2017Diabète sucré de type 2Published by: SSMG | Domus MedicaLast published: 2017Prediabetes
SIGNS / SYMPTOMS
Patients with prediabetes often have no specific differentiating signs or symptoms.
Diabetes mellitus, type 1
SIGNS / SYMPTOMS
Onset often at age <35 years, but can occur in older individuals.[2]
Many patients do not have obesity.[2]
More commonly presents with symptoms (polyuria, polydipsia, weight loss, generalized weakness, blurred vision) and ketosis, rather than being detected by screening.[82]
INVESTIGATIONS
Urine ketones are often present in type 1 diabetes, but may also be positive in type 2 diabetes if there is severe volume depletion.
Low (<0.2 nmol/L) or absent C-peptide level.[83]
One or more autoantibodies (anti-glutamic acid decarboxylase 65 [GAD65] antibodies, islet cell antibodies [ICA], insulin autoantibodies, autoantibodies to the tyrosine phosphatase-related islet antigen-2 [IA-2 and IA-2beta], and zinc-transporter-8 [ZnT8] antibodies) are present in 85% of patients with type 1 at the time of diagnosis, but may disappear within a few years.[2]
Glucose screening criteria cannot be used to differentiate type 1 and type 2 diabetes, as they are identical.[2]
Latent autoimmune diabetes in adults (LADA)
SIGNS / SYMPTOMS
Typical age of onset of diabetes is over 30 years old. Patients usually do not have obesity and respond initially to lifestyle modifications and oral agents. Production of insulin gradually decreases (between 6 months and 5 years), such that treatment with insulin is required.[88]
LADA is considered a subset of autoimmune type 1 diabetes (immune-mediated diabetes); however, patients with LADA are frequently misclassified as having type 2 diabetes.
INVESTIGATIONS
Low to normal initial C-peptide level.
Autoantibodies present. May include antibodies against glutamic acid decarboxylase 65 (GAD65), islet cells (ICA), insulin, tyrosine phosphatase-related islet antigen-2 (IA-2 and IA-2 beta), and zinc-transporter-8 (ZnT8).[2]
Monogenic diabetes
SIGNS / SYMPTOMS
Maturity-onset diabetes of the young (MODY) is the most common form of monogenic diabetes and affects 1% to 2% of people with diabetes.[89]
MODY is caused by mutation of a single gene (i.e., monogenic). At least 14 gene mutations of MODY are known.[90]
It has autosomal dominant inheritance and should be suspected in cases of diabetes in young patients (adolescent or young adult) without obesity, who have a family history of diabetes in at least one first-degree relative.[90]
Presents with nonketotic, noninsulin-dependent diabetes that responds to oral glucose-lowering drugs.[91][92]
INVESTIGATIONS
C-peptide present.
Autoantibodies absent.
Genetic testing in patients with high index of suspicion identifies mutations most commonly in genes encoding glucokinase and transcription factors.[93]
Ketosis-prone diabetes
SIGNS / SYMPTOMS
Presents with unprovoked ketosis or ketoacidosis.[94]
Considered an "idiopathic diabetes," as patients have no evidence of autoimmunity. Often misclassified as type 1 diabetes, as individuals have episodic ketoacidosis and exhibit varying degrees of insulin deficiency between episodes. However, a type 2 diabetes phenotype is common (obesity, insulin resistance, metabolic syndrome).[95]
Patients are usually from a minority ethnic group, and have a positive family history of diabetes.[95]
On discontinuation of insulin therapy, the period of near-normoglycemic remission may last for a few months to several years. However, almost half will be insulin dependent 10 years after diagnosis.[94]
INVESTIGATIONS
Absent islet cell autoantibodies.
C-peptide often low or undetectable during diabetic ketoacidosis; recovery may be used as reliable predictor of insulin discontinuation.[95]
Diabetes, gestational
SIGNS / SYMPTOMS
Only occurs during pregnancy.
INVESTIGATIONS
The American Diabetes Association recommends preconception screening for undiagnosed diabetes in all women at increased risk for type 2 diabetes who are planning a pregnancy.[2]
For those who were not screened at preconception, patients at increased risk for type 2 diabetes should be screened within the first 15 weeks of pregnancy (i.e., at their first prenatal visit) with an HbA1c or a fasting blood sugar using standard diagnostic criteria.[2]
If early screening is negative, screening should be repeated at 24-28 weeks' gestation.[2]
An alternative approach is to perform preconception screening in all women of childbearing potential (universal screening), which may be increasingly appropriate in populations with a high prevalence of risk factors and/or undiagnosed diabetes. Likewise, universal screening for undiagnosed type 2 diabetes may be considered at the first prenatal visit for all pregnant women, assuming they have not already been screened preconception.[2]
Diabetes related to disorders of the exocrine pancreas ("pancreatic diabetes")
SIGNS / SYMPTOMS
Occurs in individuals who have had a loss of pancreatic mass for a variety of reasons (pancreatitis, trauma, surgery, cystic fibrosis, hemochromatosis).
INVESTIGATIONS
Diagnosis based on clinical criteria including clinical history, as well as diagnostic testing for disorders such as cystic fibrosis and hemochromatosis. The American Diabetes Association recommends screening people for diabetes within 3-6 months of an episode of acute pancreatitis and annually thereafter.[2] Screening for diabetes is recommended annually for people with chronic pancreatitis.[2] Annual screening for cystic fibrosis-related diabetes (CFRD) with an oral glucose tolerance test should begin by age 10 years in all people with cystic fibrosis not previously diagnosed with CFRD. HbA1c is not recommended as a screening test for CFRD due to low sensitivity. However, a value of ≥6.5% (≥48 mmol/mol) is consistent with a diagnosis of CFRD.[2]
Post-transplantation diabetes mellitus (PTDM)
SIGNS / SYMPTOMS
History of organ transplantation. Risk factors for PTDM include both general diabetes risks (such as age, family history of diabetes, obesity, etc) and transplant-specific factors, such as use of immunosuppressant agents.[2]
INVESTIGATIONS
A formal diagnosis of PTDM is optimally made once the individual is stable on maintenance immunosuppression (usually at least 45 days after transplantation) and in the absence of acute infection. This is because hyperglycemia is very common during the early post-transplant period, with approximately 90% of kidney allograft recipients exhibiting hyperglycemia in the first few weeks following transplant. In most cases, such stress- or steroid-induced hyperglycemia resolves by the time of discharge.[2] The oral glucose tolerance test (OGTT) is considered the gold-standard test for the diagnosis of PTDM. However, screening people with fasting plasma glucose and/or HbA1c can identify high-risk individuals who require further assessment and may reduce the number of overall OGTTs required.[2]
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