Diabetes may be primary or secondary (Table 19.1). Although secondary diabetes accounts for barely 1-2% of all new cases at presentation, it should not be missed because the cause can often be treated. Type 1 diabetes (insulin-dependent diabetes mellitus) and type 2 diabetes (non-insulin-dependent diabetes mellitus) represent two distinct diseases from the epidemiological point of view, but clinical distinction can sometimes be difficult. The two diseases should, in clinical terms, be seen as a spectrum, distinct at the two ends but overlapping to some extent in the middle (Table 19.2). Varying degrees of insulin secretory failure may be present in both forms of diabetes. For example, some patients with immune-mediated diabetes may not at first require insulin, whereas many with type 2 diabetes will eventually do so.

Type 1 diabetes mellitus

Epidemiology

Table 19-1. Causes of secondary diabetes

Pancreatic disease

Cystic fibrosis

Chronic pancreatitis

Malnutrition-related pancreatic disease

Pancreatectomy

Hereditary haemochromatosis

Carcinoma of the pancreas

Endocrine disease

Cushing’s syndrome

Acromegaly

Thyrotoxicosis

Phaeochromocytoma

Glucagonoma

Drug-induced disease

Thiazide diuretics

Corticosteroid therapy

Atypical antipsychotics

Antiretroviral protease inhibitors

Insulin-receptor abnormalities

Congenital lipodystrophy

Acanthosis nigricans

Genetic syndromes

Friedreich’s ataxia

Dystrophia myotonica

Table 19-2. The spectrum of diabetes: a comparison of type 1 and type 2 diabetes mellitus

	Type 1 (insulin dependent)	Type 2 (non-insulin dependent)
Epidemiology	Younger (usually < 30 years of age)	Older (usually > 30 years of age)
	Usually lean	Often overweight
	Increased in those of Northern European ancestry	All racial groups. Increased in peoples of Asian, African, Polynesian and American-Indian ancestry
	Seasonal incidence
Heredity	HLA-DR3 or DR4 in > 90%	No HLA links
	30-50% concordance in identical twins	∼ 50% concordance in identical twins
Pathogenesis	Autoimmune disease:	No immune disturbance
	Islet cell autoantibodies	Insulin resistance
	Insulitis
	Association with other autoimmune diseases
	Immunosuppression after diagnosis delays beta-cell destruction
Clinical	Insulin deficiency	Partial insulin deficiency
	May develop ketoacidosis	May develop hyperosmolar state
	Always need insulin	Many come to need insulin when beta-cells fail over time
Biochemical	Eventual disappearance of C-peptide	C-peptide persists

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