Type T: prior kidney transplant.An early age of onset or long-standing disease comes with greater risks, hence the first three subtypes.Two other sets of criteria are available for diagnosis of gestational diabetes, both based on blood-sugar levels.Criteria for diagnosis of gestational diabetes, using the 100 gram Glucose Tolerance Test, according to Carpenter and Coustan:
Fasting 95 mg/dl
1 hour 180 mg/dl
2 hours 155 mg/dl
3 hours 140 mg/dlCriteria for diagnosis of gestational diabetes according to National Diabetes Data Group:
Fasting 105 mg/dl
1 hour 190 mg/dl
2 hours 165 mg/dl
3 hours 145 mg/dl

Risk factors
Classical risk factors for developing gestational diabetes are:
Polycystic ovary syndrome
A previous diagnosis of gestational diabetes or prediabetes, impaired glucose tolerance, or impaired fasting glycaemia
A family history revealing a first-degree relative with type 2 diabetes
Maternal age – a womans risk factor increases as she gets older (especially for women over 35 years of age). Paternal age – one study found that a fathers age over 55 years was associated with GD
Ethnicity (those with higher risk factors include African-Americans, Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people originating from South Asia)
Being overweight, obese or severely obese increases the risk by a factor 2.1, 3.6 and 8.6, respectively. A previous pregnancy which resulted in a child with a macrosomia (high birth weight: >90th centile or >4000 g (8 lbs 12.8 oz))
Previous poor obstetric history
Other genetic risk factors: There are at least 10 genes where certain polymorphism are associated with an increased risk of gestational diabetes, most notably TCF7L2.In addition to this, statistics show a double risk of GDM in smokers.
Because ML I is classified as a sialidosis, it is sometimes referred to as sialidosis type II. A rarer form of sialidosis – sialidosis type 1– occurs in children and adolescents and is often referred to as the juvenile form of the disorder. Children usually begin to show symptoms during the second decade of life, and myoclonus and cherry-red macules are often the initial symptoms. Patients usually develop seizures and progressive deterioration of coordinated muscular and mental activities. Pathophysiology
The role of sialidase is to remove a particular form of sialic acid (a sugar molecule) from sugar-protein complexes (referred to as glycoproteins), which allows the cell to function properly. Because the enzyme is deficient, small chains containing the sugar-like material accumulate in neurons, bone marrow, and various cells that defend the body against infection. Diagnosis
The detection of high urinary sialyl oligosaccharides and the confirmation of lysosomal enzyme deficiency in leukocytes or cultured fibroblasts make the diagnosis. Management
Treatment of sialidosis is similar to the other progressive myoclonic epilepsy disorders, which consists of managing seizures and myoclonus along with palliative, supportive, and rehabilitative care. See also
Fucosidosis
Sialic acid
Neuraminidase
Mucolipidosis
Lysosomal storage disease

Notes
References
mucolipidoses at NINDS - article derived from detail sheet available here

External links

Sialidosis type 1 and 3 at NIHs Office of Rare Diseases
Sialidosis at NIHs Office of Rare Diseases