Pemphigoid is a group of rare autoimmune blistering diseases of the skin, and mucous membranes. As its name indicates, pemphigoid is similar in general appearance to pemphigus, but, unlike pemphigus, pemphigoid does not feature acantholysis, a loss of connections between skin cells.Pemphigoid is more common than pemphigus, and is slightly more common in women than in men. It is also more common in people aged over 70 years than it is in younger people. Classification
IgG
The forms of pemphigoid are considered to be connective tissue autoimmune skin diseases. There are several types:

Gestational pemphigoid (PG) (formerly called Herpes gestationis)
Bullous pemphigoid (BP) Rarely affects the mouth
Mucous membrane pemphigoid (MMP) or (cicatricial pemphigoid), (No skin involvement)Bullous and mucous membrane pemphigoid usually affect persons who are over age 60. Gestational pemphigoid occurs during pregnancy, typically in the second or third trimester, or immediately following pregnancy. IgA
Pemphigoid is usually considered to be mediated by IgG, but IgA-mediated forms have also been described.IgA-mediated immunobullous diseases can often be difficult to treat even with usually effective medications such as rituximab. Bullous pemphigoid
Bullous pemphigoid is a rare and chronic autoimmune disorder characterised by large sub-epidermal blisters called bullae, that predominantly involves the skin and less commonly the mucous membranes. It is the most common type of the pemphigoid group, representing 80% of sub-epidermal immunobullous cases. It is more commonly known as cutaneous pemphigoid. Presentation
Primary lesions of small and large blisters, known as vesicles and bullae, are found on the skin and sometimes on the mucous membranes.
Infants from diabetic mothers usually have several blastogenic malformations. Diabetic embryopathy is therefore an etiological subgroup of defects of blastogenesis that present different monotopic and polytopic developmental defects. Abortion and perinatal deaths
Diabetic embryopathy may result in early or late spontaneous abortion and stillbirth. In maternal diabetes, 90% of pregnancy losses happen in the first trimester due to oxidative stress. Diabetic embryopathy abortions in the second-trimester are most likely due to severe birth defect, maternal metabolic derangement, placental insufficiency and fetal hypoxia due to membrane rupture. Pathogenesis
The development of birth defects associated with maternal hyperglycemia is multi-factorial. Environmental factors and genetic predisposition (paternal, maternal and offspring genome) are important in diabetic embryopathy. The diets of diabetic mothers impacts the rate at which malformations form in their offspring. Furthermore, there is evidence that resistance to certain malformations caused by diabetes is genetic. Epigenetics and its relationship with various environmental factors such as metabolism and diet play a significant role in teratogenesis. Hyperglycemia and associated teratogenic mediators influence DNA methylation, non-coding RNA expression, histone modifications and other epigenetic regulation mechanisms. Research is focused on exploring the impact of diabetic embryopathy on methylation signatures, which could potentially serve as a diagnostic biomarker for the condition. Prevention
Preconception
The probability of major birth defects in offspring of mothers with diabetes is 0.7-4.4% for glycohemoglobin levels <7%. For glycohemoglobin levels >10% the probability of major birth defects is 16.1-100% with an average of 26.6%.