Linear IgA bullous dermatosis is a rare immune-mediated blistering skin disease frequently associated with medication exposure, especially vancomycin, with men and women being equally affected. : 135   It was first described by Tadeusz Chorzelski in 1979 and may be divided into two types:: 587 
Adult linear IgA disease is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance. This disease can often be difficult to treat even with usually effective medications such as rituximab. Childhood linear IgA disease (also known as "Chronic bullous disease of childhood") is an acquired, self-limited bullous disease that may begin by the time the patient is age 2 to 3 and usually remits by age 13. See also
Skin lesion
List of cutaneous conditions
List of target antigens in pemphigoid
List of immunofluorescence findings for autoimmune bullous conditions

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Symptoms include upper gastrointestinal tract dysfunction such as delayed gastric emptying or lower gastrointestinal dysfunction, such as constipation and prolonged stool transit time.Urinary retention, waking at night to urinate, increased urinary frequency and urgency, and over- or underactive bladder are common in people with synucleinopathies. Sexual dysfunction usually appears early in synucleinopathies, and may include erectile dysfunction, and difficulties achieving orgasm or ejaculating. Diagnosis
Differential diagnosis
Persons with PD are typically less caught up in their visual hallucinations than those with DLB. There is a lower incidence of tremor at rest in DLB than in PD, and signs of parkinsonism in DLB are more symmetrical. In MSA, autonomic dysfunction appears earlier and is more severe, and is accompanied by uncoordinated movements, while visual hallucinations and fluctuating cognition are less common than in DLB. Urinary difficulties are one of the earliest symptoms with MSA, and are often severe. DNA damage
Alpha-synuclein modulates DNA repair processes, including the repair of DNA double-strand breaks by the non-homologous end joining pathway. The DNA repair function of alpha-synuclein appears to be compromised in Lewy body inclusion bearing neurons, and this may trigger cell death. Study of synucleinopathy mouse models of Parkinson’s disease indicates that alpha-synuclein pathogenesis is associated with increased DNA damage and activation of the DNA damage response. See also
Proteopathy
Lewy body


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