In general, levels below 350mcg/dL are associated with more mild iron poisoning while upper levels above 500mcg/dL are associated with more severe iron poisoning. Measuring electrolyte levels, kidney function, serum glucose, liver function tests (enzymes and bilirubin), complete blood count, clotting time via prothrombin and partial thromboplastin time, anion gap for metabolic acidosis, should be conducted for clinical monitoring and confirmation of iron poisoning.The deferoxamine challenge test is a diagnostic test for confirming iron poisoning, however it is no longer recommended for diagnostic purposes due to concerns regarding the accuracy. Deferoxamine can be administered intramuscularly as a single dose where it then binds to free iron in the blood and is excreted into the urine turning it to a "brick orange" or pink/red/orange color. Radiographs are no longer used for diagnosis due to the lack of connection between severity of iron toxicity and the presence of radiopaque iron tablets in the stomach on X-rays. This method also requires that the ingested tablet to be radiopaque which most iron preparations are not. Treatment
Management of acute iron poisoning involves providing a patient with respiratory support and intravenous deferoxamine. Patients exhibiting severe symptoms in the gastrointestinal phase should receive volume resuscitation to prevent hypovolemic shock from the loss of blood volume. Normal saline is administered intravenously to maintain adequate volume of fluid in the body. Deferoxamine is a drug that is used in cases of serious iron poisoning.
Pemphigus foliaceus is an autoimmune blistering disease (bullous disorder) of the skin. Pemphigus foliaceus causes a characteristic inflammatory attack at the subcorneal layer of epidermis, which results in skin lesions that are scaly or crusted erosions with an erythematous (red) base. Mucosal involvement is absent even with widespread disease.If there is an autoimmune IgG buildup in the epidermis, then nearly all of the antibodies are aimed against desmoglein 1. The effect of the antibodies and the immunological pathway is most likely one of three mechanisms:

Steric hindrance of the desmoglein 1: The antibody caps off the site for intracellular binding to another keratinocyte. Activation of an endocytic pathway: The antibody activates a pathway which causes an internalization of desmogleïn 1, which in turn causes a loss of adhesion. Disruption of function: In this case, the antibody blocks the desmoglein 1 from being formed into a desmosome. This in turn causes a loss of adhesion with acantholysis as a result. Cause
The National Institute of Arthritis and Musculoskeletal and Skin Diseases describes it like this:
Normally, our immune system produces antibodies that attack viruses and harmful bacteria to keep us healthy. In people with pemphigus, however, the immune system mistakenly attacks the cells in the epidermis, or top layer of the skin, and the mucous membranes. The immune system produces antibodies against proteins in the skin known as desmogleins. These proteins form the glue that keeps skin cells attached and the skin intact.