Type I antithrombin deficiency
Type I antithrombin deficiency is characterized by a decrease in both antithrombin activity and antithrombin concentration in the blood of affected individuals. Type I deficiency was originally further divided into two subgroups, Ia and Ib, based upon heparin affinity. The antithrombin of subgroup Ia individuals showed a normal affinity for heparin while the antithrombin of subgroup Ib individuals showed a reduced affinity for heparin. Subsequent functional analysis of a group of 1b cases found them not only to have reduced heparin affinity but multiple or pleiotrophic abnormalities affecting the reactive site, the heparin binding site and antithrombin blood concentration. In a revised system of classification adopted by the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis, type Ib cases are now designated as type II PE, Pleiotrophic effect.Most cases of type I deficiency are due to point mutations, deletions or minor insertions within the antithrombin gene. These genetic mutations result in type I deficiency through a variety of mechanisms:

Mutations may produce unstable antithrombins that either may be not exported into the blood correctly upon completion biosynthesis or exist in the blood for a shortened period of time, e.g., the deletion of 6 base pairs in codons 106–108. Mutations may affect mRNA processing of the antithrombin gene. Minor insertions or deletions may lead to frame shift mutations and premature termination of the antithrombin gene. Point mutations may also result in the premature generation of a termination or stop codon e.g.
Phlyctenular keratoconjunctivitis is an inflammatory syndrome caused by a delayed (aka type-IV) hypersensitivity reaction to one or more antigens. The triggering antigen is usually a bacterial protein (particularly from Staphylococcus aureus), but may also be a virus, fungus (particularly Candida albicans), or nematode. Symptoms
Irritation 
Discomfort or pain 
Foreign-body sensation 
Tearing 
Blepharospasm
Photophobia
Mucopurulent discharge (rarely) In cases where the cornea is affected, pain and photophobia are more likely, and corneal scarring can occur (potentially impairing vision). Presentation
The syndrome is marked by the appearance of characteristic lesions, known as phlyctenules, on the cornea and/or conjunctiva. These usually manifest as small (1 - 3 or 1 - 4 mm) raised nodules, pinkish-white or yellow in color, which may ulcerate (or, more rarely, necrose) and are often surrounded by dilated blood vessels. Corneal lesions are usually triangular in shape, with the base at the limbus and the apex pointing towards the center of the cornea. Diagnosis
Clinical findings of Corneal lesion or  corneal ulceration. Treatment
The symptoms of phlyctenular keratoconjunctivitis are primarily treated with application of an appropriate corticosteroid eye drop, such as prednisolone acetate (Pred Forte) or loteprednol (Lotemax). Loteprednol is increasingly preferred due to its lower risk of elevating intraocular pressure. The corticosteroid suppresses the immune response, reducing inflammation and improving most symptoms.The causative agent (i.e. the source of the antigen that triggered the hypersensitive immune response) should also be identified. Staphylococcus aureus is usually the primary suspect, along with Mycobacterium tuberculosis in areas where TB is endemic, followed by Chlamydia trachomatis.