Biological agents, such as anti-tissue necrosis factors (anti-TNF), is a well-established treatment of systemic inflammatory diseases, Infliximab and Adalimumab are TNF blockers for treating RA-associated PUK. However, the high cost and uncertainty of long-term side effects are the possible drawbacks. Surgical treatment
In terms of surgical treatment, conjunctival resection is a common procedure, which can temporarily remove local inflammatory mediators and collagenases and therefore slow down the disease progression. Other surgical management includes corneal gluing, or keratoplasty procedures. Corneal transplantation is a management option when there is severe corneal melting or perforation although one possible disadvantage is the risk of rejection.Surgical treatment helps maintain the integrity of the globe, but it is usually complementary because it alone cannot influence the underlying immunological process. Therefore, medical and surgical treatments are commonly used in conjunction. Choice of treatment
The choice of treatment may be different depending on the nature of PUK, infectious or noninfectious. Selection of the right targeted antimicrobial therapy for infectious PUK is based on clinical judgement and culture results. For example, the appropriate treatment for bacterial infections is antibiotics, such as fluoroquinolones. As for Moorens ulcers, 56% of unilateral PUK and 50% of bilateral PUK in one eye showed recovery with intensive topical steroids. Only 18% of patients with bilateral ulcers occurring simultaneously in both eyes show improvements with topical steroids alone; therefore a combination of immunosuppressive agents and systemic steroids should be given in early courses of management. Corticosteroids are the first line of therapy, but side effects may arise from long-term usage.
In some cases, there are significant differences in the activity of the mutant gene product that contribute to variations in the clinical features of the diabetes (such as degree of insulin deficiency or age of onset). Diagnosis
The following characteristics suggest the possibility of a diagnosis of MODY in hyperglycemic and diabetic patients:
Mild to moderate hyperglycemia (typically 130–250 mg/dL, or 7–14 mmol/L) discovered before 30 years of age. However, anyone under 50 can develop MODY. A first-degree relative with a similar degree of diabetes. Absence of positive antibodies or other autoimmunity (e.g., thyroiditis) in patient and family. However, Urbanova et al. found that about one quarter of Central European MODY patients are positive for islet cell autoantibodies (GABA and IA2A). Their expression is transient but highly prevalent. The autoantibodies were found in patients with delayed diabetes onset, and in times of insufficient diabetes control. The islet cell autoantibodies are absent in MODY in at least some populations (Japanese, Britons). Persistence of a low insulin requirement (e.g., less than 0.5 u/kg/day) past the usual "honeymoon" period. Absence of obesity (although overweight or obese people can get MODY) or other problems associated with type 2 diabetes or metabolic syndrome (e.g., hypertension, hyperlipidemia, polycystic ovary syndrome). Insulin resistance very rarely happens. Cystic kidney disease in patient or close relatives. Non-transient neonatal diabetes, or apparent type 1 diabetes with onset before six months of age.