Iridocorneal endothelial (ICE) syndromes are a spectrum of diseases characterized by slowly progressive abnormalities of the corneal endothelium and features including corneal edema, iris distortion, and secondary angle-closure glaucoma. ICE syndromes are predominantly unilateral and nonhereditary. The condition occurs in predominantly middle-aged women. Signs and symptoms
Many cases are asymptomatic, however patients many have decreased vision, glare, monocular diplopia or polyopia, and noticeable iris changes. On exam patients have normal to decreased visual acuity, and a "beaten metal appearance" of the corneal endothelium, corneal edema, increased intraocular pressure, peripheral anterior synechiae, and iris changes. Mechanism
The exact mechanism is unknown, however there appears to be a component of abnormal corneal endothelium that proliferates onto the iris forming a membrane that then obstructs the trabecular meshwork, leading to iris distortion. Nodule formation can also occur when the abnormal corneal endothelium causes contractions around the iris stroma. Herpesvirus DNA has been identified in some patients following keratoplasty, suggesting the possibility that herpes simplex virus may induce the abnormal endotheliazation in the anterior chamber angle and on the surface of the iris. Variations
The Chandler variant of ICE is characterized by pathology on the inner surface of the cornea leading to abnormal endothelial pump function. Other features include possible mild iris changes, corneal edema, and normal to slight elevations in intraocular pressure.Cogan-Reese variant is characterized by multiple pigmented iris nodules. This variant is most commonly unilateral and seen in middle-aged females. Diagnosis
Treatment
Penetrating karatoplasty and endothelial keratoplasty can be used as treatments for severe cases of ICE.
People who excessively consume alcohol are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, which further depletes phosphate, and the stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above). Malabsorption – This includes gastrointestinal damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids. Intravenous iron (usually for anemia) may cause hypophosphatemia. The loss of phosphate is predominantly the result of renal wasting.Primary hypophosphatemia is the most common cause of non-nutritional rickets. Laboratory findings include low-normal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism.Hypophosphatemia decreases 2,3-bisphosphoglycerate (2,3-BPG) causing a left shift in the oxyhemoglobin curve.Other rarer causes include:

Certain blood cancers such as lymphoma or leukemia
Hereditary causes
Liver failure
Tumor-induced osteomalacia

Pathophysiology
Hypophosphatemia is caused by the following three mechanisms:

Inadequate intake (often unmasked in refeeding after long-term low phosphate intake)
Increased excretion (e.g. in hyperparathyroidism, hypophosphatemic rickets)
Shift of phosphorus from the extracellular to the intracellular space. This can be seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g. hungry bone syndrome) and acute respiratory alkalosis. Diagnosis
Hypophosphatemia is diagnosed by measuring the concentration of phosphate in the blood. Concentrations of phosphate less than 0.81 mmol/L (2.5 mg/dL) are considered diagnostic of hypophosphatemia, though additional tests may be needed to identify the underlying cause of the disorder.