Drug-related glaucoma

Introduction to drug-related glaucoma Drug-related glaucoma is mainly corticosteroid glaucoma, which is usually associated with topical application of corticosteroids in the eye, and can also be seen in systemic administration. In recent years, there has been a gradual increase. Corticosteroids cause open-angle glaucoma in glaucoma, which occurs after the use of corticosteroids in the eye or system, including eye drops or eye ointment, periocular injection, external skin, systemic inhalation, and oral or injection. Increased intraocular pressure after prolonged use is called corticosteroid glaucoma, also known as glucocorticoid induced glaucoma (GIG), referred to as hormonal glaucoma. basic knowledge The proportion of illness: 0.0025% Susceptible people: no special people Mode of infection: non-infectious Complications: cataracts, ptosis

Drug-related glaucoma etiology

Glycosaminoglycan theory (45%):

GAGS has strong water absorption. It is normally present in a small amount in the interstitial space of the trabecular meshwork network. It can be hydrolyzed by hyaluronidase. GC can stabilize the lysosomal membrane, thereby inhibiting the release of hyaluronidase, resulting in excessive GAGS. Accumulation in the horn tissue, causing physiological edema, obstructing the outflow of aqueous humor, and increasing the intraocular pressure. This theory does not explain the difference in sensitivity of individuals to GC and the intraocular pressure does not recover in some advanced GIG patients after GC is stopped. phenomenon.

Phagocytic theory (15%):

The trabecular endothelial cells have phagocytic function, which can help remove debris in the aqueous humor. GC can inhibit the phagocytosis, and the debris in the aqueous water can be deposited in the trabecular meshwork, which hinders the outflow of aqueous humor. This hypothesis gives the ultrastructural study of the corner. Support, that is, there are amorphous, fibrous and linear material deposition on the GIG trabeculae, but it can not explain the phenomenon that the trabecular ultrastructure does not change when the animal has high intraocular pressure.

Genetic theory (40%):

Some people think that the intraocular pressure response to GC is determined by genetics. Human genes can be divided into GC high response gene PH and low response gene PL. If it is PHPH, it has a high intraocular pressure reaction. If it is PLPL, it is low. Intraocular pressure response or no reaction, 66% to 70% of normal people are PLPL, 26% to 29% are PHPL, and 4% to 5% are PHPH. POAG is not only particularly sensitive to GC, but almost all are moderate to high. The reaction, genetic hypothesis is inconsistent with the results of studies on twins and repeated tests of GC-induced high intraocular pressure response.

Progress in the pathogenesis of GIG

(1) Relationship between glucocorticoid receptor (GR) and cell sensitivity: The sensitivity of cells to GC is affected by cell variability, GR modification factor, GR activity, quantity and GR self-regulation mechanism. For leukemia cells, the sensitivity to GC has changed.

The difference in sensitivity to GC may be related to the amount and affinity of GR in the aqueous outflow tract cells and the difference in other tissues of the body. The GR in rabbit iris, ciliary body cells and liver cells was determined, and the amount of GR in the former was found to be about The effect was 2 times, but the affinity was the same. Paul et al. used cortisol to influence the 3H-thymidine incorporation as an indicator of cell sensitivity to GC. As a result, there was no difference in GC sensitivity between the two groups. Some studies on trabecular culture of POAG patients. When cortisone is metabolized in cells, it is found that the decrease of 3-oxidoreductase activity leads to the accumulation of 5- hydrocortisone, which promotes GR-induced nuclear transfer, thereby significantly enhancing cell-to-GC. Sensitivity.

Some scholars have used radioimmunoassay to measure the glucocorticoid receptor binding sites in normal people, primary open angle glaucoma and glucocorticoid glaucoma, and the peripheral blood lymphocyte glucocorticoid receptor binding sites. Tissue glucocorticoid receptor sites were significantly higher than normal, suggesting that this may be one of the important factors for their high sensitivity to glucocorticoids. In addition, there are glucocorticoid receptor genes in normal human and open-angle glaucoma trabecular cells. Studies have found that there is no difference in the genetic structure of the two, and it is speculated that glucocorticoid-induced glaucoma is not caused by changes in the glucocorticoid receptor gene, but due to changes in the molecular structure of the glucocorticoid receptor, which may be Somatic regulation of gene expression is associated with abnormal levels of transcriptional translation.

(2) Specific proteins and enzymes induced by GC: After GC and GR are combined, it can induce the synthesis of various proteins and enzymes, thus participating in the regulation of intraocular pressure. It has been confirmed that the degree of GR nuclear transfer caused by dexamethasone is caused by GC in living body. The trend of elevated intraocular pressure is consistent. Recent studies have found that dexamethasone can induce cultured human trabecular mesh cells to synthesize 35S-labeled 35,65,70kD cellular proteins and 40,90,100kD secreted proteins, which induce scleral fibroblasts to synthesize 70kD cellular proteins.

Among the proteins or enzymes induced by GC, some are involved in the metabolism of prostaglandins. Parridge et al. used 10-7 mol of dexamethasone to incubate with human trabecular cells and scleral fibroblasts, and found that 60% prostaglandin synthesis was inhibited. Weinreb et al. Radioimmunoassay showed that dexamethasone could inhibit the synthesis of prostaglandin F2 and E2, and PGE2 and PGF2 played an important role in aqueous humor outflow. It is speculated that dexamethasone-induced 70kD cell protein is associated with the inhibition of the synthesis of these two prostaglandins. It is shown that GC inhibits prostaglandins by inducing the synthesis of lipoprotein, which is an inhibitor of phospholipase A2, which catalyzes the synthesis of arachidonic acid.

GC can also induce the synthesis of certain extracellular matrix proteins. When indirect immunofluorescence is used to analyze the effect of GC on cultured human trabecular mesenchymal proteins, it is found that a large amount of elastin and dots appear in the interstitial after dexamethasone treatment. A stagnation (probably an unknown mixture of proteins), which was not observed in the control group, and speculated that the presence or increase of these substances in the stroma may be responsible for the increased glucocorticoid glaucoma aqueous outflow resistance.

Drug-related glaucoma prevention

First of all, pay attention not to abuse corticosteroids, especially for patients with primary open angle glaucoma and their children, high myopia and hypersensitive to corticosteroids, should be more careful, for patients with conditions, while using corticosteroids Pay attention to the intraocular pressure and choose a corticosteroid drug that has less effect on intraocular pressure to prevent corticosteroid glaucoma.

Drug-related glaucoma complications Complications of cataract

Long-term use of glucocorticoids can also cause the following ocular changes, including: posterior subcapsular cataract, ptosis, dilated pupils, eyelid skin atrophy, eye infections, delayed wound healing, and corneal ulcers, including posterior subcapsular cataract For the most common performance.

Drug-related glaucoma symptoms Common symptoms Visual field changes, elevated intraocular pressure, high intraocular pressure edema

Elevated intraocular pressure with corticosteroids can be elevated as early as 1 week after administration or as late as several years. For patients who have been treated with corticosteroids for a long time, intraocular pressure must be observed regularly. Sadly, many patients with corticosteroid glaucoma It is often used for long-term application of hormones due to minor problems in the eye without any vigilance. In addition, there are still anti-inflammatory eye drops containing hormones (dexamethasone) in the domestic market. Doctors are required to give prescriptions for long-term administration of such drugs to red-eye patients. The patient may be at risk of developing an increase in intraocular pressure, and the patient is required to measure intraocular pressure on a regular basis.

Corticosteroid glaucoma is usually very similar to open-angle glaucoma. Its clinical manifestations vary with the age of the patient. If it occurs in infants and young children, it can be similar to congenital glaucoma. The corneal diameter increases, it is foggy edema, and the post-elasticity The layer is broken and the optic disc physiological sag is enlarged. On the contrary, typical glaucomatous optic disc and visual field changes can occur in the late adult, while the angle of the anterior chamber is open. Individual patients may have symptoms of acute glaucoma, but the angle of the lens is normal, such as When corticosteroids are applied to the whole body or both eyes, the intraocular pressure of both eyes is increased, and if it is used for single eye drops, the intraocular pressure of the eye is increased.

Drug-related glaucoma examination

No special laboratory tests.

Intraocular pressure measurement: intraocular pressure showed a slower rising trend, and consistent with the hormone dosage and time course, the corner mirror examination showed that the angle was open.

Visual field examination, there will be many harms after glaucoma, one of the damages is the reduction of visual field, so the visual field is also to be checked. Now the visual field examination is a fully automatic visual field examination, which can reflect the changes of very weak visual field.

Drug-related glaucoma diagnosis

diagnosis

1. Diagnostic points

1 There is a clear history of local or systemic use of glucocorticoids.

2 The increase in intraocular pressure, amplitude and visual function damage were consistent with the amount of glucocorticoids.

3 The intraocular pressure returned to normal after several days to several weeks after the glucocorticoid was stopped.

Other damages caused by glucocorticoids, such as posterior capsule cataracts, can be found in the eyes.

5 Excluded other secondary open angle glaucoma, especially uveitis secondary to glaucoma, pigmented glaucoma, exfoliation syndrome, retrograde glaucoma.

In some clinical cases, the intraocular pressure continues to increase after the long-term use of glucocorticoids. Some patients have normalized intraocular pressure after stopping the drug, but long-term high intraocular pressure has left different degrees of visual function. And optic nerve damage, these cases are easily confused with the primary open angle glaucoma that happens to use glucocorticoids.

2. Classification

After the analysis of clinical data in China, the following identification and classification schemes are proposed:

Type I:

1 eye topical medication> 3 months;

2 has clinical manifestations similar to primary open angle glaucoma;

3 The degree of optic nerve damage is basically commensurate with the time of administration;

4 may or may not be associated with posterior capsule cataract;

5 After the drug is stopped, the intraocular pressure can return to normal.

Type II: Same type I, the intraocular pressure decreased after stopping the drug but could not return to normal level, and most of them were accompanied by posterior capsule cataract.

Type III: The duration of medication and visual function damage are not commensurate, that is, the medication time is short, the visual function damage is heavy; both eyes are used at the same time, and in the case of the same medication time and dose, the binocular visual function damage is obviously asymmetrical; the intraocular pressure is not after the drug is stopped. Decline, even progressively.

The use of this classification basically excludes primary open angle glaucoma in type I and II, and only in cases of type III may be associated with primary open angle glaucoma, a classification that guides glucocorticoid glaucoma The treatment is meaningful.

Differential diagnosis

In addition to the identification points mentioned in the above diagnostic classification and primary open angle glaucoma, the following should be identified:

1. Uveitis secondary to glaucoma: Because uveitis can also cause elevated intraocular pressure, and it requires glucocorticoid treatment, glucocorticoids on the one hand inhibit the inflammation to increase the production of aqueous humor, in addition to the above glucocorticoid Hormone-induced glaucoma leads to an increase in intraocular pressure. In this case, it is difficult to make a differential diagnosis. If it is highly suspected that the intraocular pressure is elevated due to glucocorticoids, other less elevated intraocular pressure may be used. Corticosteroid preparations, decreased intraocular pressure after dressing change may indicate high intraocular pressure caused by glucocorticoids. If there is no change in intraocular pressure, uveitis is more likely to be secondary to glaucoma.

2. Traumatic angle of the anterior recoil, exfoliation syndrome, pigment dissemination syndrome: There is the possibility of glaucoma, and there is also the possibility of high sensitivity to glucocorticoids. If the above cases of elevated intraocular pressure should be excluded first No use of glucocorticoids, if the history of useful drugs should be discontinued to observe the intraocular pressure and then make a diagnosis.

3. Others: In some cases, due to the unclear use of glucocorticoids, there has been a history of elevated intraocular pressure, and cases with normal intraocular pressure at the time of treatment may also be stimulating with glucocorticoids.

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