Toxic optic neuropathy

Linezolid Prevents bacterial protein synthesis by binding to the 23S ribosomal RNA of 50S subunit Bacteriostatic activity against susceptible bacteria Infections caused by methicillin-resistant staphylococci and vancomycin-resistant enterococci Oral, IV hepatic clearance (half-life 6 h) dosed twice-daily Toxicity Duration-dependent bone marrow suppression, neuropathy, and optic neuritis serotonin-syndrome may occur when coadministered with other serotonergic drugs (eg, selective serotonin reuptake inhibitors)... 

Toxic optic neuropathy can occur and may underlie various reports of sudden blindness in patients taking glucocorticoids. In one case, transient visual loss occurred on several occasions, each time after administration of a glucocorticoid (SEDA-17, 447). In another case, blindness occurred suddenly and paradoxically after glucocorticoid injections into the nasal turbinates (78). Although glucocorticoids are sometimes used successfully to relieve... 

Lehman NL, Johnson LN. Toxic optic neuropathy after concomitant use of melatonin, Zoloft, and a high-protein diet. J Neuroophthalmol 1999 19(4) 232-4. 

Bi Eortified breads, cereals, pasta, whole grains (especially wheat germ), lean meats (especially pork), fish, dried beans, peas, soybeans, nuts, and seeds Toxic optic neuropathy Beriberi... 

Bi2 Meat, dairy, eggs, seafood Toxic optic neuropathy Optic nerve atrophy (in Leber s disease)... 

Nntritional and toxic optic neuropathy refers to vision loss secondary to degenerative changes of the optic nerve fibers in response to exogenous metabolic stimuli. There are four primary causes of toxic optic neuropathy (1) exposure to substances within the work environment, (2) ingestion of foods containing toxic substances, (3) elevated systemic drug levels, and (4) deficiencies of... 

The clinician should suspect toxic optic neuropathy in any case of bilateral painless and symmetric loss of vision with normal or sluggish pupils. Because of the symmetric nature of the accumulation of toxins in the optic nerve head, pupillary fibers of either eye are equally affected and thus no RAPD is produced. 

A review of certain chemicals is essential. Ethylene glycol is an antifreeze used for gasoline engines and may produce somnolence, imreactive pupils, disc swelling, and kidney failure. Systemic lead poisoning produces headaches, coma, cranial nerve palsies, and papilledema. Wood alcohol, or methanol, may produce severe toxic neuropathy and disc edema. Drugs known to produce toxic optic neuropathy include amiodarone (an antiar-rhythmic), quinine, aminoquinolines, ibuprofen, ethambutol, isoniazid, and chloramphenicol. 

Bilateral acute visual loss, possibly due to toxic optic neuropathy, was observed after 4 weeks of treatment with ciprofloxacin 1.5 g/day and improved after withdrawal (16). 

Adams JW, Bofenkamp TM, Kobrin J, Wirtschafter JD, Zeese JA. Recurrent acute toxic optic neuropathy secondary to 5-FU. Cancer Treat Rep 1984 68(3) 565-6. 

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

A serious toxicity of didanosine is pancreatitis, which may be fatal (see Warnings). Other important toxicities include lactic acidosis/severe hepatomegaly with steatosis retinal changes and optic neuritis and peripheral neuropathy (see Warnings and Precautions). 

CNS toxicity occurs because isoniazid has structural similarities to pyridoxine (vitamin Be) and can inhibit its actions. This toxicity is dose-related and more common in slow acetylators. Manifestations include peripheral neuropathy, optic neuritis, ataxia, psychosis and seizures. The administration of pyridoxine to patients receiving INH does not interfere with the tuberculostatic action of INH but it prevents and can even reverse neuritis. Hematological effects include anaemia which is also responsive to pyridoxine. In some 20% of patients antinuclear antibodies can be detected but only in a minority of these patients drug-induced lupus erythematosus becomes manifest. 

Peripheral neuropathy, potentially fatal pancreatitis, retinal changes, and optic neuritis are the major toxic effects. 

The principal toxicity of linezolid is hematologic—reversible and generally mild. Thrombocytopenia is the most common manifestation (seen in approximately 3% of treatment courses), particularly when the drug is administered for longer than 2 weeks. Anemia and neutropenia may also occur, most commonly in patients with a predisposition to or underlying bone marrow suppression. Cases of optic and peripheral neuropathy and lactic acidosis have been reported with prolonged courses of linezolid. These side effects are thought to be related to linezolid-induced inhibition of mitochondrial protein synthesis. 

Iodoquinol should be taken with meals to limit gastrointestinal toxicity. It should be used with caution in patients with optic neuropathy, renal or thyroid disease, or nonamebic hepatic disease. The drug should be discontinued if it produces persistent diarrhea or signs of iodine toxicity (dermatitis, urticaria, pruritus, fever). It is contraindicated in patients with intolerance to iodine. 

The major dose-limiting toxicides of didanosine include peripheral neuropathy and pancreatitis. The neuropathy is typically symmetrical distal sensory neuropathy, which is reversible, and typically causes paresthesias, numbness and pain in lower extremities. Didanosine also causes retinal changes and optic neuritis. Other adverse effects include diarrhea, skin rash, headache, insomnia, seizures, hepatic toxicity, elevated hepatic transaminases and asymptomatic hyperuricemia. 

Other toxic effects of drugs can be associated with almost every organ system. The stiffness of the joints accompanied by damage to the optic nerve (SMON—subacute myelo-optic neuropathy) that was common in Japan in the 1960s was apparently a toxic side effect of chloroquinol (Enterovioform), an antidiarrhea drug. Teratogenosis... 

Flammable Liquid, Poison SAFETY PROFILE A human poison by ingestion. Poison experimentally by skin contact. Moderately toxic experimentally by intravenous and intraperitoneal routes. Mildly toxic by inhalation. Human systemic effects changes in circulation, cough, dyspnea, headache, lachrymation, nausea or vomiting, optic nerve neuropathy, respiratory effects, visual field changes. An experimental teratogen. Experimental reproductive effects. An eye and skin irritant. Human mutation data reported. A narcotic. 

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