Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were conducted to assess potential handling hazards from the pesticidal use of HCN-liberating "cyanide fumigation powders". Simulations were conducted in enclosed chambers on the release of HCN vapor from wetted powder containing 40% NaCN/60% kaolin at application rates of 1 g powder/m3 of space (usual rate) and 5 g/m3 (overuse condition). With the overuse situation, HCN vapor concentrations may be rapidly attained that produce serious or lethal toxicity; with the lower application rate minor signs and symptoms of HCN vapor exposure toxicity may develop. The acute peroral LD50 (rat and rabbit) of fumigant formulation is reduced in proportion to the kaolin content, but kaolin does not modify the inherent toxicity of NaCN. A typical cyanide hazard exists from swallowing cyanide fumigant powder formulations. Lethal systemic toxicity was produced by contamination of the eye (rabbit) with powder formulation, which also caused a rapid onset of moderately severe conjunctivitis and keratitis. Applied to dry intact skin (rabbit) neither NaCN nor its kaolin formulation produced systemic toxicity. However, on moistened intact skin lethal amounts of cyanide were absorbed; but the kaolin content reduced the hazard in comparison with NaCN-alone applied to moist skin. With abraded dry skin there was no difference in lethal toxicity between NaCN-alone and its formulation; also, the toxicity of the formulation on abraded skin was three times that on intact moist skin. These finds indicate that the use of cyanide fumigant powder formulations may be hazardous by contact of powder with moist or abraded skin, contamination of the eye, swallowing, and inhalation of evolved HCN. There is a clear need for respiratory, cutaneous, and ocular protection when handling cyanide fumigant powder formulations.
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PMID:Toxicology and hazard evaluation of cyanide fumigation powders. 284 35

Keratosis follicularis spinulosa decalvans (KFSD) is a rare X-linked disorder of keratinization of the hair follicle associated with corneal dystrophy. The clinical picture is characterized by solid follicular hyperkeratosis, especially on the exposed skin, sparse eyebrows/eyelashes, follicular scaling and scarring alopecia of the scalp, dry skin and ocular symptoms with keratitis and photophobia. We describe the three stages of the disease: onset, inflammation and partial remission and the treatment appropriate in each. Two patients in the inflammatory stage of KFSD, with recurrent deep, fibrosing folliculitis and perifolliculitis followed by spreading and scarring alopecia on the scalp, responded to oral therapy with retinoids. In both cases there was a distinct and lasting remission of the inflammation and stabilization of the spreading alopecia after treatment with etretinate (Tigason), up to 0.8 mg/kg body weight, or isotretinoin (Roaccutan), 0.5 mg/kg body weight, for 12 weeks. The follicular spinulous hyperkeratosis became softer, but persisted. Thus, oral therapy with retinoids appears helpful in the inflammatory stage of KFSD, even though there is little improvement in the follicular hyperkeratosis.
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PMID:[Keratosis follicularis spinulosa decalvans. Therapy with isotretinoin and etretinate in the inflammatory stage]. 837 8

Sulfur mustard is an alkylating agent that reacts with ocular, respiratory, cutaneous, and bone marrow tissues, resulting in early and late toxic effects. We compare these effects based on the experience in Iranian veterans exposed to the agent during the Iran-Iraq conflict (1983-88). The first clinical manifestations of sulfur mustard poisoning occurred in the eyes with a sensation of grittiness, lacrimation, photophobia, blepharospasm, and corneal ulceration. Respiratory effects appeared as rhinorhea, laryngitis, tracheobronchitis, and dyspnoea. Skin lesions varied from erythema to bullous necrotization. Initial leukocytosis and lymphopenia returned to normal within four weeks in recovered patients, but marked cytopenia with bone marrow failure occurred in fatal cases. Late toxic effects of sulfur mustard were most commonly found in lungs, skin and eyes. Main respiratory complications were chronic obstructive pulmonary disease, bronchiectasis, asthma, large airway narrowing, and pulmonary fibrosis. Late skin lesions were hyperpigmentation, dry skin, atrophy, and hypopigmentation. Fifteen of the severely intoxicated patients were diagnosed with delayed keratitis, having corneal vascularization, thinning, and epithelial defect. Respiratory complications exacerbated over time, while cutaneous and ocular lesions decreased or remained constant. Both the severity and frequency of bronchiectatic lesions increased during long-term follow-up. The only deteriorating cutaneous complication was dry skin. The maximum incidence of delayed kaeratitis was observed 15 to 20 years after initial exposure. Being suggested as the main cause ofassociated with malignancies and recurrent infections, natural killer cells were significantly lower 16 to 20 years after intoxication.
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PMID:Comparison of early and late toxic effects of sulfur mustard in Iranian veterans. 1704 Feb 11

The widespread use of sulphur mustard (SM) as an incapacitating chemical warfare agent in the past century has proved its long-lasting toxic effects. It may also be used as a chemical terrorist agent. Therefore, all health professionals should have sufficient knowledge and be prepared for any such chemical attack. SM exerts direct toxic effects on the eyes, skin, and respiratory tissue, with subsequent systemic action on the nervous, immunological, haematological, digestive, and reproductive systems. SM is an alkylating agent that affects DNA synthesis, and, thus, delayed complications have been seen since the First World War. Cases of malignancies in the target organs, particularly in haematopoietic, respiratory, and digestive systems, have been reported. Important delayed respiratory complications include chronic bronchitis, bronchiectasis, frequent bronchopneumonia, and pulmonary fibrosis, all of which tend to deteriorate with time. Severe dry skin, delayed keratitis, and reduction of natural killer cells with subsequent increased risk of infections and malignancies are also among the most distressing long-term consequences of SM intoxication. However, despite a lot of research over the past decades on Iranian veterans, there are still major gaps in the SM literature. Immunological and neurological dysfunction, as well as the relationship between SM exposure and mutagenicity, carcinogenicity, and teratogenicity are important fields that require further studies, particularly on Iranian veterans with chronic health effects of SM poisoning. There is also a paucity of information on the medical management of acute and delayed toxic effects of SM poisoning-a subject that greatly challenges health care specialists.
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PMID:Chronic health effects of sulphur mustard exposure with special reference to Iranian veterans. 2246 Feb 16