Gene/Protein Disease Symptom Drug Enzyme Compound
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This Guidance Article is an update of an article published in a special issue of Health Devices entitled "Lasers in Medicine--An Introduction" (13[8], June 1984). Although surgical lasers have a good overall safety record, they do expose patients, physicians, and other clinical staff to serious risks. Laser hazards can cause injury, disability, or even death: hospital staff have been burned by misdirected laser beams, technicians and maintenance personnel have received eye injuries while working on lasers and have been exposed to hazardous chemicals while changing laser dyes, and patients have died from injuries resulting from fires ignited by laser energy. Laser accidents most commonly result from misdirection of the laser beam. Direct or reflected radiation can burn skin, hair, or, more seriously, the cornea or retina, causing permanent damage. Misdirected laser energy can also cause ignition of surgical drapes, tracheal tubes, or the patient's hair. Also, a frequent by-product of laser-tissue interactions is laser plume, or smoke. Its acrid smell and particulate matter irritate the eyes, nose, and lungs and cause nausea; it is also a suspected vector for transmitting infectious materials, such as the human papilloma virus (HPV) associated with condyloma (a wartlike lesion) and cervical cancer. The risks are not limited to patients and those directly involved in using and maintaining lasers. Many laser procedures are performed in areas outside the controlled environment of the surgical suite; patients in a waiting area or even passersby could conceivably walk into an accessible laser treatment room, such as a doctor's office, and inadvertently be exposed to a direct or reflected beam.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Laser use and safety. 142 1

Precise knowledge of the undesirable effects of chloroquine and hydroxychloroquine allows better exploitation of their therapeutic effects. Retinopathy can be avoided by observing a maximum daily dosage of 3.5-4 mg/kg ideal body weight for chloroquine and 6-6.5 mg/kg for hydroxychloroquine. In this way, both can be used for long-term therapy. The pharmacokinetics of chloroquine (storage in deep compartments with long plasma half-life) means that it can cumulate, especially with higher dosages and in the presence of renal or hepatic insufficiency. A high plasma concentration reinforces the side-effects without reinforcing the therapeutic effects. Besides subjective symptoms (e.g. anorexia, diarrhoea, nausea), the following undesirable reactions are significant. On the skin exanthema, hyperpigmentation and photodynamic reactions can develop. The hair can become white in blonde and red-haired men. In the eye, chloroquine deposits in the cornea and disturbances of accommodation can occur, besides retinopathy. Neuromyopathy and central nervous system disturbances (e.g. psychosis) are rare, as is impairment of auditory function or blood cells. During pregnancy there is a risk of potential fetal damage (hearing loss, abortion). An acute overdose is extremely dangerous: the lethal dose is 1 g for children and 4 g for adults. As death occurs rapidly, chloroquine has to be stored where it is absolutely inaccessible to children.
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PMID:[Chloroquine and hydroxychloroquine: side effect profile of important therapeutic drugs]. 205 62

We report ophthalmological findings in 15 cases of nephropathia epidemica. The patients, 13 men and 2 women, were 20 to 62 (mean 30) years of age. The onset of the disease was characterized by high fever, nausea, headache, abdominal pain, backache, somnolence, red throat, proteinuria, and oliguria. The symptoms subsided rapidly during the polyuria stage. Transitory myopia occurred in 8 patients (53%). Conjunctival injection and haemorrhages were seen in 3 patients (20%). One patient had acute glaucoma with oedema in the cornea and shallowing of the anterior chamber, with subsequent anterior uveitis and haemorrhages in the ocular fundus, and another patients had acute glaucoma. Three patients had photophobia which occurred in 2 patients without any glaucoma or anterior uveitis.
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PMID:Ophthalmological findings in nephropathia epidemica in Lapland. 653 41

A 25 years old sergeant of Dicrocoeliidae infection was studied. This patient was not a spurious infection case and diagnosis was based on rocovery of the characteristic eggs consistently in the feces for 2 month. This case had no history of ingestion of ingestion of ants, land snail of grasshopper. In this case with complaints of flatulence, nausea, loss of appetite and dizziness, physical examination reveald no pathological findings except pale cornea. Liver function tests were observed to be normal and there was slight eosinophilia.
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PMID:One case of dicrocoeliidae infection. 1291 17

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Fabry disease (FD) is a recessive monogenic inheritance disease linked to chromosome X, secondary to mutations in the GLA gene. Its prevalence is estimated between 1:8,454 and 1:117,000 among males and is probably underdiagnosed. Mutations in the GLA gene lead to the progressive accumulation of globotriaosylceramide (Gb3). Gb3 accumulates in lysosomes of different types of cells of the heart, kidneys, skin, eyes, central nervous system, and gastrointestinal system, and may lead to different clinical scenarios. The onset of symptoms occurs during childhood, with acroparesthesia, heat intolerance, and gastrointestinal symptoms, such as nausea, vomiting, abdominal pain, and neuropathic pain. Subsequently, symptoms related to progressive impairment appear, such as angiokeratomas, cornea verticillata, left ventricular hypertrophy, myocardial fibrosis, proteinuria, and renal insufficiency. The latter being the main cause of death in FD. The gold standard for diagnosis is the genetic analysis in search of mutation, in addition to family history. In homozygous patients, the enzyme activity can also be used. Once the diagnosis is confirmed, the patient and their family should receive genetic counseling. The treatment, in turn, currently focuses mainly on replacing the enzyme that is absent or deficient by means of enzyme replacement therapy, with the purpose of avoiding or removing deposits of Gb3. Chaperones can also be used for the treatment of some cases. It is considered that the specific treatment should be initiated as soon as a diagnosis is obtained, which can change the prognosis of the disease.
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PMID:Fabry disease: genetics, pathology, and treatment. 3193 30