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There are several populations that have a higher risk for contracting coccidioidomycosis and developing the advanced disseminated version of the disease. Populations with exposure to the airborne arthroconidia working in agriculture and construction have a higher risk. Outbreaks have also been linked to earthquakes, windstorms and military training exercises where the ground is disturbed. Historically an infection is more likely to occur in males than females, although this could be attributed to occupation rather than gender specific. Women who are pregnant and immediately postpartum are at a high risk of infection and dissemination. There is also an association between stage of pregnancy and severity of the disease, with third trimester women being more likely to develop dissemination. Presumably this is related to highly elevated hormonal levels, which stimulate growth and maturation of spherules and subsequent release of endospores. Certain ethnic populations are more susceptible to disseminated coccioidomycosis. The risk of dissemination is 175 times greater in Filipinos and 10 times greater in African Americans than non-Hispanic whites. Individuals with a weakened immune system are also more susceptible to the disease. In particular, individuals with HIV and diseases that impair T-cell function. Individuals with pre-existing conditions such as diabetes are also at a higher risk. Age also affects the severity of the disease, with more than one third of deaths being in the 65-84 age group.
Preventing Valley fever is challenging because it is difficult to avoid breathing in the fungus should it be present, however, the public health effect of the disease is essential to understand in areas where the fungus is endemic. Enhancing surveillance of Coccidiodomycosis is key to preparedness in the medical field in addition to improving diagnostics for early infections. Currently there are no completely effective preventive measures available for people who live or travel through Valley Fever -endemic areas. Recommended preventive measures include avoiding airborne dust or dirt, but this does not guarantee protection against infection. People in certain occupations may be advised to wear face masks. The use of air filtration indoors is also helpful, in addition to keeping skin injuries clean and covered to avoid skin infection.
In 1998-2011, there were 111,117 cases of coccidioidomycosis in the U.S. that were logged into the National Notifiable Diseases Surveillance System (NNDSS). Since many U.S. states do not require reporting of coccidioidomycosis, the actual numbers can be higher. The United States' Centers for Disease Control and Prevention (CDC) called the disease a "silent epidemic" and acknowledged that there is no proven anticoccidioidal vaccine available. Studies done in the past show that the cost benefit of a vaccine is most notable among infants, teens, and immigrant adults, with negative cost-benefit results among older age groups.
Raising both surveillance and awareness of the disease while medical researchers are developing a human vaccine can positively contribute towards prevention efforts. Research demonstrates that patients from endemic areas who are aware of the disease are most likely to request diagnostic testing for coccidioidomycosis. Presently, Meridian Bioscience manufactures the so-called "EIA test" to diagnose the Valley fever, which however is known for producing a fair quantity of false positives. Currently, recommended prevention measures can include type-of-exposure-based respirator protection for persons engaged in agriculture, construction and others working outdoors in endemic areas. Dust control measures such as planting grass and wetting the soil, and also limiting exposure to dust storms are advisable for residential areas in endemic regions.
It is not practical to test or decontaminate most sites that may be contaminated with "H. capsulatum", but the following sources list environments where histoplasmosis is common, and precautions to reduce a person's risk of exposure, in the three parts of the world where the disease is prevalent. Precautions common to all geographical locations would be to avoid accumulations of bird or bat droppings.
The US National Institute for Occupational Safety and Health (NIOSH) provides information on work practices and personal protective equipment that may reduce the risk of infection. This document is available in English and Spanish.
Authors at the University of Nigeria have published a review which includes information on locations in which histoplasmosis has been found in Africa (in chicken runs, bats and the caves bats infest, and in soil), and a thorough reference list including English, French, and Spanish language references.
"Histoplasmosis capsulatum" is found throughout the world. It is endemic in certain areas of the United States, particularly in states bordering the Ohio River valley and the lower Mississippi River. The humidity and acidity patterns of soil are associated with endemicity. Bird and bat droppings in soil promote growth of "Histoplasma". Contact with such soil aerosolizes the microconidia, which can infect humans. It is also common in caves in southern and East Africa. Positive histoplasmin skin tests occur in as many as 90% of the people living in areas where "H. capsulatum" is common, such as the eastern and central United States.
In Canada, the St. Lawrence River Valley is the site of the most frequent infections, with 20-30 percent of the population testing positive.
In India, the Gangetic West Bengal is the site of most frequent infections, with 9.4 percent of the population testing positive. "Histoplasma capsulatum capsulatum" was isolated from the local soil proving endemicity of histoplasmosis in West Bengal.
Individuals with a weak immune system are most at risk. This includes individuals taking immunosuppressive medication, cancer patients, HIV patients, premature babies with very low birth weight, the elderly, etc.
People who are at an increased risk of acquiring particular fungal infections in general may also be at an increased risk of developing fungal meningitis, as the infection may in some cases spread to the CNS. People residing in the Midwestern United States, and Southwestern United States and Mexico are at an increased risk of infection with "Histoplasma" and "Coccidioides", respectively.
Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for "Candida" meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for "Aspergillus" and coccidioidal infections is poor.
Paracoccidioidomycosis has been reported as an autochthonous disease from southern Mexico to northern Argentina. No cases have been reported from Belize and Nicaragua in Central America, or from Chile, French Guiana, Guiana, and Suriname in South America. Paracoccidioidomycosis is prevalent in Brazil, Colombia, Venezuela, and Argentina, and is classically associated with individuals from rural areas. The typical patient is a man aged 30 to 50 years.
"P. brasiliensis" is a thermally dimorphic fungus distributed in Brazil and South America. The habitat of the infectious agent is not known, but appears to be aquatic. In biopsies, the fungus appears as a polygemulating yeast with a pilot's wheel-like appearance.
With treatment, most types of bacterial pneumonia will stabilize in 3–6 days. It often takes a few weeks before most symptoms resolve. X-ray finding typically clear within four weeks and mortality is low (less than 1%). In the elderly or people with other lung problems, recovery may take more than 12 weeks. In persons requiring hospitalization, mortality may be as high as 10%, and in those requiring intensive care it may reach 30–50%. Pneumonia is the most common hospital-acquired infection that causes death. Before the advent of antibiotics, mortality was typically 30% in those that were hospitalized.
Complications may occur in particular in the elderly and those with underlying health problems. This may include, among others: empyema, lung abscess, bronchiolitis obliterans, acute respiratory distress syndrome, sepsis, and worsening of underlying health problems.
Pneumonia can cause respiratory failure by triggering acute respiratory distress syndrome (ARDS), which results from a combination of infection and inflammatory response. The lungs quickly fill with fluid and become stiff. This stiffness, combined with severe difficulties extracting oxygen due to the alveolar fluid, may require long periods of mechanical ventilation for survival.
Sepsis is a potential complication of pneumonia but occurs usually in people with poor immunity or hyposplenism. The organisms most commonly involved are "Streptococcus pneumoniae", "Haemophilus influenzae", and "Klebsiella pneumoniae". Other causes of the symptoms should be considered such as a myocardial infarction or a pulmonary embolism.
Pregnant women are more severely affected by influenza, hepatitis E, herpes simplex and malaria. The evidence is more limited for coccidioidomycosis, measles, smallpox, and varicella. Pregnancy may also increase susceptibility for toxoplasmosis.
During the 2009 H1N1 pandemic, as well as during interpandemic periods, women in the third trimester of pregnancy were at increased risk for severe
disease, such as disease requiring admission to an intensive care unit or resulting in death, as compared with women in an earlier stage of pregnancy.
For hepatitis E, the case fatality rate among pregnant women has been estimated to be between 15% and 25%, as compared with a range of 0.5 to 4% in the population overall, with the highest susceptibility in the third trimester.
Primary herpes simplex infection, when occurring in pregnant women, has an increased risk of dissemination and hepatitis, an otherwise rare complication in immunocompetent adults, particularly during the third trimester. Also, recurrences of herpes genitalis increase in
frequency during pregnancy.
The risk of severe malaria by "Plasmodium falciparum" is three times as high in pregnant women, with a median maternal mortality of 40% reported in studies in the Asia–Pacific region. In women where the pregnancy is not the first, malaria infection is more often asymptomatic, even at high parasite loads, compared to women having their first pregnancy. There is a decreasing susceptibility to malaria with increasing parity, probably due to immunity to pregnancy-specific antigens. Young maternal age and increases the risk. Studies differ whether the risk is different in different . Limited data suggest that malaria caused by "Plasmodium vivax" is also more severe during pregnancy.
Severe and disseminated coccidioidomycosis has been reported the occur in increased frequency in pregnant women in several reports and case series, but subsequent large surveys, with the overall risk being rather low.
Varicella occurs at an increased rate during pregnancy, but mortality is not higher than that among men and non-pregnant women.
Listeriosis mostly occurs during the third trimester, with Hispanic women appearing to be at particular risk. Listeriosis is a vertically transmitted infection that may cause miscarriage, stillbirth, preterm birth, or serious neonatal disease.
Some infections are vertically transmissible, meaning that they can affect the child as well.
"Listeria monocytogenes" infection in infants can cause potentially fatal disseminated granulomas, called granulomatosis infantiseptica, following "in utero" infection.
Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue and can occur after an untreated Group A Beta-hemolytic streptococcal pharyngeal infection. It is believed to be caused by antibody cross-reactivity.
There are several potential risk factors or causes to this increased risk:
- An increased immune tolerance in pregnancy to prevent an immune reaction against the fetus
- Maternal physiological changes including a decrease in respiratory volumes and urinary stasis due to an enlarging uterus.
- The presence of a placenta for pathogens to use as a habitat, such as by "L. monocytogenes" and "P. falciparum".
The second most common cause of SJS and TEN is infection, particularly in children. This includes upper respiratory infections, otitis media, pharyngitis, and Epstein-Barr virus, Mycoplasma pneumoniae and cytomegalovirus infections. The routine use of medicines such as antibiotics, antipyretics and analgesics to manage infections can make it difficult to identify if cases were caused by the infection or medicines taken.
Viral diseases reported to cause SJS include: herpes simplex virus (debated), AIDS, coxsackievirus, influenza, hepatitis, and mumps.
In pediatric cases, Epstein-Barr virus and enteroviruses have been associated with SJS.
Recent upper respiratory tract infections have been reported by more than half of patients with SJS.
Bacterial infections linked to SJS include group A beta-hemolytic streptococci, diphtheria, brucellosis, lymphogranuloma venereum, mycobacteria, "Mycoplasma pneumoniae", rickettsial infections, tularemia, and typhoid.
Fungal infections with coccidioidomycosis, dermatophytosis, and histoplasmosis are also considered possible causes. Malaria and trichomoniasis, protozoal infections, have also been reported as causes.
Conditions which commonly involve hemoptysis include bronchitis and pneumonia, lung cancers and tuberculosis. Other possible underlying causes include aspergilloma, bronchiectasis, coccidioidomycosis, pulmonary embolism, pneumonic plague, and cystic fibrosis. Rarer causes include hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome), Goodpasture's syndrome, and granulomatosis with polyangiitis. In children, hemoptysis is commonly caused by the presence of a foreign body in the airway. The condition can also result from over-anticoagulation from treatment by drugs such as warfarin.
Blood-laced mucus from the sinus or nose area can sometimes be misidentified as symptomatic of hemoptysis (such secretions can be a sign of nasal or sinus cancer, but also a sinus infection). Extensive non-respiratory injury can also cause one to cough up blood. Cardiac causes like congestive heart failure and mitral stenosis should be ruled out.
The origin of blood can be identified by observing its color. Bright-red, foamy blood comes from the respiratory tract, whereas dark-red, coffee-colored blood comes from the gastrointestinal tract. Sometimes hemoptysis may be rust-colored.
The most common cause of minor hemoptysis is bronchitis.
- Lung cancer, including both non-small cell lung carcinoma and small cell lung carcinoma.
- Sarcoidosis
- Aspergilloma
- Tuberculosis
- Histoplasmosis
- Pneumonia
- Pulmonary edema
- Pulmonary embolism
- Foreign body aspiration and aspiration pneumonia
- Goodpasture's syndrome
- Granulomatosis with polyangiitis
- Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
- Bronchitis
- Bronchiectasis
- Pulmonary embolism
- Anticoagulant use
- Trauma
- Lung abscess
- Mitral stenosis
- Tropical eosinophilia
- Bleeding disorders
- Hughes-Stovin Syndrome and other variants of Behçet's disease
- Squamous Cell Carcinoma Of Esophagus
Parasitic infestations, stings, and bites in humans are caused by several groups of organisms belonging to the following phyla: Annelida, Arthropoda, Bryozoa, Chordata, Cnidaria, Cyanobacteria, Echinodermata, Nemathelminthes, Platyhelminthes, and Protozoa.
- "Acanthamoeba" infection
- Amebiasis cutis
- Ant sting
- Arachnidism
- Baker's itch
- "Balamuthia" infection
- Bedbug infestation (bedbug bite, cimicosis)
- Bee and wasp stings
- Blister beetle dermatitis
- Bombardier beetle burn
- Bristleworm sting
- Centipede bite
- Cheyletiella dermatitis
- Chigger bite
- Coolie itch
- Copra itch
- Coral dermatitis
- Creeping eruption (cutaneous larva migrans)
- Cutaneous leishmaniasis (Aleppo boil, Baghdad boil, bay sore, Biskra button, Chiclero ulcer, Delhi boil, Kandahar sore, Lahore sore, leishmaniasis tropica, oriental sore, "pian bois, uta")
- "Cysticercosis" cutis
- Demodex mite bite
- Dogger Bank itch
- Dracunculiasis (dracontiasis, guinea worm disease, Medina worm)
- Echinococcosis (hydatid disease)
- Elephantiasis tropica (elephantiasis arabum)
- Elephant skin
- Enterobiasis (oxyuriasis, pinworm infection, seatworm infection)
- "Erisipela de la costa"
- Feather pillow dermatitis
- Funnel web spider bite
- Gamasoidosis
- Gnathostomiasis (larva migrans profundus)
- Grain itch (barley itch, mattress itch, prairie itch, straw itch)
- Grocer's itch
- Head lice infestation (cooties, pediculosis capitis)
- Hookworm disease (ancylostomiasis, ground itch, necatoriasis, uncinariasis)
- Human trypanosomiasis
- Hydroid dermatitis
- Irukandji syndrome
- Jellyfish dermatitis
- Ked itch
- Larva currens
- Latrodectism (widow spider bite)
- Leech bite
- Leopard skin
- Lepidopterism (Caripito itch, caterpillar dermatitis, moth dermatitis)
- Lizard bite
- Lizard skin
- Loaiasis (Calabar swelling, fugitive swelling, "loa loa", tropical swelling)
- Loxoscelism (brown recluse spider bite, necrotic cutaneous loxoscelism)
- "Mal morando"
- Millipede burn
- Mosquito bite
- Mucocutaneous leishmaniasis (espundia, leishmaniasis americana)
- Myiasis
- Nairobi fly dermatitis (Kenya fly dermatitis, Nairobi eye)
- Nematode dermatitis
- Norwegian scabies (crusted scabies)
- Onchocerciasis
- Ophthalmia nodosa
- Paederus dermatitis
- Pediculosis corporis (pediculosis vestimenti, Vagabond's disease)
- Pediculosis pubis (crabs, phthirus pubis, pthirus pubis, pubic lice)
- Pneumocystosis (often classified as fungal)
- Portuguese man-of-war dermatitis
- Post-kala-azar dermal leishmaniasis (post-kala-azar dermatosis)
- Protothecosis
- Pulicosis (flea bites)
- Reduviid bite
- Scabies (itch mite infestation, seven-year itch)
- Scorpion sting
- Sea anemone dermatitis
- Seabather's eruption (sea lice)
- Sea urchin injury
- Seaweed dermatitis
- Snake bite
- Sowda
- Sparganosis
- Spider bite
- Stingray injury
- Swimmer's itch (cercarial dermatitis, schistosome cercarial dermatitis)
- Tarantula bite
- Tick bite
- Toxoplasmosis
- Trichinosis
- Trichomoniasis
- Tungiasis ("bicho de pie", chigoe flea bite, jigger bite, "nigua, pique")
- Visceral leishmaniasis (dumdum fever, "kala-azar")
- Visceral schistosomiasis (bilharziasis)
- Viscerotropic leishmaniasis
- Wheat warehouse itch
The condition may be a sign of various disease states, including but not exclusive to the following:
- Cancers
- Lymphoma
- Leukemia
- Infections
- HIV/AIDS
- Tuberculosis
- Mycobacterium avium-intracellulare infection
- Infectious mononucleosis
- Fungal infections (histoplasmosis, coccidioidomycosis)
- Lung abscess
- Infective endocarditis
- Brucellosis
- Pneumocystis pneumonia (most often - in immunocompromised individuals)
- Endocrine disorders
- Menopause
- Premature ovarian failure
- Hyperthyroidism
- Diabetes mellitus (nocturnal hypoglycemia)
- Endocrine tumors (pheochromocytoma, carcinoid)
- Orchiectomy
- Rheumatic disorders
- Takayasu's arteritis
- Temporal arteritis
- Other
- Obstructive sleep apnea
- Gastroesophageal reflux disease
- Chronic fatigue syndrome
- Fibromyalgia
- Granulomatous disease
- Chronic eosinophilic pneumonia
- Lymphoid hyperplasia
- Diabetes insipidus
- Prinzmetal's angina
- Anxiety
- Pregnancy
- Drugs
- Antipyretics (salicylates, acetaminophen)
- Antihypertensives
- Dinitrophenol - a common side effect
- Phenothiazines
- Drug withdrawal: ethanol, benzodiazepines, heroin (and other opiates),
- Over-bundling
- Autonomic over-activity
- IBD (inflammatory bowel disease) - Crohn's disease/ulcerative colitis
Treatment depends on the underlying cause. Treatments include iced saline, and topical vasoconstrictors such as adrenalin or vasopressin. Selective bronchial intubation can be used to collapse the lung that is bleeding. Also, endobronchial tamponade can be used. Laser photocoagulation can be used to stop bleeding during bronchoscopy. Angiography of bronchial arteries can be performed to locate the bleeding, and it can often be embolized. Surgical option is usually the last resort, and can involve, removal of a lung lobe or removal of the entire lung. Non–small-cell lung cancer can also be treated with erlotinib or gefitinib. Cough suppressants can increase the risk of choking.
Eosinophilia can be idiopathic (primary) or, more commonly, secondary to another disease. In the Western World, allergic or atopic diseases are the most common causes, especially those of the respiratory or integumentary systems. In the developing world, parasites are the most common cause. A parasitic infection of nearly any bodily tissue can cause eosinophilia.
Diseases that feature eosinophilia as a sign include:
- Allergic disorders
- Asthma
- Hay fever
- Drug allergies
- Allergic skin diseases
- Pemphigus
- Dermatitis herpetiformis
- IgG4-related disease
- Parasitic infections
- Addison's disease and stress-induced suppression of adrenal gland function
- Some forms of malignancy
- Acute lymphoblastic leukemia
- Chronic myelogenous leukemia
- Eosinophilic leukemia
- Clonal eosinophilia
- Hodgkin lymphoma
- Some forms of non-Hodgkin lymphoma
- Lymphocyte-variant hypereosinophilia
- Systemic mastocytosis
- Systemic autoimmune diseases
- Systemic lupus erythematosus
- Kimura disease
- Eosinophilic granulomatosis with polyangiitis
- Eosinophilic fasciitis
- Eosinophilic myositis
- Eosinophilic esophagitis
- Eosinophilic gastroenteritis
- Cholesterol embolism (transiently)
- Coccidioidomycosis (Valley fever), a fungal disease prominent in the US Southwest.
- Human immunodeficiency virus infection
- Interstitial nephropathy
- Hyperimmunoglobulin E syndrome, an immune disorder characterized by high levels of serum IgE
- Idiopathic hypereosinophilic syndrome.
- Congenital disorders
- Hyperimmunoglobulin E syndrome
- Omenn syndrome
- Familial eosinophilia
Tobacco smoking is by far the main contributor to lung cancer. Cigarette smoke contains at least 73 known carcinogens, including benzo["a"]pyrene, NNK, 1,3-butadiene and a radioactive isotope of polonium, polonium-210. Across the developed world, 90% of lung cancer deaths in men during the year 2000 were attributed to smoking (70% for women). Smoking accounts for about 85% of lung cancer cases.
Passive smoking—the inhalation of smoke from another's smoking—is a cause of lung cancer in nonsmokers. A passive smoker can be defined as someone living or working with a smoker. Studies from the US, Europe and the UK have consistently shown a significantly increased risk among those exposed to passive smoke. Those who live with someone who smokes have a 20–30% increase in risk while those who work in an environment with secondhand smoke have a 16–19% increase in risk. Investigations of sidestream smoke suggest it is more dangerous than direct smoke. Passive smoking causes about 3,400 deaths from lung cancer each year in the USA.
Marijuana smoke contains many of the same carcinogens as those in tobacco smoke. However, the effect of smoking cannabis on lung cancer risk is not clear. A 2013 review did not find an increased risk from light to moderate use. A 2014 review found that smoking cannabis doubled the risk of lung cancer.
Virus-related cutaneous conditions are caused by two main groups of viruses–DNA and RNA types–both of which are obligatory intracellular parasites.
- Alphavirus infection
- Asymmetric periflexural exanthem of childhood (unilateral laterothoracic exanthem)
- B virus infection
- Boston exanthem disease
- Bovine papular stomatitis
- Bowenoid papulosis
- Buffalopox
- Butcher's wart
- Chikungunya fever
- Condylomata acuminata
- Congenital rubella syndrome
- Cowpox
- Cytomegalic inclusion disease
- Dengue (Break-bone fever)
- Disseminated herpes zoster
- Eczema herpeticum (Kaposi's varicelliform eruption)
- Eczema vaccinatum
- Epidermodysplasia verruciformis
- Eruptive pseudoangiomatosis
- Erythema infectiosum (fifth disease, slapped cheek disease)
- Exanthem of primary HIV infection (acute retroviral syndrome)
- Farmyard pox
- Generalized vaccinia
- Genital herpes (herpes genitalis, herpes progenitalis)
- Gianotti–Crosti syndrome (infantile papular acrodermatitis, papular acrodermatitis of childhood, papulovesicular acrolocated syndrome)
- Giant condyloma acuminatum (Buschke–Löwenstein tumor, giant condyloma of Buschke–Löwenstein tumor)
- Hand-foot-and-mouth disease
- Heck's disease (focal epithelial hyperplasia)
- Hemorrhagic fever with renal syndrome
- Hepatitis B
- Hepatitis C
- Herpangina
- Herpes gladiatorum (scrum pox)
- Herpes simplex
- Herpes zoster oticus (Ramsay–Hunt syndrome)
- Herpetic keratoconjunctivitis
- Herpetic sycosis
- Herpetic whitlow
- HIV-associated pruritus
- Human monkeypox
- Human T-lymphotropic virus 1 infection
- Human tanapox
- Immune reconstitution inflammatory syndrome (immune recovery syndrome)
- Infectious mononucleosis (glandular fever)
- Inflammatory skin lesions following zoster infection (isotopic response)
- Intrauterine herpes simplex
- Kaposi sarcoma
- Lassa fever
- Lipschütz ulcer (ulcus vulvae acutum)
- Measles (rubeola, morbilli)
- Milker's nodule
- Modified varicella-like syndrome
- Molluscum contagiosum
- Myrmecia
- Neonatal herpes simplex
- Ophthalmic zoster
- Orf (contagious pustular dermatosis, ecthyma contagiosum, infectious labial dermatitis, sheep pox)
- Orf-induced immunobullous disease
- Orolabial herpes (herpes labialis)
- Papular purpuric gloves and socks syndrome
- Pigmented wart
- Postherpetic neuralgia (zoster-associated pain)
- Post-vaccination follicular eruption
- Progressive vaccinia (vaccinia gangrenosum, vaccinia necrosum)
- Pseudocowpox
- Recurrent respiratory papillomatosis (laryngeal papillomatosis)
- Rift Valley fever
- Roseola infantum (exanthem subitum, exanthema subitum, sixth disease)
- Roseola vaccinia
- Rubella (German measles)
- Sandfly fever (Pappataci fever, phlebotomus fever)
- Sealpox
- Varicella (chickenpox)
- Variola major (smallpox)
- Verruca plana (flat wart)
- Verruca plantaris (plantar wart)
- Verruca vulgaris (wart)
- Verrucae palmares et plantares
- Viral-associated trichodysplasia (ciclosporin-induced folliculodystrophy)
- Wasting syndrome
- West Nile virus infection
- Zoster (herpes zoster, shingles)
- Zoster sine herpete
Although SJS can be caused by viral infections and malignancies, the main cause is medications. A leading cause appears to be the use of antibiotics, particularly sulfa drugs. Between 100 and 200 different drugs may be associated with SJS. No reliable test exists to establish a link between a particular drug and SJS for an individual case. Determining what drug is the cause is based on the time interval between first use of the drug and the beginning of the skin reaction. Drugs discontinued more than 1 month prior to onset of mucocutaneous physical findings are highly unlikely to cause SJS and TEN. SJS and TEN most often begin between 4 and 28 days after culprit drug administration. A published algorithm (ALDEN) to assess drug causality gives structured assistance in identifying the responsible medication.
SJS may be caused by adverse effects of the drugs vancomycin, allopurinol, valproate, levofloxacin, diclofenac, etravirine, isotretinoin, fluconazole, valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil, lamotrigine, nevirapine, pyrimethamine, ibuprofen, ethosuximide, carbamazepine, bupropion, telaprevir, and nystatin.
Medications that have traditionally been known to lead to SJS, erythema multiforme, and toxic epidermal necrolysis include sulfonamide antibiotics, penicillin antibiotics, cefixime (antibiotic), barbiturates (sedatives), lamotrigine, phenytoin (e.g., Dilantin) (anticonvulsants) and trimethoprim. Combining lamotrigine with sodium valproate increases the risk of SJS.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a rare cause of SJS in adults; the risk is higher for older patients, women, and those initiating treatment. Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. Similar to NSAIDs, paracetamol (acetaminophen) has also caused rare cases of SJS. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.
Outdoor air pollutants, especially chemicals released from the burning of fossil fuels, increase the risk of lung cancer. Fine particulates (PM) and sulfate aerosols, which may be released in traffic exhaust fumes, are associated with slightly increased risk. For nitrogen dioxide, an incremental increase of 10 parts per billion increases the risk of lung cancer by 14%. Outdoor air pollution is estimated to account for 1–2% of lung cancers.
Tentative evidence supports an increased risk of lung cancer from indoor air pollution related to the burning of wood, charcoal, dung or crop residue for cooking and heating. Women who are exposed to indoor coal smoke have about twice the risk and a number of the by-products of burning biomass are known or suspected carcinogens. This risk affects about 2.4 billion people globally, and is believed to account for 1.5% of lung cancer deaths.
Allergic reactions to drugs are a common cause of eosinophilia, with manifestations ranging from diffuse maculopapular rash, to severe life-threatening drug reactions with eosinophilia and systemic symptoms (DRESS). Drugs that have been shown to cause DRESS are aromatic anticonvulsants and other antiepileptics, sulfonamides, allopurinol, nonsteroidal anti-inflammatory drugs (NSAIDs), some antipsychotics such as risperidone, and certain antibiotics. Phenibut, an analogue of the neurotransmitter GABA, has also been implicated in high doses. The reaction which has been shown to be T-cell mediated may also cause eosinophilia-myalgia syndrome.