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The treatment of the acute manic phase is usually undertaken in the hospital, since it is imperative to protect patients from their own misdeeds. If family members are supportive, however, and believe they can control the situation, treatment can be started outside the hospital. Lithium is not useful for the acute management of mania, and if the patient is severely agitated, sedation is necessary. Although general physicians rarely initiate treatment of acute mania, they often have patients who are taking lithium. Lithium effectively prevents relapses in most bipolar illnesses; it is slightly more effective in preventing manic than depressive episodes. Chronic medical illnesses, especially renal insufficiency, can contraindicate use of the agent. Lithium carbonate is available in 300 mg tablets or capsules, and a 300-mg slow-release tablet is also available. The starting dose of lithium carbonate in acute mania is generally 300 mg three or four times per day. Its specific therapeutic effectiveness is not evident until at least 4 to 10 days after institution of therapy. The dosage should be adjusted upward by a full or half tablet after the serum level is checked during this time period. It is necessary to monitor the serum level of lithium; adequate levels for acute illness are in the range of 0. Once maintenance levels are reached, patients usually can be maintained for long periods with minimal surveillance. Side effects in the long-term use of lithium include the development of mild leukocytosis, hypothyroidism, diabetes insipidus, and renal tubular damage. Many patients have a tremor that can be embarrassing and that occasionally interferes with activities. Preliminary evidence suggests that lamotrigine, gabapentin, and topiramate may also have efficacy in the suppression of recurrence of bipolar disorder. Manic or depressive episodes produce major disruptions of psychological, social, and vocational function. Moreover, the symptoms of some bipolar patients do not fully resolve; chronic symptoms often produce permanent psychosocial deterioration. When panic attacks occur, however, they are qualitatively different from generalized anxiety. There is also a spectrum of related mental disorders, which includes anxious features, such as the phobias and post-traumatic stress disorder. The underlying neurophysiology and neurochemistry of the anxiety disorders implicate overactivity of noradrenergic systems projecting from the locus caeruleus into forebrain regions. Panic attacks are characterized by the sudden onset of intense apprehension, fear, or a sense of impending doom. Either four attacks have occurred within a 4-week period or one or more attacks have been followed by a period of at least a month of persistent fear of having another attack. If there is any situational quality to the generalized anxiety symptoms, other therapeutic measures should be considered before benzodiazepines are prescribed. Reassurance may be tried, relaxation exercises, hypnosis, and a variety of other psychotherapies. Antihistamines such as diphenhydramine, 25 mg three times a day, can be tried for some patients. Buspirone is a non-benzodiazepine anti-anxiety agent that sometimes provides relief at doses of 5 mg twice a day initially (see Table 450-6). For all patients on maintenance benzodiazepine dosing, there should be constant surveillance for opportunities to taper or reduce the dosing regimen. Conversion disorders may be episodic, as in conversion seizures, or chronic and persistent, as in the case of sensory loss or weakness.
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Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Genome-wide association study identifies loci influencing concentrations of liver enzymes in plasma. Discovery of active enhancers through bidirectional expression of short transcripts. Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians. Rapamycin activates autophagy in Hutchinson-Gilford progeria syndrome: implications for normal aging and age-dependent neurodegenerative disorders. Correlation of rare coding variants in the gene encoding human glucokinase regulatory protein with phenotypic, cellular, and kinetic outcomes. Genome-wide association study identified novel loci associated with circulating phosphor-and sphingolipid concentrations. Genetic analysis of hematological paraments in incipient lines of the collaborative cross. Genome-wide screen for metabolic syndrome susceptibililty loci reveals strong lipid gene contribution but no evidence for common genetic basis for clustering of metabolic syndrome traits. Novel loci for adiponectin levels and their influence on type 2 diabetes and metabolic traits: a multi-ethnic meta-analysis of 45,891 individuals. A genome-wide approach accounting for body mass indes identifies genetic variants influencing fasting glycemic traits and insulin resistance. Genome-wide association for abdominal subcutaneous and visceral adipose reveals a novel locus for visceral fat in women. Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes. Large-scale association analyses identify new loci influencing glycemic traits and provide insight into the underlying biological pathways. The mammalian gene function resource: the international knockout mouse consortium. Genome-wide association study for type 2 diabetes in Indians identifies a new susceptibility locus at 2q21. Exome array analysis identifies new loci and low-frequency variants influencing insuling processing and secretion. Genome-wide association study identifies a novel locus contributing to type 2 diabetes susceptibility in Sikhs of Punjabi origin from India. Use of microarray hybrid capture and next-generation sequencing to identify the anatomy of a transgene. Causal relationship between obesity and vitamin D status: bidirectional Mendelian randomization analysis of multiple cohorts. Trans-ethnic fine-mapping of lipid loci identifieds population-specific signals and allelic heterogeneity that increases the trait variance explained. Association of ketone body levels with hyperglycemia and type 2 diabetes in 9,398 Finnish men. Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture. Household air pollution in low- and middle-income countries: health risks and research priorities. Sex-stratified genome-wide association studies including 270,000 individuals show sexual dimorphism in genetic loci for anthropometric traits. Mendelian randomisation studies do not support a causal role for reduced circulating adiponectin levels in insulin resistance and type 2 diabetes. Meta-analysis of gene-level associations for rare variants based on single-variant statistics.
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Myocardial hypertrophy may not be present before the adolescence growth spurt in children at risk, but a normal two-dimensional echocardiogram in young adults will virtually exclude the diagnosis. Atrial or ventricular arrhythmias may be asymptomatic, but their presence indicates an increased likelihood of sudden death. The genes known to be involved include those encoding for beta myosin heavy chain, cardiac troponin T, alpha tropomyosin and myosin binding protein C. These are sarcomeric proteins known to be essential for cardiac muscle contraction. Mutation analysis is not routine, but mutation detection allows presymptomatic predictive testing in family members at risk, identifying those relatives who require follow up. Mutations in the cardiac alpha actin gene have been found in some autosomal dominant families and an X-linked form (Barth syndrome) is associated with skeletal myopathy, neutropenia and abnormal mitochondria due to mutations in the X-linked taffazin gene. Dystrophinopathy, caused by mutations in the X-linked gene causing Duchenne and Becker muscular dystrophies can sometimes present as isolated cardiomyopathy in the absence of skeletal muscle involvement. Restrictive cardiomyopathy may be due to autosomal recessive inborn errors of metabolism that lead to accumulation of metabolites in the myocardium, to autosomal dominant familial amyloidosis or to autosomal dominant familial endocardial fibroelastosis. Haemophilia A is the most common bleeding disorder affecting 1 in 5000 to 1 in 10 000 males. Activity of 1% leads to severe disease that occurs in about half of affected males and may present at birth. Activity of 15% leads to moderate disease, and 525% to mild disease that may not require treatment. Affected individuals have easy bruising, prolonged bleeding from wounds, and bleeding into muscles and joints after relatively mild trauma. Repeated bleeding into joints causes a chronic inflammatory reaction leading to haemophiliac arthropathy with loss of cartilage and reduced joint mobility. Up to 15% of treated individuals develop neutralising antibodies that reduce the efficiency of treatment. Prior to 1984, haemophiliacs treated with blood products were exposed to the human immunodeficiency virus which resulted in a reduction in life expectancy to 49 years in 1990, compared to 70 years in 1980. Mutation analysis is used effectively in carrier detection and prenatal diagnosis. The mutation rate in males is much greater than in females so that most mothers of isolated cases are carriers. This is because they are more likely to have inherited a mutation occurring during spermatogenesis transmitted by their father, than to have transmitted a new mutation arising during oogenesis to their sons. Mutations in this gene are usually point mutations or small deletions or duplications. It is one of the most common genetic diseases in humans and the incidence may be as high as 1 in 1000. There is considerable variation in the age at which end stage renal failure is reached and the frequency of hypertension, urinary tract infections, and hepatic cysts. An increased prevalence of 45% for intracranial aneurysms has been suggested, compared to the prevalence of 1% in the general population. All affected individuals have renal cysts detectable on ultrasound scan by the age of 30. Screening young adults at risk will identify those asymptomatic individuals who are affected and require annual screening for hypertension, urinary tract infections and decreased renal function. Children diagnosed under the age of one year may have deterioration of renal function during childhood, but there is little evidence that early detection in asymptomatic children affects prognosis. Mutation analysis is not routinely undertaken, but linkage studies may be used in conjunction with ultrasound scanning to detect asymptomatic gene carriers. Of genetic cases, approximately 66% are autosomal recessive, 31% are autosomal dominant, 3% are X linked recessive. Mutation analysis in affected children enables carrier detection in relatives, early diagnosis in subsequent siblings and prenatal diagnosis if requested. These channels play a role in potassium homeostasis in the cochlea which is important for inner ear function. C cell membrane N intracellular Pendred syndrome Pendred syndrome is an autosomal recessive form of deafness due to cochlear abnormality that is associated with a thyroid goitre. Not all patients have thyroid involvement at the time the deafness is diagnosed and the perchlorate discharge test has been used in diagnosis.
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Overexpression of transforming growth factor beta1 in head and neck epithelia results in inflammation, angiogenesis, and epithelial hyperproliferation. Molecular links between tumor angiogenesis and inflammation: inflammatory stimuli of macrophages and cancer cells as targets for therapeutic strategy. Contributory role of 5-lipoxygenase and its association with angiogenesis in the promotion of inflammation-associated colonic tumorigenesis by cigarette smoking. Acute inflammation induced by the biopsy of mouse mammary tumors promotes the development of metastasis. Characterization of the host proinflammatory response to tumor cells during the initial stages of liver metastasis. P-selectin cell adhesion molecule in inflammation, thrombosis, cancer growth and metastasis. Macrophages: obligate partners for tumor cell migration, invasion, and metastasis. Src family kinases as mediators of endothelial permeability: effects on inflammation and metastasis. Mesenchymal stem cells in inflammation microenvironment accelerates hepatocellular carcinoma metastasis by inducing epithelial-mesenchymal transition. Iron-ascorbate-mediated lipid peroxidation causes epigenetic changes in the antioxidant defense in intestinal epithelial cells: impact on inflammation. Higher methylation levels in gastric mucosae significantly correlate with higher risk of gastric cancers. Inflammation-mediated cytosine damage: a mechanistic link between inflammation and the epigenetic alterations in human cancers. Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy. Use of Fourier-transform infrared spectroscopy to rapidly diagnose gastric endoscopic biopsies. Diagnosis of prostatic inflammation: efficacy of needle biopsies versus tissue blocks. Assessment of pre-diagnosis biomarkers of immune activation and inflammation: insights on the etiology of lymphoma. Utility of routine hematological and inflammation parameters for the diagnosis of cancer in involuntary weight loss. Granulomatous inflammation detected by endobronchial ultrasound-guided transbronchial needle aspiration in patients with a concurrent diagnosis of cancer: a clinical conundrum. However, the extent to which chemical exposures contribute to cancer incidence was not fully appreciated until population-based studies documented differing organ-specific cancer rates in geographically distinct populations and in cohort studies such as those that linked smoking to lung cancer. Experimental studies have been instrumental in replicating hypotheses generated from human studies and identifying pathobiologic mechanisms. For example, animal experiments confirmed the carcinogenic and cocarcinogenic properties of cigarette smoke and identified bioactive chemical and gaseous components. Dietary factors that enhance or inhibit cancer development and the contribution of obesity to specific organ sites have been identified in models of chemical carcinogenesis, and alterations in diet and obesity are expected to result in reduced cancer risk. Experimental animal studies are the mainstay of risk assessment as a screening tool to identify potential carcinogens in the workplace and the environment, although these studies do not prove specific chemical etiologies as a cause of human cancer because of interspecies differences and the use of maximally tolerated doses that do not replicate human exposure. For additional information, the reader is referred to agency documents and publications. As expected from this chemistry, genotoxic carcinogens can be potent mutagens and particularly adept at causing nucleotide base mispairing or small deletions, leading to missense or nonsense mutations. Others may cause macrogenetic damage, such as chromosome breaks and large deletions. In some cases, such genotoxic damage may result in changes in transcription and translation that affect protein levels or function, which in turn alter the behavior of the specific host cell type. This is best typified by the signature mutations detected in the p53 gene caused by ingested aflatoxin in human liver cancer22 and by polycyclic aromatic hydrocarbons human lung cancer caused by the inhalation of cigarette smoke. In general, these agents are carcinogenic in laboratory animals at high doses and require prolonged exposure. Synthetic pesticides and herbicides fall within this group, as do a number of natural products that are ingested. The mechanism of action by nongenotoxic carcinogens is not well understood, and may be related in some cases to toxic cell death and regenerative hyperplasia.
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Radiotherapy for early glottic carcinoma (T1N0M0): results of prospective randomized study of radiation fraction size and overall treatment time. Parameters that predict local control after definitive radiotherapy for squamous cell carcinoma of the head and neck. Preradiotherapy computed tomography as a predictor of local control in supraglottic carcinoma. Can pretreatment computed tomography predict local control in T3 squamous cell carcinoma of the glottic larynx treated with definitive radiotherapy? The evaluation of treatment of patients with extensive squamous cancer of the vocal cords. The steepness of the dose response curve both for tumor cure and normal tissue injury. Carcinoma of the supraglottic larynx: treatment results with radiotherapy alone or with planned neck dissection. Laryngofissure and cordectomy for early cordal carcinoma: outcome in 182 patients. Evaluation of pretreatment computed tomography as a predictor of local control in T1/T2 pyriform sinus carcinoma treated with definitive radiotherapy. Pharyngeal wall cancer: an analysis of treatment results complications and patterns of failure. Radiotherapy alone in patients with advanced nasopharyngeal cancer: comparison with an intergroup study. Retrospective analysis of 5037 patients with nasopharyngeal carcinoma treated during 1976-1985: overall survival and patterns of failure. Treatment results of 1070 patients with nasopharyngeal carcinoma: an analysis of survival and failure patterns. Volumetric analysis of tumor extent in nasopharyngeal carcinoma and correlation with treatment outcome. Significant prognosticators after primary radiotherapy in 903 nondisseminated nasopharyngeal carcinoma evaluated by computer tomography. Does altered fractionation influence the risk of radiation-induced optic neuropathy? Radiation therapy for esthesioneuroblastoma: rationale for elective neck irradiation. Radiation therapy in inverted papillomas of the nasal cavity and paranasal sinuses. Radiation retinopathy after external-beam irradiation: analysis of time-dose factors. The incidence of neoplastic versus inflammatory disease in major salivary gland masses diagnosed by surgery. Outcomes of postoperative concurrent chemoradiotherapy for locally advanced major salivary gland carcinoma. Systemic therapy in the management of metastatic or locally recurrent adenoid cystic carcinoma of the salivary glands: a systematic review. Southwest Oncology Group study of mitoxantrone for treatment of patients with advanced adenoid cystic carcinoma of the head and neck. Imatinib mesylate as treatment for adenoid cystic carcinoma of the salivary glands: report of two successfully treated cases. Poster presented at: 2005 3rd International Symposium in Targeted Anticancer Therapies; March 35, 2005; Amsterdam. Lyden, and Marc Haxer introduction Progress has been made in the past several years with survival for patients with head and neck cancer. Conservation surgery, radiation strategies, autogenous revascularized tissue transplantation, and treatment selection protocols continue to be used in an attempt to maintain or reestablish functional speech, voice, and swallowing in head and neck cancer patients. The ideal multidisciplinary team requires interaction among the surgical oncologists, radiation oncologists, medical oncologists, reconstructive surgeons, speech pathologists, physical therapists, occupational therapists, maxillofacial prosthodontists, dental oncologists, nutritionists, nurse oncologists, psychologists, audiologists, and social workers during pretreatment assessment and posttreatment intervention. Because radiation and chemotherapy protocols are being initiated in smaller centers, steps must be taken to ensure that the patient benefits from a multidisciplinary approach to treatment. Pretreatment counseling is essential for all patients with aerodigestive tract cancer. Patients benefit from discussions regarding swallowing, voice, and speech difficulties that can result from radiation and chemotherapy regimens. Regrettably, patients who undergo radiation and chemotherapy protocols often are inadequately counseled, if at all.
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Elevated serum tumor marker levels in gastric cancer before chemotherapy may reflect not just tumor burden but also biology of disease. Chromoendoscopy helps identify mucosal abnormalities through topical mucosal stains. Narrow band imaging affords enhanced visualization of the mucosal microvasculature. Confocal laser endomicroscopy permits in vivo, three-dimensional microscopy including subsurface structures with diagnostic accuracy, sensitivity, and specificity of 97%, 90%, and 99. However, the combined assessment of N stage and serosal invasion identified 77% of the patients at risk of disease-related death after curative resection. The sensitivity, specificity, and accuracy for lymph node metastasis were 86%, 76%, and 82%, respectively. Current noninvasive modalities used in preoperative staging of gastric cancer have sensitivities significantly lower than 100%, particularly in cases of low-volume peritoneal carcinomatosis. Staging laparoscopy also allows for assessment of peritoneal cytology and laparoscopic ultrasound. Laparoscopic staging is done to spare nontherapeutic operations and for potential stratification in various trials. Several groups confirmed these findings and concluded that staging laparoscopy with peritoneal cytology can change the management of gastric cancer in 6. When performed as a separate procedure, laparoscopy has the disadvantage of the additional risks and expense of a second general anesthetic. There were no significant differences between mean sensitivities and specificities. Clearly, not all patients benefit from preoperative laparoscopic staging; therefore, future studies should address the issue of selective laparoscopy based on noninvasive staging. Staging laparoscopy with or without cytology should be considered only if therapy will be altered consequent to information obtained by laparoscopy. The relationship between T stage, the overall stage, and survival is well defined (see. Nodal stage (N) is based on the number of involved lymph nodes, a criterion that may predict outcome more accurately than the location of involved lymph nodes. The use of numerical thresholds for nodal classification has gained increasing acceptance, although the extent of lymphadenectomy and rigor of pathologic assessment may affect results. Practice of oncology survival decreases as the number of metastatic lymph nodes increases,103,104 and that survival significantly decreases at three or more involved103 lymph nodes and again at seven or more involved lymph nodes. It may minimize the confounding effects of regional variations in the extent of lymphadenectomy and pathologic evaluation on lymph node staging and thereby 620 Practice of oncology / Cancers of the Gastrointestinal Tract reduce stage migration. These findings were confirmed by several investigators reporting on approximately 2,000 patients treated by R0 gastrectomy. In the combined superficial types, the type occupying the largest area should be described first, followed by the next type. The Japanese system extensively classifies 18 lymph node regions into four N categories (N0 to N3) depending on their relationship to the primary tumor and anatomic location. Lymph nodes situated along the proximal left gastric artery (station 7), common hepatic artery (station 8), celiac axis (station 9), splenic artery (station 11), and proper hepatic artery (station 12) are defined as group N2. However, some lymph nodes, even perigastric nodes for specific tumor locations, can be regarded as M1 disease. This is because their involvement in antral tumors is rare and portrays a poor prognosis. The assignment of tumors to one of these subtypes is based on morphology and the anatomic location of the epicenter of the tumor. In contrast, the lymphatic drainage from the cardia and subcardial regions is caudad. Thus, the Siewert classification provides a practical means for choosing among surgical options. The frequency and anatomic distribution of nodal disease are related to the depth of tumor invasion. In contrast, in the subset of >2,000 patients with tumors that invaded the submucosa, the frequencies of lymph node involvement for tumors 1. Thus, once tumors penetrate into the submucosa, the risk for nodal metastasis increases with tumor size. However, the use of more sensitive techniques such as serial sectioning of individual lymph nodes, immunohistochemistry, or reverse transcriptase-polymerase chain reaction may increase the frequency of detection of occult micrometastatic disease.
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Even in those instances where dramatic responses have been achieved, in most cases resistance eventually develops. Furthermore, while driver mutations can sometimes clearly play a major role in cancer growth, alterations in many of the other hallmarks of cancer are less amenable to treatment, at least at this time. Hence the state of affairs is that we have identified a few factors that have prognostic value (at least in some clinical settings), but it is spotty and explains only a small amount of the actual observed outcomes. The prognosis is inherently linked to a specific clinical scenario and to the outcome of interest. The ability to individualize is limited because we do not have sufficient detail of all of the other factors of the group to assess how well the group fits with the individual. Even if we had more and more detail, the more specific we get, the more limited the dataset available to derive the prediction becomes, and thus the greater the uncertainty about the prediction. Finally, the data we base the prediction on is inherently based on past observation, yet the prediction is for the future, and thus cannot take into account new developments that inevitably occur. It must remain relatively static and be used in a consistent uniform manner; the classification we assign to a particular extent of tumor today must be the same as what we assign to the same extent next year or else it is a useless nomenclature. However, prognostication is inherently fluid and constantly changing as advances occur and the setting changes. Stage classification must be consistent and definitive while prognostic prediction is inherently speculative and uncertain. The prediction must be specific to the clinical scenario and the outcome of interest. In sum, development of a prognostic model is very complex, situation specific, and constantly changing. We have only a rudimentary understanding at this point, and no overarching system of how to develop a universal prognostic prediction model. However, there have been major advances in understanding these, and solid scientific data regarding which interventions work best and in which individuals. Nicotine acts in an area of the brain associated with a sense of "safety" and "survival functions. This struggle and the illogical nature of it, combined with the stigmatism associated with smoking, lead to feelings of shame, helplessness, and depression that further aggravate the problem. It is important to use a sophisticated, evidence-based approach and an organized smoking cessation program to achieve the best results. Tobacco dependence is best managed in a chronic disease model with repeated intervention over time. In addition, seven first-line medications reliably increase long-term smoking abstinence rates (bupropion, varenicline, nicotine patch, gum, lozenges, inhaler, and nasal spray). Specifically, it is safe (and beneficial) for patients to stop smoking even a short time. Primary prevention has the greatest overall potential to minimize lung cancer risk, and smoking cessation is still the most powerful intervention to diminish lung cancer risk in persons who smoke. Smoking cessation even into the seventh decade of life results in a decrease in lung cancer incidence, and so it is never too late to quit. In theory, chemical agents might prevent these changes by a variety of proposed mechanisms, such as detoxifying carcinogens and modifying pathways that influence cell growth and behavior. Epidemiologic and animal studies had suggested that derivatives of the antioxidant vitamins A and E might be protective against lung cancer. However, large clinical trials of alpha-tocopherol and beta carotene in subjects at risk of developing lung cancer failed to demonstrate any benefit, and two studies suggested that beta carotene was actually associated with an increased incidence of lung cancer as well as cardiovascular disease. This preponderance of advanced disease, where prognosis is poor even with treatment, is a major contributor to the dismal overall 5-year survival rate of 18%; this contrasts starkly with breast, colon, and prostate cancers, the next three leading causes of cancer death, whose 5-year survival rates over the past several decades have increased to 90%, 65%, and nearly 100%, respectively. An effective screening tool for early detection of lung cancer has been an elusive goal for decades. Several large randomized trials performed during the 1960s and 1970s evaluating lung cancer screening with chest radiography with or without sputum analysis at varying time intervals failed to demonstrate any mortality benefit,8589 and a Cochrane meta-analysis90 concluded that there was no evidence to support the use of chest radiography or sputum cytology as a lung cancer screening modality. More recently, chest radiography was re-examined as a lung cancer screening tool in the Prostate, Lung, Colorectal and Ovarian trial, which enrolled 154,901 participants aged 55 to 74 years from 1993 to 2001. Together, these studies clearly demonstrate that there is no mortality benefit associated with serial chest radiography as a screening tool.
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Another provocative open use test involves the application of the product to the skin of the forearm, which is then left untouched and observed for 5 to 10 days for a reaction. An example is for a patient to apply mascara to one set of eyelashes and to leave the other eye bare, to observe for dermatitis. Thus according to this broad definition, it is not unusual for individuals to apply dozens of personal hygiene products to their skin on a daily basis including a plethora of cosmetics, each with a unique formulation of synthetic or natural ingredients. Such products can include emollients for day and night use, hair care products (shampoos, conditioners, pomade, relaxers, sprays, gels, mousses, foams), nail products (acrylic nails, polishes, hardeners, repair agents, extenders, wraps), traditional cosmetics (eye liners, mascara, eye shadow, foundation, lipstick, lip liners), concealers, shave creams and gels, antiperspirants and deodorants, toothpastes, dentifrices, hand creams, and barrier creams. Consideration must also be given to dermatitis where the allergen is transferred between partners, parent or child. Despite this extensive use, typical contact allergens contained in these products tend to be clustered in a few important classes, including fragrances, preservatives, formulation excipients, nickel, and sun blocks. Fragrances are regularly present in cosmetics and personal care products, household products, and medicaments, either to achieve an appealing scent or to mask unpleasant odors. Fragrance-free products are typically free of classic fragrance ingredients and are generally acceptable for the allergic patient. Caution should be exercised when substitute products, which are labeled fragrance free, contain large numbers of botanical extracts used for the purpose of improving odor characteristics. Clear demarcation of eczematous dermatitis on the neck where perfume is sprayed may be an obvious indication of fragrance allergy. The addition of other commonly used fragrance ingredients (ylang ylang oil, narcissus oil, and sandalwood oil) may increase the yield up to 96%. Current labeling laws do not always require manufacturers to label a specific fragrance present in a product and regulation of fragrance ingredients in cosmetics exempts fragrance formulas as "trade secrets. Use testing and slow reintroduction of some fragrance products may allow for the detection of intolerance to specific cosmetic agents. It may be possible to identify the presence of specific fragrance ingredients by communicating directly with product manufacturers. Preservatives and antibacterials are present in most aqueousbased cosmetics and personal hygiene products to prevent rancidity and microbial contamination. Preservatives tend to be grouped into 2 broad categories: formaldehyde releasers (products that emit formaldehyde) and nonformaldehyde releasers. In the United States, approximately 20% of cosmetics and personal care products (stay-on and rinse-off products) contain a formaldehyde releaser. Provocation tests may also be performed to determine relevance to this particular patient. Among nonformaldehyde releaser preservatives, methlydibromo gluteronitrile (also known as 1,2-dibromo-2,4-dicyanobutane and is the sensitizing ingredient in Euxyl K 400) has emerged as an important cosmetic allergen in recent years. In Europe, several groups have documented frequency of allergy to this preservative of approximately 1. The rate of sensitization to parabens in patients with chronic leg ulcers is higher than that of the general population. Unfortunately, in cosmetics, product labeling may not list essential oils as fragrances. Propolis is found in many "all natural' products, including lip balms, cosmetics, lotions and ointments, shampoos, conditioners, and toothpastes. Synonyms for propolis include bee glue, bee bread, hive doss, propolis balsam, propolis resin, and propolis wax. It is important that patients who are allergic to fragrance also be made aware of the potential dangers of cosmetics containing plant extracts and patients should be counseled that "natural products" does not equate with safety. Although it is less irritating than the older polar surfactants such as sodium lauryl sulfate,161,162 it is more sensitizing. Although hair dye is the main source of exposure,164 other routes of exposure include body painting and temporary tattooing. Alternatives include henna (giving a reddish tint for any hair color), lead oxide (which oxidizes to darken gray hair but has not been adequately evaluated for its toxicity), and temporary coloring agents (which only last for a few washes). However, semipermanent dyes may not be as cosmetically elegant and require more frequent application. Hence, those individuals who are allergic to it may continue to have skin eruptions weeks after application of the perm, and hairdressers allergic to it may be unable to cut or shape permanent waved hair.