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W2099947519 abstract "InstructionsCredit can now be obtained, free for a limited time, by reading the review articles in this issue. Please note the instructions listed below:1. Review the target audience, learning objectives and author disclosures.2. Complete the pre-test online at www.jacionline.org (click on the Online CME heading).3. Follow the online instructions to read the full version of the article, including the clinical vignette and review components.4. Complete the post-test. At this time, you will have earned 1.00 AMA PRA Category 1 CME Credit™.5. Approximately 4 weeks later you will receive an online assessment regarding your application of this article to your practice. Once you have completed this assessment, you will be eligible to receive 2 MOC Part II Self-Assessment credits from the American Board of Allergy and Immunology.Date of Original Release: October 2012. Credit may be obtained for these courses until September 30, 2014.Copyright Statement: Copyright © 2012-2014. All rights reserved.Target Audience: Physicians and researchers within the field of allergic disease.Accreditation/Provider Statements and Credit Designation: The American Academy of Allergy, Asthma & Immunology (AAAAI) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The AAAAI designates these educational activities for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity.List of Design Committee Members: Martin Steinhoff, MD, PhD, Ferda Cevikbas, PhD, Iwei Yeh, MD, Kim Chong, MD, Jörg Buddenkotte, PhD, and Akihiko Ikoma, MD, PhD (authors), and James T. Li, MD, PhD (series editor)Activity Objectives1. To identify clinical features that can guide the clinician to the diagnosis of the primary cause of chronic pruritus.2. To apply knowledge of the differential diagnoses of chronic pruritus to formulate a desired diagnostic strategy.3. To use the most effective management for each type of chronic pruritus.Recognition of Commercial Support: This CME activity has not received external commercial support.Disclosure of Significant Relationships with Relevant CommercialCompanies/Organizations: M. Steinhoff has received grants from the National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases. The rest of the authors declare that they have no relevant conflicts of interest. J. T. Li has consulted for Abbott. Credit can now be obtained, free for a limited time, by reading the review articles in this issue. Please note the instructions listed below: 1. Review the target audience, learning objectives and author disclosures. 2. Complete the pre-test online at www.jacionline.org (click on the Online CME heading). 3. Follow the online instructions to read the full version of the article, including the clinical vignette and review components. 4. Complete the post-test. At this time, you will have earned 1.00 AMA PRA Category 1 CME Credit™. 5. Approximately 4 weeks later you will receive an online assessment regarding your application of this article to your practice. Once you have completed this assessment, you will be eligible to receive 2 MOC Part II Self-Assessment credits from the American Board of Allergy and Immunology. Date of Original Release: October 2012. Credit may be obtained for these courses until September 30, 2014. Copyright Statement: Copyright © 2012-2014. All rights reserved. Target Audience: Physicians and researchers within the field of allergic disease. Accreditation/Provider Statements and Credit Designation: The American Academy of Allergy, Asthma & Immunology (AAAAI) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The AAAAI designates these educational activities for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity. List of Design Committee Members: Martin Steinhoff, MD, PhD, Ferda Cevikbas, PhD, Iwei Yeh, MD, Kim Chong, MD, Jörg Buddenkotte, PhD, and Akihiko Ikoma, MD, PhD (authors), and James T. Li, MD, PhD (series editor) Activity Objectives 1. To identify clinical features that can guide the clinician to the diagnosis of the primary cause of chronic pruritus. 2. To apply knowledge of the differential diagnoses of chronic pruritus to formulate a desired diagnostic strategy. 3. To use the most effective management for each type of chronic pruritus. Recognition of Commercial Support: This CME activity has not received external commercial support. Disclosure of Significant Relationships with Relevant Commercial Companies/Organizations: M. Steinhoff has received grants from the National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases. The rest of the authors declare that they have no relevant conflicts of interest. J. T. Li has consulted for Abbott. A 53-year-old woman was initially referred to our clinic by her primary care physician for evaluation of daily episodes of severe pruritus affecting the face, neck, arms, hands, and legs that had started about 6 months prior. Pruritus was most intense in early morning and late evening. She reported “itchy hands” when having contact with vegetables or fruits in the kitchen. Pruritus often kept her scratching until the skin bled. She was sometimes inclined to put her hands into hot water so that heat-induced sharp pain could inhibit her pruritus. Occasional application of corticosteroid ointments to the pruritic skin areas provided her with moderate but short relief of pruritus and skin lesions. She had no fever, arthritis, or evidence of systemic/cutaneous infections. Scabies was excluded based on physical examination. She was taking thiazides for hypertension, which she began after her pruritus and skin eruption started. Her family history was positive for atopic diseases, such as asthma (mother) and allergic rhinitis (father). Physical examination was notable for eczematous skin lesions on her face, frontal neck, arms, and legs (see Fig E1, A). She also presented with papulovesicular eruptions with excoriation, fissures, and lichenifications on the backs of her hands and lower legs. Her palms/soles were dry, and her palm lines were deep. Her lateral eyebrows were diminished. Otherwise, results of her physical examination, including examination of her eyes, were unremarkable. Blood work showed increased eosinophil counts (8% [normal = 1% to 5%]) and IgE levels (1112 IU [normal = ≤100]). Skin prick testing revealed immediate hypersensitivity against house dust mite allergens (Dermatophagoides pteronyssinus) and latex. Patch testing showed no positive reactions to standard allergens. Skin biopsy from a papular skin lesion in the lower leg demonstrated irregular parakeratosis, acanthosis, and spongiosis in the epidermis, as well as lymphomonocytic infiltrate and prominent intravascular eosinophils in the upper dermis (see Fig E2, A). No epidermal invasion of lymphocytes or epidermotropism was observed on histology. She was given a diagnosis of atopic dermatitis and was advised to eliminate trigger factors, apply a corticosteroid ointment (mometasone furoate 0.1%), and use moisturizing emollients twice daily constantly on the skin lesions until the eczematous lesions disappeared and then to taper the corticosteroid slowly (daily for 1 week and then every other day for 1 week). In addition, use of high doses of oral antihistamines (180 mg/d fexofenadine and 10 mg/d cetirizine) significantly improved both pruritus scores and skin lesions within 4 weeks and was successfully followed by a maintenance therapy with emollients. However, 1 year after her initial presentation, the patient presented with classic atopic dermatitis lesions combined with pruritic nodules on her arms, legs, and back (see Fig E1, B), which was defined as prurigo nodularis. Histology of a skin biopsy specimen from a nodular lesion in her lower leg showed thick hyperkeratosis, parakeratosis, acanthosis, and an inflammatory cell infiltrate without epidermotropism, as well as a lymphomonocytic infiltrate, vasodilatation, and prominent intravascular eosinophils in the upper dermis (see Fig E2, B). Laboratory work-up revealed increased blood urea nitrogen (28 mg/dL) and creatinine (1.7 mg/dL) levels. She was referred to a nephrologist, who further assessed the patient with abdominal ultrasound and urine tests and concluded that she had chronic renal insufficiency secondary to type II diabetes mellitus, which consequently required initiation of hemodialysis a year later. Concurrent with the treatment regimen from 1 year prior (topical corticosteroid, emollients, and high-dosage oral antihistamines: morning, 180 mg of fexofenadine; afternoon, 10 mg of cetirizine), we added oral paroxetine (20 mg/d in the morning) and doxepin (10 mg/d at night). As a result, her overall pruritus severity score (range, 0-10; 0, no pruritus; 10, worst pruritus imaginable) reduced from 9 to 6 within 2 weeks. For therapy-resistant nodules, a lidocaine 5% patch was applied at 12-hour intervals, which resulted in an additional reduction in the overall pruritus severity score to 2 within another 2 weeks. The pruritus score was thereafter successfully maintained with a topical calcineurin inhibitor (pimecrolimus 1% cream) applied twice a week to her remaining skin lesions. The full version of this article, including a review of relevant issues to be considered, can be found online at www.jacionline.org. If you wish to receive CME or MOC credit for the article, please see the instructions above. Because of the many different origins of chronic pruritus, for which different therapeutic approaches are required, adequate management of chronic pruritus starts with a thorough diagnostic work-up. Pruritus or itch is defined as an unpleasant sensation eliciting the urge to scratch. According to the International Forum for the Study of Itch, chronic pruritus is itch lasting for 6 or more weeks.E1Weisshaar E. Szepietowski J.C. Darsow U. Misery L. Wallengren J. Mettang T. et al.European guideline on chronic pruritus.Acta Derm Venereol. 2012; ([Epub ahead of print])Google Scholar It is often underestimated that severe chronic pruritus has a significant effect on patients' quality of life because of sleep disturbance, impaired concentration, depressed mood, nervousness, and impaired socializing. For more information on the etiology of chronic pruritus, see Fig E3.E2Ikoma A. Steinhoff M. Ständer S. Yosipovitch G. Schmelz M. The neurobiology of itch.Nat Rev Neurosci. 2006; 7: 535-547Crossref PubMed Scopus (767) Google Scholar, E3Cevikbas F. Steinhoff M. Ikoma A. Role of spinal neurotransmitter receptors in itch: new insights into therapies and drug development.CNS Neurosci Ther. 2011; 17: 742-749Crossref PubMed Scopus (54) Google Scholar, E4Oaklander A.L. Neuropathic itch.Semin Cutan Med Surg. 2011; 30: 87-92Crossref Scopus (65) Google Scholar, E5Pfab F. Valet M. Napadow V. Tölle T.R. Behrendt H. Ring J. et al.Itch and the brain.Chem Immunol Allergy. 2012; 98: 253-265Crossref Scopus (3) Google Scholar Chronic pruritus accompanies various skin diseases, including inflammatory, infectious, autoimmune, and malignant diseases (Fig E3, A). In addition, many systemic diseases and other noncutaneous abnormalities, including metabolic, hematologic, neuropathic, autoimmune, and malignant diseases, are known to be accompanied by chronic pruritus (Fig E3, B). Among peripheral pruritogens in human subjects, histamine is the best known and indeed causes pruritus in patients with most subtypes of urticaria. However, antihistamines (histamine H1 receptor blocker) at normal dosages are hardly effective against chronic pruritus of different origins. There are many other peripheral pruritogens/pruriceptors that have been reported to potentially play a significant role in pruritic diseases, including protease-activated receptors (eg, protease-activated receptors 2 and 4), neurotrophins (eg, nerve growth factor), neuropeptides, serotonin, acetylcholine, and interleukins (eg, IL-31). Even algogens, such as bradykinin, can sometimes cause pruritus (ie, alloknesis) because of itch sensitization. Thus multiple peripheral substances can cause pruritus in one disease, and different itch mediators might be responsible for the induction of itch in the various subtypes of itch. Recent studies established a significant involvement of various central and spinal neurosubstances and neuroreceptors in patients with pruritus.E3Cevikbas F. Steinhoff M. Ikoma A. Role of spinal neurotransmitter receptors in itch: new insights into therapies and drug development.CNS Neurosci Ther. 2011; 17: 742-749Crossref PubMed Scopus (54) Google Scholar, E5Pfab F. Valet M. Napadow V. Tölle T.R. Behrendt H. Ring J. et al.Itch and the brain.Chem Immunol Allergy. 2012; 98: 253-265Crossref Scopus (3) Google Scholar The spinal μ-opioid receptor is the best known because spinal administration of morphine frequently causes segmental pruritus as an adverse effect, and in contrast, κ-opioid receptor agonists have been developed as novel antipruritic drugs for hemodialysis- and cholestasis-associated pruritus. The spinal gastrin-releasing peptide receptor has recently been reported as a novel pruritus-selective pathway. Of note, the pathomechanisms of chronic pruritus are not limited to pruritogens/pruriceptors, as observed in neuropathic pruritus associated with herpes zoster, multiple sclerosis, notalgia paresthetica, and other small fiber neuropathies. It can be also caused by psychiatric or psychosomatic disorders, which is described as somatoform pruritus. For more information on determination of the origin of chronic pruritus, see Fig E4. Multiple origins can coexist in the same patient. Moreover, chronic pruritus of noncutaneous origin can cause a secondary skin lesion because of scratching, which then becomes another origin of chronic pruritus. Thus it is not always possible to narrow down to only 1 origin of chronic pruritus. On the contrary, it is crucial to identify and list all potential causes of pruritus in a patient to establish the most effective therapeutic strategy. The first step must be obtaining a complete medical history, which then should be followed by a thorough physical examination. It is crucial to know from the physical examination whether skin lesions or abnormalities, including erythema, papules, wheals, vesicles, and dry skin, exist together with pruritus and, if so, whether these skin lesions are generalized, localized, or perhaps located in the limited area the patient can scratch to speculate about the primary origin of pruritus. One should also consider the possibility that skin lesions emerge only during a certain time of the day and are not visible when the patient presents, as is often the case with urticaria. A magnifier should be used to closely examine the skin, so that small but significant abnormalities, such as tunnels made by scabies or other microbes, are not overlooked. Further diagnostic work-up should include, depending on the history and clinical appearance, various blood tests, stool tests, allergy tests (skin prick tests, patch tests, or both), histologic examination of affected skin, direct/indirect immunofluorescence, and radiologic imaging (magnetic resonance imaging and computed tomography). A malignancy work-up is recommended if results of the above-described initial tests are unremarkable or if any risk factors of malignancy, such as aging, B symptoms, anemia, or blood variations, are present. Because pruritus can precede a malignant process by years, regular monitoring (every 6-12 months) is recommended in the case of chronic pruritus with unknown origin. Diagnostic approaches to chronic pruritus should sometimes be managed in a multidisciplinary collaboration including primary care physicians, dermatologists, allergists, nephrologists, hepatologists, neurologists, psychologists, and oncologists. Needless to say, curing the origin of pruritus is the fundamental issue in the treatment of chronic pruritus. For example, anti-inflammatory treatment with topical corticosteroids or tacrolimus/pimecrolimus along with emollients is certainly required to inhibit pruritus in patients with atopic dermatitis. Moreover, pruritus caused by obstructive or autoimmune cholestasis or renal insufficiency should optimally be treated by treating the underlying cause. However, it is not always possible to determine the primary origin of chronic pruritus or to cure the origin of pruritus even if the cause has been determined, as is often the case with malignancy and chronic insufficiencies of internal organs, such as liver cancer, primary sclerotic cholangitis, or chronic renal failure. Moreover, even if the origin of pruritus is known and a specific treatment is available, supplementary treatments against the secondary skin lesions caused by scratching are often needed. Although both H1R and H4R among the 4 histamine receptors seem to be involved in pruritus, only H1R antagonists are currently approved to treat pruritus. H1R antagonists include sedating first-generation antagonists, which have stronger anticholinergic side effects and might be beneficial at night. In general, the nonsedating or poorly sedating second-generation H1R antagonists, which also have other anti-inflammatory effects (eg, blocking release of neuropeptide and leukotrienes), are preferable during the day. However, their effects on pruritic diseases, except for urticaria, have been verified poorly by using randomized, double-blind, placebo-controlled clinical trials. Sedating antihistamines are often superior to nonsedating H1R blockers in patients with certain pruritic diseases, such as atopic dermatitis,E8Buddenkotte J. Maurer M. Steinhoff M. Histamine and antihistamines in atopic dermatitis.Adv Exp Med Biol. 2010; 709: 73-80Crossref Scopus (38) Google Scholar but are rarely applicable during the day. Therefore the “add-on” approach is generally recommended rather than the replacement strategy, such as starting with a nonsedative H1R blocker in the morning (eg, fexofenadine and loratadine) followed by a nonsedative or mildly sedative antihistamine in the afternoon (eg, azelastine and cetirizine) and a mildly sedating or sedating antihistamine in the evening/at night (first-generation antihistamines). In contrast to morphine, which has analgesic effects but frequently causes pruritus as a side effect, μ-opioid receptor antagonists, such as naltrexone and nalmafene, have antipruritic effects in patients with pruritic diseases, such as atopic dermatitis, psoriasis, bullous pemphigoid, and cholestasis. μ-Opioid receptor antagonists should be started at a low dosage (eg, 10 mg/d for nalmefene and 25 mg/d for naltrexone) and titrated every 3 to 7 days to minimize side effects, such as dizziness, fatigue, and nausea. κ-Opioid receptor agonists, such as butorphanol and nalfurafine, also seem to have antipruritic potential because nalfurafine reportedly has no severe side effects except for insomnia (>5%) and has recently been approved in Japan for the treatment of renal pruritus. Some antidepressants, including selective serotonin reuptake inhibitors and tricyclic/tetracyclic antidepressants, seem to be effective in patients with chronic pruritus, such as sertraline (a serotonin reuptake inhibitor, 75-100 mg/d) for cholestasis-induced and T-cell lymphoma–induced pruritus, doxepin (a tricyclic antidepressant sedative anti-histamine, 10-100 mg/d) for renal pruritus or atopic dermatitis, and mirtazapine (a tetracyclic antidepressant, 15-30 mg/d) for various subtypes of chronic pruritus and morphine-induced pruritus. Attention has to be paid to possible side effects, such as sedation, insomnia, and edema. Among anticonvulsants, gabapentin and pregabalin, which are also known for their analgesic effects on neuropathic pain, have been reported to have antipruritic effects for various subtypes of chronic pruritus, especially for neuropathic pruritus, such as postherpetic pruritus, brachioradial pruritus, and notalgia paresthetica. Gabapentin and pregabalin should be started at a low dosage (300-600 mg/d for gabapentin and 75-150 mg/d for pregabalin) and gradually titrated (up to 3600 mg for gabapentin and up to 300 mg for pregabalin) to minimize side effects, such as dizziness and sedation. Off-label usage of up to 600 mg per day has been described. Another novel neuromodulator with antipruritic effects is the neurokinin-1 receptor antagonist (eg, aprepitant) because the results of recent reports and studies have verified its effectiveness in patients with chronic pruritus reviewed in Steinhoff et al with references.E7Steinhoff M. Cevikbas F. Ikoma A. Berger T.G. Pruritus: management algorithms and experimental therapies.Semin Cutan Med Surg. 2011; 30: 127-137Crossref Scopus (49) Google Scholar Of note, emollients are not only effective in patients with classical pruritic skin diseases, such as atopic dermatitis, in which an impaired skin barrier is a key factor, but also in patients with many subtypes of chronic pruritus because dry skin is an important trigger of pruritus in those with many systemic diseases and in elderly patients in general. In addition, administration of moisturizing emollients can hardly cause side effects unless they have potential allergens as ingredients. Several barrier-improving topical agents are available that contain various lipids, such as triglycerides, free fatty acids, cholesterol, phospholipids, ceramides, squalene, and phytosterols. Other humectants, such as petrolatum or urea, also work efficiently. Emollients are more effective when lifestyle modifications are also used, such as avoiding the excessive use of soaps. Menthol, a naturally occurring cyclic terpene alcohol originating from plants, elicits a cooling sensation when applied to the skin and mucous membrane by acting on the ion channel transient receptor potential melastatin 8. Menthol is empirically known to have antipruritic effects, such as cooling, and is approved by the US Food and Drug Administration for over-the-counter gels, creams, ointments, and foams. These are fairly safe but can cause irritant contact dermatitis and dry skin at higher concentrations. Capsaicin, a naturally occurring alkaloid from hot chili peppers, binds to transient potential receptor vanilloid 1 and causes a burning pain sensation and release of neuropeptides. The antipruritic effects of topical capsaicin have been speculated to derive from receptor desensitization or neuropeptide depletion of transient potential receptor vanilloid 1–positive nerve fibers. The main side effects are burning sensation, erythema, and increased pruritus, but these can be minimized by starting at lower concentrations, such as 0.006% or 0.025%, and gradually increasing the dosage, usually up to 1% to 2%. Four to 5 applications per day are recommended to have the maximum effect. We sometimes successfully apply a 10% to 20% capsaicin ointment for 10 minutes against intractable scalp pruritus, followed by a complete wash-off of the compound. Topical anesthetics, such as lidocaine 2.5% to 5%, prilocaine 2.5%, pramoxine 1%, and polidocanol 3%, have been shown to have antipruritic effects to a certain extent. Lidocaine and prilocaine reportedly treated notalgia paresthetica, pruritus ani, and postburn pruritus successfully. Pramoxine was effective for xerosis- and psoriasis-caused pruritus, as well as uremic pruritus. Polidocanol formulated with 5% urea reduced pruritus in patients with atopic dermatitis, contact dermatitis, psoriasis, and idiopathic pruritus. Attention must be paid to the risk of allergic contact dermatitis, as well as methemoglobinemia for lidocaine and prilocaine, which necessitates avoidance in infants and pregnant patients. Effects of topical amitriptyline/ketamine combinations have also been described in patients with certain subforms of chronic pruritus. Except for some specific skin conditions, such as atopic dermatitis, lichen planus, or psoriasis, anti-inflammatory agents should not be used as first-line antipruritic agents because they are only effective in pruritus caused by skin inflammation and have risks of various long-term side effects, as observed in topical glucocorticosteroids or topical calcineurin inhibitors. Doxepin, a tricyclic antidepressant, also has antihistaminergic and anticholinergic effects. It is available as a 5% cream, and is US Food and Drug Administration approved to treat moderate pruritus in adult patients with atopic dermatitis, although there is a reported risk of contact dermatitis and sedation when large skin areas are treated. In general, topical antihistamines are less effective antipruritic agents compared with sedative oral antihistamines. Effects of various UV therapies (UVA, UVA1, broad-band UVB, narrow-band UVB, and psoralen UV) on chronic pruritus have been reported. Their immunomodulatory effects make phototherapies especially useful for treating chronic pruritus caused by inflammatory dermatoses, such as atopic dermatitis, psoriasis, or solar urticaria. Phototherapies might also induce reduction of nerve fibers in the epidermis and result in inhibition of pruritus, as reported in patients with chronic pruritus derived from renal failure, prurigo nodularis, solar urticaria, aquagenic pruritus, cutaneous T-cell lymphoma, Hodgkin lymphoma, polycythemia vera, HIV infection, and pregnancy. Pruritus is enhanced by mental stress and other psychiatric disorders, such as depression. Psychological interventions (“coping with itch”) focused on body relaxation and controlling the desire to scratch are reportedly effective in patients with pruritic diseases, including atopic dermatitis. A randomized controlled trial has shown that patients with atopic dermatitis receiving cognitive-behavioral treatment and autogenic training for relaxation demonstrate a significant reduction in pruritus and scratching behavior after 1 year (reviewed in Hong et al).E6Hong J. Buddenkotte J. Berger T.G. Steinhoff M. Management of itch in atopic dermatitis.Semin Cutan Med Surg. 2011; 30: 71-86Crossref PubMed Scopus (107) Google Scholar In her initial visit the patient was given a diagnosis of atopic dermatitis based on the multiple supportive features, such as chronic pruritus, typical clinical appearance and distribution of skin lesions, family history, and increased IgE levels, together with ichthyosiform hand lines, Hertoghe sign of the lateral eyebrows, Dennie-Morgan fold, and histology showing a spongiotic dermatitis with lymphocytic infiltrate. However, she later had disseminated nodular pruritic lesions (ie, prurigo nodularis), and a further assessment revealed that she also had diabetes-induced renal insufficiency, another potential cause of her chronic pruritus. Although the histologic results were negative in this patient, patients with diabetes mellitus and renal insufficiency are susceptible to reactive perforating collagenosis, a subform of acquired perforating dermatosis with clinical features similar to prurigo nodularis, and although the onset of pruritus before drug initiation was not evidenced in this patient, prurigo nodularis can be a subform of drug eruptions. Thus if prurigo nodularis is present, as in this case, both prurigo caused by uncontrolled chronic scratching and prurigo caused by drug eruptions or reactive perforating collagenosis have to be considered. This case highlights the importance of a thorough medical history exploration in conjunction with physical examination findings to narrow down the differential diagnoses in patients with chronic pruritus. As seen in this case, several causes can underlie chronic pruritus, such as atopic dermatitis, prurigo nodularis, and renal insufficiency. On the other hand, the potential development of secondary pruritic skin lesions caused by uncontrolled scratching emphasizes the importance of an effective prevention and maintenance therapy to stop the itch-scratch vicious cycle. In this case antidepressants and local anesthetic patches, in addition to systemic high-dosage antihistamines and topical anti-inflammatory agents, were effective in stopping the patient's vicious itch-scratch cycle. Thus sometimes more complex antipruritic treatments rather than simple classical antipruritic treatments are needed in patients with chronic pruritus. However, when multiple medications are used, it is important to consider the potential side effect profiles of each topical and systemic antipruritic drug used.E7Steinhoff M. Cevikbas F. Ikoma A. Berger T.G. Pruritus: management algorithms and experimental therapies.Semin Cutan Med Surg. 2011; 30: 127-137Crossref Scopus (49) Google Scholar, E8Buddenkotte J. Maurer M. Steinhoff M. Histamine and antihistamines in atopic dermatitis.Adv Exp Med Biol. 2010; 709: 73-80Crossref Scopus (38) Google Scholar, E9Elmariah S.B. Lerner E.A. Topical therapies for pruritus.Semin Cutan Med Surg. 2011; 30: 118-126Crossref Scopus (65) Google Scholar, E10Tey H.L. Yosipovitch G. Targeted treatment of pruritus: a look into the future.Br J Dermatol. 2011; 165: 5-17Crossref PubMed Scopus (73) Google ScholarFig E2Histology (hematoxylin and eosin staining) of skin specimens from papular/nodular skin lesions of the patient's leg. A, Histology from a papular lesion at the initial visit. Irregular parakeratosis, acanthosis, and spongiosis in the epidermis and lymphomonocytic infiltrate and prominent intravascular eosinophils (arrows) in the upper dermis are shown. B, Histology from a prurigo nodularis lesion in the second visit a year later. Thick hyperkeratosis, parakeratosis, acanthosis, and an inflammatory cell infiltrate, as well as a lymphomonocytic infiltrate, vasodilatation, and prominent intravascular eosinophils (arrows) in the upper dermis, are shown.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E3Potential causes of chronic pruritus. A, Skin disease causing chronic pruritis. B, Systemic and other noncutaneous diseases causing chronic pruritis. ACE, Angiotensin-converting enzyme; PPPP, puritic papules and pustules of pregnancy.Modified from Hong et al.E6Hong J. Buddenkotte J. Berger T.G. Steinhoff M. Management of itch in atopic dermatitis.Semin Cutan Med Surg. 2011; 30: 71-86Crossref PubMed Scopus (107) Google ScholarView Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E4Diagnostic algorithm to determine the origins of chronic pruritus. ALT, Alanine aminotransferase; AP, alkaline phosphatase; AST, aspartate aminotransferase; BUN, blood urea nitrogen; DIF, direct immunofluorescence; GI, gastrointestinal.Modified from Steinhoff et al.E7Steinhoff M. Cevikbas F. Ikoma A. Berger T.G. Pruritus: management algorithms and experimental therapies.Semin Cutan Med Surg. 2011; 30: 127-137Crossref Scopus (49) Google ScholarView Large Image Figure ViewerDownload Hi-res image Download (PPT)" @default.
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W2099947519 title "Evaluation and management of a patient with chronic pruritus" @default.
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