Matches in SemOpenAlex for { <https://semopenalex.org/work/W289774433> ?p ?o ?g. }
Showing items 1 to 75 of
75
with 100 items per page.
- W289774433 endingPage "654" @default.
- W289774433 startingPage "651" @default.
- W289774433 abstract "Original ArticlesAlopecia Areata and Associated Diseases in Saudi Patients Marwan Al-KhawajahMD Marwan Al-Khawajah Address reprint requests and correspondence to Dr. Al-Khawajah: Division of Dermatology, Department of Medicine (38), College of Medicine, King Saud University, P.O. Box 2925, Riyadh 11461, Saudi Arabia. From the Department of Medicine, College of Medicine, King Saud University, Riyadh. Search for more papers by this author Published Online:1 Nov 1991https://doi.org/10.5144/0256-4947.1991.651SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutAbstractAlopecia areata is a common presentation of Saudi patients seen at dermatology clinics. Although autoimmune factors have been suggested as pathogenic factors, alopecia areata remains a disease of unknown etiology. We investigated 92 patients with alopecia areata as compared to 88 sex-and age-matched healthy control subjects for the prevalence of associated diseases as well as abnormalities of thyroid function, and for the frequency of anti-thyroid antibodies. We found that atopy and psychological stress constitute the most commonly associated disorders in our series. Except for two female patients with diabetes mellitus, none of the remaining patients displayed clinical evidence of endocrine or autoimmune disease. Only one patient had high T3 and T4 values and five (5.4%) had low titers of anti-thyroid antibodies, an acceptable finding for the normal population.IntroductionAlopecia areata accounts for 1 to 2% of new dermatological outpatient visits [1, 2], but it remains a disease of unknown cause with unsatisfactory treatment. Psychological and physical stress [3–6], bacterial and viral infections [7, 8], as well as genetic [9], endocrine [3], and autoimmune factors [10–12] have been suggested as pathogenic factors. Alopecia areata is frequently found in association with a number of diseases showing alteration of autoimmunity, the most common ones being thyroid it is [13], diabetes mellitus [14], vitiligo [11], and atopic disease [15]. There is an abundance of conflicting data about the association of alopecia areata with circulating organ-specific autoantibodies. Some investigators have found these autoantibodies to be more common in patients with alopecia areata. The autoantibodies most commonly detected are those directed against the thyroid (microsomes and thyroglobulin) [16–18]. However, a number of investigators have been unable to confirm the association with circulating autoantibodies [19–21].Alopecia areata is a common presentation of Saudi patients seen in dermatology clinics [2]. To our knowledge there have been no studies on the clinical and laboratory associations of alopecia areata in the Saudi population. In this study we have tried to elucidate the significance of some of these associations.MATERIAL AND METHODSNinety-two consecutive patients with alopecia areata of different severity, including total loss of scalp hair (alopecia totalis) and complete loss of all body hair (alopecia universalis), who had been referred to the dermatology clinics of King Khalid University Hospital (KKUH) and King Abdulaziz University Hospital (KAUH) were studied (Table 1.) The diagnosis was first established by history and clinical findings of well-circumscribed round to oval areas of alopecia that were discrete or confluent without evidence of underlying inflammatory or scarring conditions. Other systemic causes of alopecia were ruled out by history.Table 1. Distribution by sex, age and disease extent in patients with alopecia areata.Table 1. Distribution by sex, age and disease extent in patients with alopecia areata.All patients had clinically active disease, as defined by ongoing hair loss from nonscarring patches of alopecia at the time of diagnosis. None had received topical or systemic therapy for at least one month prior to investigation. A full history was taken with special emphasis on past or family history of organ-specific autoimmune disease. Pregnant women as well as patients on drugs such as contraceptive pills or hydantoin, which may interfere with thyroid function tests, were excluded. The extent and activity of the alopecia were noted and the patients were carefully examined for signs of other diseases. Laboratory evaluations were conducted for patients as well as for the control population. These included radioimmunoassay of triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH). These tests were run using standard batch testing at KKUH or KAUH, depending on where the patient was seen. Serum antithyroglobulin and antimicrosomal antibodies were measured semiquantitatively using Thymune-T and Thymune-m kits, respectively. These tests are based on Boyden's passive hemagglutination system. The control population consisted of normal healthy subjects matched for sex and, where possible, age (exceptions were controls for the four children in the study who were aged one to four years). Blood samples were obtained from patients and control subjects after fully informed consent was received.RESULTSThe patients’ ages ranged from 1 to 44 years (mean, 18.9 ±11.2 years). There were 47 female and 45 male patients (Table 1). The duration of disease ranged from 1 to 18 months (mean, 7.3 ± 5.2 months).Association with Other Diseases in Patients and RelativesSeven female patients (14.9%) had atopic disease and two had diabetes mellitus. Five male patients (11.1%) had atopic disease. In addition, eight female and five male patients had had either acute psychological trauma or long-standing emotional difficulties. Twelve female (25.5%) and eight male (17.8%) patients gave a history of alopecia areata in members of their family. Eleven patients had relatives with atopic disease, two with diabetes mellitus, one with hyperthyroidism, and one with vitiligo. A summary of findings is given in Table 2.Table 2. Prevalence of other diseases in patients with alopecia areata and in their relativesaTable 2. Prevalence of other diseases in patients with alopecia areata and in their relativesaPrevalence of Antithyroid Antibodies and Thyroid Function AbnormalitiesOf the 92 patients, only one had abnormal thyroid function tests (serum levels of T3 and T4 higher than normal). Five (5.4%) had antithyroid (two antithyroglobulin and three antimicrosomal) antibodies. None of the controls had abnormal thyroid function tests and only two had antithyroid antibodies. The difference between the patients and controls did not achieve statistical significance by Fisher's exact test. Findings are summarized in Table 3.Table 3. Antithyroid antibodies and abnormal thyroid function tests (T3, T4, and TSH) in patients with alopecia areata and controls.Table 3. Antithyroid antibodies and abnormal thyroid function tests (T3, T4, and TSH) in patients with alopecia areata and controls.DISCUSSIONOur findings confirm that there is an increased prevalence of atopy in patients with alopecia areata and in their families. Ikeda [5] found that 10% of her patients were atopic, while later studies suggested a much higher prevalence of atopy in alopecia areata [22]. Our figure of 13% lies in the middle. A significant family history of alopecia areata was found in the disease group (21.7%), and this agrees with the observations of Friedman [17] and Sauder [9].Despite the strong evidence in the literature for a statistical association between alopecia areata and organ-specific autoimmune disorders such as vitiligo, diabetes mellitus, and thyroid disease [3,13,20], our findings failed to show such an association. Disease heterogeneity in terms of quantitative and qualitative differences (e.g., variance in degree of disease activity and disease extent [17] or the existence of different subsets of disease as proposed by Rook [1]) is one possible explanation for these inconsistencies [23]. In her survey of 1,989 patients with alopecia areata, Ikeda [15] found that the autoimmune group constituted only 3% of the whole, and occurred in patients over the age of 40. In our study group, only three patients were over 40. It is therefore entirely possible that bur series of relatively young patients (mean age, 18.9 ± 11.2 years) might not have included any of the autoimmune type, and may have represented mainly the common (idiopathic) and atopic types described by Ikeda.Thirteen (14.1%) of our patients (as compared to two [2.2%] of the controls) had considerable emotional stress (e.g., jealousy from a newborn, fear of an examination, financial difficulties) as a possible etiological factor in their disorder, as judged from the coincidence of onset of alopecia with the emotional incident and their parallel courses in remission and relapses (e.g., “seasonal” alopecia areata recurring at examination time in two students in our study). The role of psychological stress in the pathogenesis of alopecia areata remains controversial. In the past, psychological stress has been a popular etiological explanation for alopecia areata [4,5,24,25]. Mac Alpine [26], however, found no evidence to suggest that emotional factors play a significant role in the disease. Nevertheless, it does remain possible, as shown in a 1984 study [27], that severe emotional stress could be a precipitating factor in certain cases. This does not totally contradict an immunological view of its pathogenesis, since alterations of immune function can occur under conditions of severe psychological stress [28, 29].Finally, although some workers have shown an increased frequency of circulating antithyroid (antithyroglobulin and antimicrosomal) antibodies in patients with alopecia areata [16–18], like most authors [19–21,30], we have been unable to confirm such an association. The figure of 5.4% in our patients with antithyroid antibodies does not differ significantly from that observed for the control group (3.4%), and is in accordance with that reported for the normal population studies conducted in other parts of the world [31,32]. Moreover, the titers of positive tests were similar to those observed in the normal population, i.e., < 1:20 for antithyroglobulin antibody and < 1:400 for antimicrosomal antibody [31].ARTICLE REFERENCES:1. Rook A, Wilkinson DS. In: Rook A, Wilkinson DS, Ebling FJG, et al., eds. Textbook of dermatology, ed 4. Oxford: Blackwell, 1986; 53: 1985–92. Google Scholar2. Sherif AB. Spectrum of common dermatoses in Riyadh. Saudi Arabia . Proceedings of the Sixth Annual Ain Shams Medical Congress, March1983, pp 419–28. Google Scholar3. Muller SA, Winkelmann RK. Alopecia areata . Arch Dermatol. 1963; 88: 290–7. Google Scholar4. Greenberg SI. Alopecia areata: psychiatric survey . Arch Dermatol. 1955; 72: 454–7. Google Scholar5. Reinhold M. Relationship of stress to the development of symptoms in alopecia areata and chronic urticaria . Br Med J. 1960; 1: 846–9. Google Scholar6. Toback C, Rajkumar S. The emotional disturbance underlying alopecia areata, alopecia totalis and trichotillomania . Child Psychiatry Hum Dev. 1979; 10: 114–7. Google Scholar7. Williams N, Riegert AL. Epidemic alopecia areata . J Occup Med. 1971; 13: 535–42. Google Scholar8. Stankler L. Synchronous alopecia areata in two siblings: possible viral etiology . Lancet. 1979; 1: 1303–4. Google Scholar9. Sauder DN, Bergfeld WF, Krakauer RS. Alopecia areata: an inherited autoimmune disease. In: Brown AC, Crounse RG, eds. Hair, trace elements, and human illness. New York: Praeger Publishers, 1980; 343–7. Google Scholar10. Klein U, Weinheimer B, Zaun H. Simultaneous occurrence of alopecia areata and immunothyroiditis . Int J Dermatol. 1974; 13: 116–8. Google Scholar11. Thompson DM. Alopecia areata, vitiligo, scleroderma, and ulcerative colitis . Proc R Soc Med. 1974; 67: 1010–2. Google Scholar12. Brown AC. Autoimmune gonadal disease and alopecia areata. In: Brown AC, Crounse RG, eds. Hair, trace elements, and human illness. New York; Praeger Publishers, 1980; 313–33. Google Scholar13. Cunliffe WJ, Hall R, Stevenson CJ, et al. Alopecia areata, thyroid disease, and autoimmunity . Br J Dermatol. 1969; 81: 877–81. Google Scholar14. Aw TC, Cheah JS. Diabetes mellitus presenting with alopecia totalis . Lancet. 1978; 1: 268–9. Google Scholar15. Ikeda T. A new classification of alopecia areata . Der-matologica. 1965; 131: 421–45. Google Scholar16. Schenk EA, Schneider P, Brown AC. Autoantibodies in alopecia areata and vitiligo. In: Brown AC, Crounse RG, eds. Hair, trace elements, and human disease. New York; Praeger Publishers, 1980; 334–42. Google Scholar17. Friedmann PS. Alopecia areata and auto-immunity . Br J Dermatol. 1981; 105: 153–7. Google Scholar18. Herzer P, Czarnetzki BM, Holzmann H, et al. Immunological studies in patients with alopecia areata . Int Arch Allergy Appl Immunol. 1979; 58: 212–8. Google Scholar19. Muller HK, Rook AJ, Kubba R. Immunohistology and autoantibody studies in alopecia areata . Br J Dermatol. 1980; 102: 609–10. Google Scholar20. Klaber MR, Munro DD. Alopecia areata: immunofluorescence and other studies . Br J Dermatol. 1978; 99: 383–6. Google Scholar21. Conchran REI, Thomson J, MacSween RNM. An autoantibody profile in alopecia totalis and diffuse alopecia . Br J Dermatol. 1976; 95: 61–5. Google Scholar22. Penders AJM. Alopecia areata and atopy . Dermatologica. 1978; 156: 306–8. Google Scholar23. Mitchell AJ, Krull EA. Alopecia areata: pathogenesis and treatment . J Am Acad Dermatol. 1984; 11: 763–75. Google Scholar24. Anderson I. Alopecia areata: a clinical study . Br Med J. 1950; 2: 1250–2. Google Scholar25. Irwin D. In: Wittkower E, Russell B, eds. Emotional factors in skin disease. New York: Paul B. Hoeber, 1953; 176–89. Google Scholar26. MacAlpine I. Is alopecia areata psychosomatic? Br J Dermatol. 1958; 70: 117–31. Google Scholar27. Perini GI, Fornasa V, Cipriani R, et al. Life events and alopecia areata . Psychother Psychosom. 1984; 41: 48–52. Google Scholar28. Bartrop RW, Lazarus L, Luckhurst E, et al. Depressed lymphocyte function after bereavement . Lancet. 1977; 1: 834–6. Google Scholar29. Monjan M, Collector MI. Stress-induced modulation of the immune response . Science. 1977; 196: 307–8. Google Scholar30. Betterle C, Peserico A, Del Prete G, et al. Autoantibodies in alopecia areata . Arch Dermatol. 1975; 111: 927–8. Google Scholar31. Cayzer I, Chalmers SR, Doniach D, et al. An evaluation of two new haemagglutination tests for the rapid diagnosis of autoimmune thyroid disease . J Clin Pathol. 1978; 31: 1147–51. Google Scholar32. Tunbridge WMG, Evered DC, Hall R, et al. The spectrum of thyroid disease in a community: the Whickham Survey . Clin Endocrinol. 1977; 7: 481–93. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 11, Issue 6November 1991 Metrics History Accepted17 December 1990Published online1 November 1991 InformationCopyright © 1991, Annals of Saudi MedicinePDF download" @default.
- W289774433 created "2016-06-24" @default.
- W289774433 creator A5036580666 @default.
- W289774433 date "1991-11-01" @default.
- W289774433 modified "2023-10-13" @default.
- W289774433 title "Alopecia Areata and Associated Diseases in Saudi Patients" @default.
- W289774433 cites W1963668098 @default.
- W289774433 cites W1964389872 @default.
- W289774433 cites W1966623202 @default.
- W289774433 cites W1970739888 @default.
- W289774433 cites W1995333913 @default.
- W289774433 cites W2014247012 @default.
- W289774433 cites W2014385555 @default.
- W289774433 cites W2016366029 @default.
- W289774433 cites W2016555275 @default.
- W289774433 cites W2028231965 @default.
- W289774433 cites W2036183981 @default.
- W289774433 cites W2040421698 @default.
- W289774433 cites W2047434528 @default.
- W289774433 cites W2059525780 @default.
- W289774433 cites W2065837774 @default.
- W289774433 cites W2085621256 @default.
- W289774433 cites W2093103981 @default.
- W289774433 cites W2094843221 @default.
- W289774433 cites W2148113299 @default.
- W289774433 cites W2162218048 @default.
- W289774433 doi "https://doi.org/10.5144/0256-4947.1991.651" @default.
- W289774433 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17590818" @default.
- W289774433 hasPublicationYear "1991" @default.
- W289774433 type Work @default.
- W289774433 sameAs 289774433 @default.
- W289774433 citedByCount "9" @default.
- W289774433 countsByYear W2897744332012 @default.
- W289774433 countsByYear W2897744332013 @default.
- W289774433 countsByYear W2897744332016 @default.
- W289774433 countsByYear W2897744332019 @default.
- W289774433 countsByYear W2897744332020 @default.
- W289774433 countsByYear W2897744332023 @default.
- W289774433 crossrefType "journal-article" @default.
- W289774433 hasAuthorship W289774433A5036580666 @default.
- W289774433 hasBestOaLocation W2897744331 @default.
- W289774433 hasConcept C16005928 @default.
- W289774433 hasConcept C17744445 @default.
- W289774433 hasConcept C199539241 @default.
- W289774433 hasConcept C2777524370 @default.
- W289774433 hasConcept C2779473830 @default.
- W289774433 hasConcept C71924100 @default.
- W289774433 hasConceptScore W289774433C16005928 @default.
- W289774433 hasConceptScore W289774433C17744445 @default.
- W289774433 hasConceptScore W289774433C199539241 @default.
- W289774433 hasConceptScore W289774433C2777524370 @default.
- W289774433 hasConceptScore W289774433C2779473830 @default.
- W289774433 hasConceptScore W289774433C71924100 @default.
- W289774433 hasIssue "6" @default.
- W289774433 hasLocation W2897744331 @default.
- W289774433 hasLocation W2897744332 @default.
- W289774433 hasOpenAccess W289774433 @default.
- W289774433 hasPrimaryLocation W2897744331 @default.
- W289774433 hasRelatedWork W2044090606 @default.
- W289774433 hasRelatedWork W2054859753 @default.
- W289774433 hasRelatedWork W2068981453 @default.
- W289774433 hasRelatedWork W2395623616 @default.
- W289774433 hasRelatedWork W2404906068 @default.
- W289774433 hasRelatedWork W2766455916 @default.
- W289774433 hasRelatedWork W2941516307 @default.
- W289774433 hasRelatedWork W3106353918 @default.
- W289774433 hasRelatedWork W2460135485 @default.
- W289774433 hasRelatedWork W3166178439 @default.
- W289774433 hasVolume "11" @default.
- W289774433 isParatext "false" @default.
- W289774433 isRetracted "false" @default.
- W289774433 magId "289774433" @default.
- W289774433 workType "article" @default.