Mirosława Gałęcka, *Anna M. Basińska, Anna Bartnicka
Pruritus ani – causes and treatment-supporting diagnostics
Świąd odbytu – przyczyny i diagnostyka wspomagająca leczenie
Institute of Microecology, Poznań
Streszczenie
Doniesienia literaturowe sugerują, że problem świądu odbytu może dotyczyć nawet 5% populacji. Wiadomo, iż świąd odbytu może być objawem bardzo zróżnicowanych chorób, zarówno zapalnych, nowotworowych, zakażeń (bakteryjnych, grzybiczych, pasożytniczych), może być też spowodowany chorobami dermatologicznymi, alergicznymi lub ogólnoustrojowymi (np. cukrzycą), a nawet zaburzeniami psychicznymi. Badania epidemiologiczne związane z ustaleniem częstości występowania świądu odbytu oraz jego przyczynami są prowadzone rzadko. Niestety u wielu pacjentów trudno jest wskazać konkretną przyczynę uporczywych i obniżających jakość życia dolegliwości. W związku z tym często pacjent jest leczony objawowo, a nie przyczynowo. W takich przypadkach zasadne jest zatem rozważenie przeprowadzenia rozszerzonej diagnostyki, w oparciu o szczegółowy wywiad oraz najnowsze doniesienia literaturowe. Zastosowanie nowych metod diagnostycznych związanych z oceną mikrobioty jelitowej, również grzybów pleśniowych i drożdżopodobnych, oraz parametrów odporności śluzówkowej i stanu zapalnego może zdecydowanie pomóc w ustaleniu przyczyn świądu odbytu oraz jego leczeniu. Dodatkowo indywidualnie dobrana dieta i celowana probiotykoterapia mogą korzystnie wspomagać leczenie zasadnicze, np. pacjentów proktologicznych.
Summary
Literature reports suggest that the problem of pruritus ani may affect up to 5% of population. It is a known fact that anal pruritus may be a sign of a variety of diseases, including inflammation, cancer, infections (bacterial, fungal or parasitic), as well as skin conditions, allergic, systemic (e.g. diabetes), and even mental diseases. Epidemiological research to determine the incidence and the causes of pruritus ani is sparse. Unfortunately, it is difficult to identify the cause of these persistent, life quality lowering symptoms in many cases. Therefore, patients often receive symptomatic instead of causative treatment. It seems reasonable to consider extended diagnosis in such cases, based on a detailed medical history and the latest literature reports. The use of new diagnostic methods involving an assessment of intestinal microbiota, including moulds and yeast-like fungi, as well as mucosal immunity and inflammatory parameters may definitely help determine the causes of pruritus ani and allow for treatment initiation. Furthermore, the primary treatment may be supported by an individually composed diet and targeted probiotic therapy e.g. in proctological patients.
Introduction
Pruritus ani is a distressing problem for patients and a very important symptom for doctors, which should not be underestimated. Due to the location of areas affected by itching, patients often conceal their symptoms, which causes the problem to grow. According to dermatologists, the described symptom represents the most common anogenital condition. Epidemiological research on the factors predisposing to pruritus ani is sparse. It has been suggested that the condition affects 1-5% of population and is four times more common among men, usually aged 40-70 years (1, 2). However, pruritus ani may occur in different age groups due to a variety causes. Pruritus ani of unknown aetiology, which unfortunatlely accounts for the majority of cases (almost 75%), is classified as idiopathic. The fact that anal pruritus is often treated symptomatically rather than causatively is concerning (3). In addition to idiopathic pruritus ani, pruritus due to undiagnosed allergy is also classified as primary.
The most common causes of secondary pruritus include:
– proctological conditions, such as anal fissure, haemorrhoidal disease, anal abscess and anal fistula, rectal prolapse, colon and anal cancers, postoperative complications, such as “wet anus” and sphincter incompetence,
– perianal bacterial and fungal infections,
– viral and parasitic perianal skin infections, e.g. pruritus in anal warts, enterobiosis, ascariasis, scabies, and pubic lice,
– hypersensitivity or allergy to personal and intimate hygiene products, toilet paper,
– primary skin conditions, such as psoriasis, lichen, eczema, leukoplakia, atopic dermatitis,
– inflammatory bowel disease and irritable bowel syndrome with persistent diarrhoea,
– metabolic diseases such as diabetes, renal or hepatic failure, jaundice, hyperthyroidism, iron deficiency,
– local and systemic immune deficiency,
– obesity, deep intergluteal cleft and excess hair around the anus promote pruritus,
– improper, i.e. insufficient or excess perineal hygiene, anal sexual intercourse and sexually-transmitted infections,
– mental disorders,
– celiac disease, dermatitis herpetiformis (4-6).
Studies by Hadasik et al. showed that contact dermatitis was diagnosed in 26 out of 55 patients with persistent pruritus ani. However, idiopathic pruritus was found in up to 14 patients, which means that the cause of pruritus remained unknown. Perianal streptococcal dermatitis was found in 5, and candidal intertrigo in another 5 patients. Inverse psoriasis, genital warts, erythrasma, enterobiosis and paraneoplastic pruritus were identified in other patients (2). In younger patients, persistent pruritus ani is often associated with pinworms. Despite improved hygiene habits, pinworms are the most common parasites, with annual rates of 18% in Poland. Pruritus ani may be also caused by other gastrointestinal parasites, such as Ascaris lumbricoides and tapeworm (7). Other causes may include improper hygiene, i.e. insufficient hygiene, such as in children or patients with limited mobility, or excess hygiene leading to the loss of natural protective barrier and increased susceptibility to infections. Additionally, it should be emphasised that pruritus ani may occur as a complication after proctological procedures and invasive treatment, e.g. chemotherapy, which suppress patient’s immune system and may promote secondary infections (8).
Therefore, a thorough medical history, which helps select further diagnostic methods, is still an important component of clinical management aimed to identify the cause of pruritus (9). Doctors observe in their practice that some dietary restrictions have beneficial clinical effects in patients treated for pruritus (9). Dietary recommendations of experienced specialists further involve the exclusion of coffee, tea, alcohol, hot spices, chocolate and tomatoes. Furthermore, patients are suggested to avoid milk and dairy products as a source of potential allergens (3). Clinical observations indicate that pruritus ani is common among patients with celiac disease (hypersensitivity to gluten) and may be also associated with impaired intestinal microbiota. Increased permeability of the intestinal epithelium due to impaired microbiota or other diseases promotes the passage of increased protein levels from frequently consumed food products into the bloodstream and, consequently, IgG-mediated food hypersensitivity.
It should be emphasised that the problem of pruritus ani may be encountered by a variety of specialists (3), therefore it seems reasonable to discuss the latest scientific reports and diagnostic methods that could facilitate the diagnosis and treatment of affected patients.
Intestinal microbiota and its role in the development of immunity
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Piśmiennictwo
1. Daniel GL, Longo WE, Vernava AM: Pruritus ani. Causes and concerns. Dis Colon Rectum 1994; 37(7): 670-674.
2. Hadasik K, Hadasik G, Brzezińska-Wcisło L: Potential etiologic factors in patients with persistent pruritus ani. Post Nauk Med 2015; XXVIII(3): 173-176.
3. Kołodziejczak M, Jaraczewska I: Primary pruritus ani in adults. Med Rodz 2002; 3-4: 123-126.
4. Bielecki K: Intractable pruritus ani. Post Nauk Med 2006; 5: 204-206.
5. Friend WG: The cause and treatment of idiopathic pruritus ani. Dis Colon Rectum 1977; 4: 40-42.
6. Stermer E, Sukhotnic I, Shaoul R: Pruritus ani: an approach to an itching condition. J Pediatr Gastroenterol Nutr 2009; 48(5): 513-516.
7. Hadaś E, Derda M: Pasożyty – zagrożenia nadal aktualne. Probl Hig Epidemiol 2014; 95(1): 6-13.
8. Kołodziejczak M, Talarek M: Proctologic problems in patients treated for rectal cancer. Nowa Med 2015; 3: 93-97. DOI: 10.5604/17312485.1184084.
9. Ciesielski P, Kołodziejczak M: Significance of clinical symptoms for the diagnosis of diseases of the lower gastrointestinal tract. Nowa Med 2009; 3: 163-168.
10. Mroczyńska M, Libudzisz Z, Gałęcka M, Szachta P: Mikroorganizmy jelitowe człowieka i ich aktywność metaboliczna. Prz Gastroenterol 2016; 4: 218-224.
11. Dethlefsen L, Eckburg PB, Bik EM et al.: Assembly of the human intestinal microbiota. Trends Ecol Evol 2006; 21: 517-523.
12. Ley RE, Peterson DA, Gordon JI: Ecological and evolutionary forces shaping microbial diversity in the human intestine. Cell 2006; 124(4): 837-848.
13. Louis P, Flint HJ: Diversity, metabolism and microbial ecology of butyrate-producing bacteria from the human large intestine. FEMS Microbiol Lett 2009; 294(1): 1-8.
14. Cao Y, Shen J, Ran ZH: Association between Faecalibacterium prausnitzii reduction and inflammatory bowel disease: a meta-analysis and systematic review of the literature. Gastroenterol Res Pract 2014; 2014: 872725.
15. Everard A, Belzer C, Geurts L et al.: Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci 2013; 110(22): 9066-9071.
16. MacDonald TT: The gut is still the biggest lymphoid organ in the body. Mucosal Immunol 2008; 1: 246-247.
17. Rusch K, Peters U: Jelito grube – centrum układu immunologicznego. Medycyna Biologiczna 2003; 2: 54-58.
18. Majewska M, Szczepanik M: Rola receptorów toll-podobnych (TLR) w odporności wrodzonej i nabytej oraz ich funkcja w regulacji odpowiedzi immunologicznej. Postepy Hig Med Dosw 2006; 60: 52-63.
19. Matzinger P: The danger model: a renewed sense of self. Science 2002; 296: 301-305.
20. Gałęcka M, Bartnicka A, Szewc M, Mazela J: Kształtowanie się mikrobioty jelitowej u niemowląt warunkiem zachowania zdrowia. Stand Med, Pediatr 2016; 13: 359-367.
21. Habermann W, Zimmermann K, Skarabis H et al.: The effect of a bacterial immunostimulant (human Enterococcus faecalis bacteria) on the occurrence of relapse in patients with. Arzneimittel-Forschung 2001; 51(11): 931-937.
22. Gałęcka M, Basińska AM, Bartnicka A: KyberKompaktPro – nowoczesna diagnostyka mikroflory przewodu pokarmowego i jej znaczenie dla prawidłowego funkcjonowania organizmu człowieka. Forum Zakażeń 2017; 8(2): 111-116.
23. Tlaskalová-Hogenová H, Štěpánková R, Kozáková H et al.: The role of gut microbiota (commensal bacteria) and the mucosal barrier in the pathogenesis of inflammatory and autoimmune diseases and cancer: contribution of germ-free and gnotobiotic animal models of human diseases. Cell Mol Immun 2011; 8(2): 110-120.
24. Ebel B, Lemetais G, Beney L et al.: Impact of probiotics on risk factors for cardiovascular diseases. A review. Crit Rev Food Sci Nutr 2014; 54(2): 175-189.
25. Quigley EM: New perspectives on the role of the intestinal flora in health and disease. J Gastrointest Liver 2006; 15(2): 109.
26. Kasper LH: The evolving role of the gut microbiome in human disease. FEBS let 2014; 588(22): 4101.
27. Gałecka M, Szachta P: Kyberkompakt – znaczenie nowoczesnej diagnostyki mikrobiologicznej przewodu pokarmowego. Zakażenia 2013; 13(6): 84.