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REVIEW 16. Ji JD, Cheon H, Jun JB, Choi SJ, Kim YR, Lee YH, Kim TH, Chae IJ, Song GG, Yoo DH, Kim SY, Sohn J. Effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) on the expression of inflammatory cytokines and apoptosis induction in rheumatoid synovial fibroblasts and monocytes. J Autoimmun. 2001;17(3):215-221. 17. Fahmi H, Di Battista JA, Pelletier JP, Mineau F, Ranger P, Martel-Pelletier J. Peroxisome proliferator-activated receptor gamma activators inhibit interleukin1-beta induced nitric oxide and matrix metalloproteinase 13 production in human chondrocytes. Arthritis Rheum. 2001;44:595-607. 18. Francois M, Richette P, Tsagris L, et al. Peroxisome proliferator-activated receptor gamma downregulates chondrocyte matrix metalloproteinase-1 via a novel composite element. Clin Exp Immunol. 2002;129:379- 384. 19. Jiang C, Ting AT, Seed B: PPAR-gamma agonists inhibit production of monocyte inflammatory cytokines. Nature 1998; 391:82-86. 20. Ricote M, Li AC, Wilson TM, Kelly CJ, Glass CK: The peroxisome proliferator-activated receptor gamma is a negative regulator of macrophage activation. Nature 1998; 391:79-82. 21. Kobayashi T. Notoya K. Naito T. Unno S. Nakamura A. Martel-Pelletier J. Pelletier JP. Pioglitazone, a peroxisome proliferatoractivated receptor gamma agonist, reduces the progression of experimental 8 osteoarthritis in guinea pigs. Arthritis & Rheumatism 2005;52(2):479-87. 22. Brandt KD, Braunstein EM, Visco DM, O’Connor B, Heck D, Albrecht M Anterior (cranial) cruciate ligament transection in the dog: a bona fide model of osteoarthritis, not merely of cartilage injury and repair. J Rheumatol. 1991;18:436-446. 23. Frank CB, Shrive NG, Boorman RS, Lo IKY, Hart DA: New perspectives on bioengineering of joint tissues: joint adaptation creates a moving target for engineering replacement tissues. Ann Biomed Eng. 2004;32(3):458-465. 24. Hashimoto S, Creighton-Achermann L, Takahashi K, Amiel D, Coutts RD, Lotz M. Development and regulation of osteophyte formation during experimental osteoarthritis. Osteoarthritis Cartilage. 2002;10:180-187. 25. Hellio le Graverand MP, Eggerer J, Vignon E, Otterness IG, Braclay L, Hart DA. Assessment of specific mRNA levels in cartilage regions in a lapine model of osteoarthiritis. J Orthop Res. 2002;20:535- 544. 26. Lohmander, LS, Ostenberg A, Englund M, Roos H. High prevalence of knee osteoarthritis, pain, and functional limitations in female soccer players twelve years after anterior cruciate ligament injury. Arthritis Rheum. 2004;50(10):3145-3152. 27. Sah RL, Yang AS, Chen AC, Hant JJ, Halili RB, Yodhioka M, Amiel D, Coutts RD. Physical properties of rabbit articular cartilage after transection of the Clinical application and review of typical and atypical antipsychotics in the treatment of delusional parasitiosis Nathan Y. Hoy, 1 Patricia T. Ting, MSc, MD, 2 Stewart Adams, MD 3 anterior cruciate ligament. J Orthop Res. 1997;15:197-203. 28. Setton LA, Elliott DM, Mow VC. Altered mechanics of cartilage with osteoarthritis: human osteoarthritis and an experimental model of joint degeneration. Osteoarthritis Cartilage. 1999;7:2-14. 29. Woo S, Young E, Suh J, Engevretsen, L. Acute injury to ligament and meniscus as inducers of osteoarthritis. In: Kuettner KE, Goldberg VM, eds. Osteoarthritic Disorders: American Academy of Orthopaedic Surgeons, 1995. 30. Walsh DA. Pathophysiological mechanisms of angiogenesis. Adv Clin Chem. 2007;44:187-221. 31. Bonnet CS, Walsh DA. Osteoarthritis, angiogenesis and inflammation. J Rheumatol. 2005;44(1):7-16. 32. Chimich D, et al. Water content alters viscoelastic behaviour of the normal adolescent rabbit medial collateral ligament. J Biomech. 1992; 25(8):831-837. 33. Kobayashi M, Squires GR, Mousa A, Tanzer M, Zukor DJ, Antoniou J, Feige U, Poole AR. Role of interleukin-1 and tumor necrosis factor alpha in matrix degradation of human osteoarthritic cartilage. Arthritis Rheum. 2002;52(1):128-135 34. Miller D, Forrester K, Leonard C, Hart DA, Salo P, Bray RC. Endothelial dysfunction and decreased vascular responsiveness in the anterior cruciate ligament deficient model of osteoarthritis. J Appl Physiol. 2007;102:1161-1169. 1 Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada 2 Deparment of Dermatology and Cutaneous Sciences, Department of Medicine, University of Alberta, Edmonton, Canada 3 Department of Dermatology, University of Calgary, Calgary, Canada Correspondence and reprint requests to: Nathan Hoy, #110 Beddington Co-op Mall, 8220 Centre St. N.E., Calgary, Alberta, Canada T3K 1J7, Ph: (780) 289-3383, Fax: (403) 275-1143, Email: nhoy@ualberta.ca ABSTRACT Background: Delusional parasitosis (DP) is a monosymptomatic hypochondrial psychosis characterized by a false belief that one is infected with parasites. Traditionally, treatment revolved around typical antipsychotics, especially pimozide. Pimozide’s adverse effect profile and the advent of atypical antipsychotics have made the latter the treatment of choice. Given the paucity of randomized control trials and relatively recent introduction of atypicals, little is known about their efficacy in the treatment of DP. Objective: The purpose of this study is to review the evidence for the efficacy and use of both typical and atypical antipsychotics as treatment modalities for DP, with a specific emphasis on the newer atypical pharmacologics. As well, we aim to provide suggestions on how best to implement treatment in a dermatological setting. Methods: Medline and EMBASE were searched for available literature for both University of Alberta Health Sciences Journal • April 2012 • Volume 7 • Issue 1
types of antipsychotics used in the treatment of DP. A systematic review was not completed to allow for discussion of clinical application of treatment. Results: Risperidone and olanzapine are currently the most commonly used atypical antipsychotics in DP treatment and are as efficacious as pimozide (full or partial remission rates of 68% and 90% respectively vs. pimozide average of 79%), and have fewer side effects. Other atypicals such as quetiapine, aripiprazole and paliperidone as well as risperidone long acting injections have demonstrated promising remission rates > 75% in a limited number of patients, but still require further studies to be considered first-line therapies. Conclusion: Limited clinical studies with small study populations implicate risperidone and olanzapine as first line treatments, but more randomized control trials are needed. We also review methods of how dermatologists may best initiate treatment with atypical antipsychotics. Keywords: Delusional parasitosis, atypical antipsychotics, typical antipsychotics, treatment INTRODUCTION Delusional parasitosis is a monosymptomatic hypochondrial psychosis characterized by an unwavering false belief that one is infected with parasites. 1 Thieberge first described this disorder in 1894, and the name delusional parasitosis (DP) was introduced in 1946. 2 The prevalence of DP is not well established, but is considered rare. Overall, the femaleto-male ratio of affected individuals is approximately 2:1, with the mean age of diagnosis being slightly higher for females than males (mean age, 50 years to 40 years). 3 The classification of DP is as either primary or secondary. Primary DP is characterized by a somatic delusion lasting for at least 1 month, whereby patients do not meet criterion A for schizophrenia and there can be no underlying cause of the delusion. 4 Secondary DP results from the use of a substance, organic causes, or other medical or psychiatric disorders with the most common causes being schizophrenia, diabetes, depression, cardiovascular events, and neurodegenerative disease. A comprehensive review of other secondary causes of DP is discussed by Huber et al. (2007). 5 Given that DP is a somatic delusion, patients often initially present to dermatologists instead of psychiatrists with symptoms of pruritis, crawling sensations attributed to the presence of parasites under the skin leading to secondary excoriations, lichenification, prurigo nodularis and full thickness ulcers. 6, 7 Commonly, patients bring in samples of skin in small boxes as proof that the parasites exist; this stereotypical presentation is referred to as “the matchbox sign.” 8 Furthermore, patients may attempt to rid these “parasites” with anti-scabetic permethrin cream or even perform harmful skin cleansing rituals with disinfectants or pesticides. 9 METHODS Treatment of DP requires the differentiation between the primary and secondary forms. Treatment of secondary DP relies on treating the underlying cause or cessation of the offending drug. 10 Treatment of primary DP has mostly revolved around typical and the newer atypical antipsychotics, which have differing mechanisms of action compared to typical antipsychotics. We conducted a literature search using combinations of the search terms: delusion*, parasitosis, typical, atypical, antipsychotics and treatment, in EMBASE and PubMed inclusive of studies published prior to May 1, 2010. For studies involving typical antipsychotics, only those with n≥20 (including placebo group) were reviewed, since these represent the most influential studies on which the basis of typical antipsychotic treatment is formed. Due to the relatively recent introduction of atypical antipsychotics in the treatment of DP, the n values for these studies were significantly smaller; thus sample size was not used as a definitive exclusion criterion. We included at least one study for each atypical. The criteria we considered included the size of the study, with preference being given to larger sample sizes; whether or not numerous atypicals were compared within the same study, to control for variable treatment practices; and how well the study represented the general treatment population with respect to disease severity, co-morbidities and age. RESULTS Typical antipsychotics The most common typical antipsychotic used in the treatment of DP is pimozide. 11 Pimozide is an approved treatment for Gilles de la Tourette syndrome in the United States, but it has also been shown to have a therapeutic effect for numerous offlabel disorders, such as DP. 10-19 Pimozide’s primary mechanism of action is via central Dopamine-receptor D2 antagonism. 12 One advantage of pimozide over other typical antipsychotics is its weak noradrenergic receptor blockade effect which reduces adverse side effects such as orthostatic hypotension and dizziness. 14 A number of case reports, case series, and double-blind crossover trials showing the effects of pimozide in DP have been conducted (summarized in Table 1) 15-19 . The first double-blind crossover study was performed by Hamann and Avnstorp (1982) which demonstrated that 10 out of 11 DP patients had a decrease in Brief Psychiatric Rating Scale points and improvement of delusion and itching following 6 weeks of treatment with pimozide, while only one patient from the placebo group experienced improvement in the 4 week evaluation period. 15 In 1986, another double-blind crossover study showed significant improvement in 10 DP patients administered 2-8 mg/day of pimozide for 3 weeks followed by a relapse following 2 weeks of placebo treatment and subsequent improvement when pimozide was restarted. Improvement was based on the authors’ own rating scale using symptoms of DP. 13 Although these studies used a placebo control, the results are limited by the small sample size (i.e. n=11 and n=10 13, 15 respectively). The rates of partial and full remission are variable amongst studies with pimozide. Zomer et al. (1998) found a partial to full remission rate of 61% (11 out of 18 patients) in patients treated with pimozide compared to 20% (3 out of 15) in the non-treatment group. 16 A survey conducted by Lyell (1983) demonstrated 44 of 66 patients treated with pimozide demonstrated full or partial remission (combined remission rate of 67%). 17 Partial and full remission of DP in patients treated with pimozide have been reported as high as 87% (n = 46)18 to 100% (n=10). 13 The long-term efficacy of treatment with pimozide was demonstrated in a follow-up study by Lindskov and Baadsgaard (1985). 19 Fourteen patients were followed up between 19 and 48 months after termination of pimozide treatment. Seven patients had improved, while 4 had deterioration of their symptoms and 3 had relapses that responded well to intermittent pimozide treatment. A systematic review conducted by Lepping et al. (2007) found a total of 92 patients treated with typical antipsychotics for primary DP. Of those 92, 40 (43%) had partial remission, 45 (49%) had full remission and 7 (8%) showed no improvement or were lost to follow-up. 10 Of the 53 patients treated with pimozide, 50 had either full or partial remission (94%), University of Alberta Health Sciences Journal • April 2012 • Volume 7 • Issue 1 9 REVIEW
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Page 21 and 22: Give Me Hope | by Vina Nguyen | Med
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Page 25 and 26: References 1. Brett-MacLean PJ, Cav
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Page 39 and 40: Thank you The UAHSJ wishes to thank

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