skin-manifestations-of-hepatitis-c-in-chronic-renal-disease-patient

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ACTA PSYCHOPATHOLOGICA ISSN 2469-6676 2017 Vol. 3 No. 3: 14 1 iMedPub Journals Mini Review http://www.imedpub.com DOI: 10.4172/2469-6676.100086 © Under License of Creative Commons Attribution 3.0 License | This article is available from: www.psychopathology.imedpub.com Awad Magbri Dialysis Access Center of Pitsburgh PA USA Corresponding author: Awad Magbri  elmagbrihotmail.com MD Dialysis Access Center of Pitsburgh PA USA. Tel: +1 4122715106 Citation: Magbri A. Skin Manifestatons of Hepatts C in Chronic Renal Disease Patent. Acta Psychopathol. 2017 3:3. Introducton Cutaneous manifestatons of chronic HCV infecton are found in 20-40 of patents and are ofen presented to the dermatologists for treatment. The extra-hepatc manifestatons of the virus are numerous 1 and the kidneys and skin are the most organs involved afer the liver. The extra-hepatc manifestatons of chronic hepatts C infecton are many including 1-4: • Hematological diseases such as cryoglobulinemia and lymphoma 2. • Autoimmune disorders such as thyroidits. • Renal disease. • Dermatological diseases such as lichen planus porphyria cutanea tarda skin lymphoma and vasculits 34. In this mini-review will try to shed light on the skin manifestaton of HCV infecton in patents with chronic HCV infecton. It is recognized that most extrahepatc manifestaton of HCV infecton are common in chronic kidney disease and can occur in 38 of patents 3. Essental cryoglobulinemia or type II mixed cryoglobulinemia is a lymphoproliferatve disorder which leads to depositon of circulatng immune complexes in small to medium sized blood vessels. This type of disorder is common with chronic HCV infecton. The most common clinical manifestaton of this disease includes palpable purpura arthralgia and renal disease in the form of membranoproliferatve glomerulonephrits or membranous nephropathy with hypocomplementemia. Skin involvement is ofen associated with neurological manifestaton in the form of peripheral neuropathy due to involvement of the small blood vessels in the peripheral nerves. The purpuric vasculits in the lower extremites may undergo necrosis and ulceraton. Digital necrosis and skin lymphoma may also occur. More than 90 of patents with essental cryoglobulinemia are infected with HCV 5 and patents should undergo evaluaton for HCV infecton. Skin vasculits and cryoglobulin levels may respond to treatment of HCV infecton. Plasmapheresis steroids cytotoxics and specifc ant-HCV medicatons are the mainstay therapy of HCV infecton in this conditon. The associaton of HCV infecton with monoclonal gammopathies has been inconsistent. In one study 35 are positve for HCV in patents with smoldering or multple myeloma 6. The incidence of monoclonal gammopathies increased in the age group of 60- 69 years 21. 50 of these patents are infected with HCV genotype 2a/c. In another study 12 of HCV positve patents had a monoclonal gammopathies compared to 3 of the control group 7. HCV infecton has been associated with polyclonal or oligoclonal hyperglobulinemia most ofen IgG 89. The kidneys are ofen involved in monoclonal gammopathy that is known Received: April 12 2017 Accepted: April 18 2017 Published: April 24 2017 Skin Manifestatons of Hepatts C in Chronic Renal Disease Patent Abstract Hepatts C virus is a single stranded RNA virus. It is a major cause of acute and chronic hepatts. The mode of infecton is usually through intravenous drug abuse or transfusion of infected blood or blood products. Health care workers are at risk for needle stck and other with high-risk sexual behavior is also considered a major risk factor for HCV infecton. The incidence of new cases of acute HCV infecton has sharply decreased in the United States during the past decade but the prevalence remains high with approximately 2.7 million Americans infected with the virus. Chronic HCV infecton progresses in roughly 75 of patents afer acute infecton by the virus. Chronic HCV infecton is slowly progressive disease and results in severe morbidity in 20-30 of infected persons. Keywords: Hepatts C Chronic hepatts Healthcare Drug abuse Skin lymphoma Kidney disease

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2017 ACTA PSYCHOPATHOLOGICA ISSN 2469-6676 Vol. 3 No. 3: 14 2 This article is available from: www.psychopathology.imedpub.com Alcohol estrogen iron overload and the exposure to hydrocarbons are among the triggering factors. Simultaneous HCV infecton of liver and kidney may occur. Diagnosis of PCT is typically suspected on clinical grounds and confrmed by marked elevaton of urine uroporphyrin levels. The disease can also be confrmed directly by measuring hepatc uroporphyrinogen decarboxylase actvity. All patents with PCT should be evaluated for HCV infecton HIV and iron overload e.g. hemochromatosis with HFE mutaton testng. Treatment of PCT consists of avoiding the precipitatng factors treatng iron overload and HCV infecton. Leukocytoclastc Vasculits LV Leukocytoclastc vasculits presented as palpable purpura petechiae ulceraton of the skin livido retcularis polyarthrits and myalgia 33. Leukocytoclastc vasculits usually involves the lower extremites. Skin biopsy showed cutaneous vasculits with dermal blood vessel destructon and infltraton of neutrophils around the vessel walls. Peripheral nerves may also be involved resultng in peripheral neuropathy secondary to involvement of the small vessels supplying the nerves vasa vasorum 34. Leukocytoclastc vasculits is associated with essental mixed cryoglobulinemia poly arterits nodosa erythema nodosum and erythema multforme. The kidneys are usually involved in essental cryoglobulinemia with membranoproliferatve glomerulonephrits membranous glomerulonephrits and hypertension with reduced kidney functon. Polyarterits nodosa is another disease of the small or medium sized blood vessels which is related to HBV and HCV infecton that can involve many organs including the kidneys. Polyarterits nodosa is found in approximately 10 of HBV and HCV infecton. Kidney functon can be stabilized with the sustained viral response of HCV infecton to the new antviral medicatons. Complete disappearance of arthralgia skin and liver diseases occurred with clearance of HCV infecton suggestng that urtcarial vasculits may result from HCV immune complex disease. Lichen Planus LP Lichen planus is a skin disorder characterized by fat-topped violaceous and pruritc papules with scaly base. The distributon of the lesions of LP is generalized that can involve mucus membranes hair lines and nails. The mechanism of pathogenesis of LP is not known but cell mediated immunity may play a major role 35. Skin biopsy usually showed dense lymphocytc infltraton in the upper dermis. It is estmated that 10-40 of patents with LP are positve for HCV infecton 36. It is believed that LP may be exacerbated by interferon treatment for HCV. The efect of new ant HCV drugs is not known. Sustained viral response may alleviate the symptoms of LP. Necrolytc acral erythema It is a necrolysis erythematous skin lesion on the acral parts of the body. It is characterized by pruritc psoriasis-like skin disease on sharply marginated erythematous base with hyperpigmented plaques and variable scales which can be confused with LP or psoriasis. In a series of 30 patents with the disorder all were collectvely as monoclonal gammopathy of renal signifcance. This disease can present with asymptomatc proteinuria hematuria or decline in renal functon. Kidney biopsies along with urine and serum free light chain estmaton are almost always diagnostc. B-cell Non-Hodgkins Lymphoma NHL has been associated with HCV infecton and renal involvement by the lymphoma is not uncommon. Patents with renal involvement can present with hematuria proteinuria or acute kidney injury with decline in renal functon. Direct lymphomatous infltraton of the kidney can also occur. This type of lymphoma is usually difuse large B-cell lymphoma. However marginal zone lymphoma splenic and mucosa-associated lymphoma have been reported to occur 10-20. If the NHL involved the skin it can present with raised violaceous areas of the skin and intense pruritus. Lymphoma may develop due to progression of cryoglobulinemia 19-23. Chronic stmulaton of the immune system by HCV infecton can lead to progression of lymphoproliferatve disorder. The immune system react to contnuous stmulaton of HCV-E2 protein with increased prevalence of chromosomal translocaton t1418 in the B cell- lineage 24-27. Treatments of HCV infectons with antviral therapy along with chemotherapy for the underlying lymphoma are used in these cases. In this review will highlight the most common cutaneous manifestaton of chronic hepatts C infecton with emphases on the common skin manifestatons. Skin Manifestatons of Chronic HCV Infecton Porphyria Cutanea Tarda PCT PCT develops in patents with risk factors like exposure to chemical or toxic agents drugs iron overload or excessive alcohol intake 2829. PCT is manifested as blisters vesicles on the dorsal parts of the acral sufaces especially the dorsum of the hands. Minor trauma and sun exposure can lead to erythema and the development of vesicles and bullae. Hypo or hyperpigmentaton hirsutsm and sclerodermatous changes may develop. Hypertrichosis of the temples pigmented changes scarring ulceratons and dystrophic calcifcatons can occur. These lesions are the results of skin fragility with symptoms of epidermolysis bullosa. Uroporphyrins and hepatocarboxyl porphyrins collect in skin bones and teeth afer they spell into the blood once the liver is saturated. These pigments can fuorescent on light exposure and turn the urine dark red upon urinaton. In the United States the prevalence of HCV infecton in patents with PCT is estmated at 50 30. PCT is caused by reduced actvity of the enzyme uroporphyrinogen decarboxylase causing build-up of uroporphyrinogen in the blood and urine 31. PCT can be inherited also as autosomal dominant form which has the same characteristcs as the acquired form. The skin and the liver are the two main organs afected by the disease. Chronic liver disease with steatosis fbrosis and cirrhotc changes are the next common manifestaton that may occur 32.

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3 © Under Lic ense of C r ea tiv e C ommons A ttr ibution 3.0 Lic ense 2017 Vol. 3 No. 3: 14 ACTA PSYCHOPATHOLOGICA ISSN 2469-6676 found to have antbodies to HCV 37. Skin biopsy usually shows psoriatc changes necrosis of the keratnocytes and papillomatosis. These patents may have kidney involvement in the form of proteinuria or decreased kidney functon. Treatment of HCV and topical steroids with oral zinc supplements may alleviate the disease 38-41. Cutaneous lymphoma Cutaneous lymphoma is mainly T-cell lymphoma which has no relaton to HCV infecton. However difuse B-cell lymphoma can involve the skin and subcutaneous tssue with palpable masses that may ulcerate to the skin surface. These cases may be associated with HCV infecton. The diferental diagnosis of cutaneous lymphoma should be considered in LP psoriasis or ulceraton of the skin. Treatment of HCV infecton Treatment of HCV infecton is a rapidly evolving feld guidelines by the American Associaton for the Study of Liver Disease have been updated in 2015 and 2016. The treatment depends on the genotype of the virus and the organ involved. The general treatment recommendatons include: • Determinaton of HCV genotype and subtype including quanttatve HCV load. • Complete blood count liver functon tests and renal functon tests. • Evaluaton of advanced liver fbrosis with liver biopsy imaging and/or invasive markers. • It is recommended that treatment should be carried out by healthcare provider who is expert in HCV infecton. • Treatment of skin manifestaton of HCV infecton should be coordinated with HCV specialist.

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2017 ACTA PSYCHOPATHOLOGICA ISSN 2469-6676 Vol. 3 No. 3: 14 4 This article is available from: www.psychopathology.imedpub.com References 1 Sterling RK Bralow S 2006 Extrahepatc manifestatons of Hepatts C virus. Curr Gastroenterol Rep 8: 53-59. 2 Mets J Carmichael L Kokor W Scharfenberg R 2014 Hepatts C: extrahepatc manifestatons. FF Essent 427: 32-35. 3 Fachinelli LR Silva EC Figueiredo MG Possa MS Pelegrinelli FF et al. 2012 Hepatts C and cutaneous alteratons. Rev Soc Bras Med Trop 45: 770-773. 4 Akhter A Said A 2015 Cutaneous manifestatons of viral hepatts. Curr Infect Dis Rep 17: 452. 5 Lunel F Musset L Cacoub P Frangeul L Cresta P et al. 1994 Cryoglobulinemia in chronic liver diseases: role of Hepatts C virus and liver damage. Gastroenterology 106: 1291-1300. 6 Andreone P Zignego AL Cursaro C Gramenzi A Gherlinzoni F et al. 1998 Prevalence of monoclonal gammopathies in patents with Hepatts C virus infecton. Ann Intern Med 129: 294-298. 7 Perrone A Deramo MT Spaccavento F Santarcangelo P Favoino B et al. 2001 Hepatts C virus HCV genotypes human leucocyte antgen expression and monoclonal gamopathy prevalence during chronic HCV infecton. Cytobios 106: 125-134. 8 Tsianos EV Di Bisceglie AM Papadopoulos NM Costello R Hoofnagle JH 1990 Oligoclonal immunoglobulin bands in serum in associaton with chronic viral hepatts. Am J Gastroenterol 85: 1005-1008. 9 Maruyama S Hirayama C Horie Y Yorozu K Maeda K et al. 2007 Serum immunoglobulins in patents with chronic Hepatts C: a surrogate marker of disease severity and treatment outcome. Hepatogastroenterology 54: 493-498. 10 Gisbert JP Garcia-Buey L Pajares JM Moreno-Otero R 2003 Prevalence of hepatts C virus infecton in B-cell non-Hodgkin’s lymphoma: systemic review and meta-analysis. 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Ann Intern Med 137: 571-580. 28 Bulaj ZJ Phillips JD Ajioka RS Franklin MR Grifen LM et al. 2000 Hemochromatosis genes and other factors contributng to the pathogenesis of porphyria cutanea tarda. Blood 95: 1565-1571 29 Cribier B Petau P Stoll-Keller F Schmit C Veter D et al. 1996 Porphyria cutanea tarda and hepatts C viral infecton. A clinical and virologic study. Ann Dermatol Venereol 123: 200-202. 30 Gisbert JP Garcia-Buey L Pajares JM Moreno-Otero R 2003 Prevalence of hepatts C virus infecton in porphyria cuatnea tarda: systematc review and meta-analysis. J Hepatol 39: 620-627. 31 Kushner JP Barbuto AJ Lee GR 1976 An inherited enzymatc defect in porphyria cutanea tarda: decreased uroporphyrinogen decarboxylase actvity. J Clin Invest 58: 1089-1097. 32 Di Padova C Marchesi L Cainelli T Gori G Podenzani SA et al. 1983 Efects of phlebotomy on urinary porphyrin patern and liver histology in patents with porphyria cutanea tarda. Am J Med Sci 285: 2-12.

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5 © Under Lic ense of C r ea tiv e C ommons A ttr ibution 3.0 Lic ense 2017 Vol. 3 No. 3: 14 ACTA PSYCHOPATHOLOGICA ISSN 2469-6676 33 Hamid S Cruz PD Jr Lee WM 1998 Urtcarial vasculits caused by hepatts C virus infecton: response to interferon alfa therapy. J Am Acad Dermatol 39: 278-280. 34 David WS Peine C Schlesinger P Smith SA 1996 Nonsystemic vasculitc mononeuropathy multplex cryoblobulinemia and hepatts C. Muscle Verve 19: 1596-1602. 35 Pilli M Penna A Zerbini A Vescovi P Manfredi M et al. 2002 Oral lichen planus pathogenesis: A role for the HCV-specifc cellular immune response. Hepatology 36: 1446-1452. 36 Gumber SC Chopra S 1995 Hepatts C: a multfaceted disease: review of extrahepatc manifestatons. Ann Intern Med 123: 615-620. 37 Abdallah MA Ghozzi MY Monib HA Hafez AM Hiat KM et al. 2005 Necrolytc acral erythema: a Cutaneous sign of hepatts C virus infecton. J Am Acad Dermatol 53: 247-251. 38 Khanna VJ Shieh S Benjamin J Somach S Zaim MT et al. 2000 Necrolytc acral erythema associated with hepatts C: efectve treatment with interferon alfa and zinc. Arch Dermatol 136: 755-757. 39 Abdallah MA Hull C Horn TD 2005 Necrolytc acral erythema: a patent from the United States successfully treated with oral zinc. Arch Dermatol 141: 85-87. 40 Hivnor CM Yan AC Junkins-Hopkins JM Honig PJ 2004 Necrolytc acral erythema: response to combinaton therapy with interferon and ribavirin. J AM Acad Dermatol 50: S121-S124. 41 El-Ghandour TM Sakr MA El-Sebai H El-Gammal TF El-Sayed MH 2006 Necrolytc acral erythema in Egyptan patents with hepatts C virus infecton. J Gastroenterol Hepatol 21: 1200-1206.

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