Porphyria cutanea tarda in a HIV- positive patient

Abstract

This is a case report about Porphyria cutanea tarda (PCT) and its relationship with the infection caused by the human immunodeficiency virus (HIV). Cutaneous porphyria is an illness caused by enzymatic modification that results in partial deficiency of uroporphyrinogen decarboxylase (Urod), which may be hereditary or acquired. Several studies suggest that HIV infection associated with cofactors might trigger the development of porphyria cutanea tarda. In this case report, we present a patient infected with HIV, who after the introduction of antiretroviral therapy (ART) enjoyed clinical improvement of porphyria cutanea tarda symptoms.

Role of ABCB1 and glutathione S‑transferase gene variants in the association of porphyria cutanea tarda and human immunodeficiency virus infection

“…In Argentina, PCT patients have a high incidence (16%) of human immunodeficiency virus (HIV) infection ( 11 ). However, since almost all HIV-infected patients have additional risk factors for Porphyria manifestation, it is still unclear whether HIV infection is a precipitating factor for development of PCT.…”

Case for diagnosis. Sclerodermiform manifestations of porphyria cutanea tarda secondary to hepatitis C

“…In addition to the different clinical forms of cutaneous scleroderma, sclerodermiform disorders may be secondary to graft versus host disease, drugs, silica exposure, porphyrias, silicone implants, paraneoplastic manifestations, and chronic infections. [1][2][3][4][5][6][7] The authors reported a case of porphyria cutanea tarda (PCT) -or chronic hepatic porphyria, with sclerodermiform lesions, secondary to chronic hepatitis C virus, with significant involvement of photoexposed areas (face and upper limbs). 6 The evolution of PCT with cutaneous sclerodermoid lesions and alopecia is uncommon, and is due to the delay in diagnosis.…”

Estudio del paciente con hiperferritinemia

“…Esta condición puede ser adquirida en un 80% de los casos y hereditaria en el 20% restante [102]. Entre las formas adquiridas, con mayor frecuencia en los hombres (4:1), están las asociadas con el alcoholismo crónico [103], la hepatitis viral B [104,105] y la hepatitis viral C [105,106], la infección por el citomegalovirus, el virus de la inmunodeficiencia humana [107], la diabetes mellitus [108], el lupus eritematoso diseminado [109,110], el síndrome de Sjögren [111], la hemocromatosis hereditaria [112][113][114][115][116] y medicamentos como el tamoxifeno [117] y el olmesartan [118], entre otros. En cuanto a la formas hereditarias estas se deben a un error en el metabolismo de las porfirinas, caracterizado por un déficit de la actividad enzimática de la uroporfibilinógeno descarboxilasa, lo cual conduce a la acumulación de porfirinas altamente carboxiladas en el hígado, en el plasma y en la orina [119].…”