Asunto(s)
Enfermedades del Colágeno , Humanos , Persona de Mediana Edad , Administración Cutánea , Corticoesteroides/administración & dosificación , Corticoesteroides/efectos adversos , Enfermedades del Colágeno/inducido químicamente , Enfermedades del Colágeno/tratamiento farmacológico , Enfermedades del Colágeno/patología , Glucocorticoides/administración & dosificación , Glucocorticoides/efectos adversos , Resultado del TratamientoAsunto(s)
Enfermedades del Colágeno , Panitumumab , Anciano , Femenino , Humanos , Antineoplásicos Inmunológicos/efectos adversos , Enfermedades del Colágeno/inducido químicamente , Enfermedades del Colágeno/patología , Erupciones por Medicamentos/etiología , Erupciones por Medicamentos/patología , Panitumumab/efectos adversosAsunto(s)
Adenocarcinoma del Pulmón/tratamiento farmacológico , Antineoplásicos/efectos adversos , Enfermedades del Colágeno/inducido químicamente , Clorhidrato de Erlotinib/efectos adversos , Neoplasias Pulmonares/tratamiento farmacológico , Enfermedades de la Piel/inducido químicamente , Enfermedades del Colágeno/diagnóstico , Enfermedades del Colágeno/terapia , Femenino , Humanos , Persona de Mediana Edad , Enfermedades de la Piel/diagnóstico , Enfermedades de la Piel/terapiaAsunto(s)
Enfermedades del Colágeno , Neoplasias del Colon , Enfermedades de la Piel , Enfermedades del Colágeno/inducido químicamente , Enfermedades del Colágeno/diagnóstico , Enfermedades del Colágeno/tratamiento farmacológico , Neoplasias del Colon/tratamiento farmacológico , Humanos , Hiperplasia , Panitumumab/efectos adversosRESUMEN
No disponible
Asunto(s)
Humanos , Masculino , Anciano de 80 o más Años , Sorafenib/efectos adversos , Erupciones por Medicamentos/etiología , Enfermedades del Colágeno/inducido químicamente , Enfermedades de la Piel/inducido químicamente , Inhibidores de Proteínas Quinasas/administración & dosificación , Inhibidores de Proteínas Quinasas/efectos adversos , Biopsia , Piel/efectos de los fármacos , Antagonistas de los Receptores Histamínicos/administración & dosificación , Enfermedades del Colágeno/diagnóstico , Enfermedades del Colágeno/tratamiento farmacológicoRESUMEN
We present the case of a patient with a debut of reactive perforating collagenosis associated with the use of Sorafenib for stage IV hepatocarcinoma, very successfully controlled with local corticotherapy and systemic antihistamines. This is an extremely rare side effect associated with this treatment, as only another eleven cases of acquired perforating dermatoses associated with Sorafenib or other multi-kinase inhibitors have been found in the medical literature. Given the unusual nature of this presentation, high clinical suspicion and a correct histopathological study are indispensable for its correct filiation and treatment.
Asunto(s)
Carcinoma Hepatocelular , Enfermedades del Colágeno , Neoplasias Hepáticas , Enfermedades de la Piel , Carcinoma Hepatocelular/tratamiento farmacológico , Enfermedades del Colágeno/inducido químicamente , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , Sorafenib/efectos adversosAsunto(s)
Adalimumab/efectos adversos , Antirreumáticos/efectos adversos , Artritis Juvenil/tratamiento farmacológico , Enfermedades del Colágeno/inducido químicamente , Síndromes Neoplásicos Hereditarios/inducido químicamente , Neoplasias Cutáneas/inducido químicamente , Adolescente , Artritis Juvenil/complicaciones , Enfermedades del Colágeno/complicaciones , Femenino , Humanos , Síndromes Neoplásicos Hereditarios/complicaciones , Neoplasias Cutáneas/complicacionesRESUMEN
The term, acquired perforating dermatoses (APD), represents a group of skin conditions that develop in adulthood and are characterized by transepidermal elimination of dermal connective tissue. This appears clinically as a papulonodule with a keratotic core. Although APD is typically associated with diabetes mellitus, chronic renal failure, and several other conditions causing generalized pruritus, there have been reports in the literature describing an association of APD with select drugs including sorafenib. We present a case of acquired perforating dermatosis in a patient with HIV and hepatocellular carcinoma undergoing treatment with sorafenib.
Asunto(s)
Antineoplásicos/efectos adversos , Enfermedades del Colágeno/inducido químicamente , Enfermedades de la Piel/inducido químicamente , Sorafenib/efectos adversos , Anciano , Carcinoma Hepatocelular/complicaciones , Carcinoma Hepatocelular/tratamiento farmacológico , Enfermedades del Colágeno/diagnóstico , Enfermedades del Colágeno/patología , Infecciones por VIH/complicaciones , Humanos , Neoplasias Hepáticas/complicaciones , Neoplasias Hepáticas/tratamiento farmacológico , Masculino , Enfermedades de la Piel/diagnóstico , Enfermedades de la Piel/patologíaRESUMEN
BACKGROUND: Prednisolone is a potent anti-inflammatory glucocorticoid (GC) but chronic use is hampered by metabolic side effects. Little is known about the long-term effects of GCs on gene-expression in vivo during inflammation. AIM: Identify gene signatures underlying prednisolone-induced metabolic side effects in a complex in vivo inflammatory setting after long-term treatment. MATERIALS & METHODS: We performed whole-genome expression profiling in liver and muscle from arthritic and nonarthritic mice treated with several doses of prednisolone for 3 weeks and used text-mining to link gene signatures to metabolic pathways. RESULTS: Prednisolone-induced gene signatures were highly tissue specific. We identified a short-list of genes significantly affected by both prednisolone and inflammation in liver and involved in glucose and fatty acid metabolism. For several of these genes the association with GCs is novel. CONCLUSION: The identified gene signatures may provide useful starting points for the development of GCs with a better safety profile.
Asunto(s)
Antiinflamatorios/toxicidad , Enfermedades del Colágeno/genética , Enfermedades Metabólicas/genética , Prednisolona/toxicidad , Animales , Artritis/inducido químicamente , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Enfermedades del Colágeno/inducido químicamente , Enfermedades del Colágeno/metabolismo , Ácidos Grasos/metabolismo , Expresión Génica/efectos de los fármacos , Glucosa/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Enfermedades Metabólicas/inducido químicamente , Enfermedades Metabólicas/metabolismo , Ratones , Ratones Endogámicos CBA , Músculos/efectos de los fármacos , Músculos/metabolismoAsunto(s)
Enfermedades del Colágeno/inducido químicamente , Inhibidores de Proteínas Quinasas/efectos adversos , Quinazolinas/efectos adversos , Enfermedades de la Piel/inducido químicamente , Anciano , Enfermedades del Colágeno/tratamiento farmacológico , Enfermedades del Colágeno/patología , Complicaciones de la Diabetes/complicaciones , Erupciones por Medicamentos/etiología , Clorhidrato de Erlotinib , Humanos , Masculino , Enfermedades de la Piel/tratamiento farmacológico , Enfermedades de la Piel/patologíaRESUMEN
The paper describes the case of 56 years old woman admitted to the Toxicology Department because of skin lesions, joint and muscle pain and elevated activity of transaminases and creatine phosfokinase as well in biochemical analysis. The symptoms occurred after 6 days of the Atorvastatin therapy. The clinical picture indicated side effects of the hipolipemic therapy, but the presence of the skin lesions suggested drug induced collagenosis (lupus erythrematosus, dermatomyositis). Immunological studies confirmed association with antinuclear antibodies (ANA) and anti-Mi-2 autoantibodies in the serum. Immunosuppressive therapy was ordered with clinical and biochemical improvement.
Asunto(s)
Dermatomiositis/inducido químicamente , Ácidos Heptanoicos/efectos adversos , Inhibidores de Hidroximetilglutaril-CoA Reductasas/efectos adversos , Pirroles/efectos adversos , Anticolesterolemiantes/efectos adversos , Artralgia/inducido químicamente , Atorvastatina , Autoanticuerpos/sangre , Enfermedades del Colágeno/inducido químicamente , Creatina Quinasa/metabolismo , Dermatomiositis/tratamiento farmacológico , Femenino , Humanos , Inmunosupresores/uso terapéutico , Persona de Mediana Edad , Transaminasas/metabolismoRESUMEN
A 24-year-old healthy man presented with a 6-week history of numerous umbilicated coalescing erythematous papules with some scale and crust on his anterior medial thighs. The eruption began 1 to 2 weeks after he spilled calcium chloride rock salts on his pants while salting the sidewalk during a snow storm. The salts dissolved and remained in contact with his skin for at least 4 hours until he was able to change clothes. A skin biopsy shows thick and thin collagen fibers with partial calcification in the papillary and upper reticular dermis associated with a sparse infiltrate of neutrophils, lymphocytes and mononuclear histiocytes. There are foci of transepidermal elimination of calcified fibers with adjacent epidermal hyperplasia and ortho- and parakeratosis. Von Kossa stain highlights calcification of the fibers, and trichrome stain confirms the fibers are collagen. A Verhoeff-van Gieson stain shows no abnormality of elastic fibers. The patient was treated with topical betametasone diproprionate cream twice daily for 3 weeks, as well as a short course of oral levofloxacin and topical gentamicin cream. The lesions resolved over 3 weeks with residual scarring. We report a unique case of acquired perforating calcific collagenosis secondary to topical calcium chloride exposure.
Asunto(s)
Calcinosis/inducido químicamente , Cloruro de Calcio/toxicidad , Enfermedades del Colágeno/inducido químicamente , Enfermedades de la Piel/inducido químicamente , Piel/patología , Antibacterianos/uso terapéutico , Antiinflamatorios/uso terapéutico , Betametasona/uso terapéutico , Calcinosis/tratamiento farmacológico , Calcinosis/patología , Cicatriz/patología , Enfermedades del Colágeno/patología , Quimioterapia Combinada , Tejido Elástico/patología , Humanos , Levofloxacino , Masculino , Infiltración Neutrófila , Ofloxacino/uso terapéutico , Enfermedades de la Piel/tratamiento farmacológico , Enfermedades de la Piel/patología , Muslo , Resultado del Tratamiento , Adulto JovenRESUMEN
Central giant cell granuloma is a benign lesion of the jaws which is sometimes aggressive locally. The most common treatment is curettage,which has a high recurrence rate, particularly in more aggressive lesions. Other treatments such as interferon (IFN) and calcitonin have been described. We report a patient with Stickler syndrome and an aggressive central giant cell granuloma in the mandible. Initial treatment with calcitonin was not successful. A combination of IFN and imatinib, given for 9 months, initiated regression of the lesion that continued after treatment had ceased.
Asunto(s)
Antineoplásicos/uso terapéutico , Enfermedades del Colágeno/inducido químicamente , Granuloma de Células Gigantes/tratamiento farmacológico , Enfermedades Mandibulares/tratamiento farmacológico , Adolescente , Benzamidas , Calcitonina/uso terapéutico , Combinación de Medicamentos , Femenino , Granuloma de Células Gigantes/complicaciones , Humanos , Mesilato de Imatinib , Interferón alfa-2 , Interferón-alfa/uso terapéutico , Enfermedades Mandibulares/complicaciones , Piperazinas/uso terapéutico , Polietilenglicoles/uso terapéutico , Pirimidinas/uso terapéutico , Proteínas Recombinantes , Inducción de Remisión , SíndromeRESUMEN
Sirolimus is an immunosuppressive macrolide with antineoplasic properties that is increasingly used in posttransplantation immunosuppression. The treatment is frequently associated with cutaneous side effects such as sirolimus-associated acneiform facial dermatitis, which has been observed in up to 50% of treated patients. We report a 51-year-old female with liver transplantation who developed inflammatory papules and nodules on the face and the upper chest 3 weeks after the initiation of sirolimus therapy. Sequential biopsies revealed lymphocytic infiltration of the dermis with a peculiar pattern of sebotropism, while older lesions showed acquired reactive perforating collagenosis. The lesions were responsive to hydroxychloroquine treatment despite continued sirolimus treatment.
Asunto(s)
Erupciones Acneiformes/inducido químicamente , Enfermedades del Colágeno/inducido químicamente , Erupciones por Medicamentos/etiología , Inmunosupresores/efectos adversos , Sirolimus/efectos adversos , Erupciones Acneiformes/tratamiento farmacológico , Erupciones Acneiformes/patología , Antiinflamatorios/uso terapéutico , Colágeno/análisis , Enfermedades del Colágeno/tratamiento farmacológico , Enfermedades del Colágeno/patología , Femenino , Humanos , Hidroxicloroquina/uso terapéutico , Trasplante de Hígado , Persona de Mediana Edad , Glándulas Sebáceas/patología , Sebo/química , Sirolimus/farmacocinética , Piel/patologíaAsunto(s)
Terapia Antirretroviral Altamente Activa/efectos adversos , Enfermedades del Colágeno/inducido químicamente , Infecciones por VIH/tratamiento farmacológico , Inhibidores de la Proteasa del VIH/efectos adversos , Indinavir/efectos adversos , Enfermedades de la Piel/inducido químicamente , Adulto , Enfermedades del Colágeno/patología , Humanos , Masculino , Enfermedades de la Piel/patologíaRESUMEN
Collagen-induced arthritis (CIA) in mice has been classified as a Thl-mediated disease. However, most evidence for this has been obtained by indirect experiments; for example, the administration of neutralizing anti-interferon-gamma (IFN-gamma) antibody reduced the severity of arthritis. To obtain direct evidence about the cytokine balance in CIA mice, we analyzed the cytokine-secreting cell in CIA mice at the single cell level using a dual color enzyme-linked immunospot (ELISPOT) assay, which enabled us to analyze interleukin-2 (IL-2)-secreting cells or IL-4-secreting cells or both simultaneously. Furthermore, to characterize the cytokine network in the pathogenesis of CIA, the frequency of the cells secreting IL-12, which induced the development of naive Th cells into Th1 cells, was analyzed. The results show that in the prearthritic phase, the number of IL-12-secreting cells in spleen and peritoneal exuded cells is increased, and Th1 cells in lymph node and spleen are dominant. In contrast, after the onset of clinical arthritis, the number of IL-12-secreting cells in spleen, lymph node, and peritoneal exuded cells is decreased, and there is a shift from a Thl-dominant to a Th2-dominant state in lymph node and spleen. The results indicated that the pathogenesis of CIA is associated with a disruption in the normal ratio of Th1/Th2 at cell level.
Asunto(s)
Enfermedades Autoinmunes/inmunología , Enfermedades del Colágeno/inmunología , Ensayo de Inmunoadsorción Enzimática/métodos , Interleucina-12/metabolismo , Interleucina-2/metabolismo , Interleucina-4/metabolismo , Células TH1/metabolismo , Animales , Enfermedades Autoinmunes/inducido químicamente , Enfermedades Autoinmunes/metabolismo , Bovinos , Colágeno/inmunología , Colágeno/toxicidad , Enfermedades del Colágeno/inducido químicamente , Enfermedades del Colágeno/metabolismo , Color , Progresión de la Enfermedad , Inmunización , Ganglios Linfáticos/inmunología , Ganglios Linfáticos/patología , Masculino , Ratones , Ratones Endogámicos DBA , Especificidad de Órganos , Cavidad Peritoneal/citología , Bazo/inmunología , Bazo/patología , Células TH1/inmunología , Células Th2/inmunologíaRESUMEN
The treatment of viral hepatitis or malignomas with interferon (IFN) can increase the incidence of autoimmune disease. This paper reviews published case and study reports. The incidence of overt autoimmune diseases under IFN treatment is about 3%. Autoantibodies can be detected in 23% of the patients. Autoimmune thyroid diseases are the most frequent ones, but nearly all autoimmune diseases can occur. Beside benign and reversible courses chronic developments and lethal outcomes are possible. Actual concepts concerning the pathogenesis of IFN-associated autoimmunity include induction of MHC and other molecules as well as the modulation of lymphocyte functions. Clinical and paraclinical controls are necessary under treatment with IFN and during follow-up.
Asunto(s)
Enfermedades Autoinmunes/inducido químicamente , Interferones/efectos adversos , Anemia Hemolítica Autoinmune/inducido químicamente , Enfermedades Autoinmunes/epidemiología , Enfermedades del Colágeno/inducido químicamente , Hepatitis Viral Humana/terapia , Humanos , Incidencia , Interferones/uso terapéutico , Linfocitos/efectos de los fármacos , Complejo Mayor de Histocompatibilidad/efectos de los fármacos , Neoplasias/terapia , Trombocitopenia/inducido químicamente , Tiroiditis Autoinmune/inducido químicamenteRESUMEN
Thyroid hormone preparations, especially thyroxine, are widely used either at replacement doses to correct hypothyroidism or at suppressive doses to abolish thyrotropin (thyroid-stimulating hormone) secretion in patients with differentiated thyroid carcinoma after total thyroidectomy or with diffuse/ nodular nontoxic goitre. In order to suppress thyrotropin secretion, it is necessary to administer slightly supraphysiological doses of thyroxine. Possible adverse effects of this therapy include cardiovascular changes (shortening of systolic time intervals, increased frequency of atrial premature beats and, possibly, left ventricular hypertrophy) and bone changes (reduced bone density and bone mass), but the risk of these adverse effects can be minimised by carefully monitoring serum free thyroxine and free liothyronine (triiodothyronine) measurements and adjusting the dosage accordingly. Thionamides [thiamazole (methimazole), carbimazole, propylthiouracil] are the most widely used antithyroid drugs. They are given for long periods of time and cause adverse effects in 3 to 5% of patients. In most cases, adverse effects are minor and transient (e.g. skin rash, itching, mild leucopenia). The most dangerous effect is agranulocytosis, which occurs in 0.1 to 0.5% of patients. This life-threatening condition can now be effectively treated by granulocyte colony-stimulating factor administration. Other major adverse effects (aplastic anaemia, thrombocytopenia, lupus erythematosus-like syndrome, vasculitis) are exceedingly rare.