RESUMEN
Although liver damage is a relatively rare adverse effect of oral anticoagulation with phenprocoumon, acute liver failure can be a serious treatment-associated complication. In this contribution, a patient with drug-induced liver failure during oral anticoagulation with phenprocoumon is presented. This case illustrates the need for close laboratory monitoring and suggests that phenrocoumon-induced liver damage should be considered along with other common complications of this treatment.
Asunto(s)
Fibrilación Atrial/tratamiento farmacológico , Fallo Hepático/inducido químicamente , Fallo Hepático/prevención & control , Fenprocumón/administración & dosificación , Fenprocumón/efectos adversos , Administración Oral , Anciano , Anticoagulantes/administración & dosificación , Anticoagulantes/efectos adversos , Fibrilación Atrial/complicaciones , Humanos , MasculinoRESUMEN
BACKGROUND: Mitoxantrone is highly efficacious in the treatment of severe multiple sclerosis (MS). Mitoxantrone therapy-related acute leukemia (TRAL) has recently become the focus of interest. METHODS: A case report of fatal TRAL following mitoxantrone therapy is presented with a discussion on the differential diagnosis and risk factors. The interdisciplinary development of diagnostic and therapeutic algorithms is presented from a haematological and neurological point of view. RESULTS: We describe the case of a 34-year-old MS patient who developed TRAL following mitoxantrone therapy (cumulative dose 45 mg/m(2) body surface). The patient died from endocarditis. TRAL is a rare but potentially fatal complication of mitoxantrone therapy with a wide variation of reported incidence. Thus far, no specific risk factors relating for example to preceding therapy and treatment regimens have been identified. Frequent laboratory controls and early bone marrow aspiration are mandatory for suspected TRAL as the condition is potentially curable. CONCLUSIONS: TRAL needs to be considered in the risk-benefit assessment of mitoxantrone therapy, however, the exact incidence and risk factors (e.g. dosage, treatment regimen) are still unclear. The risks are controllable under close surveillance and early diagnosis is important for prognosis. Future investigations need to concentrate on identification of potential risk factors.
Asunto(s)
Leucemia/inducido químicamente , Mitoxantrona/efectos adversos , Mitoxantrona/uso terapéutico , Esclerosis Múltiple/complicaciones , Esclerosis Múltiple/tratamiento farmacológico , Trombocitopenia/inducido químicamente , Adulto , Analgésicos/administración & dosificación , Analgésicos/efectos adversos , Humanos , Leucemia/prevención & control , Masculino , Trombocitopenia/prevención & controlRESUMEN
AIMS/HYPOTHESIS: Diabetes frequently develops in patients with chronic pancreatitis (CP). Partial pancreatectomy has emerged as a treatment option for such patients. We addressed whether the development of diabetes in CP patients is related to pancreatic beta cell area or clinical variables, and which factors predict the diabetes risk after partial pancreatectomy. METHODS: Fractional beta cell area was determined in pancreatic tissue samples obtained from 114 CP patients undergoing pancreatic surgery and related to measures of glucose control, as well as clinical and anthropometric data. Seventy-four patients without diabetes at the time of surgery were contacted again 2.5 +/- 1.0 years after partial pancreatectomy in order to obtain information about the post-operative development of diabetes. RESULTS: In the surgical samples in the whole cohort, pancreatic beta cell area was 0.40 +/- 0.06% in patients with and 0.64 +/- 0.06% in those without previously known diabetes (p = 0.039). There was an inverse non-linear relationship between pancreatic beta cell area and fasting glucose concentrations (r = 0.29) as well as HbA(1c) levels (r = 0.36). Nineteen out of 74 previously normoglycaemic patients (26%) developed diabetes over an average period of 2.5 years of follow-up. Pre-operative fasting glucose levels, HbA(1c) and BMI were identified as predictors of diabetes after partial pancreatectomy. However, pancreatic beta cell area did not differ in those who subsequently developed diabetes (0.66 +/- 0.15%) and those who did not (0.62 +/- 0.08%, p = 0.45). CONCLUSIONS/INTERPRETATION: Hyperglycaemia in CP patients is associated with reduced beta cell area. However, reduced beta cell area does not predict the development of diabetes, suggesting that other factors are more important determinants of alterations in glucose metabolism in patients with CP.
Asunto(s)
Glucemia/metabolismo , Diabetes Mellitus/etiología , Pancreatitis Crónica/complicaciones , Adulto , Diabetes Mellitus/metabolismo , Diabetes Mellitus/patología , Femenino , Estudios de Seguimiento , Humanos , Hiperglucemia/etiología , Hiperglucemia/metabolismo , Hiperglucemia/patología , Células Secretoras de Insulina/metabolismo , Células Secretoras de Insulina/patología , Masculino , Persona de Mediana Edad , Pancreatectomía , Pancreatitis Crónica/metabolismo , Pancreatitis Crónica/patología , Pancreatitis Crónica/cirugía , Análisis de RegresiónRESUMEN
We report the case of a patient with acquired pure megakaryocytic aplasia. Until today, less than 20 cases of acquired pure megakaryocytic aplasia have been reported and the disease aetiology still seems to be unclear. This report summarizes the published data concerning possible aetiologies, treatment options and outcome of patients with acquired pure megakaryocytic aplasia. Furthermore, this case report presents an example for a possible disease progression.