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Vitiligo is an acquired pigmentation disorder with different theorized etiologies, although the exact pathogenesis is still largely unknown. It presents as well-demarcated white plaques throughout the body that result from the loss of melanocytes within the epidermis. Commonly, this condition presents alongside other autoimmune conditions, and it is associated with both genetic and non-genetic factors. We present a patient with no history of autoimmune disease who developed vitiligo after receiving her vaccines against COVID-19. This first occurred within 24 hours of receiving her first vaccine and then worsened after receiving her second vaccine. The depigmented rash was localized to the face, arms, and chest. She was treated with both oral and topical steroids, as well as topical tacrolimus cream. Despite adherence to treatment, the patient only reported subjective improvement in her skin lesions overall. While vitiligo arises sporadically, the temporal relationship between vaccinations and depigmentation makes a stronger case for the vaccine as the inciting factor for this patient, though coincidence is possible. A systematic review of the literature regarding the onset of vitiligo following both infection with and vaccination against COVID-19, this case offers a unique presentation that had a sudden onset and creates a learning opportunity for clinicians to investigate the potential relationship between the receipt of the vaccine and the onset of this skin condition. The goal of this report is to help clinicians be cognizant of the possibility of developing or worsening skin diseases after infection or vaccination so that they can be addressed and treated appropriately.
RESUMO
Acute portal vein thrombosis (PVT) is a complication of liver cirrhosis. The presence of viral infections such as hepatitis B (HBV) and hepatitis C (HCV) can further increase cirrhotic patients' risk of developing PVT, especially in the rare case when there is superinfection with both HBV and HCV. We present a patient with HCV cirrhosis whose clinical condition was decompensated secondary to the development of superimposed HBV infection, who developed acute PVT during hospitalization. This case offers a unique presentation of acute PVT that developed within several days of hospitalization for decompensated liver disease, as proven by the interval absence of portal venous flow on repeat imaging. Despite the workup on the initial presentation being negative for PVT, reconsideration of differentials after the change in our patient's clinical status led to the diagnosis. Active HBV infection was likely the initial trigger for the patient's cirrhosis decompensation and presentation; the subsequent coagulopathy and alteration in the portal blood flow triggered the development of an acute PVT. The risk for both prothrombotic and antithrombotic complications remains high in patients with cirrhosis, a risk that is vastly increased by the presence of superimposedinfections. The diagnosis of thrombotic complications such as PVT can be challenging, thus stressing the importance of repeat imaging in instances where clinical suspicion remains high despite negative imaging. Anticoagulation should be considered for cirrhotic patients with PVT on an individual basis for both prevention and treatment. Prompt diagnosis, early intervention, and close monitoring of patients with PVT are crucial for improving clinical outcomes. The goal of this report is to illustrate diagnostic challenges that accompany the diagnosis of acute PVT in cirrhosis, as well as discuss therapeutic options for optimal management of this condition.
RESUMO
OBJECTIVE: Medication adherence among adolescents with cystic fibrosis (CF) is often suboptimal and this has significant impact on their health and quality of life. The purpose of the study was to evaluate the impact of frequent home pulmonary function (PFT) monitoring on medication adherence among adolescents with CF. HYPOTHESIS: We hypothesized that weekly home PFT monitoring will improve adherence while not significantly adding to the treatment burden. METHODS: Individuals aged 12-21 years with CF were provided a spirometer to measure PFTs weekly for 1 year. Results were reviewed weekly via telephone. PFT data were downloaded from the device during quarterly clinic visits. Adherence was calculated from prescription refill data and compared to the previous year. Perceptions of treatment burden were assessed using the CF questionnaire-revised (CFQ-R) quality of life measure. Health outcome measures including nutritional status and PFTs from clinic were collected for the study period and the year prior. RESULTS: Thirty-nine subjects participated in the study. Mean age was 15.89 ± 2.18 years and 54% were female. Mean adherence to weekly spirometry monitoring was 59.47 ± 24.60%. Values generated on the device showed good correlation with those obtained in clinic. Mean medication possession ratio (MPR) was 60% in the previous year and 65% during the study (P = 0.04). Mean treatment burden scaled score on the CFQ-R was 68 at enrollment and 66 at study completion (P = 0.14). CONCLUSIONS: Frequent home PFT monitoring is feasible in CF adolescents and could successfully improve medication adherence without significantly impacting treatment burden.
