A 51-year-old African American woman was referred to our tertiary care center with stage 2 hypertension. She was asymptomatic and presented on diltiazem therapy with a blood pressure of 210/110 mm Hg. Evaluation for secondary causes of hypertension was negative and her baseline alanine transaminase (ALT) (normal 9-52 IU/L), aspartate transaminase (AST) (normal 8-39 IU/L), and total bilirubin (0.1-1.3 mg/dL) levels were within normal limits. She was started on labetalol 200 mg by mouth twice daily and diltiazem was discontinued. Eight weeks into labetalol therapy, the patient's blood pressure remained elevated at 200/100 mm Hg and she remained asymptomatic. Hydrochlorothiazide (HCTZ) 25 mg once daily was added, and the labetalol was increased to 300 mg 3 times a day. After failing to keep her scheduled follow-up appointment and approximately 3 months after initiation of labetalol and 4 weeks after beginning HCTZ, she called the clinic complaining of "yellow eyes." She denied fever but further assessment revealed a history of nausea, abdominal pain, fatigue, and dark urine 1 to 2 weeks earlier. On examination, her blood pressure was >300/130 mm Hg, liver enzymes were elevated (ALT, 1102 IU/L; AST, 757 IU/L), and total bilirubin was 7.0 mg/dL. She was admitted to the hospital with a diagnosis of acute hepatitis and hypertensive emergency.The patient's differential diagnosis of hepatitis included viral, drug-induced, and autoimmune hepatitis. She reported no history of intravenous drug use, recent travel, or ethanol abuse or recent use. She also denied recent acetaminophen use or the use of any other prescription or over-thecounter medications or herbal remedies. Viral hepatitis serologies were negative for hepatitis A, B, and C. In consultation with the gastroenterology department, extensive testing for autoimmune and infectious causes of hepatitis (including antinuclear antibodies, antimitochondrial antibodies, anti-smooth muscle antibodies, cytomegalovirus, and Epstein-Barr virus) were negative (Table). Serum iron, total iron-binding capacity, copper, and ceruloplasmin were within normal limits. An ultrasound of the liver and gallbladder showed no evidence of obstruction in the portal or hepatic veins and no focal abnormalities.HCTZ was initially suspected as a cause of druginduced hepatitis due to the temporal relationship of its appearance with her symptoms. HCTZ was discontinued and trandolapril and spironolactone were added for blood pressure management. Her blood pressure improved to 150/90 mm Hg and liver enzymes, although not returning to baseline values, initially showed a downward trend after the HCTZ was discontinued. Her jaundice clinically improved. She was discharged and scheduled for follow-up with gastroenterology and the hypertension clinic.At her clinic visit, 1 week after hospital discharge, she had complaints of continued weakness, malaise, and decreased appetite. Her blood pressure was 220/110 mm Hg, and on physical examination
Obesity, now recognized as an independent risk factor for cardiovascular disease, is closely associated with hypertension. Complex mechanisms link increasing body weight with increasing blood pressure. Treatment of the obese patient with hypertension requires consideration of physiologic changes related to obesity hypertension. Lifestyle modification, including weight reduction and increased physical activity, can directly influence blood pressure levels and improve blood pressure control in obese, hypertensive patients. Clinical trials are needed to determine the most effective antihypertensive drugs for the obese, hypertensive patient. Antiobesity drugs offer viable adjunctive pharmacotherapy for obesity hypertension, but additional long-term studies are needed to support their safety and efficacy.
A 51-year-old African American woman was referred to our tertiary care center with stage 2 hypertension. She was asymptomatic and presented on diltiazem therapy with a blood pressure of 210/110 mm Hg. Evaluation for secondary causes of hypertension was negative and her baseline alanine transaminase (ALT) (normal 9-52 IU/L), aspartate transaminase (AST) (normal 8-39 IU/L), and total bilirubin (0.1-1.3 mg/dL) levels were within normal limits. She was started on labetalol 200 mg by mouth twice daily and diltiazem was discontinued. Eight weeks into labetalol therapy, the patient's blood pressure remained elevated at 200/100 mm Hg and she remained asymptomatic. Hydrochlorothiazide (HCTZ) 25 mg once daily was added, and the labetalol was increased to 300 mg 3 times a day. After failing to keep her scheduled follow-up appointment and approximately 3 months after initiation of labetalol and 4 weeks after beginning HCTZ, she called the clinic complaining of "yellow eyes." She denied fever but further assessment revealed a history of nausea, abdominal pain, fatigue, and dark urine 1 to 2 weeks earlier. On examination, her blood pressure was >300/130 mm Hg, liver enzymes were elevated (ALT, 1102 IU/L; AST, 757 IU/L), and total bilirubin was 7.0 mg/dL. She was admitted to the hospital with a diagnosis of acute hepatitis and hypertensive emergency.The patient's differential diagnosis of hepatitis included viral, drug-induced, and autoimmune hepatitis. She reported no history of intravenous drug use, recent travel, or ethanol abuse or recent use. She also denied recent acetaminophen use or the use of any other prescription or over-thecounter medications or herbal remedies. Viral hepatitis serologies were negative for hepatitis A, B, and C. In consultation with the gastroenterology department, extensive testing for autoimmune and infectious causes of hepatitis (including antinuclear antibodies, antimitochondrial antibodies, anti-smooth muscle antibodies, cytomegalovirus, and Epstein-Barr virus) were negative (Table). Serum iron, total iron-binding capacity, copper, and ceruloplasmin were within normal limits. An ultrasound of the liver and gallbladder showed no evidence of obstruction in the portal or hepatic veins and no focal abnormalities.HCTZ was initially suspected as a cause of druginduced hepatitis due to the temporal relationship of its appearance with her symptoms. HCTZ was discontinued and trandolapril and spironolactone were added for blood pressure management. Her blood pressure improved to 150/90 mm Hg and liver enzymes, although not returning to baseline values, initially showed a downward trend after the HCTZ was discontinued. Her jaundice clinically improved. She was discharged and scheduled for follow-up with gastroenterology and the hypertension clinic.At her clinic visit, 1 week after hospital discharge, she had complaints of continued weakness, malaise, and decreased appetite. Her blood pressure was 220/110 mm Hg, and on physical examination
Table of contents O1 Tumour heterogeneity: what does it mean? Dow-Mu Koh O2 Skeletal sequelae in adult survivors of childhood cancer Sue Creviston Kaste O3 Locoregional effects of breast cancer treatment Sarah J Vinnicombe O4 Imaging of cancer therapy-induced CNS toxicity Giovanni Morana, Andrea Rossi O5 Screening for lung cancer Christian J. Herold O6Risk stratification of lung nodules Theresa C. McLoud O7 PET imaging of pulmonary nodules Kirk A Frey O8 Transarterial tumour therapy Bernhard Gebauer O9 Interventional radiology in paediatric oncology Derek Roebuck O10 Image guided prostate interventions Jurgen J. Fütterer O11 Imaging cancer predisposition syndromes Alexander J. Towbin O12Chest and chest wall masses Thierry AG Huisman O13 Abdominal masses: good or bad? Anne MJB Smets O14 Hepatobiliary MR contrast: enhanced liver MRI for HCC diagnosis and management Giovanni Morana O15 Role of US elastography and multimodality fusion for managing patients with chronic liver disease and HCC Jeong Min Lee O16 Opportunities and challenges in imaging metastatic disease Hersh Chandarana O17 Diagnosis, treatment monitoring, and follow-up of lymphoma Marius E. Mayerhoefer, Markus Raderer, Alexander Haug O18 Managing high-risk and advanced prostate cancer Matthias Eiber O19 Immunotherapy: imaging challenges Bernhard Gebauer O20 RECIST and RECIST 1.1 Andrea Rockall O21 Challenges of RECIST in oncology imaging basics for the trainee and novice Aslam Sohaib O22 Lymphoma: PET for interim and end of treatment response assessment: a users’ guide to the Deauville Score Victoria S Warbey O23 Available resources Hebert Alberto Vargas O24 ICIS e-portal and the online learning community Dow-Mu Koh O25 Benign lesions that mimic pancreatic cancer Jay P Heiken O26 Staging and reporting pancreatic malignancies Isaac R Francis, Mahmoud, M Al-Hawary, Ravi K Kaza O27 Intraductal papillary mucinous neoplasm Giovanni Morana O28 Cystic pancreatic tumours Mirko D’Onofrio O29 Diffusion-weighted imaging of head and neck tumours Harriet C. Thoeny O30 Radiation injury in the head and neck Ann D King O31 PET/MR of paediatric brain tumours Giovanni Morana, Arnoldo Piccardo, Maria Luisa Garrè, Andrea Rossi O32 Structured reporting and beyond Hebert Alberto Vargas O33 Massachusetts General Hospital experience with structured reporting ...
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