Nonalcoholic steatohepatitis is a common cause of liver inflammation and is associated with obesity, insulin resistance, and hyperlipidemia. There are concerns that it may turn out to be the most common cause of liver failure as prevalence of obesity increases. It leads to increased morbidity and mortality. Other causes of liver inflammation, especially alcoholic liver disease, must be ruled out. The diagnosis is suggested by abnormalities in the blood work and metabolic panel in an obese patient. Despite advances made in our understanding regarding the pathogenesis and trials with multiple drugs targeting mechanisms in pathogenesis, there are no consistent guidelines regarding treatment. However, multiple sources advocate weight reduction, optimum blood glucose control, and elimination of medications that cause fatty infiltration. The purpose of our article is to detail advances made in identifying disease mechanisms and treatment modalities, including surgery to promote weight loss.
A 69 year old woman was referred to hospital because of a persistent dry cough and dyspnoea. She has never smoked and was taking captopril for hypertension and thyroxine for hypothyroidism. At age 20 she developed pulmonary tuberculosis which was treated with a left artificial pneumothorax. A few years later during the course of investigation into infertility she was found to have tuberculous endometriosis and salpingitis. This was treated with streptomycin injections and isoniazid.A large mass measuring 10 cm × 9 cm was seen on chest radiography (see figs 1 and 2). Computed tomography of the thorax demonstrated a solid, partially calcified 10 cm mass situated posteriorly in the left upper lobe. In addition there was loss of volume and concentric pleural thickening in the left hemithorax, probably as a result of the previous artificial pneumothorax. No metastases were evident. At bronchoscopy irregular mucosa was noted in the left upper lobe bronchus. A biopsy specimen of this showed abnormal lymphoid tissue. Staining of sputum for acid-alcohol fast bacilli and subsequent mycobacterial cultures were negative.In the meantime the patient had developed marked hypertension, spontaneous bruising, and epistaxis. Fundal haemorrhages were present. Blood tests revealed a plasma viscosity of 5.3 mpa/s (normal range 1.5-1.72), haemoglobin
Colonoscopy is rarely associated with complications such as colonic perforation. Perforation of the small bowel is extremely rare, especially if the procedure is done without therapeutic interventions. Several factors are associated with this entity. Perforation of the ileum has been reported, but proximal jejunal perforation secondary to rupture of jejunal diverticulum during colonoscopy has not been reported. We present the case of an 88-year-old patient who developed abdominal pain after undergoing colonoscopy without any additional interventions. Urgent exploration revealed perforation of the proximal jejunum secondary to rupture of a jejunal diverticulum. No therapy or biopsies were undertaken during the colonoscopy, which are known predisposing factors.
Gastric ulcer and its complications are commonly encountered by physicians. Penetration is only noted in about 20% of the cases. Penetration into the splenic artery is a very rare occurrence. Making the diagnosis early on is important in order to prevent morbidity and mortality due to the brisk bleeding that can follow. In our report we describe the case, the imaging and the interventional radiological findings which helped with management. We review the literature published including radiological findings in such cases and describe the proposed pathogenesis. Definitive treatment usually involves controlling the bleeding either by means of embolization using coils or ligating the bleeding vessel.
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