No abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the developed world. Simple hepatic steatosis is mild, but the coexistence of steatohepatitis (NASH) and fibrosis increases the risk of hepatocellular carcinoma. Proper dietary and pharmacological treatment is essential for preventing NAFLD progression. The first-line treatment should include dietary intervention and increased physical activity. The diet should be based on the food pyramid, with a choice of products with low glycemic index, complex carbohydrates in the form of low-processed cereal products, vegetables, and protein-rich products. Usage of insulin-sensitizing substances, pro- and prebiotics, and vitamins should also be considered. Such a therapeutic process is intended to support both liver disease and obesity-related pathologies, including insulin resistance, diabetes, dyslipidemia, and blood hypertension. In the pharmacological treatment of NAFLD, apart from pioglitazone, there are new classes of antidiabetic drugs that are of value, such as glucagon-like peptide 1 analogs and sodium/glucose cotransporter 2 antagonists, while several other compounds that target different pathogenic pathways are currently being tested in clinical trials. Liver biopsies should only be considered when there is a lack of decline in liver enzymes after 6 months of the abovementioned treatment. Dietary intervention is recommended in all patients with NAFLD, while pharmacological treatment is recommended especially for those with NASH and showing significant fibrosis in a biopsy.

Obesity is considered to be a 20th century pandemic, and its prevalence correlates with the increasing global pollution and the presence of chemical compounds in the environment. Excessive adiposity results from an imbalance between energy intake and expenditure, but it is not merely an effect of overeating and lack of physical activity. Recently, several compounds that alter the mechanisms responsible for energy homeostasis have been identified and called “obesogens”. This work presents the role of obesogens in the pathogenesis of obesity. We reviewed data from in vitro animal and human studies concerning the role of obesogens in the disturbance of energy homeostasis. We identified (i) the main groups and classes of obesogens, (ii) the molecular mechanisms of their action, (iii) their deleterious effect on adipose tissue function and control of appetite, and (iv) possible directions in limiting their influence on human metabolism. Obesogens have a multifactorial detrimental influence on energy homeostasis. Focusing on limiting exposure to obesogens and improving early life nutrition seems to be the most reasonable direction of action to prevent obesity in future generations.

A 44-year-old woman was admitted to hospital with end-stage renal failure, productive cough, and decreased exercise tolerance. She had owned nine cats, which resulted in long-term exposure (18 years) to silica-containing bentonite cat litter. High-resolution computed tomography of the chest showed micronodular lesions in the lungs, and mild mediastinal lymphadenopathy. A lung biopsy revealed multinucleated giant cells, some of which had birefringent material and Schaumann bodies. X-ray photoelectron spectroscopy revealed the presence of silicon in the lung biopsy specimen, as well as in the patient’s cat litter. The pulmonary condition was suggestive of sarcoid-like lung disease, rather than silicosis, sarcoidosis, or hypersensitivity pneumonitis, according to the clinicopathological findings. Renal failure appeared to be a result of chronic hypercalcemia due to extrarenal calcitriol overproduction in activated alveolar macrophages. Ultimately, the patient was diagnosed with sarcoid-like lung disease complicated by end-stage renal failure from exposure to bentonite cat litter. Therapy with steroids, in addition to elimination of the bentonite cat litter exposure, resulted in a significant improvement in the health condition. At a follow-up visit after 4 months, an almost complete resolution of the lung lesions and a significant improvement in renal function were observed.

BackgroundBentonite cat litter is one of the most popular types of litter used in cat litter boxes worldwide. One of its components is crystalline silica, which when inhaled is a risk factor for silicosis. While silicosis is considered an occupational lung disease, it seems that individuals with no occupational exposure, such as cat owners, may also be affected. In this case report we present an unusual case of chronic silicosis with sarcoid-like reaction complicated by end-stage renal failure from exposure to bentonite cat litter. Case presentationA 44-year-old woman was admitted to the hospital with end-stage renal failure, productive cough and decreased exercise tolerance. On evaluation, a transbronchial lung biopsy was performed. The X-ray photoelectron spectroscopy revealed the presence of silicon in the lung tissue specimen, as well as in the patient’s cat litter. A detailed patient’s history excluded occupational exposure to crystalline silica, however she acknowledged that she had owned 9 cats at home. In a 44m2 apartment, she had had 9 cat litter boxes, which all had been filled with bentonite cat litter for 18 years. After an extensive workup, a diagnosis of chronic silicosis with sarcoid-like reaction complicated by end-stage renal failure from exposure to bentonite cat litter was made. Renal deterioration appeared to result from chronic hypercalcemia, which was a consequence of extra-renal overproduction of calcitriol in activated alveolar macrophages, frequently seen in granulomatous diseases.ConclusionsOur patient had an abnormally large and longtime exposure, but similar health complications may occur, for example, in workers in the zoological industry. It seems reasonable to consider our case report as a strong call for bentonite cat litter manufacturers to place on the packaging information on potential health complications, along with a recommendation to use protective masks when cleaning the litter box.