Glycerol
Regulatory sources consulted
Approved indications
- Local symptomatic relief of transient occasional constipation in adults and adolescents aged 12 years or older.
Contraindications
Absolute
- Anorectal disorders, hemorrhagic proctocolitis, inflamed hemorrhoids, or signs of appendicitis, intestinal obstruction, or acute inflammatory bowel disease.
Clinical warnings
- For occasional short-term use. Seek advice for pain, bleeding, worsening, or lack of response. — CIMA AEMPS
Adverse events
Common (≥1%)
Rectal irritation
Recent literature (PubMed)
Nonalcoholic fatty liver disease (NAFLD) is common and partially heritable and has no effective treatments. We carried out a genome-wide association study (GWAS) meta-analysis of imaging (n = 66,814) and diagnostic code (3,584 cases versus 621,081 controls) measured NAFLD across diverse ancestries. We identified NAFLD-associated variants at torsin family 1 member B (TOR1B), fat mass and obesity associated (FTO), cordon-bleu WH2 repeat protein like 1 (COBLL1)/growth factor receptor-bound protein 14 (GRB14), insulin receptor (INSR), sterol regulatory element-binding transcription factor 1 (SREBF1) and patatin-like phospholipase domain-containing protein 2 (PNPLA2), as well as validated NAFLD-associated variants at patatin-like phospholipase domain-containing protein 3 (PNPLA3), transmembrane 6 superfamily 2 (TM6SF2), apolipoprotein E (APOE), glucokinase regulator (GCKR), tribbles homolog 1 (TRIB1), glycerol-3-phosphate acyltransferase (GPAM), mitochondrial amidoxime-reducing component 1 (MARC1), microsomal triglyceride transfer protein large subunit (MTTP), alcohol dehydrogenase 1B (ADH1B), transmembrane channel like 4 (TMC4)/membrane-bound O-acyltransferase domain containing 7 (MBOAT7) and receptor-type tyrosine-protein phosphatase δ (PTPRD). Implicated genes highlight mitochondrial, cholesterol and de novo lipogenesis as causally contributing to NAFLD predisposition. Phenome-wide association study (PheWAS) analyses suggest at least seven subtypes of NAFLD. Individuals in the top 10% and 1% of genetic risk have a 2.5-fold to 6-fold increased risk of NAFLD, cirrhosis and hepatocellular carcinoma. These genetic variants identify subtypes of NAFLD, improve estimates of disease risk and can guide the development of targeted therapeutics.
Trigeminal neuralgia (TN) is a disorder characterized by recurrent, unilateral brief electric shock-like pains, abrupt in onset and termination, limited to the distribution of one or more branches of the trigeminal nerve, and triggered by innocuous stimuli. The literature on the diagnosis and treatment of TN was retrieved and summarized. The diagnosis is made almost entirely based on the patient's history. In classical TN, the neurological examination is typically normal, whereas the exam in secondary TN is focused on surveilling for signs of multiple sclerosis (MS) or a cerebellopontine tumor. The appropriate imaging technique is magnetic resonance imaging (MRI) with contrast of the trigeminal ganglion, which is recommended prior to interventional procedures. The treatment of a patient with TN is a team effort and should always be multidisciplinary, addressing all dimensions of pain. Carbamazepine or oxcarbazepine are first-line medical treatments. Microvascular decompression (MVD) is the technique of choice for patients without or with minor comorbidities. Percutaneous procedures for TN are mainly radiofrequency thermocoagulation of the branches of the trigeminal nerve introduced by Sweet and Wepsic in 1965, retrogasserian glycerol injection introduced by Hakanson in 1981, and balloon compression introduced by Mullan and Lichtor in 1983. Radiofrequency treatment is recommended in elderly patients or those with major comorbidities. Other techniques such as stereotactic radiosurgery and pulsed radiofrequency treatment are also discussed. Recommendations are based on very low-quality evidence. MVD and radiofrequency are the preferred invasive treatments, although higher-quality evidence is necessary to better assess the risk-benefit ratios. Neither the excretion of guaifenesin in milk nor its effect on breastfed infants have been studied. It is unlikely that with usual maternal doses amounts in breastmilk would harm the nursing infant, especially in infants over 2 mo
Central pattern of fat distribution, especially fat accumulation within the intraabdominal cavity increases risks for cardiometabolic diseases. Portal hypothesis combined with a pathological remodeling in visceral fat is considered the major etiological factor explaining the independent contribution of visceral obesity to cardiometabolic diseases. Excessive remodeling in visceral fat during development of obesity leads to dysfunctions in the depot, characterized by hypertrophy and death of adipocytes, hypoxia, inflammation, and fibrosis. Dysfunctional visceral fat secretes elevated levels of fatty acids, glycerol, and proinflammatory and profibrotic cytokines into the portal vein directly impacting the liver, the central regulator of systemic metabolism. These metabolic and endocrine products induce ectopic fat accumulation, insulin resistance, inflammation, and fibrosis in the liver, which in turn causes or exacerbates systemic metabolic derangements. Elucidation of underlying mechanisms that lead to the pathological remodeling and higher degree of dysfunctions in visceral adipose tissue is therefore, critical for the development of therapeutics to prevent deleterious sequelae in obesity. We review depot differences in metabolic and endocrine properties and expendabilities as well as underlying mechanisms that contribute to the pathophysiological aspects of visceral adiposity in cardiometabolic diseases. We also discuss impacts of different weight loss interventions on visceral adiposity and cardiometabolic diseases.