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Mitochondrial DNA-Associated Leigh Syndrome and NARP }, authors { names ml { Thorburn DR, Rahman S } }, from book { title { name GeneReviews(R) }, authors { names std { { name ml Pagon RA, role editor }, { name ml Adam MP, role editor }, { name ml Ardinger HH, role editor }, { name ml Wallace SE, role editor }, { name ml Amemiya A, role editor }, { name ml Bean LJH, role editor }, { name ml Bird TD, role editor }, { name ml Dolan CR, role editor }, { name ml Fong CT, role editor }, { name ml Smith RJH, role editor }, { name ml Stephens K, role editor } } }, imp { date std { year 1993 }, language eng, pubstatus ppublish, history { { pubstatus pubmed, date std { year 2010, month 3, day 20 } }, { pubstatus medline, date std { year 2010, month 3, day 20 } }, { pubstatus other, date std { year 2010, month 3, day 20 } } } } }, ids { pubmed 20301352, other { db bookaccession, tag str NBK1173 } } }, abstract Mitochondrial (mt) DNA-associated Leigh syndrome and NARP (neurogenic muscle weakness, ataxia, and retinitis pigmentosa) are part of a continuum of progressive neurodegenerative disorders caused by abnormalities of mitochondrial energy generation. Leigh syndrome (or subacute necrotizing encephalomyelopathy) is characterized by onset of symptoms typically between age three and 12 months, often following a viral infection. Decompensation (often with elevated lactate levels in blood and/or CSF) during an intercurrent illness is typically associated with psychomotor retardation or regression. Neurologic features include hypotonia, spasticity, movement disorders (including chorea), cerebellar ataxia, and peripheral neuropathy. Extraneurologic manifestations may include hypertrophic cardiomyopathy. About 50% of affected individuals die by age three years, most often as a result of respiratory or cardiac failure. NARP is characterized by proximal neurogenic muscle weakness with sensory neuropathy, ataxia, and pigmentary retinopathy. Onset of symptoms, particularly ataxia and learning difficulties, is often in early childhood. Individuals with NARP can be relatively stable for many years, but may suffer episodic deterioration, often in association with viral illnesses. The diagnosis of NARP and mtDNA-associated Leigh syndrome is established using clinical criteria and molecular genetic testing. MT-ATP6, MT-TL1, MT-TK, MT-TW, MT-TV, MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND5, MT-ND6, and MT-CO3 are the mitochondrial genes in which pathogenic variants are known to cause mtDNA-associated Leigh syndrome. MT-ATP6 is the only gene in which pathogenic variants are known to cause NARP. Approximately 10% of individuals with Leigh syndrome have either the m.8993T>G or m.8993T>C MT-ATP6 pathogenic variant; approximately 10%-20% have pathogenic variants in other mitochondrial genes. The proportion of individuals with NARP who have a detectable pathogenic variant at MT-ATP6 nucleotide 8993 is unknown but likely greater than 50%; a T-to-G transversion (m.8993T>G) is most common; a T-to-C transition (m.8993T>C) has also been described. Treatment of manifestations: Supportive treatment includes use of sodium bicarbonate or sodium citrate for acidosis and antiepileptic drugs for seizures. Dystonia is treated with benzhexol, baclofen, tetrabenezine, and gabapentin alone or in combination, or by injections of botulinum toxin. Anticongestive therapy may be required for cardiomyopathy. Regular nutritional assessment of daily caloric intake and adequacy of diet and psychological support for the affected individual and family are essential. Surveillance: Neurologic, ophthalmologic, and cardiologic evaluations at regular intervals to monitor progression and appearance of new symptoms. Agents/circumstances to avoid: Sodium valproate and barbiturates, anesthesia, and dichloroacetate (DCA). Mitochondrial DNA-associated Leigh syndrome and NARP are transmitted by maternal inheritance. The father of a proband is not at risk of having the mtDNA pathogenic variant. The mother of a proband usually has the mtDNA pathogenic variant and may or may not have symptoms. In most cases, the mother has a much lower mutant load than the proband and usually remains asymptomatic or develops only mild symptoms. Occasionally the mother has a substantial mutant load and develops severe symptoms in adulthood. Offspring of males with a mtDNA pathogenic variant are not at risk; all offspring of females with a mtDNA pathogenic variant are at risk of inheriting the pathogenic variant. The risk to offspring of a female proband of developing symptoms depends on the tissue distribution and mutant load of the mtDNA pathogenic variant. Prenatal diagnosis and preimplantation genetic diagnosis for couples at increased risk of having children with mitochondrial DNA-associated Leigh syndrome and NARP is possible by analysis of mtDNA extracted from non-cultured fetal cells or from single blastomeres, respectively; however, the use of molecular genetic test results to predict long-term outcome is difficult
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Insulin Resistance }, authors { names ml { Freeman AM, Soman-Faulkner K, Pennings N } }, from book { title { name StatPearls }, authors { names ml { } }, imp { date std { year 2019, month 1 }, language eng, pubstatus ppublish, history { { pubstatus pubmed, date std { year 2018, month 6, day 26, hour 6, minute 1 } }, { pubstatus medline, date std { year 2018, month 6, day 26, hour 6, minute 1 } }, { pubstatus other, date std { year 2018, month 6, day 26, hour 6, minute 1 } } } } }, ids { pubmed 29939616 } }, abstract Insulin resistance is identified as an impaired biologic response to insulin stimulation of target tissues, primarily liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in a compensatory increase in beta-cell insulin production and hyperinsulinemia. [1][2][3]The metabolic consequences of insulin resistance can result in hyperglycemia, hypertension, dyslipidemia, visceral adiposity, hyperuricemia, elevated inflammatory markers, endothelial dysfunction, and a prothrombic state. Progression of insulin resistance can lead to metabolic syndrome, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes mellitus. Insulin resistance is primarily an acquired condition related to excess body fat, though genetic causes are identified as well. The clinical definition of insulin resistance remains elusive as there is not a generally accepted test for insulin resistance. [4][5]Clinically, insulin resistance is recognized via the metabolic consequences associated with insulin resistance as described in metabolic syndrome and insulin resistance syndrome. The gold standard for measurement of insulin resistance is the hyperinsulinemic-euglycemic glucose clamp technique. This is a research technique with limited clinical applicability; however, there are a number of clinically useful surrogate measures of insulin resistance, including HOMA-IR, HOMA2, QUICKI, serum triglyceride and triglyceride/HDL ratio. In addition, several measures assess insulin resistance based on a serum glucose and/or insulin response to a glucose challenge. The predominate consequence of insulin resistance is type 2 diabetes (T2DM). Insulin resistance is thought to precede the development of T2DM by 10 to 15 years. The development of insulin resistance typically results in a compensatory increase in endogenous insulin production. Elevated levels of endogenous insulin, an anabolic hormone, is associated with insulin resistance and results in weight gain which, in turn, exacerbates insulin resistance.[6][7] This vicious cycle continues until pancreatic beta cell activity can no longer adequately meet the insulin demand created by insulin resistance, resulting in hyperglycemia. With continued mismatch between insulin demand and insulin production, glycemic levels rise to levels consistent with T2DM. Resistance to exogenous insulin has also been described. An arbitrary but clinically useful benchmark considers patients requiring greater than 1 unit/kilogram/day of exogenous insulin to maintain glycemic control insulin resistant. Patients requiring greater than 200 units of exogenous insulin per day are considered severely insulin resistant. In addition to T2DM, the spectrum of disease associated with insulin resistance includes obesity, cardiovascular disease, nonalcoholic fatty liver disease, metabolic syndrome, and polycystic ovary syndrome(PCOS). These are all of great consequence in the United States with a tremendous burden being placed on the healthcare system to treat the direct and indirect conditions associated with insulin resistance. The microvascular complications of diabetes (neuropathy, retinopathy, and nephropathy), as well as the associated macrovascular complications (coronary artery disease [CAD], cerebral-vascular disease, and peripheral artery disease [PAD]), consume the lions share of the healthcare dollar. Lifestyle modification should be the primary focus for the treatment of insulin resistance. Nutritional intervention with calorie reduction and avoidance of carbohydrates that stimulate excessive insulin demand are a cornerstone to treatment. Physical activity helps to increase energy expenditure and improve muscle insulin sensitivity. Medications also can improve insulin response and reduce insulin demand
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Nitisinone }, from book { title { name LiverTox: Clinical and Research Information on Drug-Induced Liver Injury }, authors { names ml { } }, imp { date std { year 2012 }, language eng, pubstatus ppublish, history { { pubstatus pubmed, date std { year 2019, month 10, day 24, hour 6, minute 1 } }, { pubstatus medline, date std { year 2019, month 10, day 24, hour 6, minute 1 } }, { pubstatus other, date std { year 2019, month 10, day 24, hour 6, minute 1 } } } } }, ids { pubmed 31643958 } }, abstract Nitisinone is an inhibitor of the tyrosine catabolism that is used to treat hereditary tyrosinemia, type 1, in which accumulation of intermediates of tyrosine metabolism causes severe and progressive hepatic and renal injury. Nitisinone has been associated with mild, transient serum aminotransferase elevations, but has not been linked to instances of clinically apparent acute liver injury or jaundice
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Assessment of cardiac and vessel functions in childhood psoriasis }, authors { names ml { Saylan Cevik B, Akalin F, Erolu E, Gencosmanoglu S, Ergun T } }, from journal { title { iso-jta Turk J Med Sci, ml-jta Turk J Med Sci, issn 1303-6165, name Turkish journal of medical sciences }, imp { date std { year 2019, month 4, day 18 }, volume 49, issue 2, pages 617-623, language eng, pubstatus epublish, history { { pubstatus other, date std { year 2019, month 4, day 19, hour 6, minute 0 } }, { pubstatus pubmed, date std { year 2019, month 4, day 19, hour 6, minute 0 } }, { pubstatus medline, date std { year 2019, month 6, day 19, hour 6, minute 0 } } } } }, ids { pubmed 30997977, doi 10.3906/sag-1812-139, other { db ELocationID doi, tag str 10.3906/sag-1812-139 } } }, abstract Background/aim: Psoriasis is a chronic inflammatory disease. The effect of psoriasis on the cardiovascular system has not been studied in children before. We studied ventricular strain and vascular functions to assess early cardiovascular effects of psoriasis during childhood. Materials and methods: The study population consisted of 20 psoriatic and 20 age- and sex-matched control subjects. Two-dimensional echocardiography images, longitudinal and global strain, and carotid and brachial ultrasound studies were performed. Results: The mean age of psoriatic children was 14 +/- 0.89 years and that of the controls was 14.05 +/- 0.88. There were significant increases in terms of interventricular septum diastolic and left ventricular posterior wall diastolic diameter and decreases in mitral E, mitral A, and E/A values between groups. Tissue Doppler imaging revealed significant differences between groups in terms of lateral annulus E, A, E/A, isovolumetric contraction time, and ejection time. Aortic stiffness was significantly higher and global circumferential strain and longitudinal strain were significantly lower in the psoriasis group. Carotid intima media thickness and flow-mediated dilatation did not differ significantly between the groups. Conclusion: Cardiac left ventricular and arterial functions are affected in psoriatic children and may be an alarming sign of atherosclerotic heart disease in the long term. Early detection of these changes may be helpful for eliminating other risk factors
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Leber Hereditary Optic Neuropathy }, authors { names ml { Yu-Wai-Man P, Chinnery PF } }, from book { title { name GeneReviews(R) }, authors { names std { { name ml Pagon RA, role editor }, { name ml Adam MP, role editor }, { name ml Ardinger HH, role editor }, { name ml Wallace SE, role editor }, { name ml Amemiya A, role editor }, { name ml Bean LJH, role editor }, { name ml Bird TD, role editor }, { name ml Fong CT, role editor }, { name ml Mefford HC, role editor }, { name ml Smith RJH, role editor }, { name ml Stephens K, role editor } } }, imp { date std { year 1993 }, language eng, pubstatus ppublish, history { { pubstatus pubmed, date std { year 2010, month 3, day 20 } }, { pubstatus medline, date std { year 2010, month 3, day 20 } }, { pubstatus other, date std { year 2010, month 3, day 20 } } } } }, ids { pubmed 20301353, other { db bookaccession, tag str NBK1174 } } }, abstract Leber hereditary optic neuropathy (LHON) is characterized by bilateral, painless, subacute visual failure that develops during young adult life. Males are four to five times more likely than females to be affected. Affected individuals are usually entirely asymptomatic until they develop visual blurring affecting the central visual field in one eye; similar symptoms appear in the other eye an average of two to three months later. In about 25% of cases, visual loss is bilateral at onset. Visual acuity is severely reduced to counting fingers or worse in the majority of cases, and visual field testing shows an enlarging dense central or centrocecal scotoma. After the acute phase, the optic discs become atrophic. Significant improvements in visual acuity are rare and most persons qualify for registration as legally blind (visual acuity A, m.11778G>A, or m.14484T>C. Treatment of manifestations: Management of affected individuals is largely supportive, with the provision of visual aids, help with occupational rehabilitation, and registration with the relevant social services. ECG may reveal a pre-excitation syndrome in individuals harboring mtDNA LHON-causing mutations, but no further intervention is required in the absence of cardiac symptoms. A multidisciplinary approach to those affected individuals with extra-ocular neurologic features (ataxia, peripheral neuropathy and dystonia) should be considered to minimize the functional consequences of these complications. Agents/circumstances to avoid: Individuals harboring mtDNA LHON-causing mutations should be strongly advised to moderate their alcohol intake and not to smoke. Avoiding exposure to other putative environmental triggers for visual loss, in particular industrial toxins and drugs with mitochondrial-toxic effects, also seems reasonable. Therapies under investigation: A recent randomized controlled trial suggests that oral administration of idebenone could benefit individuals with LHON who are at an early stage of the disease process and still at high risk for further visual loss. Similarly, EPI-743 has been used in a small open-labelled study of five individuals with acute LHON with some early encouraging visual results. Leber hereditary optic neuropathy is caused by mutations in mtDNA and it is transmitted by maternal inheritance. Genetic counseling for LHON is complicated by the gender- and age-dependent penetrance of the primary mtDNA LHON-causing mutations. The mother of a proband usually has the mtDNA mutation and may or may not have symptoms. In most cases a history of visual loss affecting maternal relatives at a young age is present, but up to 40% of cases are simplex (i.e., occur in a single individual in a family). A male (affected or unaffected) with a primary LHON-causing mtDNA mutation cannot transmit the mutation to any of his offspring. A female (affected or unaffected) with a primary LHON-causing mtDNA mutation transmits the mutation to all of her offspring. Prenatal diagnosis for mitochondrial mutations is possible if the disease-causing mutation in a family is known; however, accurate interpretation of a positive prenatal test result is difficult because the mtDNA mutational load in amniocytes and chorionic villi may not correspond to that of other fetal or adult tissues, and the presence of the mtDNA mutation does not predict the occurrence of disease, age of onset, severity, or rate of disease progression. Prenatal testing may be available through laboratories offering testing for the gene of interest or custom testing
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