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Muscular Dystrophies at Different Ages: Metabolic and Endocrine Alterations  [PDF]
Oriana del Rocío Cruz Guzmán,Ana Laura Chávez García,Maricela Rodríguez-Cruz
International Journal of Endocrinology , 2012, DOI: 10.1155/2012/485376
Abstract: Common metabolic and endocrine alterations exist across a wide range of muscular dystrophies. Skeletal muscle plays an important role in glucose metabolism and is a major participant in different signaling pathways. Therefore, its damage may lead to different metabolic disruptions. Two of the most important metabolic alterations in muscular dystrophies may be insulin resistance and obesity. However, only insulin resistance has been demonstrated in myotonic dystrophy. In addition, endocrine disturbances such as hypogonadism, low levels of testosterone, and growth hormone have been reported. This eventually will result in consequences such as growth failure and delayed puberty in the case of childhood dystrophies. Other consequences may be reduced male fertility, reduced spermatogenesis, and oligospermia, both in childhood as well as in adult muscular dystrophies. These facts all suggest that there is a need for better comprehension of metabolic and endocrine implications for muscular dystrophies with the purpose of developing improved clinical treatments and/or improvements in the quality of life of patients with dystrophy. Therefore, the aim of this paper is to describe the current knowledge about of metabolic and endocrine alterations in diverse types of dystrophinopathies, which will be divided into two groups: childhood and adult dystrophies which have different age of onset. 1. Introduction There are about 30 different types of muscular dystrophies caused by alterations in diverse genes, which are characterized by the progressive loss of muscle in accordance with age of onset, severity, and the group of muscles affected [1]. The altered protein in most of these dystrophies is located in muscle fiber and is linked to other proteins, enzymes, or extracellular matrix [2]. Myopathologies are associated with different ages of onset, for example, Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) as well as Emery-Dreifuss muscular dystrophy (EDMD) demonstrating their first clinical manifestations during childhood [3], whereas some laminopathies such as myotonic dystrophy or limb-girdle muscular dystrophy are developed during adulthood [4]. This group of diseases can cause different physical symptoms such as contractures and scoliosis, respiratory impairment, swallowing and feeding difficulties, and, in some cases, metabolic alterations have been reported [4, 5]. Even so, the primordial clinical sign is muscle weakness [4, 5]. Skeletal muscle is responsible for 70–80% of whole body insulin-stimulated glucose uptake, disposal, and
Endocrine and Metabolic Disorders Associated with Human Immune Deficiency Virus Infection
C.N Unachukwu, D.I Uchenna, E.E Young
West African Journal of Medicine , 2009,
Abstract: BACKGROUND: Many reports have described endocrine and metabolic disorders in the human immunodeficiency virus (HIV) infection . This article reviewed various reports in the literature in order to increase the awareness and thus the need for early intervention when necessary. DATA SOURCE: Data were obtained from MEDLINE, Google search and other journals on ‘HIV, Endocrinopathies/Metabolic Disorders’ from 1985 till 2007. STUDY SELECTION: Studies related to HIV associated endocrinopathies and metabolic disorders in the last two decades were reviewed. DATA EXTRACTION: Information on epidemiology, pathogenesis, diagnosis and treatment of the target organ endocrinopathies and metabolic disorders in HIV/AIDS were extracted from relevant literature. RESULTS: Endocrine and metabolic disturbances occur in the course of HIV infection. Pathogenesis includes direct infection of endocrine glands by HIV or opportunistic organisms, infiltration by neoplasms and side effects of drugs. Adrenal insufficiency is the commonest HIV endocrinopathy with cytomegalovirus adrenalitis occurring in 40-88% of cases. Thyroid dysfunction may occur as euthyroid sick syndrome or sub-clinical hypothyroidism. Hypogonadotrophic dysfunction accounts for 75% of HIV-associated hypogonadism, with prolonged amenorrhoea being three times more likely in the women. Pancreatic dysfunction may result in hypoglycaemia or diabetes mellitus (DM). Highly active antiretroviral therapy (HAART) especially protease inhibitors has been noted to result in insulin resistance and lipodystrophy. CONCLUSION: Virtually every endocrine organ is involved in the course of HIV infection. Detailed endocrinological and metabolic evaluation and appropriate treatment is necessary in the optimal management of patients with HIV infection in our environment. WAJM 2009; 28(1): 293–299
Prenatal Hyperandrogenization Induces Metabolic and Endocrine Alterations Which Depend on the Levels of Testosterone Exposure  [PDF]
Sabrina Amalfi, Leandro Martín Velez, María Florencia Heber, Susana Vighi, Silvana Rocío Ferreira, Adriana Vega Orozco, Omar Pignataro, Alicia Beatriz Motta
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037658
Abstract: Prenatal hyperandrogenism is able to induce polycystic ovary syndrome (PCOS) in rats. The aim of the present study was to establish if the levels of prenatal testosterone may determine the extent of metabolic and endocrine alterations during the adult life. Pregnant Sprague Dawley rats were prenatally injected with either 2 or 5 mg free testosterone (groups T2 and T5 respectively) from day 16 to day 19 day of gestation. Female offspring from T2 and T5 displayed different phenotype of PCOS during adult life. Offspring from T2 showed hyperandrogenism, ovarian cysts and ovulatory cycles whereas those from T5 displayed hyperandrogenism, ovarian cysts and anovulatory cycles. Both group showed increased circulating glucose levels after the intraperitoneal glucose tolerance test (IPGTT; an evaluation of insulin resistance). IPGTT was higher in T5 rats and directly correlated with body weight at prepubertal age. However, the decrease in the body weight at prepubertal age was compensated during adult life. Although both groups showed enhanced ovarian steroidogenesis, it appears that the molecular mechanisms involved were different. The higher dose of testosterone enhanced the expression of both the protein that regulates cholesterol availability (the steroidogenic acute regulatory protein (StAR)) and the protein expression of the transcriptional factor: peroxisome proliferator-activated receptor gamma (PPAR gamma). Prenatal hyperandrogenization induced an anti-oxidant response that prevented a possible pro-oxidant status. The higher dose of testosterone induced a pro-inflammatory state in ovarian tissue mediated by increased levels of prostaglandin E (PG) and the protein expression of cyclooxygenase 2 (COX2, the limiting enzyme of PGs synthesis). In summary, our data show that the levels of testosterone prenatally injected modulate the uterine environment and that this, in turn, would be responsible for the endocrine and metabolic abnormalities and the phenotype of PCOS during the adult life.
Endocrine, metabolic, nutritional, and toxic disorders leading to dementia
Ghosh Amitabha
Annals of Indian Academy of Neurology , 2010,
Abstract: One of the first steps toward the correct diagnosis of dementia is to segregate out the nondegenerative dementias from possible degenerative dementias. Nondegenerative dementias could be due to traumatic, endocrine, metabolic, nutritional, toxic, infective, and immunological causes. They could also be caused by tumors, subdural hematomas, and normal pressure hydrocephalus. Many of the nondegenerative dementias occur at an earlier age and often progress quickly compared to Alzheimer′s disease and other degenerative dementias. Many are treatable or preventable with simple measures. This review aims to give an overview of some of the more important endocrine, metabolic, nutritional, and toxic disorders that may lead to dementia.
Endocrine manifestations related to inherited metabolic diseases in adults
Marie-Christine Vantyghem, Dries Dobbelaere, Karine Mention, Jean-Louis Wemeau, Jean-Marie Saudubray, Claire Douillard
Orphanet Journal of Rare Diseases , 2012, DOI: 10.1186/1750-1172-7-11
Abstract: Inborn errors of metabolism (IEM) are rare genetic diseases, which usually have a recessive mode of inheritance. They are classified into 3 main groups according to their mechanisms: cellular intoxication, energy deficiency, and degradation or synthesis defects of complex molecules [1]. This is a new and growing field in adulthood and is not yet very well known.Endocrine manifestations can be a complication of a previously diagnosed IEM. More rarely they may signal the presence of a new IEM, mostly those involving glucose metabolism and presenting with hypoglycaemia (see the related article for review). Nevertheless all types of endocrine disorders have been described in IEM (Table 1), and the endocrinologist should be aware of them when an endocrine disorder is associated with multisystem involvement, for example with neurological, muscular and/or hepatic features.Many endocrine manifestations in IEM might go unrecognized, especially with regard to subclinical dysfunctions. Otherwise, the long-term consequences of IEM on growth, bone metabolism and fertility have not been prospectively investigated.When fertility is maintained, all pregnancies in patients with a previously diagnosed IEM should be carefully planned and monitored, especially those with dietary management, such as with phenylketonuria. Preconception screening for hormone deficiency, especially hypothyroidism, is recommended in most IEM, as is investigation for gestational diabetes. Genetic counseling should be provided, even though most IEMs, except for mitochondrial diseases, are inherited in an autosomal recessive manner. Prenatal testing for high-risk pregnancies may be discussed if the disease-causing mutations in the family are known.The aim of this review is to identify the main IEMs in adults that can be revealed or complicated by an endocrine disorder other than hypoglycaemia.Hormones play an essential role in the coordination of complex functions such as growth, reproduction, metabolism and e
Pulmonary alterations in cocaine users
Terra Filho, Mário;Yen, Chen Chin;Santos, Ubiratan de Paula;Mu?oz, Daniel Romero;
Sao Paulo Medical Journal , 2004, DOI: 10.1590/S1516-31802004000100007
Abstract: context: brazilian researchers have recently recognized a marked increase in the number of people using abusable drugs and the consequences of this habit. it has become a major public health problem in a potentially productive segment of the general population. in the last few years, several medical articles have given special emphasis to pulmonary complications related to cocaine use. this review is based on this information and experience acquired with groups of cocaine users. objective: to present to physicians the pulmonary aspects of cocaine use and warn about the various effects this drug has on the respiratory system, stressing those related to long-term use. design: narrative review. method: pulmonary complications are described. these may include infections (staphylococcus aureus, pulmonary tuberculosis, acquired immunodeficiency syndrome/aids, etc.), aspiration pneumonia, lung abscess, empyema, septic embolism, non-cardiogenic pulmonary edema, barotrauma, pulmonary granulomatosis, bronchiolitis obliterans and organizing pneumonia, pneumonitis and interstitial fibrosis, pneumonitis hypersensitivity, lung infiltrates and eosinophilia in individuals with bronchial hyperreactivity, diffuse alveolar hemorrhage, vasculitis, pulmonary infarction, pulmonary hypertension and alterations in gas exchange. it is concluded that physicians should give special attention to the various pulmonary and clinical manifestations related to cocaine use, particularly in young patients.
Association of Symptoms of Gastroesophageal Reflux with Metabolic Syndrome Parameters in Patients with Endocrine Disease  [PDF]
Masatoshi Nomura,Naotaka Tashiro,Tetsuhiro Watanabe,Akie Hirata,Ichiro Abe,Taijiro Okabe,Ryoichi Takayanagi
ISRN Gastroenterology , 2014, DOI: 10.1155/2014/863206
Abstract: Background. Metabolic syndrome (MetS) and obesity are known risk factors for gastroesophageal reflux disease (GERD), which is often found in patients with endocrine disorders, such as thyroid dysfunction and hypopituitarism. To clarify the relationship of endocrine disease with GERD, we investigated the symptoms of GERD in patients with various endocrine diseases. Methods. Patients with various endocrine disorders who visited Kyushu University Hospital were included. GERD symptoms were examined using a self-administered questionnaire, the frequency scale for the symptoms of GERD (FSSG). Metabolic parameters, including body-mass index (BMI), waist circumference, blood pressure, hemoglobin A1c, total cholesterol, high-density lipoprotein cholesterol (HDL-C), and triglycerides, and values of endocrine function, including thyroid stimulating hormone, free thyroxin, cortisol, and insulin-like growth factor-1, were assessed. Results. A total of 111 consecutive patients were recruited for the study. Among these, 18 (16.2%) patients were considered to have GERD. Among the parameters, BMI ( ) and triglycerides ( ) showed a positive association and HDL-C ( ) showed an inverse association with the FSSG score. However, none of the endocrine values were associated with the FSSG score. Conclusion. Symptoms of GERD in patients with endocrine disorders might be attributed to MetS as comorbidity. 1. Introduction Metabolic syndrome (MetS) is a cluster of metabolic abnormalities defined as the presence of three or more of the following factors: abdominal obesity (increased waist circumference), elevated triglycerides, low high-density lipoprotein cholesterol (HDL-C) levels, high blood pressure, and high fasting plasma glucose levels [1]. MetS is a high risk factor for cardiovascular and other atherosclerotic diseases [2]. Obesity has been implicated in various gastrointestinal diseases, such as gastroesophageal reflux disease (GERD). The prevalence of GERD has been increasing worldwide [3], and adversely affects health-related quality of life [4]. Dyspepsia is usually defined as upper abdominal pain or retrosternal pain, discomfort, belching, abdominal bloating, nausea, or other symptoms considered to have arisen from the upper alimentary tract. Reflux symptoms (RS), such as heartburn and regurgitation, are regarded as typical symptoms of GERD. However, it is reported that other dyspeptic symptoms are also common in patients with nonerosive GERD [5, 6]. Therefore, GERD is also associated with dyspeptic manifestations other than RS. Dyspeptic symptoms that respond to
Endocrine and metabolic disorders in HTLV-1 infected patients
Alves, Cresio;Dourado, Luciano;
Brazilian Journal of Infectious Diseases , 2010, DOI: 10.1590/S1413-86702010000600011
Abstract: human t-cell leukemia virus type 1 (htlv-1) infection is endemic in japan and several countries in south america, caribbean and africa. endocrine and metabolic disorders have been variably reported to be associated with human t-cell leukemia virus type 1 (htlv-1) infection. therefore, the aim of this article was to critically evaluate the current knowledge of the endocrine and metabolic disorders associated with htlv-1 infection. the literature search used pubmed, web of science, and lilacs databases in the past 10 years, utilizing, in various combinations, the following keywords: htlv-1, adult t-cell leukemia, diabetes mellitus, glut-1, osteoporosis, hypercalcemia, autoimmune thyroid disorders, diabetes insipidus, inappropriate antidiuretic hormone secretion; pseudohypoparathyroidism; pseudopseudohypoparathyroidism. the proven endocrine manifestations of the htlv-1 infection are calcium disorders which occur in some patients with acute htlv-1/adult t-cell leukemia/lymphoma. the few reports about thyroid, parathyroid, antidiuretic hormone and diabetes mellitus are insufficient to prove a causal association with htlv-1 infection. the evidence for an association between endocrine disorders and htlv-1 infection in general, and in asymptomatic patients is lacking. given all these uncertainties, the endocrine expression of the htlv-1 infection composes a promising research line for understanding the pathophysiology of this infection
Endothelial dysfunction in cardiovascular and endocrine-metabolic diseases: an update
Davel, A.P.;Wenceslau, C.F.;Akamine, E.H.;Xavier, F.E.;Couto, G.K.;Oliveira, H.T.;Rossoni, L.V.;
Brazilian Journal of Medical and Biological Research , 2011, DOI: 10.1590/S0100-879X2011007500104
Abstract: the endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. reduced endothelium-derived nitric oxide (no) bioavailability and increased production of thromboxane a2, prostaglandin h2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. in addition, recent studies have demonstrated the role of enhanced overactivation ofβ-adrenergic receptors inducing vascular cytokine production and endothelial no synthase (enos) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. however, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased no production by enos. the present review focuses on the role of no bioavailability, enos uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. these are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations.
Prognostic value of quantitative immune alterations in melanoma patients
Andrés,R.; Mayordomo,J. I.; Isla,D.; Lasierra,P.; Godino,J.; Marcos,I.; Saenz,A.; Escudero,P.; Lambea,J.; Aguirre,E.; Millastre,E.; Larrad,L.; Tres,A.;
Oncología (Barcelona) , 2006, DOI: 10.4321/S0378-48352006000100004
Abstract: purpose: the immune response is altered in patients with neoplasms. immunosuppression has important consequences in patients with melanoma. the aim of this study was to assess quantitative immune alterations in melanoma patients.. material and methods: we obtained a peripheral blood sample in edta from 86 melanoma patients (63 of them disease-free and 23 with distant disease). total leukocytes and lymphocytes, b lymphocytes (cd19), types cd3, cd4, cd8 lymphocytes, and nk lymphocytes (cd56) were counted by determining the surface markers by flow cytometry, using a coulter epics elite (coulter corp.). iga, igg, ige and igm were assayed by nephelometric methods employing a hyland pdq laser nephelometer. results: we found significant differences between disease-free patients and those with active disease with regard to lymphocytes total count (median: 2251.57 vs. 1783.04/mm3, p=0.010), nk lymphocytes (cd56) (149.54 vs. 115.2/mm3, p=0.016), and iga levels (241.59 vs. 300.55 mg/dl, p=0.044), when taken as continuous variables. when considering each parameter as a discontinuous variable, only changes in absolute lymphocyte count retained an statistical difference depending on the presence or absence of active disease, 73.9% of the patients with active metastatic disease having a lymphocyte count below 2000 cells/mm3 versus only 36.5% of the disease-free patients (c2 pearson=9.476, df=1, p=0.002). the median survival for the 46 patients with absolute lymphocyte count above 2000 cells/mm3 was 965 days (df=65.03, ic 95%=792.72-1090.30) versus 441 days (df=75.61, ic 95%=292.81-589.19) for the 40 patients with absolute lymphocyte count below 2000 cells/mm3 (log rank=4.54, df=1, p=0.0331). conclusions: there are significant differences in some lymphocyte populations and iga levels between patients with metastases and disease-free patients. melanoma patients with absolute lymphocyte levels above 2000 cells/mm3 have a longer survival than those with a lymphocyte count below 2000 c
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