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At least 19 recordsLinked to original sources
PubMed2006

Retinal vascular manifestations of metabolic disorders.

Metabolic diseases have profound effects on the structure and function of the retinal circulation. The recent development of retinal photography and digital imaging has enabled more precise documentation of diabetic retinopathy, as well as other retinal microvascular changes, such as retinal arteriolar narrowing, venular dilation and isolated retinopathy signs in nondiabetic individuals. These retinal microvascular signs have been shown to be associated with long-term risks of type 2 diabetes and hypertension, components of the metabolic syndrome (e.g. obesity, dyslipidemia), and a range of macro- and micro-vascular conditions (e.g. stroke, cardiovascular mortality). There is evidence that endothelial dysfunction and inflammation might be possible mechanisms involved in the development of various retinal microvascular changes in patients with diabetes, hypertension and other metabolic disorders. Further understanding of how these processes influence the retinal vasculature might help to elucidate the diverse vascular manifestations of metabolic diseases.

Animals↗
PubMed2006

Inflammation and metabolic disorders.

Metabolic and immune systems are among the most fundamental requirements for survival. Many metabolic and immune response pathways or nutrient- and pathogen-sensing systems have been evolutionarily conserved throughout species. As a result, immune response and metabolic regulation are highly integrated and the proper function of each is dependent on the other. This interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease. Collectively, these diseases constitute the greatest current threat to global human health and welfare.

Adipose Tissue↗
PubMed1987

[Liver transplantation in children. Blood transfusion and metabolic disorders].

Metabolic disorders during hepatic transplantation can be partly induced by blood transfusion. A retrospective survey of perioperative biological data recorded in patients under 18 years of age having liver transplantation was performed. Blood transfusion was also studied. For this evaluation, patients were divided in a paediatric group I (n = 20; mean age: 3.7 years) and an adolescent group II (n = 11; mean age: 14.3 years). Blood transfusion was significantly (p less than 0.05) more important in group I (302 +/- 286 ml X kg-1) than in group II (148.5 +/- 156 ml X kg-1). Autotransfusion of washed red cells was performed in six patients, allowing a mean 17 +/- 7% saving in blood transfusion. Severe hypernatraemia over 152 mmol X l-1 due to blood transfusion was observed only in five patients in group I. Hyperglycaemia increasing till the revascularization of the new liver was constant in both groups, but significantly more pronounced in group II. Cardiac arrest occurred twice in group I at initial revascularization. In group I, children with biliary atresia were not significantly different from the others for the duration of operation and the volume of blood transfusion; however the latter was more abundant. Conversely, in group II, the duration of operation was longer (p less than 0.05) in patients with previous abdominal surgery than in others. Finally the paediatric group differs from the adolescent group by obvious differences in anaesthesia and intensive care and specifically in hepatic transplantation by larger volume of blood transfusion leading to severe hypernatraemia. In further studies, adolescents should be distinct from the paediatric group and included in the adult group.

Adolescent↗
PubMed2001

[Peroxisomal hereditary metabolic disorders].

Metabolic function of peroxisomes includes oxidation of wide spectrum of substances in the presence of oxygen. Hydrogen peroxide formed at the same time is either degraded by catalase or further utilized in peroxidative reactions. From the view of cellular pathology, the most important becomes alpha and beta-oxidation of carboxylic acids, particularly beta-oxidation of long-chain carboxylic acids, which undergoes selectively in peroxisomes. Mutations of peroxisomal genes result in serious metabolic disorders. At present about twenty hereditary peroxisomal diseases has been described. One group of them includes generalized forms (impairment of peroxisome biogenesis); diseases of other group result from isolated defects of individual peroxisomal enzymes. Combined incidence of peroxisomal hereditary disorders in the Western Europe is estimated to be 1:10,000. Beside the X-linked adrenoleukodystrophy, all others have the autosomal-recessive type of heredity. In phenotypic manifestation of generalized forms, as in the Zellweger syndrome, neonatal adrenoleukodystrophy, infantile Refsum disease, rhizomelic chondrodysplasia punctata, an impairment of the central nervous system, liver, and kidney dominate. Most of the patients die within one year, survival period longer than three years becomes exceptional. X-adrenoleukodystrophy, pseudoneonatal adrenoleukodystrophy, trifunctional enzyme deficiency, Refsum disease, primary hyperoxaluria, acatalasemia result from the deficiency of a single enzyme. The most frequent peroxiosomal hereditary disease, the X-adrenoleukodystrophy, has several clinical phenotypes, which most frequently manifest already in infants. The disease has also a clinically less serious form, which manifest only in adults--the adrenomyeloneuropathy. For the postnatal but also for the prenatal diagnostics, methods of biochemistry, molecular genetics, morphology, and immunocytochemistry are necessary.

Humans↗
PubMed2005

Impact of diabetes mellitus and metabolic disorders.

Metabolic and endocrine disorders are common in the perioperative surgical patient. During surgical stress and critical illness, each hormonal system reveals characteristic changes that can be of diagnostic and prognostic significance. A number of endocrinopathies,electrolyte problems, or metabolic derangements may either preexist or develop during the course of surgical treatment. Early correction and tight control of blood glucose levels was shown to improve outcome in critically ill surgical patients. However, many other pharmacological interventions to correct endocrine alterations in critical illness have proven unsuccessful, most likely because of the many overlapping actions between the endocrine and immune systems, and are not standard of care in surgical patients.

Diabetes Mellitus↗
PubMed2003

The association of metabolic disorders with the metabolic syndrome is different in men and women.

AIMS: Metabolic disorders depend on genetic, hormonal and environmental factors, whose relations may differ between genders. Therefore, we compared the contribution of metabolic disorders to the metabolic syndrome in women and men. METHODS: To this end, we used a hierarchical classification statistical method to classify subjects into similarity groups according to clinical and biological parameters. Data were collected from 3,508 men and women aged 35-64 years, from a cardiovascular disease survey. RESULTS: In both women and men, hierarchical classification identified a cluster corresponding to the metabolic syndrome representing 14 and 15% of the women's and men's sample, respectively. In women, elevated body weight (women's Z-score: 1.59 vs. men's Z-score: 1.29; p < 0.005), waist girth (1.62 vs. 1.30; p < 0.001) and low HDL cholesterol (-0.95 vs. -0.75; p < 0.05) were significantly larger contributors to the metabolic syndrome than in men. In contrast, systolic (0.59 vs. 0.95; p < 0.0001) and diastolic (0.55 vs. 0.99; p < 0.0001) blood pressure and apolipoprotein B (0.51 vs. 0.71; p < 0.0001) contributed significantly less in women than in men. Finally, insulin (n.s.), glucose (n.s.), triglycerides (n.s.) and LDL-cholesterol (n.s.) contributions were not different between genders. CONCLUSION: These results are consistent with the concept that a clustering of metabolic disorders occurs frequently in both women and men. However, the contribution of several metabolic disorders to the metabolic syndrome is different in men and women. This finding supports the concept that different criteria are necessary to define the metabolic syndrome in women and men.

Adult↗
PubMed2005

Schizophrenia and comorbid metabolic disorders.

Comorbid metabolic disorders in patients with schizophrenia are underrecognized by many health care professionals and patients. That lack of awareness can contribute to serious morbidity and mortality in patients with schizophrenia. Patients with schizophrenia may be at greater risk for metabolic disorders such as insulin resistance, lipid abnormalities, and weight gain. In addition, although the use of atypical antipsychotics in the treatment of schizophrenia offers many positive benefits and may reduce some of the factors related to the morbidity and mortality of the disorder, these drugs appear to be associated with varying degrees of comorbid metabolic disorders, such as metabolic syndrome, and more serious consequences, such as cardiovascular disease. Recent consensus guidelines recommend that metabolic risks be considered when initiating therapy with atypical antipsychotics. Thus, baseline screening and routine monitoring of patient weight, fasting lipid profile, and fasting plasma glucose are essential. In addition, optimal treatment for patients with schizophrenia and comorbid metabolic disorders is best achieved when all parties involved with patient care (mental health and medical community, caregiver/family, and patient) communicate and work together. With proper awareness and cooperation on the part of the medical community, caregivers, and patients, the detrimental consequences that may result from the metabolic disorders addressed in this article can be at least partially offset.

Antipsychotic Agents↗
PubMed1991

[CNS disorders caused by metabolic disorders].

A guideline for early diagnosis of metabolic disorders affecting central nervous system during neonatal and early infancy was presented. Clinical manifestations associated with inborn errors of metabolism in the neonatal period are poor feeding, vomiting, diarrhea, abnormalities in muscle tonus, dyspnea, convulsion, coma and so on, and these are not specific to each disorder. However, such symptoms or signs as described below have often intimate relation to metabolic disorders: (1) previous children died of undetermined causes during early infancy; (2) complication of sepsis; (3) onset in the early neonatal period; (4) developmental and growth retardation. When newborns and infants have these symptoms or signs, we should start simple screening studies immediately for metabolic disorders, including CBC, hepatic function tests, blood glucose, lactate, pyruvate, ketone bodies, ammonia, blood gas analysis, urinalysis (including non-glucose reducing substance tests and FeCl3 reaction) and so on. As for CBC, we have to make our own effort to find spherocytosis and vacuoles in lymphocytes. Family history, especially the mother's personal history, is indispensable. During physical examinations, we must pay attention to facial appearance, skin color, macroglossia, hair abnormalities, peculiar odor of the urine and hepatosplenomegaly. When abnormality is found in these clinical signs or simple laboratory examinations, we should not hesitate to start dietary treatment even if special examinations for differential diagnosis are on the way.

Blood Gas Analysis↗
PubMed2000

Familial history of metabolic disorders and the multiple metabolic syndrome: the NHLBI family heart study.

UNLABELLED: A case-control study was conducted to investigate the association between family history of obesity, hypertension, and diabetes and the co-occurrence of metabolic disorders associated with the multiple metabolic syndrome (MMS). Included were 1,448 African and European American men and women aged 48-71 who participated in both the third cohort examination of the Atherosclerosis Risk in Communities study, 1992-1994, and phase I of the Family Heart Study 1993-1995. The joint occurrence of hypertension, dyslipidemia, and diabetes or impaired fasting glucose in an individual determined his/her status of "affected" (MMS: n = 97), while the absence of these three metabolic disorders determined his/her status of "unaffected" ( CONTROL: n = 527). First-degree relatives provided the information to calculate family risk scores (FRSs) for the phenotypes under study: obesity, diabetes and hypertension. Although the majority of cases were obese (76.3%), family history of obesity was associated only weakly with the MMS, while family history of diabetes, or hypertension was associated significantly with the MMS (controlling for age, race, gender, and sampling group). Obesity of cases and controls modified the strength of these associations-odds ratios were 2.5(95% CI:1.1-6.1) and 2.9(95% CI:1.2-7.0) for the diabetes and hypertension FRSs in the non-obese, while in obese individuals the respective odds ratios were 1.6(95% CI:0.9-2.8) and 1.7(95% CI:0.9-3.1). These results may imply that obesity, whether familial or environmental in nature, is associated with the development of the MMS, while in non-obese individuals a family history of diabetes, hypertension, or obesity is a marker of genetic predisposition to components of the MMS.

Aged↗
PubMedDate not supplied

[The characteristics of histocompatibility antigen distribution in urolithiasis patients with a phosphorus metabolic disorder].

Phosphorus metabolic disturbances play a great role in the occurrence of urolithiasis. This study covered 150 patients with urolithiasis to establish correlations between the frequency of histocompatibility antigens and the increase in blood and urinary phosphorus levels. The HLA antigens were identified by the routine microlymphocytotoxic method involving a histotyping serum panel. The ABO antigens and rhesus were determined by the agglutination method by using reference sera. The study revealed specific distribution of histocompatibility antigens in urolithiasis patients with disturbed phosphorus metabolism. Hyperphosphatemia correlated with the higher frequency of HLA-B35 (chi 2 = 9.89) and E/E system rhesus (chi 2 = 8.63); hyperphosphaturia showed a negative association with the HLA-A28 antigens (chi 2 = 9.7), as well as with E/e (chi 2 = 14.69) and e/e (chi 2 = 39.36) and a positive association with HLA-B13 (chi 2 = 5.98) and B35 (chi 2 = 36.58). The highest relative risk for hyperphosphatemia associated with the B27 and B35 antigens was observed with genetic predisposition, being 3.63 and 7.13, respectively. B12- and B35-positive individuals were at higher risk for hyperphosphaturia up to 11.25. There were significant differences in antigen frequency, and sex, genetic predisposition to urolithiasis, association of phosphorus metabolic disturbances with other metabolic disorders, and their effects of parathyroid lesions, etc. The findings reveal the immunogenetically induced risk for the occurrence and development of urolithiasis with disturbed phosphorus metabolism to make goal-oriented prophylactic measures.

ABO Blood-Group System↗
PubMed1977

[Circulatory insufficiency in the light of neuroendocrine and metabolic disorders].

Certain metabolic disorders characterizing disturbances both in neuroendocrine control and in metabolic processes at the cell and tissue levels were revealed in 472 patients with rheumatic heart disease, atherosclerotic cardiosclerosis, and cor pulmonale. The disturbance in the adrenal function was of a dissociated character, manifested by increase in sympathoadrenal and decrease in glucocorticoid activity. The indices of pentosophosphate cycle and erythrocyte and blood serum enzymes studied testify to deep changes in the state of the erythron, marked both by breaks and by adaptation to hypoxia caused by circulatory insufficiency.

Adolescent↗
PubMed1998

Proton MR spectroscopy of pediatric brain metabolic disorders.

Brain metabolic disorders are a major cause of mortality and morbidity in children. Proton MR spectroscopy is a sensitive diagnostic modality for these diseases. The abnormalities in metabolite levels revealed by MR spectroscopy provide specific information in a wide range of metabolic disturbances. Continuing MR imaging and MR spectroscopy yields maximum diagnostic information in an MR examination.

Amino Acid Metabolism, Inborn Errors↗