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At least 649 records · Page 36Linked to original sources
PubMed1995

[Neuro-ophthalmological problems in the diabetic patient].

Neuro-ophthalmological complications in diabetic patients are relatively rare, and their prevalence seems to be much less important than the retinopathy and the cataract prevalence. Although the low frequency of the neuro-ophthalmological complications, these might induce severe loss of vision or oculomotor disturbance, as it is reported in acute anterior ischaemic optic neuropathy or in cranial neuropathy. The etiopathogenic mechanism is still uncertain, but actually a metabolic dysfunction seems to be the more plausible hypothesis. In absence of specific treatment, we emphasized the importance of a preventive treatment based on the best control of diabetes and the treatment of the vascular and infection risk factors.

Adult↗
PubMedDate not supplied

[Emergency therapy of neonatal hyperammonemia with high dosage glucose].

In severe neonatal hyperammonemia, therapy must be started immediately to prevent irreversible CNS damage. Endogenous ammonia production can be quickly reduced if an anabolic condition is induced by means of high-dose glucose infusion. We applied this treatment to four newborn infants with hyperammonemia, this being a symptom of an inborn error of metabolism. The dangerous metabolic dysfunction was brought under control without dialysis within 24-48 hours in all four patients.

Ammonia↗
PubMed1995

[Disorders of consciousness due to disorders of body fluid composition--case report of a female patient].

We report a female patient presenting with sepsis and multi-organ failure following eclampsia and intrauterine childdeath. In the phase of recovery, the patient developed consciousness disorder and coma characterized by fasciculation, generalized myoclonia and respiratory insufficiency. The clinical picture corresponded to that of Lance Adam's syndrome. A quick change in the composition of body fluids in the polyuric phase of renal insufficiency associated with an antidiuretic hormone deficit was a cause of that disorder. Metabolic dysfunction and hyperexcitability of neurons developed as a result. Hyperexcitability of the caudal part of the medulla oblongata was responsible for the development of myoclonia. Following the correction of that disorder, the patient completely improved.

Acute Kidney Injury↗
PubMed1996

[Monitoring of intracranial pressure].

The use of intraparenchymatous ICP sensor is becoming increasingly popular at the expense of the traditional intraventricular catheter method, in spite of the impossibility, with the former technic, to correct a possible zero drift. The decision to initiate or discontinue ICP monitoring is essentially based upon whether suggestive aspects of raised ICP are or not present on CT-scan. The degree of basal cisterns effacement is particularly informative. The same data from successive CT-scans are used to check the validity of the monitoring. Predefining critical levels of ICP and cerebral perfusion pressure (CPP) allows to establish practical guide-lines for treatment. Cerebral ischemia is considered very likely when ICP rises above 30 mmHg. Regarding CPP, the therapeutical goal is to avoid its reduction under the critical level of 60-80 mmHg. As these thresholds vary with the patients age and the type of lesion, a parallel evaluation of cerebral ischemia by other methods is mandatory. Transcranial doppler allows an easy detection of critical reduction of arterial flow. However, in case of flow hypervelocity, interpretation needs measurement of absolute cerebral blood flow values. Cerebral venous oxygen saturation monitoring, at the level of the jugular golf, shows desaturation episodes indicative of cerebral ischemia. Blood sampling for determination of arterial and jugular venous lactate concentrations allows calculation of the lactate oxygen index, a practical correlate of the degree of cerebral ischemia. ICP measurement alone is of limited value to understand the cerebral hemodynamical and metabolical situation in severe brain injury. Preceding the rise of ICP, there exists a compensation phase during which a progressive decrease of intracranial compliance is the important event. Even more earlier, posttraumatic cellular metabolic dysfunctions are to-day objectives for a neurochemical monitoring. Therefore a special technical and human environment has became mandatory to take a real benefit from ICP monitoring.

Brain Injuries↗
PubMed1996

[Effects of thermal injury on heart sialic acid content in rats].

The myocardial sialic acid content, ATPase activities, and Ca2+ level were investigated in rats with full thickness burn of 30% TBSA. The results showed that the burned rats had a decreased level of myocardial sialic acid which was only 58.8% of controls at 3 h postburn. Myocardial Na+, K(+)-ATPase, Ca2+, Mg(2+)-ATPase and Ca(2+)-ATPase activities were inhibited in burned rats. As compared to controls, the burned rats showed a higher level of Ca2+ in heart tissue. This study indicated that there were abnormal energy metabolism, dysfunction of ion pump, and paradox Ca2+ overload in burned rats, which may be associated with the decrease in sialic acid content in myocardium.

Animals↗
PubMed1997

[Anxiety, aggression, agitation and depression: psychopathologic aspects].

While clinical experience has long since shown that there are different types of depression, in particular anxious and hostile depressions, the psychopathological analysis of the various forms remains of current interest. At least four psychopathological models are currently available. The first raises the question of the continuity between reactions to separation, particularly studied in children, and the clinical expression of certain forms of depression in adults. In many aspects, the latter suggest the sequence: protest-despair-detachment. The second model raises the question of the relationship between the depressive disorder and the organization of certain personalities. The considerable comorbidity between the borderline personality and affective disorders suggest that these two different disorders share a common dimension. The third-cultural-model hypothesizes a relationship between the sociocultural prohibition of aggressive responses and the incidence of depression. The fourth model is based on the existence of a specific biological constraint related to abnormalities of serotonin metabolism, to which dysregulation of anxious and aggressive-impulsive behavior patterns during depression are considered related. In conclusion, it may be considered that several models, in particular that of reaction to separation, may, at least in part, account for "positive-expression" depression, but that at least two questions have still to be answered: that regarding the relationships between depression and personality, and that concerning the relationships between the psychopathological constraints related to serotonin metabolism dysfunction and the "positive" expressions.

Adult↗
PubMed1997

[A case of incomplete Kearns-Sayre syndrome with a stroke like episode].

A 32-year-old woman developed chronic progressive hearing impairment, trunkal ataxia, bilateral ptosis and external ophthalmoplegia. She also showed slowly progressive mild to moderate proximal dominant muscle weakness and atrophy. ECG showed incomplete right bundle branch block. An aerobic exercise test showed abnormal blood lactate elevation and muscle biopsy revealed ragged-red fibers in addition to the myopathic change. Analysis of mitochondrial DNA extracted from biopsied muscle and fibroblast samples revealed a 1,758bp deletion from the cytochrome b to ND6 coding regions. Common mutations in tRNALeu(UUR) coding region to the mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) were not present. She was diagnosed as having incomplete Kearns-Sayre syndrome (KSS). Since the age of 35, she developed complex partial seizure attacks with secondary generalization frequently and at the age of 42, she had a severe generalized seizure with delayed consciousness loss followed by left hemiplegia. MRI showed wide T2-high signal lesions in the right temporo-parieto-occipital area. The proton MR-spectroscopy showed prominent increase of lactate beyond the lesions detected by MRI, indicating diffuse aerobic metabolic dysfunction in the central nervous system. We reviewed two other KSS cases with a stroke like episode, who also had epilepsy and large deletion but no tRNALeu(UUR) mutation, in mitochondrial DNA. Patients with KSS who have seizure may develop the stroke-like episode as seen in MELAS patients.

Adult↗
PubMed1997

10 years experience in performing Shouldice operation.

206 male patients were operated for primary direct and indirect inguinal hernia, or both, by Shouldice technique at general surgical departments of Madadeni Hospital, Newcastle, South Africa, Pásztó Hospital and Szolnok MAV Hospital, Hungary between 1986 and 1996. Mean age was 51 yrs +/- 15 yrs (17-91 yrs). The operations were performed by the original way of Shouldice described that type of hernia repair in 1945. 175 patients had spinal and 31 patients had local anesthesia with intravenous fluid and sedation respectively. Studies indicate that collagen metabolic dysfunction plays a major rule in the etiology of groin hernia. Until this is more clearly defined, surgeons will continue to repair groin hernias constitute 15% of operations in general surgery. In approach to groin hernia, the best view for examination of the inguinal region can be obtained by Shouldice technique to decide the proper surgical intervention to repair groin hernia. With low recurrence rate and rapid rehabilitation, author reports 2% of recurrence rate, the Shouldice operation highly recommended.

Adolescent↗
PubMed1998

[Studies of pathogenicity and characterization of molecular phenotype caused by mutations in human mitochondrial DNA].

Mitochondrial DNA evolves and accumulates mutations more rapidly than nuclear DNA. These nucleotide variation may produce neutral polymorphisms or affect to functional conserved positions being very deleterious. On the other hand the relation between the type of mutation (genotype) and the observed clinical symptoms (phenotype) is nowadays practically unknown. Therefore it is very important to demonstrate clearly that the new described mutations are pathogenic and understanding the molecular mechanisms responsible for the energetic metabolism dysfunction produced by these mutations at cellular level. In the last years several procedures have been developed, including in situ hybridization, single-fiber PCR and the use of patient myoblast, fibroblast and lymphoblast cell culture lines. Specially relevant is the cybrid technology that allow repopulate a cell line depleted of mtDNA with mitochondria obtained from patient fibroblasts, producing transmitochondrial cell lines. The use of these methodology in the last few years has been very important to understand the pathogenic mechanism of some of the classical mutations associated to mitochondrial pathology.

Bone Neoplasms↗
PubMed2000

Altered metabolism causes cardiac dysfunction in perfused hearts from diabetic (db/db) mice.

Contractile function and substrate metabolism were characterized in perfused hearts from genetically diabetic C57BL/KsJ-lepr(db)/lepr(db) (db/db) mice and their non-diabetic lean littermates. Contractility was assessed in working hearts by measuring left ventricular pressures and cardiac power. Rates of glycolysis, glucose oxidation, and fatty acid oxidation were measured using radiolabeled substrates ([5-(3)H]glucose, [U-(14)C]glucose, and [9,10-(3)H]palmitate) in the perfusate. Contractile dysfunction in db/db hearts was evident, with increased left ventricular end diastolic pressure and decreased left ventricular developed pressure, cardiac output, and cardiac power. The rate of glycolysis from exogenous glucose in diabetic hearts was 48% of control, whereas glucose oxidation was depressed to only 16% of control. In contrast, palmitate oxidation was increased twofold in db/db hearts. The hypothesis that altered metabolism plays a causative role in diabetes-induced contractile dysfunction was tested using perfused hearts from transgenic db/db mice that overexpress GLUT-4 glucose transporters. Both glucose metabolism and palmitate metabolism were normalized in hearts from db/db-human insulin-regulatable glucose transporter (hGLUT-4) hearts, as was contractile function. These findings strongly support a causative role of impaired metabolism in the cardiomyopathy observed in db/db diabetic hearts.

Animals↗
PubMed2001

Cubilin dysfunction causes abnormal metabolism of the steroid hormone 25(OH) vitamin D(3).

Steroid hormones are central regulators of a variety of biological processes. According to the free hormone hypothesis, steroids enter target cells by passive diffusion. However, recently we demonstrated that 25(OH) vitamin D(3) complexed to its plasma carrier, the vitamin D-binding protein, enters renal proximal tubules by receptor-mediated endocytosis. Knockout mice lacking the endocytic receptor megalin lose 25(OH) vitamin D(3) in the urine and develop bone disease. Here, we report that cubilin, a membrane-associated protein colocalizing with megalin, facilitates the endocytic process by sequestering steroid-carrier complexes on the cellular surface before megalin-mediated internalization of the cubilin-bound ligand. Dogs with an inherited disorder affecting cubilin biosynthesis exhibit abnormal vitamin D metabolism. Similarly, human patients with mutations causing cubilin dysfunction exhibit urinary excretion of 25(OH) vitamin D(3). This observation identifies spontaneous mutations in an endocytic receptor pathway affecting cellular uptake and metabolism of a steroid hormone.

Animals↗
PubMed2005

Alzheimer's disease--a dysfunction in cholesterol and lipid metabolism.

1. Strong etiological association exists between dysfunctional metabolism of brain lipids, age-related changes in the cerebral vasculature and neurodegenerative features characteristic of Alzheimer's disease (AD) brain. 2. In this short review, recent experimental evidence for these associations is further discussed below.

Alzheimer Disease↗
PubMed2002

[Dysfunction of calcium metabolism following resection of the thyroid gland. An analysis of important risk factors].

PURPOSE: Dysfunction of the parathyroid glands is a typical complication following thyroid surgery. Risk factors for the development of postoperative symptomatic hypocalcemia were retrospectively analyzed. METHODS: 308 consecutive thyroid resections (women n = 236, men n = 72, mean age 53 years) performed in 1996 and 1997 were evaluated. Main diagnosis was non-toxic nodular goiter (n = 234, 76 %), 28 patients (9 %) had thyroid carcinoma. The most common operation performed was bilateral functional thyroid resection (n = 116, 38 %), the proportion of thyroidectomies was 14 % (n = 44). The patients with postoperative symptomatic hypocalcemia were followed for a median of 32 months. RESULTS: Clinical symptoms of hypocalcemia were observed in 18 patients (6 %) postoperatively. Three patients developed transient (n = 1) or permanent hypothyroidism (n = 2). In univariate analysis, the underlying thyroid disease, the method of operative therapy, removal, identification and autotransplantation of parathyroid glands, in multivariate analysis, thyroidectomy (relative risk 6.9) and removal of parathyroid glands (relative risk 23.9) were proved to be significant risk factors for the development of postoperative symptomatic hypocalcemia (p < 0.05). CONCLUSIONS: Patients with thyroidectomy, operation for thyroid carcinoma and intraoperative removal of parathyroid glands should be closely followed for postoperative hypocalcemia. Exact surgical technique provided, permanent hypoparathyroidism is rare, particularly if several parathyroid glands were identified intraoperatively and autotransplanted, if necessary.

Adolescent↗
PubMed2026

MASLD Exacerbates Chronic Low-dose PM2.5-induced Lung Injury, Inflammation, and Fibrosis.

BACKGROUND/AIM: Fine particulate matter (PM2.5) and metabolic dysfunction-associated steatotic liver disease (MASLD) are independent risk factors for respiratory disease. However, the combined impact of chronic, low-dose PM2.5 exposure and Western diet (WD)-induced metabolic dysfunction on pulmonary health remains poorly understood. We investigated whether this metabolic state exacerbates PM2.5-driven pathologies using an environmentally relevant PM2.5 dosage (~50 &#x3bc;g/m3). MATERIALS AND METHODS: C57BL/6J mice were fed a WD or normal diet (ND) for 28 weeks and concurrently received intratracheal instillations of PM2.5 (0.5 mg/kg diesel particulate matter) or vehicle three times per week. The MASLD phenotype was confirmed through metabolic and histological analyses. Pulmonary injury, fibrosis, and inflammation were assessed via histology (hematoxylin and eosin, and Masson's trichrome staining) and cytokine quantification in both bronchoalveolar lavage fluid using Luminex multiplex assay and lung tissue using enzyme-linked immunosorbent assay and quantitative polymerase chain reaction. RESULTS: The WD successfully induced MASLD characterized by weight gain, hepatic steatosis, and dyslipidemia. While PM2.5 exposure did not significantly worsen the primary features of MASLD, its combination with a WD markedly exacerbated pulmonary injury and fibrosis compared to PM2.5 exposure alone. This exacerbation was driven by a surge in pro-inflammatory chemokines, including C-X-C motif chemokine ligands 1 and 2 (CXCL1 and CXCL2), and C-C motif chemokine ligand 5 (CCL5), confirmed by Luminex analysis of lavage fluid and mRNA/protein quantification in lung tissue. CONCLUSION: Diet-induced metabolic dysfunction primes the lung for a hyper-inflammatory response to chronic PM2.5 exposure. These findings identify individuals with MASLD as a population with heightened susceptibility to air pollution-related respiratory diseases and underscore the critical interplay between metabolic health and environmental toxicology.

Animals↗
PubMed1989

The metabolism and excretion of trimethadione in patients with percutaneous transhepatic biliary drainage and renal dysfunction.

The metabolism and excretion of trimethadione (TMO) following an oral dose of 4 mg/kg has been examined in patients with percutaneous transhepatic biliary drainage (PTBD) and renal dysfunction. Biliary excretion as the total amount of TMO and its metabolite, dimethadione (DMO) was 2.0% of the dose during 0 to 48 h after TMO administration in patients with PTBD. Total urinary excretion (0-48 h) was 2.8% and 3.0% of the dose in healthy volunteers and patients with renal dysfunction, respectively. The serum DMO/TMO ratio at 4 h after oral dosing in patients of PTBD and renal dysfunction was not significantly changed in comparison with the ratio reported previously in healthy volunteers. The elimination half-life of TMO was also not altered in patients with PTBD in comparison with that reported previously in volunteers. These results suggest that metabolism and urinary and biliary excretion of TMO are not changed in patients with PTBD and renal dysfunction.

Adult↗
PubMed1988

Exercise training in patients with severe left ventricular dysfunction. Hemodynamic and metabolic effects.

We studied the effects of exercise training in patients with chronic heart failure attributed to left ventricular dysfunction (ejection fraction, 24 +/- 10%). Twelve ambulatory patients with stable symptoms underwent 4-6 months of conditioning by exercising 4.1 +/- 0.6 hr/wk at a heart rate corresponding to 75% of peak oxygen consumption. Before and after training, patients underwent maximal bicycle exercise testing with direct measurement of central hemodynamic, leg blood flow, and metabolic responses. Exercise training resulted in a decrease in heart rate at rest and submaximal exercise and a 23% increase in peak oxygen consumption from 16.8 +/- 3.8 to 20.6 +/- 4.7 ml/kg/min (p less than 0.01). Heart rate, arterial lactate, and respiratory exchange ratio were unchanged at peak exercise after training. Maximal cardiac output tended to increase from 8.9 +/- 2.7 to 9.9 +/- 3.2 1/min and contributed to improved peak oxygen consumption in some patients, although this change did not reach statistical significance (p = 0.13). Rest and exercise measurements of left ventricular ejection fraction, left ventricular end-diastolic volume, and left ventricular end-systolic volume were unchanged. Right atrial, pulmonary arterial, pulmonary capillary wedge, and systemic arterial pressures were not different after training. Training induced several important peripheral adaptations that contributed to improved exercise performance. At peak exercise, systemic arteriovenous oxygen difference increased from 13.1 +/- 1.4 to 14.6 +/- 2.3 ml/dl (p less than 0.05). This increase was associated with an increase in peak-exercise leg blood flow from 2.5 +/- 0.7 to 3.0 +/- 0.8 l/min (p less than 0.01) and an increase in leg arteriovenous oxygen difference from 14.5 +/- 1.3 to 16.1 +/- 1.9 ml/dl (p = 0.07). Arterial and femoral venous lactate levels were markedly reduced during submaximal exercise after training, even though cardiac output and leg blood flow were unchanged at these workloads. Thus, ambulatory patients with chronic heart failure can achieve a significant training effect from long-term exercise. Peripheral adaptations, including an increase in peak blood flow to the exercising leg, played an important role in improving exercise tolerance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2006

Prevalence of erectile dysfunction in patients with metabolic syndrome.

AIM: We wished to investigate the relationship between metabolic syndrome and erectile dysfunction (ED). MATERIALS AND METHODS: A total of 268 patients were included in this study. All of the patients were asked to fill in an International Index for Erectile Function (IIEF) questionnaire. The presence of metabolic syndrome was determined when any three or more of the five risk factors were present according to the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP)-III. The relationship between risk factor for metabolic syndrome and ED status was determined according to logistic regression analysis. RESULTS: Eighty-nine patients (33%) constituted the metabolic syndrome group. IIEF-EF domain scores of patients with and without metabolic syndrome were 17.7 +/- 7.9 and 21.7 +/- 7.5, respectively (P < 0.001). Seventy-four percent of patients with metabolic syndrome and 50% of patients without metabolic syndrome had ED (P < 0.001; odds ratio 2.9; 95% CI 1.7-5.0). Erectile function domain scores significantly decreased as the number of metabolic risk factors increased (P < 0.001). Patients with the risk factor of fasting blood glucose (FBG), waist circumference (WC), or hypertension (HT) had lower erectile function domain scores than the patients with other metabolic risk factors. Logistic regression analysis revealed that FBG and WC were the most important criteria for ED. CONCLUSIONS: Metabolic syndrome seems to be a potential risk factor for ED. We recommend patients with metabolic syndrome should be questioned about ED, and WC measurement might take part in the evaluation of ED.

Erectile Dysfunction↗