The hyper-methemoglobinemia causes the oxygen transfer disorder. The clinical symptoms depends on the level of methemoylobinemia. Hypermethemoglobinemia can be congenital or acquired hypermethemoglobinemia. The congenital hypermethemoglobinemia caused by partial or total methemoglobine reeducates deficiency in patients with rare genetic heterozygous enzyme deficiency due to the abnormal hemoglobin. The acquired hypermethemoglobinemia occurred after exposure to colour compound, food and drinking water with nitrate or drugs. The determination of causative agent of hypermethemoglobin help treating more effectively
Methemoglobin ; Hemoglobins, Abnormal ; Therapeutics ; Methemoglobinemia

No abstract available.
Administration, Intravesical* ; Humans ; Reflex, Abnormal*

Humans ; Hemoglobinopathies ; Hemoglobins, Abnormal/genetics*

The vibratory inhibition index(V.I.I.) of H-reflex, H/M(mean H-reflex amplitude / mean M wave amplitude) and F/M(mean F wave amplitude / mean M wave amplitude) ratios were measured in patients of hyperreflexia with or without spasticity. These data were compared with age-matched control subjects. In comparison to normals, V.I.I. And F/M ratios were increased at statistically significant levels(versus normal : V.I.I. P<0.001, F/M p<0.005) in patient group. And V.I.I.'s were inclined to be correlated with F/M ratios without statistical significance(r=0.27, p=0.21). H /M ratios showed no significant difference between patient and control groups. In these patients, the normal significant correlation between mean F wave amplitude and M wave amplitudes was maintained(p<0.01). F/M ratios were negatively correlated with rnotor nerve conductoion velocity(r= -0.72, p<0.01).These results indicate that V.I.I. And F/M ratios increase in patients with hyperreflexia and/or spasticity. Although mechanisms differ, the data are consistent with a similar physiological responses of H-reflex and F wave to spasticity.
H-Reflex* ; Humans ; Muscle Spasticity* ; Reflex, Abnormal

PURPOSE: We classified DH(detrusor hyperreflexia) into variable urodynamic findings as DHIC(detrusor hyperreflexia with impaired contractility), DHDP(detrusor hyperreflexia with dyssynergia pattern), and NCDDH(non-impaired contractility < non-dyssynergia pattern detrusor hyperreflexia). The aim of this study was to elucidate the reliability of the difference among the classified DH through a urodynamic study. MATERIALS AND METHODS: Sixty-nine patients showed DH, which was defined as an involuntary detrusor contraction of more than 15cmH2O with involuntary urine leakage with only a cerebrovascular accident (CVA), by urodynamic study. We classified DH(n=69) into three subgroups as DHIC(n=22)(Pdet.max<30cmH2O, Qmax<12ml/s), DHDP (n=19)(Pdet.max>50cmH2O, Qmax<12ml/s), and NICNDP-DH(n=28). RESULTS: Mean fraction of voided volume of DHIC(41.7+/-1.8%) and DHDP (38.3+/-2.2%) were significantly less than that of NCDDH (98.5+/-3.2%) according to the urodynamic study (p<0.01). Mean voiding pressure was 25.8+/-0.7cmH2O in DHIC, which was significantly less. However, 96.3+/-10.4cmH2O in DHDP was significantly more than that of NCDDH(p<0.01). Mean age was 83.8+/-1.2 years old in DHIC, which was significantly older than the mean age of the other groups(p=0.01). CONCLUSIONS: Variable findings of the urodynamic study were found in patients with DH as clinical parameters. Thus, we must treat the DH patients with individual therapy based on urodynamic findings.
Ataxia ; Humans ; Reflex, Abnormal* ; Stroke* ; Urodynamics*

No abstract available.
Autonomic Nervous System ; Hypohidrosis* ; Reflex, Abnormal*

Abnormal lipid metabolism associated with various renal diseases has been known for a long time. Hypercholesterolemia is one of the characteristic features of nephotic syndrome, and hypertriglyceridemia is often observed in chronic renal failure (CRF). The role of lipid abnormalities in the pathogenesis of renal diseases has been variously discussed. However, direct evidence only recently became possible when more sophisticated analyses of renal histopathology as well as an application of molecular biology were introduced in the field of clinical nephrology. The recent identification of lipoprotein nephropathy (LPG), reported most often by Japanese authors since 1989, is particularly noteworthy. The detailed analysis of lipid profiles and renal histology has been instrumental in clarifying the relationship between lipids and the kidney not only in LPG but also in other disease entities such as familial-type dyslipidemias, CRF, focal glomerulosclerosis, and diabetic nephropathy. Dyslipidemias common to these diseases, together with the presence of hypertension, cause systemic atherosclerotic lesions (including lesions in the kidney) and terminal renal failure.
seconds ; Kidney Diseases ; lipid metabolism ; Abnormal ; Lipids

Hemoglobins, Abnormal ; Humans ; Singapore/epidemiology* ; alpha-Thalassemia

Humans ; Hemoglobinopathies ; Hemoglobins, Abnormal/genetics* ; Oxygen

The clinical and urodynarnic studies for urinary dysfunction were performed in 35 patients with idiopathic parkinson's disease who admitted at Hanyang University Hospital from January, 1988 to June, 1990. The results are as follows; 1. Urinary dysfunction was noted in 9 patients (25.7%) with idiopathic parkinson's disease Their cysto / uroflowmetry showed detrusor hyperreflexia in 6 patients, and detrusor hyporeflexia in 3 patients. The common urinary symptoms were frequency, incontinence, hesitency, decreased urinary force, and retention in that order. 2. The mean time-interval from the onset of initial parkinsonian symptoms to the development of urinary symptoms was 22.6 months (ranged from 3 to 48 months). Urinary dysfuncion showed no correlation with clinical severity of parkinson's disease. 3. The frequency of urinary dysfunction was greater in rigidity-predominant parkinsonian group than patients with tremor. Cysto / uroflowmetry in the former showed detrusor hyperreflexia more frequently than detrusor hyporeflexia. 4. It was suggested that urinary dysfunction in idiopathic parkinson's disease probably result from multifactorial causes such as the change of neuronal effect, dysautonomia, and skeletal rigidity.
Humans ; Neurons ; Parkinson Disease* ; Primary Dysautonomias ; Reflex, Abnormal ; Tremor