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At least 19 recordsLinked to original sources
PubMed2005

Fursultiamine, a vitamin B1 derivative, enhances chondroprotective effects of glucosamine hydrochloride and chondroitin sulfate in rabbit experimental osteoarthritis.

OBJECT AND DESIGN: The therapeutic effect of glucosamine hydrochloride (GH) and chondroitin sulfate (CS) in combination with fursultiamine, a vitamin B1 derivative, on the development of cartilage lesions was investigated in an animal model of osteoarthritis (OA). METHODS: The OA model was created by partial medial meniscectomy of the right knee joint (day 0). The rabbits were placed into three experimental groups: operated (OA) rabbits that received placebo treatment, OA rabbits that received GH (1000 mg/kg) + CS (800 mg/kg), and OA rabbits that received GH + CS + fursultiamine (100 mg/kg). Each treatment was initiated on day 3 and continued for 8 weeks. Macroscopic and histologic analyses were performed on the cartilage. The level of MMP-1 in OA cartilage chondrocytes was evaluated by immunohistochemistry. RESULTS: Only the group receiving combined treatment with GH + CS + fursultiamine showed a significant reduction in the severity of macroscopic and histologic lesions on tibial plateau, which is the weight bearing cartilage surface of the tibia, compared with placebo-treated OA rabbits. This treatment group also revealed a small, but significant, decrease in the body weight gain of the rabbits. In cartilage from placebo-treated OA rabbits, a significantly higher percentage of chondrocytes in superficial layer stained positive for MMP-1 compared with unoperated control. Rabbits treated with the GH + CS + fursultiamine revealed a significant reduction in the level of MMP-1. CONCLUSION: These results suggest that the chondroprotective effect of GH + CS is enhanced by the addition of fursultiamine in experimental OA. This effect was associated with a reduction in the level of MMP-1, which are known to play an important role in the pathophysiology of OA lesions.

Animals↗
PubMed1991

[A case of beriberi heart--with special reference to the rapid effect of fursultiamine on hemodynamics].

A 33-year-old man was admitted to Kushiro City General Hospital on February 27, 1989, because of palpitation, shortness of breath and anasarca. Eight months previously he had noted the onset of pretibial edema, which had progressed to anasarca. He had had a meal only once a day for nine months. Physical examination revealed a blood pressure of 114/46 mmHg and pulse rate of 80/min. The 3rd sound was audible. No rales in the chest and no hepatosplenomegaly were noted. Ascites, pretibial edema and anasarca were present. Vibration sensation was diminished, and the deep tendon reflexes were absent in the legs. The blood thiamine level on the 4th day of hospitalization decreased to 2.9 micrograms/dl. The red cell transketolase activity and TPP effect on the 10th hospital day were 0.76 IU/gHb and 11%, respectively. A chest roentogenogram showed pulmonary congestion and cardiomegaly (CTR 61.3%). The electrocardiogram showed non-specific T wave changes. On the echocardiogram, remarkable pericardial effusion and diffuse hypertrophy of the left ventricular wall were observed. In addition, the left ventricular wall motion showed a hyperkinetic state. On the basis of these findings, the diagnosis of beriberi heart was made. The hemodynamic study performed on the 10th hospital day showed a remarkable high cardiac output (CO) of 10.7 l/min and an extremely reduced total peripheral resistance (TPR) of 352 dynes.sec.cm-5. 15 min after intravenous administration of Fursultiamine 100 mg, CO decreased to 7.24 l/min and TPR increased to 848 dynes.sec.cm-5. Following the administration of Fursultiamine 75 mg, po/day, his symptoms and abnormal findings of clinical examination data rapidly improved.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Comparative bioavailability of various thiamine derivatives after oral administration.

In a multiple change-over study the bioequivalence of 3 thiamine preparations, used therapeutically as neurotropic agents for the treatment of polyneuropathies, was tested in a collective of 7 volunteers. After ingestion of a single dose of either 100 mg benfotiamin CS-benzoylthiamine-o-monophosphate), fursultiamin (thiamintetrahydrofurfuryldisulfide) or thiaminedisulfide, thiamine blood levels were analyzed for a 10-hour period. Thiamine was measured by HPLC after precolumn derivatization to thiochrome. The maximal thiamine concentration Cmax and its time (tmax) in plasma and hemolysate, the area under concentration time curve (AUC), and thiamine excretion in 24-hour urine were assessed as criteria of bioavailability. Additionally the erythrocytic transketolase activity (ETK) and alphaETK were determined as indicators of the cellular thiamine availability. After benfotiamin ingestion a more rapid and earlier increase of thiamine in plasma and hemolysate was observed in contrast to fursultiamin and the disulfide. All biokinetic data demonstrated a significantly improved thiamine bioavailability from benfotiamin compared with the other preparations. The lowest bioavailability was detected with thiamindisulfide. From our results it can be concluded that oral administration of benfotiamin is best suitable for therapeutical purposes owing to its excellent absorption characteristics.

Administration, Oral↗
PubMed1996

Thiamine therapy in Alzheimer's disease.

Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function. Only mildly impaired subjects showed cognitive improvement. Alzheimer patients' blood levels of thiamine before the trial were within the normal range. No adverse reactions were observed and all patients tolerated the trial well. TTFD could afford an alternate treatment to large doses of thiamine hydrochloride in Alzheimer patients. However, further investigations of the therapeutic implications of thiamine and its possible etiologic clues to Alzheimer's disease are necessary.

Aged↗
PubMed1995

[Olfactory disturbance caused by chronic sinusitis].

Sinusitis has been reported to be one of the major causative etiologies of olfactory disorder. According to our data during last 3 years, 47.5% of all cases of olfactory disorder were attributed to sinusitis. Persistent olfactory disturbance was often critical even after resection of the pathological sinus mucosa by surgery for chronic sinusitis. Accordingly, olfactory epithelial inflammation involved in sinusitis may be considered another important causative factor disturbing the restoration of olfactory acuity. To elucidate this hypothesis, the following experimental and clinical studies were carried out. (1) A morphological study was done with specimens taken from the olfactory cleft of rabbits with experimentally induced sinusitis to analyze the inflammatory effects, and the degree of inflammatory damage was compared, histopathologically between olfactory and respiratory epithelium. SEM observation in the morphological study showed delayed healing in the olfactory portion in comparison with the respiratory portion (p < 0.01). Cell proliferation activity as determined by immunohistochemical study with bromodeoxyuridine (BrdU) was significantly greater in the respiratory area of the cases with sinusitis than in the control (p < 0.01). Cell proliferation status may play a significant role in this delay. (2) Olfaction tests were performed in patients with sinusitis accompanied with olfactory disturbance. In addition to both T&T olfactometry and intravenous olfactometry using fursultiamine (Alinamin Test), Smell Identification Test (SIT) and Threshold Test by graded Phenyl Ethyl Alchol (PEA) were applied to estimate the olfactory acuity of the patients with sinusitis. The results of SIT and PEA tended to parallel not the Alinamin Test but T&T olfactometry. Results showed that the olfactory disorder caused by sinusitis tended to be severe. The results showed that the epithelial factor is important in explaining olfactory disorder etiologically in cases of sinusitis. In particular, olfactory disturbance tended to persist.

Animals↗
PubMed2003

[Acute encephalopathy due to thiamine deficiency with hyperammonemia in a chronic hemodialysis patient: a case report].

Hemodialysis(HD) patients are at risk for thiamine deficiency because of low intake and accelerated loss of thiamine during HD. We report here an HD patient, an 82-year-old woman, who developed acute encephalopathy due to thiamine deficiency with hyperammonemia. She was admitted to Nishikawa Town Hospital due to pneumonia and was treated with ABPC/SBT for one week. While she was cured of pneumonia, she had a persistently poor appetite. On the twenty-fourth day after admission, HD with intradialytic parenteral nutrition(IDPN), which consisted of 10% glucose 500 ml, in order to correct her malnutrition, was started. She suddenly presented confusion, speech disturbance and ophthalmoplegia. HD with IDPN was stopped after two hours because of her symptoms. Laboratory studies disclosed plasma glucose of 186 mg/dl and serum ammonium of 155 micrograms/dl. Arterial blood gas analysis(inhaling 3 l/min O2) showed severe metabolic acidosis and respiratory acidosis (pH 7.138, pCO2 44.8 mmHg, pO2 108.9 mmHg, HCO3- 15.1 mmol/l). Her malnutrition, unexplained metabolic acidosis and neurological presentation raised the suspicion of acute encephalopathy due to thiamine deficiency. Fursultiamine 100 mg was administered intravenously. After two hours, metabolic acidosis disappeared (pH 7.437, pCO2 33.9 mmHg, pO2 161.0 mmHg, HCO3- 22.9 mmol/l), and she regained her clear consciousness and serum ammonium decreased at 16 micrograms/dl on the next morning. Serum lactate and thiamine level were shown later to be 57.5 mg/dl and 27 nmol/l, respectively. Her clinical course suggests that the glucose load including IDPN may have caused deterioration of the neurological disorder under the condition of thiamine deficiency. Furthermore, it is possible that a relationship exists between thiamine deficiency and hyperammonemia.

Acidosis, Lactic↗
PubMed1990

Thiamine tetraphydrofurfuryl disulfide in nutritional polyneuropathy.

An open trial with thiamine tetrahydrofurfuryl disulphide (TTFD) was carried out on 44 patients with nutritional polyneuropathy who were admitted to the Neurological Department, Dr. Soetomo Hospital, Surabaya, Indonesia, Thirty-four patients showed improvement of their motor functions (P less than 0.01) with slight restoration of sensory function and reflexes (P less than 0.1). Of the 18 patients who were re-examined electrophysiologically 3 months later, 6 showed remarkable improvements. No side-effects were observed during TTFD treatment. It seemed that nutritional polyneuropathy in our low socio-economic patients was mostly caused by thiamine deficiency.

Adolescent↗
PubMed1996

Effects of thiamine supplementation on exercise-induced fatigue.

High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue. Sixteen volunteer male athletes volunteer, 8 with a blood thiamine level of 40 ng/ml or more (normal thiamine group) and 8 with levels below that level (low thiamine group) were selected as subjects. They exercised on a bicycle ergometer and the effects of thiamine supplementation were compared with placebo. Blood thiamine level markedly increased following supplementation of thiamine for 3 days before exercise. Exercise-induced changes in hemodynamic parameters and cardiopulmonary function indicated the onset of fatigue. Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items.

Adult↗
PubMed1998

Inhibition of the delayed rectifier K current in guinea-pig cardiomyocytes by thiamine tetrahydrofurfuryl disulfide.

We examined effect of thiamine tetrahydrofurfuryl disulfide on electrophysiological characteristics of single atrial myocytes, obtained by digestion of guinea-pig heart, using collagenase. Membrane potential and ion channel current in the atrial myocytes were recorded by the patch clamp method. Thiamine tetrahydrofurfuryl disulfide prolonged action potentials at cycle lengths from 250 to 10,000 ms. The degree of thiamine tetrahydrofurfuryl disulfide-induced prolongation was similar among these cycle lengths. Thiamine tetrahydrofurfuryl disulfide inhibited the delayed rectifier K+ current, without affecting Ca2+ current and inward-rectifier K+ current. Thiamine tetrahydrofurfuryl disulfide blocked the delayed rectifier K+ current in voltage- and time-independent manner, indicating that thiamine tetrahydrofurfuryl disulfide blocked both subtypes of the delayed rectifier K+ current (rapid and slow components). Thiamine, the parent molecule of thiamine tetrahydrofurfuryl disulfide, blocked the delayed rectifier K+ current only when thiamine was applied intracellularly. Thiamine tetrahydrofurfuryl disulfide may be converted to thiamine in the cytoplasm, and then may block the the delayed rectifier K+ channel from the intracellular side. Although thiamine tetrahydrofurfuryl disulfide (or thiamine) has some of the properties of class III antiarrhythmics agents, thiamine tetrahydrofurfuryl disulfide did not exhibit reverse use-dependent prolongation of action potential.

Action Potentials↗
PubMed1997

The effect of a thiamin derivative on exercise performance.

The purpose of this study was to investigate the effect of a thiamin derivative, thiamin tetrahydrofurfuryl disulfide (TTFD), on oxygen uptake (VO2), lactate accumulation and cycling performance during exercise to exhaustion. Using a randomized, double-blind, cross-over design with a 10-day washout between trials, 14 subjects ingested either 1 g.day-1 of TTFD or a placebo (PL) for 4 days. On day 3, subjects performed a progressive exercise-test to exhaustion on a cycle ergometer for the determination of VO2submax, VO2peak, lactate concentration ([La-]), lactate threshold (ThLa) and heart rate (fc). On day 4, subjects performed a maximal 2000-m time trial on a cycle ergometer. A one-way analysis of variance (ANOVA) with repeated measures was used to determine significant differences between trials. There were no significant differences detected between trials for serial measures of VO2submax, [La-] or fc. Likewise, VO2peak [PL 4.06 (0.19) TTFD 4.12 (0.19) l.min-1, P = 0.83], ThLa [PL 2.47 (0.17), TTFD 2.43 (0.16) l.min-1, P = 0.86] and 2000-m performance time [PL 204.5 (5.5), TTFD 200.9 (4.3).s, P = 0.61] were not significantly different between trials. The results of this study suggest that thiamin derivative supplementation does not influence high-intensity exercise performance.

Adult↗
PubMed2006

Neuromagnetic changes of brain rhythm evoked by intravenous olfactory stimulation in humans.

To identify the changes in the respective frequency band and brain areas related to olfactory perception, we measured magnetoencephalographic (MEG) signals before and after instilling intravenously thiamine propyl disulfide (TPD) and thiamine tetrahydrofurfuryl disulfide monohydrochloride (TTFD), which evoked a strong and weak sensation of odor, respectively. For the frequency analysis of MEG, a beamformer program, synthetic aperture magnetometry (SAM), was employed and event-related desynchronization (ERD) or synchronization (ERS) was statistically determined. Both strong and weak odors induced ERD in (1) beta band (13-30 Hz) in the right precentral gyrus, and the superior and middle frontal gyri in both hemispheres, (2) low gamma band (30-60 Hz) in the left superior frontal gyrus and superior parietal lobule, and the middle frontal gyrus in both hemispheres, and (3) high gamma band 2 (100-200 Hz) in the right inferior frontal gyrus. TPD induced ERD in the left temporal, parietal and occipital lobes, while TTFD induced ERD in the right temporal, parietal and occipital lobes. The results indicate that physiological functions in several regions in the frontal lobe may change and the strength of the odor may play a different role in each hemisphere during olfactory perception in humans.

Adult↗
PubMed2006

Myopathy in thiamine deficiency: analysis of a case.

BACKGROUND: Tenderness in the limb muscles has been reported anecdotally in patients with beriberi neuropathy, but clinical effects of thiamine deficiency on skeletal muscle have received little attention. OBJECTIVE: To describe a patient with thiamine deficiency who manifested myopathic symptoms and responded well to thiamine supplementation. PATIENT: A 26-year-old woman with neuropathy and heart failure associated with thiamine deficiency also complained of myalgia and weakness, most troublesome in the proximal portions of the limbs. RESULTS: Serum creatine kinase, myoglobin, and aldolase concentrations were abnormally elevated. Magnetic resonance imaging of lower limb muscles demonstrated areas of high signal intensity in T2-weighted images and showed Gd-DTPA enhancement. A biopsy specimen from the quadriceps muscle showed myopathic changes without neurogenic changes. Abnormalities improved well with thiamine administration. CONCLUSION: Myopathy may occur in patients with thiamine deficiency.

Adult↗
PubMed1998

Thiamine and its derivatives inhibit delayed rectifier potassium channels of rat cultured cortical neurons.

We examined the effects of thiamine and its derivatives on voltage-gated ion channels of neuronal cells isolated from fetal forebrain cortex and cultured for 6-14 days. Under the whole-cell voltage clamp, thiamine tetrahydrofurfuryl disulfide (TTFD), a membrane-permeable derivative of thiamine, inhibited the delayed rectifier K+ current (IK) in a concentration-dependent manner (10(-4)-10(-3) M). The IK-suppressing effect was also observed by internal perfusion with 1 mM thiamine, but not by the external application of thiamine, indicating the poor permeability of thiamine through the cell membrane. However, thiamine which was applied directly to the intracellular side of patch membranes in the inside-out configuration failed to decrease the open probability of the single IK channel. In contrast, thiamine diphosphate decreased both the open probability and the open-time of the channel without changing the single channel conductance. These results suggest that phosphorylated thiamine can function as an endogenous K+ channel blocker in neuronal cells. TTFD, when applied extracellularly at a concentration of 1 mM, prolonged the action potential (AP) duration of neurons (172.8 +/- 6.6%) without changing the resting membrane potential or AP amplitude, while the same concentration of thiamine did not influence any parameters of the AP, implying that TTFD may cause the potentiation of neuronal AP through the inhibition of IK.

Animals↗
PubMed2002

Taste disturbance after tonsillectomy.

Of the 3583 outpatients treated at our taste disorder clinic over a period of 15 years, 11 (0.31%) complained of taste disorder after tonsillectomy. The cause of taste disorder was identified in 8 of the 11 cases: in 3 cases it was caused by direct or indirect damage to the lingual branch of the glossopharyngeal nerve; in 2 cases it was attributable to medication taken by the patient after tonsillectomy; and in 3 cases taste disturbance was caused by a lack of dietary zinc, even though this was identified at the time of tonsillectomy. These findings indicate the importance of (i) informing patients when consent for tonsillectomy is obtained that there is a risk of postoperative taste disorder; (ii) measuring the patient's taste threshold and serum zinc level preoperatively; and (iii) obtaining a thorough drug history, including details of non-prescription medications habitually taken by the patient.

Adult↗
PubMed1982

Effect of thiamine tetrahydrofurfuryl disulfide on audiogenic seizures in DBA/2J mice.

Weanling mice of the DBA/2J strain are spontaneously audiogenically seizure prone between 19 and 24 days. Thereafter, susceptibility declines rapidly within the next 7-10 days. It was found that thiamine tetrahydrofurfuryl disulfide (TTFD) significantly delayed the natural disappearance of seizure proneness in male animals compared with controls treated with identical doses of saline. There was no significant difference between treated females and controls. Evidence is presented that suggests that TTFD is cholinergic in its action and has pharmacologic effects other than a simple vitamin replacement. The difference between males and females found in this strain of mouse in this experiment is consistent with previous information which indicates that sex-related differences exist in their response to stress.

Acoustic Stimulation↗
PubMed1981

Erythrocyte transketolase activity in the Wernicke-Korsakoff syndrome.

Erythrocyte transketolase activity and the effect of adding thiamine pyrophosphate (% TPP effect) were measured in subjects suffering from Wernicke-Korsakoff syndrome both before and during treatment with thiamine and/or thiamine tetrahydrofurfuryldisulphide (TTFD). Transketolase activity was significantly lower in untreated patients than in healthy volunteers. Treatment with either thiamine or with TTFD restored enzyme levels to control values but TTFD produced a greater increase than thiamine in enzyme activity. In a group of seven patients there was no correlation between duration of TTFD therapy and either increase in erythrocyte transketolase activity or % decrease in the TPP effect. However, when three patients were followed at intervals during treatment with TTFD, their erythrocyte transketolase increased progressively. Neither thiamine nor TTFD produced clinical improvement in the mental symptoms of Wernicke-Korsakoff psychosis unless administered early in the course of the disease.

Alcohol Amnestic Disorder↗
PubMed1981

Wernicke-Korsakoff syndrome in monozygotic twins: a biochemical peculiarity.

A pair of monozygotic twins, one suffering from the Wernicke-Korsakoff syndrome, verified at autopsy, and the other healthy, was studied biochemically. The erythrocyte transketolase of each twin showed abnormalities, though these differed in the two individuals. In the healthy twin, the basal transketolase was low, but responded normally to thiamine pyrophosphate (TPP) added in vitro. In the twin with the Wernicke-Korsakoff syndrome the basal level of the enzyme and its response in vitro were normal, but a period of treatment with thiamine tetrahydrofurfuryldisulphide, led to loss of the in vitro response. It is suggested that, initially, an inborn error of metabolism may have been common to both twins.

Alcohol Amnestic Disorder↗