SEARCH · PubMed Health

Results for “HYDROXOCOBALAMIN”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

PubMed2000

Antidotes--inappropriate timely availability.

The aim of this study was to determine the availability of antidotes to poisons in Wales and the South West of England. A stocklist of antidotes that are available to accident and emergency departments was requested and was compared with recommendations from the International Programme on Chemical Safety (IPCS). Chief pharmacists were invited to complete a short questionnaire regarding knowledge of existing guidelines. Thirty-four of 43 centres replied (response rate 77%). No department held all 36 antidotes (mean 13, range 7-33). All departments held antidotes that were frequently used. Ninety-one percent of departments held one cyanide antidote. Eighty-eight percent held one heavy metal chelating agent. The remaining antidotes were variably stocked. New agents such as 4-methylpyrazole, hydroxocobalamin and the heavy metal chelating agents DMSA and DMPS were infrequently held. Twenty of 34 chief pharmacists were unfamiliar with existing UK guidelines. A trend exists whereby larger departments stocked more antidotes. Some antidotes to poisons are not available in a timely fashion in Wales and the South West of England. There is a lack of awareness of existing guidelines. New recommendations relevant to clinical need and local practice should ideally be developed.

Antidotes↗

PubMed1976

Cobalamins in fibroblasts cultured from normal control subjects and patients with methylmalonic aciduria.

The intracellular content and proportional distribution of B12 (cobalamin) derivatives in fibroblasts cultured from patients with various forms of methylmalonic aciduria, as well as from normal control subjects, has been determined by a two-dimensional chromatobioautographic technique. Each line of fibroblasts was grown in the presence of four concentrations of cobalamin, ranging from the 0.04-0.07 pmol/ml contained in the basal medium to 74 pmol/ml (100 ng/ml), added in form of hydroxocobalamin (OH-CHl). Control cells grown in the basal medium contained substantial proportions of both methylcobalamin (MeCbl) and adenysylcobalamin (AdoCbl), with the former predominating. As increasing concentrations of OH-CBl were added to the growth medium, the total cellular cobalamin content increased without marked changes in the relative proportions of MeCbl, AdoCbl, and OH-Cbl. Three different patterns were discernable in the cobalamin distributions of the cells cultured from patients with methylmalonic aciduria (Table 1 and Fig. 1).

Amino Acid Metabolism, Inborn Errors↗

PubMed1997

A 44-month clinical-brain MRI follow-up in a patient with B12 deficiency.

We report a 51-year-old woman with vitamin B12 deficiency who presented with slight megaloblastic anemia and severe neurologic deficits associated with multiple focal and confluent T2-weighted white matter hyperintensities on brain MRI. Forty-four months after initiation of hydroxocobalamin therapy, there was clinical improvement and striking reduction in the MRI abnormalities. B12 deficiency should be considered in the differential diagnosis of neurologic disorders associated with multiple areas of white matter hyperintensities on T2-weighted brain MRI.

Brain↗

PubMed2006

Pediatric cyanide poisoning: causes, manifestations, management, and unmet needs.

Confirmed cases of childhood exposure to cyanide are rare despite multiple potential sources including inhalation of fire smoke, ingestion of toxic household and workplace substances, and ingestion of cyanogenic foods. Because of its infrequent occurrence, medical professionals may have difficulty recognizing cyanide poisoning, confirming its presence, and treating it in pediatric patients. The sources and manifestations of acute cyanide poisoning seem to be qualitatively similar between children and adults, but children may be more vulnerable than adults to poisoning from some sources. The only currently available antidote in the United States (the cyanide antidote kit) has been used successfully in children but has particular risks associated with its use in pediatric patients. Because hemoglobin kinetics vary with age, methemoglobinemia associated with nitrite-based antidotes may be excessive at standard adult dosing in children. A cyanide antidote with a better risk/benefit ratio than the current agent available in the United States is desirable. The vitamin B12 precursor hydroxocobalamin, which has been used in Europe, may prove to be an attractive alternative to the cyanide antidote kit for pediatric patients. In this article we review the available data on the sources, manifestations, and treatment of acute cyanide poisoning in children and discuss unmet needs in the management of pediatric cyanide poisoning.

Adolescent↗

PubMed1998

Peripheral neuropathy with nucleoside antiretrovirals: risk factors, incidence and management.

Distal symmetrical peripheral neuropathy is a common adverse experience in persons with HIV infection. This condition, which presents as a pain, numbness. burning and/or dysaethesia initially in the feet, is often multi-factorial in its origin. Nucleoside analogue reverse transcriptase inhibitors represent an important contributor to peripheral neuropathy. Specifically, around 10% of patients receiving stavudine or zalcitabine and 1 to 2% of didanosine recipients may have to discontinue therapy with these agents due to neuropathy. Prompt withdrawal of these therapies enables gradual resolution of signs and symptoms in most patients, although a period of symptom intensification may occur shortly after withdrawal. Risk factors for developing peripheral neuropathy during nucleoside analogue therapy include low CD4+ cell count (<100 cells/mm3), a prior history of an AIDS defining illness or neoplasm, a history of peripheral neuropathy, use of other neurotoxic agents including high alcohol (ethanol) consumption and nutritional deficiencies such as low serum hydroxocobalamin levels. Thus, patients at increased risk of peripheral neuropathy should potentially avoid the use of the neurotoxic nucleoside analogues or be more carefully monitored during therapy. Management of this problem includes patient education. prompt withdrawal of the likely causative agent (giving consideration not to leave the patient on a sub-optimal therapy regimen) and simple analgesia. with augmentation with tricyclic antidepressants or anticonvulsant agents when pain is severe. New agents that may assist in managing this condition include levacecarnine (acetyl-L-carnitine) and nerve growth factors such as recombinant human nerve growth factor.

Clinical Trials, Phase I as Topic↗

PubMed1996

Measurement of joint aspirate dilution by a spectrophotometer capillary tube system.

The amount of synovial fluid in small joints which is available for analysis of endogenous compounds is usually very limited and saline washings are therefore commonly required. However, since the washing fluid is not fully recovered and, furthermore, dilutes the synovial fluid in the joint aspirate, the true synovial fluid concentration of a particular substance is unknown. In the present study we validate the use of vitamin B12 (hydroxocobalamin, 1 mg ml-1) as an internal standard to determine this dilution, since its strong red colour lends itself to spectroscopic measurement by a capillary tube system requiring only 3 microliter per sample. The absorbance of different dilutions of the stock solutions (25, 33 and 50% vitamin B12 in saline) by saline, plasma and hyaluronan was measured in order to establish the optimal wavelength, the lower limit of detection and the interference by plasma or hyaluronan in the absorbance. Furthermore, the interaction of vitamin B12 in the analyses of interleukin-1 beta, serotonin and glucose was investigated. The optimal wavelength was found to be 350 nm and the limit of detection 0.5-0.9% dilution of the vitamin B12 solution. Hyaluronan or plasma did not influence the absorbance measurements and the minute interaction of vitamin B12 in the photometric measurements could be compensated for.

Biopsy, Needle↗

PubMed1995

Nutrition and optic nerve disease.

The syndrome characterized by papillomacular bundle damage, central or cecocentral scotoma, and reduction of color vision can be produced by toxic, nutritional, or hereditary causes. Patients who present with such a picture should be evaluated for toxic sources such as tobacco or alcohol use. Nutritional deficiencies must be considered and a good family history should be obtained to explore hereditary factors. DNA mutation analysis is available to detect genetic abnormalities. A trial of nutritional replacement may be advisable even in the face of normal laboratory values. Previous reports have shown dramatic visual improvement with intramuscular hydroxocobalamin and other oral vitamin B complexes, even when specific deficiencies are not found.

Alcohol Drinking↗

PubMed1981

Cyanide poisoning.

In recent years, the increasing use of laetrile has been added to the traditional sources of exposure to cyanide in industry, chemistry labs, and fumigation. The events in Jonestown in 1978 were a grim reminder of the lethality of cyanide. Nonetheless, advancement in new modes of treatment has been slow. The traditional method of treatment used in the United States is effective, but not without its own morbidity and mortality. Using two case reports as models, we review here the topic of cyanide poisoning including sources of exposure, pathophysiology, clinical manifestations of both acute and chronic exposure, and modes of treatment. Although there is currently no accepted alternate treatment in this country, review of the literature shows promise in other modalities being investigated in Europe, including hydroxocobalamin, cobalt salts, and particularly aminophenols.

Adult↗

PubMed1981

Vitamin B12 administration for milk fat synthesis in lactating dairy cows fed a low fiber diet.

Thirty lactating Holstein cows were in two groups in a study of effects of vitamin B12 injections on milk fat synthesis. All cows were fed a normal fiber diet for the first 28 days after calving and then adjusted gradually to a low fiber diet over the next 28 days. After adjustment to the low fiber diet, in a single reversal trail, cows received either 150 mg of vitamin B12 in the form of hydroxocobalamin intramuscularly every 7 days for 21 days or no treatment for 21 days. Daily milk yield (kg), percent milk fat, and milk fat yield (g) for the normal fiber, low fiber adjustment, low fiber control, and low fiber plus vitamin B12 treatments were 29.6, 3.59, 1192; 31.5, 2.85, 840; 28.0, 2.58, 715; and 28.8, 2.65, 760. Injections of vitamin B12 did not correct the milk fat depression associated with the low fiber diets. In addition, there was no consistent relationship between blood B12 and milk fat production. Milk fat production was highly correlated with molar percent acetate in the rumen .63 and with blood acetate concentration .74.

Animal Feed↗

PubMed1982

The mechanism of in sutu reactivation of glycerol-inactivated coenzyme B12-dependent enzymes, glycerol dehydratase and diol dehydratase.

In the previous paper (S. Honda, T. Toraya, and S. Fukui, J. Bacteriol., 143, 1458-1465 (1980)), we reported that the glycerol-inactivated holoenzymes of adenosylcobalamin-dependent glycerol dehydratase and diol dehydratase are rapidly and continually reactivated in toluene-treated cells (in situ) by adenosine 5'-triphosphate (ATP) and divalent metal ions in the presence of free adenosylcobalamin. To elucidate the mechanism of this in situ reactivation, the nature of the binding of various irreversible cobalamin inhibitors to the dehydratases in situ was investigated. In the presence of ATP and Mn2+, enzyme-bound hydroxocobalamin, cyanocobalamin and methylcobalamin were rapidly displaced by added adenosylcobalamin. Without ATP and Mn2+, such displacement did not take place. In contrast, enzyme-bound adeninylbutylcobalamin and adenosylethylcobalamin were essentially not displaceable by the free coenzyme even in the presence of ATP and Mn2+. Inosylcobalamin was a very weak inhibitor irrespective of the presence of ATP and Mn2+. These results indicate that the relative affinity of the enzymes in situ for the cobalamins with simple Co beta ligands was markedly lowered in the presence of ATP and Mn2+, whereas that for the cobalamins with adenine-containing ligands was not. When the glycerol-inactivated holoenzymes in situ were dialyzed against a buffer containing ATP and Mg2+, the inactivated coenzyme moiety dissociated from the enzymes leaving apoproteins. Kinetic evidence was also obtained with the dehydratases in situ that continual displacement of the inactivated coenzyme moiety by adenosylcobalamin takes place during the glycerol dehydration reaction in the presence of ATP and Mn2+. Since the adenosyl group of the bound coenzyme is irreversibly removed from the cobalamin moiety during inactivation by glycerol, all of these data constitute clear evidence that the inactivated holo-dehydratases are reactivated in situ in the presence of ATP and Mn2+ by displacement of the modified coenzyme moiety by free intact adenosylcobalamin (i.e. selective B12-exchange mechanism).

Adenosine Triphosphate↗

PubMed1984

Assay, purification and characterization of cob(I)alamin adenosyltransferase of Protaminobacter ruber.

A simple spectrophotometric method for assay of ATP: cob(I)alamin Co-beta-adenosyltransferase was established. By using this method, specific activity of the enzyme in Protaminobacter ruber was found to be the highest in the logarithmic growth phase. The enzyme was highly purified from the cells in that phase and characterized. The molecular weight of the enzyme was estimated as 44,000 by gel filtration. The optimal pH and temperature were about 8.0 and 50 degrees C, respectively. Among divalent metal ions tested, only Mg2+ was effective for the enzyme activity. Km values for ATP and hydroxocobalamin were 250 microM and 26.3 microM, respectively. Substrate analogs such as GTP and CTP had only small activity in the enzymatic reaction.

Alkyl and Aryl Transferases↗

PubMed1990

Occurrence and tissue distribution of both NADH- and NADPH-linked aquacobalamin reductases in some vertebrates.

To elucidate the synthesis of cobalamin coenzymes in view of comparative biochemistry, tissue distribution of activity of aquacobalamin reductase [EC 1.6.99.8] catalyzing the reduction of hydroxocobalamin to cob(II)alamin was studied in some vertebrates. Activity of NADH- or NADPH-linked aquacobalamin reductase (or both) was found in some tissues of monkey, rat, cow, hog, chicken, fish, and frog. The liver homogenates of these vertebrates contained both NADH- and NADPH-linked enzymes. Monkey and rat livers accounted for more than 80% of total activities of both NADH- and NADPH-linked enzymes. Ratios of activities of the liver NADH- and NADPH-linked enzymes were above 1.0 in some land animals (monkey, rat, cow, and hog) but below 1.0 in water animals (sea and freshwater fishes). These different ratios are presumably due to the difference in the metabolisms of cobalamin and/or in the other cellular components between land and water animals.

Animals↗

PubMed2026

Case Report: Persistent isolated hyperhomocysteinemia in an adolescent with celiac disease and homozygous MTHFR c.665C>T polymorphism: a multifactorial disturbance of one-carbon metabolism.

UNLABELLED: Hyperhomocysteinemia in adolescence typically prompts investigation for classical inborn errors of sulfur amino acid metabolism, including cystathionine β-synthase deficiency and cobalamin-dependent remethylation disorders. However, persistent elevations may also arise from interactions between common genetic polymorphisms and acquired nutritional conditions that alter one-carbon metabolism. CASE PRESENTATION: We report an 18-year-old male with type 1 diabetes mellitus, celiac disease on a strict gluten-free diet, congenital unilateral sensorineural hearing loss, and persistent isolated hyperhomocysteinemia. At age 16, he presented with an acute visual field disturbance and right occipital cortical MRI changes suggestive of ischemia. Plasma homocysteine was persistently between 50 and 65 μmol/L.Extensive metabolic and genetic investigations, including targeted gene panels, whole-exome and research whole-genome sequencing, mitochondrial DNA sequencing, mitochondrial complex activities in fibroblasts, and fibroblast complementation, excluded classical homocystinuria and remethylation defects. Sequential trials of pyridoxine, hydroxocobalamin, and high-dose betaine produced modest or transient improvement. Re-analysis of exome data showed homozygosity for the common MTHFR c.665C>T (p.Ala222Val) variant. Family testing revealed that his father (TT) and mother (CT) had normal homocysteine (10.9 and 10.4 μmol/L), indicating that MTHFR TT alone is insufficient to cause a biochemical phenotype and functions as a susceptibility factor. Combined oral methylfolate (1,000 µg daily) and vitamin B12 (cyanocobalamin 1,000 µg daily) reduced homocysteine from 66 to 24.6 μmol/L in 8 weeks. CONCLUSION: This case illustrates multifactorial hyperhomocysteinemia arising from interactions between celiac disease-related micronutrient vulnerability and reduced MTHFR activity. Recognition of gene-nutrient interactions is important when classical metabolic disorders are excluded and may guide targeted therapy.

MTHFR polymorphism↗

PubMed1976

[An enzymic assay for the determination of vitamin B12 (author's transl)].

A procedure which extends the very sensitive propanediol-dehydratase reaction for 5'-deoxy-5'-adenosylcobalamine determination to cyanocobalamine and hydroxocobalamine is described. In this procedure, the cobalamines are adenosylated by vitamin B12 coenzyme synthetase and the resulting 5'-deoxy-5'-adenosylcobalamine can be determined by the propanediol-dehydratase reaction. Aldehyde, the product of the latter, can be registered by the alcohol dehydrogenase reaction.

Adenosine↗

PubMed1999

[Smoke poisoning].

SYSTEMIC AND LOCAL EFFECT: Smoke inhalation causes systemic and local, mainly respiratory, toxicity due to the asphyxiant and irritant properties of toxic gases. OXYGEN DEPRIVATION AND INTOXICATION: The syndrome of oxygen deprivation and intoxication by asphyxiant gases is caused by combustion-induced oxygen deprivation and exposure to carbon monoxide (CO) and cyanide (CN), but also to other toxic gases. A loss of consciousness is a good sign of systemic toxicity; however, the respective role of CO, CN and other toxic gases cannot be determined. The presence of apnea, lactic acidosis, and severe cardiovascular disturbances is consistent with CN poisoning. A correlation exists between blood CO concentration determined on a sample obtained at the site of the fire, and the occurrence and severity of the clinical disorders. IRRITANT GASES INTOXICATION: This syndrome explains the mucosal injury affecting the eyes and the lungs. These complications are better diagnosed by clinical examination rather than by various investigations such as chest X-ray or fiberoptic bronchoscopy. Dysphonia is always a sign of severe poisoning. CLINICAL COURSE: In non-burned victims, delayed neurological and respiratory complications can be observed. Oxygen administration is the cornerstone supportive therapy. Hyperbaric oxygen should be discussed according to the severity of the syndrome of oxygen deprivation and intoxication by asphyxiant gases. In case of cyanide poisoning, a safe and effective antidote should be given; hydroxocobalamine seems to be the drug of choice. Supportive treatment is efficient to treat respiratory failure. Endotracheal intubation should be considered in patients exhibiting early dysphonia associated with dyspnea.

Asphyxia↗

PubMed2000

Emergency management of poisoning in Hong Kong.

The emergency management of poisoning is important in reducing the risk of mortality and morbidity in poisoned patients. This article reviews the Hong Kong system of prehospital and emergency care of poisoning, with reference to recent advances in this field. Administering activated charcoal is recommended for the gastro-intestinal decontamination of most poisons, unless doing so is contra-indicated. Gastric lavage should be considered only in life-threatening cases of poisoning that present within the first hour. Newer antidotes that are available in Hong Kong accident and emergency departments include hydroxocobalamin, stonefish and snake antevenenes, digoxin-specific antibodies, esmolol hydrochloride, and octreotide. The 'golden hour' concept of gastro-intestinal decontamination is advocated and ways to ensure that decontamination is performed within the 'golden hour' are suggested.

Antidotes↗

PubMed2001

[Availability of antidotes in French emergency medical aid units].

OBJECTIVE: To study the availability of antidotes in French emergency medical aid units (SAMU). METHODS: The physicians or nurses responsible for antidotes in French emergency medical aid units (SAMU) were interviewed by phone. The study involved 102 SAMU in metropolitan France. Four answers on availability of 37 antidotes were possible: the antidote was available in the emergency vehicle used for interventions; the antidote was available in the hospital-located SAMU; the antidote was available in the referral hospital (emergency unit, intensive care unit, operating room, pharmacy); the antidote was not available or not known to be available. RESULTS: Adrenaline and atropine were available in all the intervention vehicles. Nine other antidotes were available in more than two-thirds of the vehicles: 30% glucose (101/102), isoprenaline (100/102), dobutamine (98/112), sodium bicarbonate (97/102), naloxone (95/102), calcium chloride or bicarbonate (89/102), flumazénil (83/102), sodium lactate (77/102), and magnesium sulfate (66/102). Among the other antidotes, hydroxocobalamine and propranolol were available in 24/102 intervention vehicles and activated charcoal in 22/102. Antidigitalic antibodies and 4-methylpyrazole were not available in any vehicle, and were available in less than 25% of the hospitals. CONCLUSION: There is a great disparity of antidote availability. Certain essential antidotes, for which there is no alternative, are not available in emergency intervention vehicles and even in the hospital. The SAMU should develop an economically acceptable departmental management scheme for exceptional-use antidotes.

Ambulances↗

PubMed2001

Early-onset combined methylmalonic aciduria and homocystinuria: neuroradiologic findings.

BACKGROUND AND PURPOSE: Combined methylmalonic aciduria and homocystinuria (MMA-HC) is caused by impaired hepatic conversion of dietary cobalamin to methylcobalamin and adenosylcobalamin, resulting in decreased activity of methylmalonyl-CoA mutase and methionine synthase. Patients with the early-onset variety present within 12 months of age with severe neurologic, hematologic, and gastrointestinal abnormalities. We describe the neuroradiologic features of early-onset MMA-HC and discuss related pathophysiological mechanisms. METHODS: Twelve infants with hypotonia, failure to thrive, poor feeding, and hematologic abnormalities were diagnosed with MMA-HC on the basis of a typical plasmatic and urinary metabolic profile and enzyme activity in fibroblastic cultures. Complementation studies were performed in two cases, and yielded a CblC result. MR imaging was performed at presentation in four cases and later in the others. All patients showed prompt biochemical improvement with intramuscular hydroxocobalamin administration, and most had moderate neurologic improvement. RESULTS: Diffuse supratentorial white matter edema and dysmyelination was the typical MR picture at presentation, whereas white matter bulk loss characterized later stages of the disease. Nucleocapsular areas of gliosis were an additional finding in one case. One patient had tetraventricular hydrocephalus at presentation. CONCLUSION: White matter damage is probably caused by reduced methyl group availability and nonphysiological fatty acids toxicity, whereas focal gliosis results from homocysteine-induced toxicity to the endothelium. Hydrocephalus may result from diffuse intracranial extracerebral arterial stiffness, known as reduced arterial pulsation hydrocephalus. MR imaging features at presentation and at follow-up are nonspecific.

Brain↗