Intravenous Methylcobalamin Treatment for Uremic and Diabetic Neuropathy in Chronic Hemodialysis Patients.

Kuwabara, Satoshi; Nakazawa, Ryoichi; Azuma, Nakanobu; Suzuki, Masatoshi; Miyajima, K; Fukutake, Toshio; Hattori, Takamichi

doi:10.2169/internalmedicine.38.472

Cited by 75 publications

(40 citation statements)

References 11 publications

(10 reference statements)

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“…This effect has been attributed to the effect of vitamin B12 on axonal conduction (Wang et al, 2005). In the treatment of patients presenting with diabetic polyneuropathy, treatment with vitamin B12 led to a reduction in pain and paresthesia along with significant improvement of ulnar motor and median nerve conduction velocities (Kuwabara et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Nunes¹,

Jr²,

Goldberg³

et al. 2013

RNIJ

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Section: Discussionmentioning

confidence: 99%

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Nunes¹,

Jr²,

Goldberg³

et al. 2013

RNIJ

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“…In this regard, "functional" deficiency of Cbl has recently been suggested in the pathogenesis of both Alzheimer disease and AIDS myelopathy. 43,44 Moreover, pharmacologic doses of methylcobalamin can improve measures of both cardiac autonomic dysfunction and peripheral neuropathy in diabetic subjects, [45][46][47] and high doses of methylcobalamin also accelerate nerve regeneration in rats with acrylamide neuropathy. 48 The observation that methylcobalamin can serve as a methyl donor in vitro in the DNA methylase reaction provides one possible mechanism for a pharmacologic effect of Cbl therapy.…”

Section: Discussionmentioning

confidence: 99%

Cobalamin-responsive disorders in the ambulatory care setting: unreliability of cobalamin, methylmalonic acid, and homocysteine testing

Solomon

2005

Blood

136

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IntroductionWhile cobalamin (Cbl) deficiency classically causes macrocytic anemia, anemia can occur without macrocytosis, and both neurologic and cognitive dysfunction often develop in the absence of hematologic changes. 1-5 Symptoms consistent with Cbl deficiency, including paresthesias, unsteady gait, fatigue, and impaired memory, are commonly encountered in the ambulatory care setting, and early recognition of Cbl deficiency is important to prevent progressive, irreversible neurologic and cognitive impairment. 6,7 Although treatment with Cbl is often initiated after the finding of a low serum Cbl level, many patients with low Cbl levels are not Cbl deficient. 8,9 As a result, measurements of the Cbl-dependent metabolites, methylmalonic acid (MMA) and homocysteine (HCys), have recently been used to confirm the presence of Cbl deficiency. Retrospective studies of patients at academic medical centers with low serum Cbl levels and clinically overt Cbl deficiency found MMA and/or HCys levels more than 3 standard deviations (SD) above the normal mean in almost all patients. 8,10-12 Thus, algorithms for the diagnosis of Cbl deficiency were developed that suggest initial measurement of serum Cbl followed by determination of MMA and HCys when Cbl levels are intermediate or when suspicion of clinically significant Cbl deficiency is high. 8,[13][14][15][16][17][18][19][20] However, because little attention has been given to the study of patients with clinical findings consistent with Cbl deficiency but normal vitamin and metabolite levels, the negative predictive value of these tests is uncertain. Indeed, Cbl levels are normal in some patients with overt deficiency, 11 and currently available Cbl assay kits may not be reliable. 21,22 Moreover, because studies from academic centers usually employed special diagnostic or research laboratory facilities, their findings may not be representative of those obtainable in other ambulatory care settings.Thus, a retrospective review of patients evaluated for Cbl deficiency during a 10-year period at a staff model HMO utilizing a national commercial laboratory was performed. Initially, only patients with low serum Cbl levels or elevated metabolite levels received therapeutic trials of Cbl. However, in the seventh year of the study period, one patient with total absence of vibratory sensation in the iliac crest, knees, and ankles had complete recovery following 2 months of Cbl therapy despite normal Cbl, MMA, and HCys levels. Thereafter, therapy was offered to all patients with hematologic or neurologic abnormalities consistent with Cbl deficiency regardless of the results of screening studies. Patients, materials, and methods Laboratory methodsSerum Cbl was measured by the ADVIA Centaur chemiluminescence assay (Bayer Diagnostics, Tarrytown, NY). Normal Cbl values were 200 to 1100 pg/mL, but higher reference ranges have been suggested, 11,13,16,17,20,23,24 and the statement "patients with values less than 300 pg/mL may experience unexplained neuropsychiatric or hematologic abnormali...

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“…The effects of high-dose intravenous administration of the vitamin B 12 analog methylcobalamin (500 µg 3 times per week) over a 6-month period was evaluated in chronic hemodialysis patients presenting diabetic neuropathy. The authors reported reduction in pain and paresthesia along with significant improvement of ulnar motor and median nerve conduction velocities [27]. Methylcobalamin was also shown to be effective in the treatment of diabetic neuropathy at oral doses of 500 mg; treatment resulted in improvement in pain as well as somatosensory and autonomic symptoms [28,29].…”

Section: Discussionmentioning

confidence: 99%

Symptomatic improvement in an acute, non-traumatic spine pain model with a combination of uridine triphosphate, cytidine monophosphate, and hydroxocobalamin

Mibielli¹,

Nunes²,

Scussel³

et al. 2014

PST

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Intravenous Methylcobalamin Treatment for Uremic and Diabetic Neuropathy in Chronic Hemodialysis Patients.

Cited by 75 publications

References 11 publications

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Cobalamin-responsive disorders in the ambulatory care setting: unreliability of cobalamin, methylmalonic acid, and homocysteine testing

Symptomatic improvement in an acute, non-traumatic spine pain model with a combination of uridine triphosphate, cytidine monophosphate, and hydroxocobalamin

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