scholarly journals Vitamin B12 deficiency in captive monkeys and its effect on the nervous system and the blood

1970 ◽  
Vol 4 (1) ◽  
pp. 1-12 ◽  
Author(s):  
C. E. Oxnard ◽  
W. Thomas Smith ◽  
I. Torres

Monkeys fed vegetarian diets develop neurological and haematological abnormalities; paralysis can occur though the neural lesions (cerebral degeneration, posterior and lateral column degeneration of the spinal cord, segmental and wallerian degeneration of the peripheral nerves) are usually not evident during life. It is clearly important that the diet given to captive animals should contain an adequate amount of vitamin B12, and that newly captive monkeys should not be used for research purposes unless shown to have normal serum levels of the vitamin.

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Alberto Fragasso ◽  
Clara Mannarella ◽  
Angela Ciancio ◽  
Oronzo Scarciolla ◽  
Nicoletta Nuzzolese ◽  
...  

Background. Measurement of serum cobalamin (Cbl) levels is the standard investigation for assessing vitamin B12 deficiency. Falsely increased values of Cbl can be caused by alcoholic liver disease. Measurement of total vitamin B12 serum levels might be misleading in alcoholics, because a tissue metabolic deficiency is possible even with normal serum Cbl levels. Holotranscobalamin (HoloTC), the Cbl metabolically active fraction, is considered as a better index of vitamin B12 deficiency.Methods. For assessing vitamin B12 status, we evaluated 22 adult alcoholic male patients by measuring in parallel serum Cbl, serum folate and red blood cell folate levels, HoloTC levels by the AxSYM assay.Results. HoloTC values were reduced in 3 alcoholics with borderline-low Cbl values. Significant positive correlations were found between serum Cbl and HoloTC levels, serum Cbl and gamma-glutamyl transpeptidase (GGT).Conclusion. HoloTC measurement is a useful option for assessing vitamin B12 status in alcoholics, particularly in the subjects with borderline Cbl values and may be considered an early marker of vitamin B12 deficiency.


2019 ◽  
Vol 12 (10) ◽  
pp. e232319 ◽  
Author(s):  
Sanjeev Khera ◽  
Suman Kumar Pramanik ◽  
Saroj Kumar Patnaik

Transcobalamin (TC) deficiency is a rare autosomal recessive inborn error of cobalamin transport which clinically manifests in early infancy. We describe a child with TC deficiency who presented with classical clinical and lab stigmata of inborn error of vitamin B12 metabolism except normal serum B12 levels. He was started on empirical parenteral cobalamin supplements at 2 months of age; however, the definitive diagnosis could only be established at 6 years of age when a genetic evaluation revealed homozygous nonsense variation in exon 8 of the TCN2 gene (chr22:g.31019043C>T).


2021 ◽  
Vol 104 (2) ◽  
pp. 003685042110076
Author(s):  
Nazmi Mutlu Karakaş

Background: In this study, the aim was to evaluate the prevalence of vitamin D, vitamin B12, ferritin, and folate deficiencies in adolescence to clarify the need for early diagnosis and therapy. Methods: The medical records of adolescents between 10 and 18 years of age between 01 September 2018 and 28 February 2019 as healthy with non-specific complaints, or due to well-child care visits, were analyzed retrospectively. Results: A total of 1847/2507 (73.6%) adolescents were included in the study. The prevalence of vitamin D deficiency was 25.7% (n: 178/691). Vitamin B12 deficiency prevalence was 69.2% (n: 753/1088). The prevalence of anemia and ferritin deficiency was 4.8% and 13.26%. The prevalence of folate deficiency was 37.9% (n: 413/1088). VDD prevalence was statistically significantly higher in females than males (F/M:116/62). VB12D prevalence, the number and mean age of females with hemoglobin deficiency, and low ferritin levels was found to be statistically significantly higher in females than males. Conclusions: The prevalence of vitamin D, vitamin B12, folate deficiency and low ferritin levels was found to be high among adolescents. In particular, adolescents admitting with non-specific complaints and for control purposes in big cities must be considered to be at risk for the deficiency of these vitamins and low level of ferritin.


2021 ◽  
pp. bmjnph-2020-000193
Author(s):  
Darby Martin ◽  
Jeet Thaker ◽  
Maria Shreve ◽  
Lois Lamerato ◽  
Kartazyna Budzynska

ObjectivesOur study investigated the use of vitamin B12 testing in a large cohort of patients on metformin and assesses appropriateness and benefits of screening recommendations for vitamin B12 deficiency.DesignThis retrospective cohort study included insured adult patients who had more than 1 year of metformin use between 1 January 2010 and 1 October 2016 and who filled at least two consecutive prescriptions of metformin to establish compliance. The comparison group was not exposed to metformin. Primary outcome was incidence of B12 deficiency diagnosed in patients on metformin. Secondary outcome was occurrence of B12 testing in the patient population on metformin. Records dated through 31 December 2018 were analysed.SettingLarge hospital system consisting of inpatient and outpatient data base.ParticipantsA diverse, adult, insured population of patients who had more than 1 year of metformin use between 1 January 2010 and 1 October 2016 and who filled at least two consecutive prescriptions of metformin.ResultsOf 13 489 patients on metformin, 6051 (44.9%) were tested for vitamin B12 deficiency, of which 202 (3.3%) tested positive (vs 2.2% of comparisons). Average time to test was 990 days. Average time to test positive for deficiency was 1926 days. Factors associated with testing were linked to sex (female, 47.8%), older age (62.79% in patients over 80 years old), race (48.98% white) and causes of malabsorption (7.11%). Multivariable logistic regression showed older age as the only factor associated with vitamin B12 deficiency, whereas African-American ethnicity approached significance as a protective factor.ConclusionsBased on our study’s findings of vitamin B12 deficiency in patients on metformin who are greater than 65 years old and have been using it for over 5 years, we recommend that physicians consider screening in these populations.


Author(s):  
Ralph Green ◽  
Joshua W. Miller

AbstractPrevalence rates for folate deficiency and hyperhomocysteinemia have been markedly reduced following the introduction of folic acid fortification in the United States. We report the prevalence of hyperhomocysteinemia in a population of community-dwelling elderly Latinos in the post-folic acid fortification era. We measured homocysteine, total vitamin B


2018 ◽  
Vol 49 (2) ◽  
pp. 143-144
Author(s):  
Ashok Kumar Pannu ◽  
Dinesh Raja Palanisamy

A combination of anaemia and knuckle pigmentation should always raise concern for megaloblastic anaemia. As the terminal ileum is the site of vitamin B12 absorption and also the commonest site of abdominal tuberculosis, a clinical triad of prolonged fever, knuckle pigmentation and right lower quadrant abdominal tenderness should suggest ileocaecal tuberculosis in endemic areas.


Author(s):  
Nishant Kumar Singh ◽  
Hirni J. Patel ◽  
Mohit Buddhadev ◽  
S P Srinivas Nayak ◽  
Gunosindhu Chakraborthy

Peripheral nerves are susceptible to damage by a wide array of toxins, medications, and vitamin deficiencies. Vitamin B12 (VB12) deficiency neuropathy is a rare debilitating disease that affects mostly the elderly. It is important to consider these etiologies when approaching patients with a variety of neuropathic presentations in this review were have included most relevant and latest information on mechanisms causing Peripheral neuropathy in VB12 deficiency. We also have included cardiovascular disorders and their management. Hyperhomocysteinemia has been implicated in endothelial dysfunction and cardiovascular disease. The association of homocysteine (Hcy) and VB12 with cardiovascular risk factors in patients with coronary artery disease (CAD) has also been studied Keywords: Peripheral Neuropathy, Vitamin B12 Deficiency, Cardiovascular Disease and Homocysteine.


Author(s):  
Saskia LM van Loon ◽  
Anna M Wilbik ◽  
Uzay Kaymak ◽  
Edwin R van den Heuvel ◽  
Volkher Scharnhorst ◽  
...  

Background Methylmalonic acid (MMA) can detect functional vitamin B12 deficiencies as it accumulates early when intracellular deficits arise. However, impaired clearance of MMA from blood due to decreased glomerular filtration rate (eGFR) also results in elevated plasma MMA concentrations. Alternative to clinical trials, a data mining approach was chosen to quantify and compensate for the effect of decreased eGFR on MMA concentration. Methods Comprehensive data on patient’s vitamin B12, eGFR and MMA concentrations were collected ( n = 2906). The relationship between vitamin B12, renal function (eGFR) and MMA was modelled using weighted multiple linear regression. The obtained model was used to estimate the influence of decreased eGFR on MMA. Clinical impact was examined by comparing the number of patients labelled vitamin B12 deficient with and without adjustment in MMA. Results Adjusting measured MMA concentrations for eGFR in the group of patients with low-normal vitamin B12 concentrations (90–300 pmol/L) showed that the use of unadjusted MMA concentrations overestimates vitamin B12 deficiency by 40%. Conclusions Through a data mining approach, the influence of eGFR on the relation between MMA and vitamin B12 can be quantified and used to correct the measured MMA concentration for decreased eGFR. Especially in the elderly, eGFR-based correction of MMA may prevent over-diagnosis of vitamin B12 deficiency and corresponding treatment.


2012 ◽  
Vol 4 (2) ◽  
pp. 326-328
Author(s):  
M Wadhwani ◽  
S Beri ◽  
A Saili ◽  
S Garg

Background: Homocystinuria is a rare metabolic disorder charcterised by excess homocysteine in the urine. Vitamin B12 deficiency has diverse cutaneous, nervous and ophthalmic manifestations. Objective: To report a case of homocystinuria masquerading as vitamin B 12 deficiency. Case: We hereby are presenting an interesting case of a 4 year old boy who was being treated for Vitamin B 12 deficiency on the basis of history of delayed milestone, abdominal pain and hyperpigmentation of skin which was diagnosed as homocystinuria. Conclusion: It is important to carry out ophthalmological examination in every case of megaloblastic anemia if associated with blurring of vision and mental retardation.DOI: http://dx.doi.org/10.3126/nepjoph.v4i2.6554 Nepal J Ophthalmol 2012; 4 (8): 326-328


2008 ◽  
Vol 99 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Shuhei Ebara ◽  
Motoyuki Nakao ◽  
Mayuko Tomoda ◽  
Ryoichi Yamaji ◽  
Fumio Watanabe ◽  
...  

The aim of the present study was to elucidate the mechanism of the vitamin B12 deficiency-induced changes of the serine dehydratase (SDH) and tyrosine aminotransferase (TAT) activities in the rat liver. When rats were maintained on a vitamin B12-deficient diet, the activities of these two enzymes in the liver were significantly reduced compared with those in the B12-sufficient control rats (SDH 2·8 (sd 0·56) v. 17·5 (sd 6·22) nmol/mg protein per min (n 5); P < 0·05) (TAT 25·2 (sd 5·22) v. 41·3 (sd 8·11) nmol/mg protein per min (n 5); P < 0·05). In the B12-deficient rats, the level of SDH induction in response to the administration of glucagon and dexamethasone was significantly lower than in the B12-sufficient controls. Dexamethasone induced a significant increase in TAT activity in the primary culture of the hepatocytes prepared from the deficient rats, as well as in the cells from the control rats. However, a further increase in TAT activity was not observed in the hepatocytes from the deficient rats, in contrast to the cells from the controls, when glucagon was added simultaneously with dexamethasone. The glucagon-stimulated production of cAMP was significantly reduced in the hepatocytes from the deficient rats relative to the cells from the control rats. Furthermore, the glucagon-stimulated adenylyl cyclase activity in the liver was significantly lower in the deficient rats than in the controls. These results suggest that vitamin B12 deficiency results in decreases in SDH and TAT activities correlated with the impairment of the glucagon signal transduction through the activation of the adenylyl cyclase system in the liver.


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