scholarly journals Sensory Neuronopathy Revealing Severe Vitamin B12 Deficiency in a Patient with Anorexia Nervosa: An Often-Forgotten Reversible Cause

Nutrients ◽  
2017 ◽  
Vol 9 (3) ◽  
pp. 281 ◽  
Author(s):  
Jérôme Franques ◽  
Laurent Chiche ◽  
Stéphane Mathis
Keyword(s):  
Anorexia Nervosa ◽  
Vitamin B12 ◽  
Vitamin B12 Deficiency ◽  
Sensory Neuronopathy ◽  
Severe Vitamin ◽  
B12 Deficiency

scholarly journals Severe Vitamin B12 Deficiency in Pregnancy Mimicking HELLP Syndrome

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Shravya Govindappagari ◽  
Michelle Nguyen ◽  
Megha Gupta ◽  
Ramy M. Hanna ◽  
Richard M. Burwick
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Thrombotic Microangiopathy ◽  
Hellp Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Elevated Liver Enzymes ◽  
B12 Deficiency ◽  
In Pregnancy

Severe vitamin B12 deficiency may present with hematologic abnormalities that mimic thrombotic microangiopathy disorders such as hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We report a patient diagnosed with severe vitamin B12 deficiency, following termination of pregnancy for suspected preeclampsia and HELLP syndrome at 21 weeks’ gestation. When hemolysis and thrombocytopenia persisted after delivery, testing was performed to rule out other etiologies of thrombotic microangiopathy, including atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and vitamin B12 deficiency. This work-up revealed undetectable vitamin B12 levels and presence of intrinsic factor antibodies, consistent with pernicious anemia. Parenteral B12 supplementation was initiated, with subsequent improvement in hematologic parameters. Our case emphasizes the importance of screening for B12 deficiency in pregnancy, especially in at-risk women with unexplained anemia or thrombocytopenia. Moreover, providers should consider B12 deficiency and pernicious anemia in the differential diagnosis of pregnancy-associated thrombotic microangiopathy.

scholarly journals Life-threatening Pseudo-thrombotic Microangiopathy Caused by Severe Vitamin B12 Deficiency

2021 ◽  
Vol 9 (11) ◽  
pp. 532-534
Author(s):  
Ziad Abuhelwa ◽  
Talal Khan ◽  
Rana Daas ◽  
Sami Ghazaleh ◽  
Ragheb Assaly
Keyword(s):  
Vitamin B12 ◽  
Thrombotic Microangiopathy ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Life Threatening ◽  
B12 Deficiency

Chronic diarrhea in a patient with severe vitamin B12 deficiency: a rare clinical manifestation

2016 ◽  
Vol 51 (6) ◽  
pp. 763-764 ◽  
Author(s):  
Antonio Mirijello ◽  
Carla Vallone ◽  
Salvatore De Cosmo ◽  
Raffaele Landolfi ◽  
Giovanni Addolorato
Keyword(s):  
Vitamin B12 ◽  
Clinical Manifestation ◽  
Chronic Diarrhea ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
B12 Deficiency

scholarly journals Folic acid metabolism in vitamin B12-deficient sheep. Depletion of liver folates

1973 ◽  
Vol 136 (2) ◽  
pp. 279-293 ◽  
Author(s):  
Richard M. Smith ◽  
William S. Osborne-White
Keyword(s):  
Urinary Excretion ◽  
Vitamin B12 ◽  
Acid Metabolism ◽  
Vitamin B12 Deficiency ◽  
Deficient Diet ◽  
Severe Vitamin ◽  
Quantitative Estimates ◽  
Folic Acid Metabolism ◽  
B12 Deficiency ◽  
Microbiological Assays

1. Metabolism of folate was studied in six ewes in an advanced state of vitamin B12 deficiency as judged by voluntary food intake and in their pair-fed controls receiving vitamin B12. A group of four animals that were maintained throughout the experiment at pasture was also studied. 2. After 34–40 weeks on the cobalt-deficient diet urinary excretion of formiminoglutamate by four deficient animals was about 3.2mmol/day and this was not significantly decreased by injection of three of them with about 4.5μg of [2-14C]folate/kg body weight per day for 5 days. Three days after the last injection retention of [2-14C]folate by the livers of the deficient animals (5.5% of the dose) was lower than that of their pair-fed controls (26% of the dose) but there was no evidence of net retention of injected folate in the livers of either group. Urinary excretion of 14C indicated that renal clearance of folate may have been impaired in very severe vitamin B12 deficiency. 3. As estimated by microbiological assays total folates in the livers of animals at pasture (12.9μg/g) included about 24% of 5-methyltetrahydrofolate as compared with about 72% of a total of 12.5μg/g in three further ewes fed on a stock diet of wheaten hay-chaff and lucerne-chaff. Liver folates of vitamin B12-deficient animals (0.5μg/g) included about 88% of 5-methyltetrahydrofolate as compared with about 51% of a total of 5.2μg/g in pair-fed animals treated with vitamin B12. 4. Chromatography of liver folates of the pair-fed animals permitted quantitative estimates of the pteroylglutamates present. The results showed that the vitamin B12-deficient livers were more severely depleted of tetrahydrofolates and formyltetrahydrofolates than of methyltetrahydrofolates and that as the deficiency developed they were more severely depleted of the higher polyglutamates than of the monoglutamate within each of these classes. Results from animals injected with [2-14C]folate indicated an impairment of the exchange between pteroylmonoglutamates and pteroylpolyglutamates in the livers of deficient animals. 5. In vitamin B12-deficient animals with food intakes below 200g/day some of the liver folates were not completely reduced and some degradation of pteroylpolyglutamates was detected. The latter condition may have been associated with fatty liver. 6. The results are discussed in relation to current theories of vitamin B12–folate interactions.

Neuropathic Bladder in Setting of Severe Vitamin B12 Deficiency

1995 ◽  
pp. 199-200 ◽  
Author(s):  
Joseph V. Campellone ◽  
Thomas M. Bosley ◽  
Terrence R. Malloy
Keyword(s):  
Vitamin B12 ◽  
Vitamin B12 Deficiency ◽  
Neuropathic Bladder ◽  
Severe Vitamin ◽  
B12 Deficiency
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