1: Am Fam Physician
Oh RC, Brown DL.
Army Health Clinic,
Darmstadt, Germany and USA, Madigan Army Medical Center, Fort Lewis,
Vitamin B12 (cobalamin)
deficiency is a common cause of macrocytic anemia and has been implicated
in a spectrum of neuropsychiatric disorders. The role of B12 deficiency in
hyperhomocysteinemia and the promotion of atherosclerosis is only now
being explored. Diagnosis of vitamin B12 deficiency is typically based on
measurement of serum vitamin B12 levels; however, about 50 percent of
patients with subclinical disease have normal B12 levels. A more sensitive
method of screening for vitamin B12 deficiency is measurement of serum
methylmalonic acid and homocysteine levels, which are increased early in
vitamin B12 deficiency. Use of the Schilling test for detection of
pernicious anemia has been supplanted for the most part by serologic
testing for parietal cell and intrinsic factor antibodies. Contrary to
prevailing medical practice, studies show that supplementation with oral
vitamin B12 is a safe and effective treatment for the B12 deficiency
state. Even when intrinsic factor is not present to aid in the absorption
of vitamin B12 (pernicious anemia) or in other diseases that affect the
usual absorption sites in the terminal ileum, oral therapy remains
2: Clin Lab Med 2002
approaches to the investigation of vitamin B12 deficiency.
Department of Pathology and
Laboratory Medicine, University of Minnesota, Duluth School of Medicine,
10 University Drive, Duluth, MN 55812, USA. email@example.com
The classic workup of a
patient for possible PA is revisited in light of the vanishing Schilling
test. The vagaries of testing for B12 and blocking antibodies are
reexamined. The advantages and disadvantages of newer tests such as MMA
and serum gastrin levels are catalogued. At this juncture in the evolution
of new test strategies, there is a considerable controversy regarding the
significance of high MMA levels in the face of normal B12 levels,
particularly in the elderly. Hopefully, this controversy will soon be
resolved and the newer crop of tests will be proven and accepted in the
workplace. Still, the words of Alexander Pope spring to mind: "Be not the
first by whom the new are tried, Nor yet the last to lay the old aside."
3: Ann Pharmacother 2002
of vitamin b(12)-deficiency anemia: oral versus parenteral therapy.
Lane LA, Rojas-Fernandez C.
College of Pharmacy, The
University of Oklahoma Health Sciences Center, Norman Regional Hospital,
Norman, OK, USA. firstname.lastname@example.org
OBJECTIVE: To evaluate the
use of oral cyanocobalamin therapy in the treatment of cobalamin (vitamin
B(12))-deficient anemia. DATA SOURCES: Primary and review articles were
identified by MEDLINE search (1966-May 2000) and through secondary
sources. DATA SYNTHESIS: Cobalamin-deficient anemia is among the most
common diagnoses in older populations. Cobalamin-deficient anemia may be
diagnosed as pernicious anemia, resulting from the lack of intrinsic
factor required for cobalamin absorption or as protein malabsorption from
the inability to displace cobalamin from protein food sources. Several
studies provide evidence that daily oral cyanocobalamin as opposed to
monthly parenteral formulations may adequately treat both types of
cobalamin-deficient anemias. CONCLUSIONS: Daily oral cyanocobalamin at
doses of 1000-2000 microg can be used for treatment in most cobalamin-deficient
patients who can tolerate oral supplementation. There are inadequate data
at the present time to support the use of oral cyanocobalamin replacement
in patients with severe neurologic involvement.
4: Neurology 2002 May
B12 deficiency can occur in women of child bearing age supplemented with
Drazkowski J, Sirven J, Blum
Department of Neurology
Comprehensive Epilepsy Program, Mayo Clinic, Scottsdale,
AZ 85259, USA. email@example.com
5: Adv Exp Med Biol
vitamin B-12 deficiency during lactation on maternal and infant health.
Department of Nutrition,
University of California, Davis 95616, USA.
6: Mayo Clin Proc 2002
completo en formato PDF]
myelopathy in a 34-year-old man with vitamin B12 deficiency.
Pittock SJ, Payne TA, Harper
Department of Neurology, Mayo
Clinic, Rochester, Minn 55905, USA. firstname.lastname@example.org
Vitamin B12 deficiency is
common, with most patients lacking classic features of advanced severe
deficiency. Early diagnosis and treatment prevent severe anemia and
irreversible damage to the nervous system. We describe a 34-year-old man
with pernicious anemia who presented with clinical and radiologic features
of early myelopathy and borderline low serum levels of vitamin B12. Prompt
diagnosis based on the measurement of serum methylmalonic acid and
treatment with cyanocobalamin injections led to rapid resolution of
clinical manifestations and magnetic resonance imaging abnormalities. We
review the literature of magnetic resonance imaging in vitamin B12
deficiency myelopathy and discuss the issues relating to diagnosis and
early treatment of this potentially reversible condition.
7: Postgrad Med 2001
Jul;110(1):99-105; quiz 106
to vitamin B12 deficiency. Early treatment may prevent devastating
Dharmarajan TS, Norkus EP.
Division of Geriatrics, Our
Lady of Mercy Medical Center, 4141 Carpenter Ave, Bronx, NY 10466, USA.
Vitamin B12 deficiency is a
common problem that affects the general population and the elderly in
particular. Persons with the deficiency may be asymptomatic or may have
hematologic or neuropsychiatric signs and symptoms. If the disorder is
untreated, complications may cause significant morbidity. In this article,
Drs Dharmarajan and Norkus discuss approaches to screening and diagnosis
as well as the nontoxic, low-cost treatments now available.
8: J Pediatr 2001
deficiency in children and adolescents.
Rasmussen SA, Fernhoff PM,
Division of Birth Defects,
Child Development, and Disability and Health, National Center for
Environmental Health, Atlanta, Georgia, USA.
9: Hematol Oncol Clin North
Am 2000 Oct;14(5):1079-100, viii
and laboratory features and sequelae of deficiency of folic acid (folate)
and vitamin B12 (cobalamin) in pregnancy and gynecology.
Frenkel EP, Yardley DA.
Department of Internal
Medicine, University of Texas Southwestern Medical Center at Dallas, USA.
Classically, deficiency of
folic acid (folate) or vitamin B12 (cobalamin) was recognized by the
presence of a macrocytic anemia resulting from megaloblastic changes in
the bone marrow. A markedly changing paradigm has identified both new
mechanisms for altered folate and cobalamin status and new sequelae and
clinical interrelationships that include altered mechanisms of absorption,
a changing pattern of neurologic deficits, an increased risk of vascular
occlusive lesions, and an important relationship with the mechanisms of
neoplastic transformation. Several of these newer characterizations relate
to issues of neoplasia in the nonpregnant woman and to issues in
pregnancy, such as the potential for developmental abnormalities of the
fetal nervous system.