Prevalence of Iron,
Folate, and Vitamin B12 Deficiency Anemia after Laparoscopic
Roux-en-Y Gastric Bypass
Vargas-Ruiz AG, et al.
Obes Surg, 2008 Jan 23; [Epub ahead of print]
One of the most common bariatric operations is the
laparoscopic Roux-en-Y gastric bypass (LRYGBP) in which the
gastric capacity is restricted and the absorption by the
small intestine is reduced. The objective of this study was
to
evaluate the incidence of iron, folate, and vitamin B12
deficiency anemia in patients undergoing LRYGBP. Clinical
records of 30 patients who underwent LRYGBP between July
2003 and January 2005 and had a minimum follow up of
24 months at our outpatient clinic were included.
Multivitamin supplementation was prescribed to all patients.
The
complete blood cell count, plasma iron, total iron-binding
capacity, transferrin saturation, serum folate, and
cobalamin
levels before surgery, 6 months, 1, 2, and 3 years after the
surgery were analyzed. There were 25 women (83.4%) and
five men (16.6%) with ages from 21 to 56 years. Before
surgery, two patients (6.6%) presented ferropenic anemia.
Iron
deficiency was seen in 40 and 54.5% 2 and 3 years after
surgery, respectively. Cobalamin deficiency was observed in
33.3% at 2 years and in 27.2% at 3 years. At 2-year
follow-up, 46.6% of the patients had already developed
anemia and63.6% at 3 years. Folate deficiency was not
observed in any patient. Our routine scheme of vitamin
supplementation isnot sufficient to prevent iron and vitamin
B12 deficiencies in most patients.
Dietary Zinc
Supplementation during Pregnancy Prevents Spatial and Object
Recognition Memory Impairments Caused by Early Prenatal
Ethanol Exposure
Summers BL, et al.
Behav Brain Res, 2008 Jan 25 ;186(2) :230-8.
Alcohol-induced zinc (Zn) deficiency is one of the
mechanisms proposed as a cause of ethanol teratogenicity.
Subcutaneous Zn treatment with ethanol in early pregnancy
has been shown to prevent birth abnormalities and memory
impairments in mice. This study examined whether dietary Zn
supplementation throughout pregnancy can prevent cognitive
impairments caused by early ethanol exposure. Pregnant
C57BL/6J mice were fed either a control (35 microg Zn/g) or
Zn-supplemented (200 microg Zn/g) diet throughout pregnancy.
On gestational day (GD) 8 mice received two intraperitoneal
injections (4h apart) of either saline or 25% ethanol (0.015
mL/g). All offspring were screened for physical and
behavioral defects (e.g. growth, visual, exploratory,
anxiety, motor deficits). Twenty-four phenotypicallynormal
offspring were randomly selected from each of the four
treatment groups (saline +/- Zn-supplementation, ethanol +/-
Zn supplementation) and tested at 60 d of age using a
cross-maze escape task for spatial learning and memory
impairments, and an object recognition task. While no
differences were observed between treatments for spatial
learning, offspring exposed to ethanol demonstrated spatial
memory impairments at both 12 and 28 d after learning an
escape task, with less correct trials and increased escape
latency scores compared with saline-treated mice.
Furthermore, these mice also exhibited impairments in object
recognition memory. In comparison, ethanol-exposed
offspring from dams fed a Zn-supplemented diet throughout
pregnancy did not display spatial memory or object
recognition deficits, performing at the same level as
saline-treated offspring. Therefore, dietary
Zn-supplementation
during pregnancy prevents spatial and object recognition
memory impairments caused by ethanol exposure during early
pregnancy.
Hypocupremia and Bone Marrow Failure
Haddad AS, et al.
Haematologica, 2008 Jan ; 93(1) :e1-5.
Copper deficiency associated
with neurological disorders is a well documented condition.
However,
hypocupremia is less often recognized as a cause of
cytopenias or bone marrow failure. We report an illustrative
series of three new cases of bi-lineage cytopenia associated
with copper deficiency. We have analyzed clinical
features of current and historical cases to identify clues
that could facilitate application of appropriate laboratory
testing and heighten the level of clinical suspicion. By
maintaining an appropriately high level of suspicion for
potential copper deficiency and obtaining a serum copper
level, bone marrow failure due to this condition can be
correctly diagnosed and treated. We suggest that copper
deficiency be included in the differential diagnosis of
reversible causes of bone marrow failure syndromes including
myelodysplastic syndrome.
Magnesium in
Skin Allergy
Błach J, et al.
Postepy Hig Med Dosw ; 2007 Oct 8 ;61 :548-54 (article in
Polish).
Magnesium is involved in many biological processes within
the body. Magnesium deficiency causes many disorders,
including impairment of immunity. This review summarizes
present knowledge on the relationship between magnesium
and skin allergy reactions. Special focus is on allergy
types I and IV. At present the best knowledge is on allergy
1.
Magnesium deficiency in experimental animals, mainly rats,
leads to characteristic hyperemia, an increase in IgE,
neutrophilia and eosinophilia, an increase in the level of
proinflammatory cytokines, mastocyte degranulation,
histaminemia, and splenomegaly. These symptoms observed in
hypomagnesemic rats are similar to those in atopic
patients. Data on the relationship between magnesium and
other types of allergy are scarce. Clinical observations
show the beneficial effect of topical and oral
administration of magnesium salts in patients with skin
allergy. All the presented data point to an important role
of magnesium in allergy reactions. Other studies are needed
to better understand the mechanism of magnesium's action.
Well-controlled clinical protocols should also be conducted
to assess the efficiency of magnesium supplementation in
patients with skin allergy.
Prevention of Upper Aerodigestive Tract Cancer in
Zinc-Deficient Rodents:
Inefficacy of Genetic or Pharmacological Disruption of
COX-2
Fong LY, et al .
Int J Cancer ; 2008 Mar 1 ;122(5) :978-89.
Zinc deficiency in humans is associated with an
increased risk of upper aerodigestive tract (UADT)
cancer. In rodents,
zinc deficiency predisposes to carcinogenesis by causing
proliferation and alterations in gene expression. We
examined whether in zinc deficient rodents, targeted
disruption of the cyclooxygenase (COX)-2 pathway by the
COX-2 selective inhibitor celecoxib or by genetic
deletion prevent UADT carcinogenesis. Tongue cancer
prevention studies were conducted in zinc-deficient rats
previously exposed to a tongue carcinogen by celecoxib
treatment with or without zinc replenishment, or by zinc
replenishment alone. The ability of genetic COX-2
deletion to protect against chemicallyinduced
forestomach tumorigenesis was examined in mice on zinc
deficient versus zinc-sufficient diet. The expression of
3 predictive biomarkers COX-2, nuclear factor (NF)-kappa
B p65 and leukotriene A(4) hydrolase (LTA(4)H) was
examined by immunohistochemistry. In zinc-deficient
rats, celecoxib without zinc replenishment reduced
lingual tumor multiplicity but not progression to
malignancy. Celecoxib with zinc replenishment or zinc
replenishment alone significantly lowered lingual
squamous cell carcinoma incidence, as well as tumor
multiplicity. Celecoxib alone reduced overexpression of
the 3 biomarkers in tumors slightly, compared with
intervention with zinc replenishment. Instead of being
protected, zinc-deficient COX-2 null mice developed
significantly greater tumor multiplicity and forestomach
carcinoma incidence than wild-type controls.
Additionally, zinc deficient COX-2-/- forestomachs
displayed strong LTA(4)H immunostaining, indicating
activation of an alternative pathway under zinc
deficiency when the COX-2
pathway is blocked. Thus, targeting only the COX-2
pathway in zinc-deficient animals did not prevent UADT
carcinogenesis. Our data suggest zinc supplementation
should be more thoroughly explored in human prevention
clinical trials for UADT cancer. (c) 2007 Wiley-Liss,
Inc.
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