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Thiamin (B1) (Aneurine) :
Its stable in hot acid solution but rapidly
destroyed by heat in neutral or alkaline
solutions .
Functions:
1. Oxidative decarboxylations of αketoacids (e.g α-ketoglutarate,
pyruvate, and the α-keto analogs of
leucine, isolleucine and valine).
2. Transketolase reactions ( e.g in the
pentose phosphate pathway
After absorption of thiamin in the jejunum and ileum, thiamin
is phosphorelated to active form which is thiamin
pyrophosphate(TPP) which is coenzyme involved in
decarboxylation of pyruvate(end product of glycolysis) to
Acetyl coA .
Also thiamin diphosphate cooperate in biosynthesis of
branched A.A such as leucine, isoleucine and valine).
The active form of thiamin ,thiamin pyrophosphate(TPP) also
involved in transketolation which occur in pentose-phosphate
cycle which an important direct oxidative pathway in
metabolism of glucose in RBC .
In neurological cell and myelinated structure of nervous
system, failure in transketolation lead to accumulation of
pentose-5-phosphate substrate energy, metabolism of CNS is
mostly dependent upon CHO, this explain neurological
disorders associated with thiamin deficiency .
Thiamine's biologic half-life is approximately 10 to 20 days; due to limited
tissue storage, continuous supplementation is required . Thiamine and all
of its metabolites are excreted in the urine. Losses depend on cooking
method, length, alkalinity of cooking medium
Deficiency :Thiamine deficiency has been associated with three disorders:
1-Beriberi (infantile and adult)
There are two major types of beriberi:
Wet beriberi affects the cardiovascular system.
Dry beriberi affect the nervous system.
If you eat a normal, healthy diet, you should get enough thiamine. Today,
beriberi occurs mostly in patients who abuse alcohol. Drinking heavily can
lead to poor nutrition, and excess alcohol makes it harder for the body to
absorb and store thiamine. Beriberi can occur in breast-fed infants when
the mother's body is lacking in thiamine. The condition can also affect
infants who are fed unusual formulas that don't have enough thiamine.
Getting dialysis and taking high doses of diuretics raise your risk of
beriberi
2-Wernicke-Korsakoff syndrome &
3-Leigh's syndrome
Infantile beriberi — becomes clinically apparent between the ages
of two and three months. The infant becomes Buffy and edematous
with diminution of urine excretion with tenderness of muscles .
These signs may developed to a fulminant cardiac failure with
cardiomegaly, tachycardia, cyanosis, dyspnea, convulsion, coma
,death ,within 24-48 hours .
Adult beriberi — Adult beriberi is described as dry (neurological) or
wet (cardiac).
Dry beriberi: Is called dry because of absence of edema or edema is
less obvious, is the chronic form of the disease & is characterized by
progressive, peripheral neuropathy due to continuous and milder
thiamin deficiency, poly neuropathy is bilateral and symmetrical
with involvement of motor and sensory nerve fibers resulting in
ankle drop, wrist drop, loss of tendon reflexes and parasthesia. Foot
drop is accompanied by loss of sensation in the feet & absent knee
jerk reflexes.
Wet beriberi : this type characterized by appearance of non-specific fever,
anorexia and constipation with increase of muscles tenderness and
weakness, parasthesia are common, tendon reflexes are usually present
and may be exaturated, the rapidly increasing edema extend from leg to
trunk and face with pericardial , plural and other serous effusions .
is the acute form of the disease& is cc. by high output cardiac failure ,
bounding pulse , warm extremities, peripheral edema, and cardiac
palpitation.
•Wernicke-Korsakoff syndrome :
•Is exclusively seen in chronic alcoholics who have a poor thiamin diet, it
characterized by: confusion (low level of consciousness), ataxia (poor
coordination), ophthalmoplegia and nystagmus due to paralysis of one or
more of the external movement of the eyes which is a diagnostic criteria.
Korsakoffs psychosis is impaired short term memory often follows
encephalopathy(amnesia).
•Leigh's syndrome : Leigh's subacute necrotizing encephalomyopathy It is
manifested with ataxia, dysarthria, movement disorders, muscle atrophy,
and weakness.
Diagnosis of beriberi :
•Glucose load test: The rise in fasting pyruvate
following a loading dose of 100 mg of glucose.
This test non specific to thiamin deficiency
because The blood pyruvate increase in other
conditions besides thiamin deficiency including
severe heart failure, and other causes of
anoxemia.
•Erythrocyte-Transketolase test : is more
sensitive than first test .
•Urinary excretion of thiamin : its unreliable
diagnostic test but is useful to assessment of
thiamin nutrition for populations .
Treatment of beriberi : should be urgently in case of wet
beriberi .
•Complete rest in bed
•Parenteral thiamin (I.M injection) is given immediately,
the dose is 25 mg twice daily for 3 days .
•In extreme cases, the dose is 100 mg for life saving .
•The maintain therapy is 10 mg trice daily should be
given until recovery .
•Toxicity : there is no toxicity of vitamin B1 even in large
doses since the kidneys can rapidly clear almost all
excess thiamine, but anaphylaxis could occur after
sensitization through injection of vitamin B1 .
RDA : average daily intake 2mg/day for men & 1.54
mg/day for woman
•Some conditions may need extra vitamin B1:
• increase physical activity, pregnancy, lactation, Fever, hyperthyroidism .
•Good food sources :
Rich: pork
Important: cereals, grains, beans
•Prognosis :Untreated, beriberi is often deadly. With treatment, symptoms usually
improve quickly. Heart damage is usually reversible, and a full recovery is
expected. However, if acute heart failure has already occurred, the outlook is
poor. Nervous system damage is also reversible, if caught early. If it is not
caught early, some symptoms (such as memory loss) may remain even with
treatment.
•Prevention :1-Eating a proper diet that is rich in thiamine and other vitamins will prevent
beriberi.
2-Nursing mothers should make sure that their diet contains all vitamins and
be sure that infant formulas contain thiamine.
3-People who drink heavily should try to cut down or quit, and take B
vitamins to make sure their body is properly absorbing and storing thiamine.
vitamin B2 (Riboflavin) :
its destroyed under alkaline conditions , by heat, and by exposure to
sunlight . Because riboflavin is destroyed by exposure to light, foods
with riboflavin should not be stored in glass containers that are
exposed to light.
Levels are low in staple cereals but germination increases its content.
FUNCTION :
• promotion of normal growth .
•assist synthesis of steroid , red blood cell and glycogen
• maintenance of mucous membranes , skin , eyes and nervous system
•aiding Fe absorption
Deficiency :
1-Lesions of the mucosal surfaces of mouth(lesion of lips)
2- chelliosis :angular stomatitis (Cracks at corners of mouth); ,
3-Glossitis(Magenta tongue),
4-Localized seborrhoeic dermatitis , and follicular keratosis, vascularization of the
cornea . surface lesions of genitalia,
Diagnosis of vitamin B2 deficiency :
•Urinary excretion is generally used as guide to riboflavin
intake in nutritional survey of populations group. This
test is of a little diagnostic value .
Treatment of vitamin B2 deficiency :
in case of deficiency of vitamin B2 we give B- complex in
addition to B2 .
food sources of Riboflavin :
Rich: milk
Important: milk products, breakfast cereals, bread .
Toxicity is not reported and Average daily intake :
•men is 2.1mg\day &
•female 1.6mg\day
Vitamin B3 NIACIN
(nicotinamide , nicotinic acid, pellagra-preventing factor(PPF)
Function :
is a nontoxic component of the toxic alkaloid nicotine of
tobacco ,promotes healthy skin and nerves, synthesis of
insulin, sex hormones, cortisone, and thyroxin
.nicotinamide is an essential part of the two pyridine
nucleotides, nicotinamide adenine dinucleotide (NAD)
and nicotinamide adenine dinucleotide phosphate
(NADP), which are essential in all cells for energy
production and metabolism. NADH and NADPH are
the reduced forms of NAD and NADP; they carry a
hydrogen ion. .
Niacin can be synthesized in the body in limited
amounts from the amino acid tryptophan.
Tryptophan
B6
niacin
Niacin in many foods, particularly those from
animal sources, consists mostly of the coenzyme
forms NAD and NADP, each of which must be
digested to release the absorbed forms
(nicotinamide
and
nicotinic
acid)
,The
physiological active form is nicotinamide
Many foods derived from plants, particularly
grains( corn), contain niacin in covalently bound
complexes with small peptides and carbohydrates
that are not released during digestion. These
forms (niacytin) are not biologically available but
can become bioavailable through alkaline
hydrolysis. Thus the Central American tradition of
soaking maize in lime water to increases the
bioavailability of niacin in what otherwise would
be considered a low niacin food.
Note:
the protein of the corn is called (maize) which is
free tryptophan or low niacin food.
•Deficiency :
An inability to absorb niacin or the amino acid tryptophan may
cause pellagra, a disease characterized by scaly sores(dermatitis),
mucosal
changes
(diarrhea),
and
mental
symptoms
(dementia).pathologically the clinical signs that occur in skin and
mucous membrane also occur in the gut from mouth to anus,
similar conditions occur in vulva and vagina in addition there is non
specific scattered lesions of nervous system especially
demyelination of spinal cord. In endemic area pellagra tend to be
seasonal .
Etiology of pellagra :
pellagra is a disease of poverty caused by multiple deficiency of
protein and vitamins especially those of vitamin B group and
predominantly of niacin . secondary pellagra occur with alcoholism,
malabsorption syndrome, low-protein diet intake and in case of
treatment of T.B by INH drug which is antagonist to vitamin B6 and
hence interfere with conversion of tryptophan to niacin .
Pellagra is caused by
• having too little niacin or tryptophan in the diet.
•It can also occur if the body fails to absorb these nutrients.
•It may develop after gastrointestinal diseases
•or with alcoholism.
•The disease is common in parts of the world where people have
a lot of corn in their diet.
clinical features of pellagra :
typical dermatitis : when it appear its diagnostic, is localized in
area exposed to sunlight start as an itching, burning sensation on
skin, and erythema, skin may vesiculated and ulcerated and
becomes infected, in chronic pellagra, skin becomes thick, rough,
dry and pigmented.
Stomatitis, glossitis, and urogenital
syndrome with painful inflammation. Diarrhea also occur and
responsible for more malnutrition. Mental symptoms include
depression and there is excitement of patient, confusion and
delirium.
Treatment : specific treatment by nicotinamide with
improvement in diet especially protein energy .
Multivitamins treatment for non specific conditions . nicotinamide
in 300-500 mg/day lead to dramatic improvement within 24 hours
,treatment should be continue for 7 days followed by multivitamin
preparation .
Toxicity of niacin :
Large therapeutic doses of niacin lead to transient vasodilatation
with flushing , feeling warmth, redness, itching or tingling of the
face, neck, arms or upper chest .
RDA :
•
15 - 20 mg per day for adult males,
•and 13 - 15 mg per day for adult females
Food sources :
Protein foods containing tryptophan, in addition to whole grain,
cereals, legumes, leafy green vegetables, meat and dairy products .