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CORD BLOOD

CORD BLOOD BANKING – TRANSFUSION, USES, BANKING, INDICATIONS, ADVANTAGES AND DISADVANTAGES OF CORD BLOOD BANKING

CORD BLOOD TRANSFUSION

Cord blood is the blood obtained from placenta and in the attached umbilical cord. Sources of stem cells include bone marrow, peripheral blood, umbilical cord blood, fetal organs and artificially produced human embryos in vitro.

Cord blood is a rich source of multipotent stem cells. They are less likely to mount immunological reactions. Cord blood stem cell infusion is becoming more popular.

Use of blood collected from the umbilical cord after delivery as a source of stem cells has become an established procedure within the past 15 years. Cord blood contains large number of granulocyte-macrophage progenitor stem cells, sufficient enough to re-populate marrows of irradiated subjects. This has paved the way for organized cord blood banking. There are several blood banks undertaking storage and delivery of cord blood, all over the developed countries. There are a few privately-owned cord blood banks in the world. Cord blood can be cryopreserved in the viable state for many years. The services provided include:

1. Use of cord blood as a source of stem cells and

2. Preservation of the cord blood indefinitely for long periods, for use in the same individual if a need for stem cells arises. The donor is charged for this service.

Uses of Cord Blood

1. Allogenic transplant

2. Autologous transplant

3. As a source of multipotent stem cells for reconstitution and repair of damaged tissues such as the heart, after myocardial infarction.

The immunological properties of cord blood stem cells differ from those of adult marrow or peripheral blood.

Cord blood contains a higher proportion of T-cells expressing (C D 45 R A +/ C D 45 R A O) and CD 62 L+. These cells are immunologically naïve and therefore graft versus host disease is less common.

The chemokine receptor C C R5 expressed by Th-1 T lymphocytes is less abundant in cord blood T-cells compared to adult T-cells.

Cord Blood Banking

Pregnant women are recruited as donors after obtaining informed consent, and excluding common communicable diseases. Blood is collected from the placental side of the severed umbilical cord either in utero before the delivery of the placenta or ex-utero after its delivery. Long-term storage is done under temperatures below –180° C and released for use on demand after proper cross-matching.

Indications for Cord Blood Transfusions

a. Stem cell replenishment in hematological malignancies—acute leukemias, chronic myeloid leukemia and myelodysplastic syndrome.

b. Non-malignant conditions-aplastic anemia, thalassemias, hemoglobinopathies, immunodeficiency states.

ADVANTAGES AND DISADVANTAGES OF CORD BLOOD

Advantages of cord blood are its availability, lower incidence of graft versus host disease (GVHD) and good success rate even if mismatched for two antigens. The waiting period for transplantation is also shorter.

Disadvantages are the higher infection rates with cord blood stem cells, compared to preparations from bone marrow or peripheral blood from adult donors.

Future strategies for improving the service include:

1. Pooling of cord blood

2. Cord blood expansion using cytokines which stimulate stem cell proliferation

3. Combining cord blood and haplo-identical bone marrow transplants

4. Non myeloablative or reduced intensity conditioning regimen.

CORD BLOOD BANKING – TRANSFUSION, USES, BANKING, INDICATIONS, ADVANTAGES AND DISADVANTAGES OF CORD BLOOD BANKING
CORD BLOOD BANKING – TRANSFUSION, USES, BANKING, INDICATIONS, ADVANTAGES AND DISADVANTAGES OF CORD BLOOD BANKING

ZINC AND SELENIUM

ZINC AND SELENIUM – SOURCES, SYNDROME AND SUPPLEMENTS

ZINC

Zinc is present in many enzymes. Highest concentration occurs in the liver, voluntary muscle, bone, prostate, and ocular structures. Foods such as meat, fish, peas and cereals contain zinc. Daily requirement is not clearly known, but is around 15 mg. Dietary deficiency is very rare. Zinc deficiency leads to impairment of maturation and immunodeficiency. In malnourished subjects zinc deficiency may result in thymic atrophy.

A syndrome of dwarfism and hypogonadism seen in Egypt and Iran has been attributed to zinc deficiency. Oral zinc sulphate corrected this clinical picture. Acrodermatitis enteropathica is an inherited disorder resulting from the malabsorption of zinc, probably due to an enzymic defect.

Administration of zinc sulphate 30-150 mg/day results in complete remission. Oral zinc sulphate 100 mg/day has been found to stimulate the growth of granulation tissue in chronic ulcers. Oral supplementation of zinc 10 mg (5mg) in children less than 1 year of age for 16 months reduced overall all-cause mortality by 7%.

SELENIUM

Selenium is a constituent of selanoproteins. It has structural and enzyme roles and it acts as an important antioxidant. It is a catalyst for the production of thyroid hormone. Other functions include: (1) proper functioning of the immune system, (2) sperm motility, (3) maintenance of proper mood and mental state, (4) resistance against cancer. Selenium retards the progress of AIDS. Daily requirement is 400-450 μg/day. Dietary sources include Brazil nuts, kidney, crab, liver, shellfish, fish, meat, poultry, wheat and some vegetables. In animal foods selenium is present as sclenocystine. In vegetable sources it occurs as sclenomethionine.

ZINC AND SELENIUM – SOURCES, SYNDROME AND SUPPLEMENTS
ZINC AND SELENIUM – SOURCES, SYNDROME AND SUPPLEMENTS

YELLOW FEVER

YELLOW FEVER – Etiology, Distribution and Incidence, Distribution and Incidence, Transmission and Epidemiology, Pathogenesis and Pathology, Clinical Features, Diagnosis, Treatment and Prevention

Yellow fever is an acute mosquito-borne infection of varying severity characterized by the triad of hepatitis, hemorrhagic diathesis and proteinuria.

Etiology

The causative virus is an arbo virus belonging to the genus Flavivirus, in the family Flaviviridae.

Distribution and Incidence

Yellow fever is prevalent in many parts of Africa, tropical parts of South America and Panama. The presence of the efficient vector Aedes aegypti mosquitoes and the non-immune population pose a threat of the disease spreading, if the virus is introduced.

Transmission and Epidemiology

Epidemic (urban) yellow fever is transmitted from human to human by Aedes aegypti mosquitoes. Infected monkeys and the vector mosquitoes maintain the reservoir of infection in the jungle. These act as a source of infection when the humans intrude into endemic areas.

Pathology and Pathogenesis

The incubation period after an infectious mosquito bite is 3 to 6 days. Liver and kidneys show maximal lesions but hemorrhage may occur in all organs. Hepatic changes include widespread necrosis, and degeneration of liver cells. Renal changes include acute tubular necrosis and subcapsular hemorrhages. Bleeding diathesis is due to depletion of hepatic clotting factors, intravascular coagulation, and platelet abnormalities. Direct damage to the myocardium, kidneys and other organs and the effects of vasoactive cytokines, lead to fatal complications such as multi-organ failure and shock.

CLINICAL FEATURES

In the majority of cases, the disease is a self limited with fever and myalgia. 25 to 50% of cases may develop the full syndrome with complications such as hemorrhages, jaundice, renal involvement and shock.

The first stage (i.e. period of infection) is due to the direct effect of the virus. It starts abruptly with fever, headache and myalgia. In severe illness there is nausea vomiting, abdominal pain and distressing pain in the back, and limbs. There is relative bradycardia. This stage lasts about 3 days and by 4th day the temperature comes down and the second stage (period of remission) starts.

Many cases recover without going to the third stage. Some progress to the third stage (period of intoxication). It starts after a day or a few days, with resumption of high fever, body pains, nausea, vomiting, abdominal pain and changes in the level of consciousness. Bradycardia, jaundice, wide spread hemorrhages and renal failure may supervene. Death is due to hepatic or renal failure and shock.

Diagnosis

In endemic areas, fever, leukopenia and proteinuria with or without jaundice should suggest the possibility of yellow fever. Specific diagnosis is established by the isolation of the virus from the blood in the first few days of fever or demonstration of rising titer of antibodies in serum.

Treatment

There is no specific antiviral treatment. Symptomatic and supportive measures should be instituted. Hepatic and renal failure has to be anticipated and managed accordingly.

Prevention

Vaccination using live attenuated vaccine (17D strain) is very effective. Vaccination gives immunity starting from ten days and full protection for 10 years. Though side effects are generally negligible, children below 9 months may develop encephalitis. Pregnancy is not a contraindication for vaccination. Many countries insist on yellow fever vaccination for persons entering the country or remaining during transit, if they come from endemic areas. Persons travelling to endemic areas have to take vaccination.

YELLOW FEVER – Etiology, Distribution and Incidence, Distribution and Incidence, Transmission and Epidemiology, Pathogenesis and Pathology, Clinical Features, Diagnosis, Treatment and Prevention
YELLOW FEVER – Etiology, Distribution and Incidence, Distribution and Incidence, Transmission and Epidemiology, Pathogenesis and Pathology, Clinical Features, Diagnosis, Treatment and Prevention

X-linked Inheritance

X-linked Inheritance – Sex Chromosome Related Disorders, X-linked Recessive Inheritance and X-linked Dominant Inheritance

Sex Chromosome Related Disorders

In all females one of the ‘X’ chromosome derived from either parent undergoes inactivation at the early period of gestation, in a random manner governed by the laws of probability Lyon’s hypothesis (1961). Females, therefore contain a mosaic of tissue cells containing either the maternal or the paternal X-chromosome. Inactivation of the X-chromosome is effected by the action of a gene called the X-inactivation specific transcript which is located in the long arm of the X-chromosomes. Since 50% of the X-chromosomes in carrier females are normal, they do not manifest signs of the disease, but male offsprings suffer from the disease.

X-linked Recessive Inheritance

1. There is ‘oblique’ transmission, i.e., in the pedigree a line drawn through the affected persons is oblique.

2. Only males are affected, females are only carriers.

3. For the offsprings of a carrier female there is a 50% chance of sons being affected and a 50% chance of daughters being carriers.

4. Among offsprings of an affected male, none of the sons will carry the trait, while all the daughters will be carriers.

A female may manifest an X-linked trait if the normal X-chromosome is inactivated during early fetal life or if she is the offspring of a carrier female and affected male, or if the unaffected X-chromosome is structurally abnormal, as in Turner’s syndrome, e.g., hemophilia, Christmas disease, pseudohypertrophic muscular dystrophy.

X-linked Dominant Inheritance

1. The number of females affected is double the number of affected males.

2. The affected male passes Y-chromosome to his sons (and not the X-chromosome). Therefore, all sons of an affected male are normal, whereas all daughters of an affected male are abnormal.

3. The affected female passes the mutant X-chromosome to half her daughters and to half her sons and, therefore, half the daughters and half the sons are affected.

The disease is usually milder in the female, because of the normal gene on the other X-chromosome, e.g. hypophosphatemic type of vitamin D resistant rickets.

X-linked Inheritance - Sex Chromosome Related Disorders, X-linked Recessive Inheritance and X-linked Dominant Inheritance
X-linked Inheritance – Sex Chromosome Related Disorders, X-linked Recessive Inheritance and X-linked Dominant Inheritance

WHOOPING COUGH – PERTUSSIS

WHOOPING COUGH – PERTUSSIS – Definition, Pathology, Clinical Manifestations, Diagnosis, Treatment and Prevention

DEFINITION

The term pertussis, which means intensive cough, is an acute respiratory infection, seen more commonly in young children. The disease is also more serious in them. The term “whooping cough” is derived from the occurrence of progressive repetitive paroxysms of cough followed by inspiratory whoop. Natural pertussis infection and vaccination do not produce life-long immunity. The immunity wanes over a few decades. Since there is almost complete coverage of DPT vaccination in children, adolescents and adults may become susceptible to infection increasingly. It is therefore possible that adults develop pertussis infection.

Pertussis is caused by Bordetella pertussis which is highly infective. Bordetella parapertussis and B. bronchiseptica are members of the same genus, rarely causing disease in man. Maximum incidence is seen in children below five years and the mortality is highest for children below 1 year of age. The organisms are spread by droplet infection and the route of entry is the respiratory tract.

The infectious period is the catarrhal prodrome and for three weeks after the onset of illness. Bordetella are small gram-negative coccobacilli, exclusively pathogenic to humans. The genome of B.pertussis has been sequenced.

Pathology

The mucosal lining of the respiratory tract shows inflammation. Peribronchial lymphoid hyperplasia occurs initially and this is followed by necrosis of the midzonal and basilar layers of the bronchial epithelium. This leads to the accumulation of tenacious mucus, atelectasis and eventually bronchiectasis.

Clinical Manifestations

The incubation period is usually 7-14 days but may be prolonged to 20 days. Three stages can be distinguished—catarrhal, paroxysmal and convalescent—each lasting up to 2 weeks so that the course of the disease extends to 6-8 weeks.

The catarrhal stage manifests with rhinorrhea, mild fever, and cough. During this stage, clinical recognition of the disease is difficult. This is the most infective stage.

In the paroxysmal stage cough starts, increases in severity, and becomes repetitive and explosive. Each paroxysm is followed by a whoop produced by a sudden massive inspiratory effort through a narrowed glottis. During the paroxysms of cough the infant develops facial congestion, distension of neck and scalp veins, lacrimation, cyanosis, and clouding of consciousness. The paroxysm ends with the onset of vomiting. The whoop may not be distinctly made out in younger infants, but they may become asphyxiated and develop anoxic convulsions. Physical examination may reveal periorbital edema. In the uncomplicated cases lung signs are usually absent. Pertussis occurring in adults causes prolonged cough. With increasing age the manifestations also become more severe.

Convalescence is marked by the decrease in frequency and severity of the paroxysms. Vomiting subsides and the patient’s appetite improves. At this stage the child is very susceptible to develop superinfections by other respiratory pathogens and this may lead to recurrence of the

paroxysms of cough. When this occurs it may last for several months.

Complications

Complications are common to develop

A. Respiratory:

Otitis media, especially in infants

Bronchitis

Bronchopneumonia

Atelectasis (segmental or lobar)

Interstitial or subcutaneous emphysema or pneumothorax due to rupture of alveoli

Bronchiectasis

Flare-up of tuberculosis

Sudden death of the infant may occur

B. Central nervous system:

Convulsions may occur due to anoxia, encephalopathy or rarely intracranial hemorrhage.

C. Gastrointestinal:

Severe vomiting with dehydration, tetany, ulceration of the frenum of the tongue (due to biting during a paroxysm), prolapse rectum, hernia.

D. Hemorrhages:

Epistaxis

Subconjunctival hemorrhage

Hemoptysis, hematemesis

E. Malnutrition:

Severe emaciation occurs in most of the affected children. In poor communities it is the starting point for marasmus and kwashiorkor.

Diagnosis

The disease has to be suspected clinically, particularly in an unimmunized child with known contact with the disease. Total leucocyte count is elevated to 20,000 to 50,000/cmm with absolute lymphocytosis. A leukemoid reaction may sometimes occur. Chest X-ray may show perihilar infiltrates or segmental collapse. Bacteriological diagnosis is established by culturing the organism obtained from nasopharyngeal swabs. Fluorescent antibody staining of pharyngeal specimens provides a rapid and specific diagnosis. PCR using nasopharyngeal aspirate reveals the organisms. In cases with duration above two weeks IgG antitoxic antibody can be demonstrated in serum.

Treatment

Supportive care is important to maintain nutrition, prevent aspiration into the respiratory tract and maintain the airway. The airway is cleared by suction of the exudates. Anoxic convulsions are managed by administration of oxygen and anti-convulsants. Small, frequent feeds are tolerated if given soon after a paroxysm of cough.

Intravenous fluids may be required if the child is dehydrated. In general, administration of antibiotics does not shorten the paroxysmal stage, once it is established. Erythromycin 50 mg/kg/day given for 5-7 days will reduce the period of communicability. It may even abort or prevent the progress of the disease if given in the catarrhal stage. Ampicillin, chloramphenicol and cotrimoxazole may also be used as alternative drugs. Azithromycin 250-500 mg po, od for 7-10 days is effective in controlling the infection if started early. Clarithromycin is a suitable alternative.

Antibodies are not transferred transplacentally in the case of whooping cough. In most patients, a single attack confers life-long immunity.

Prevention

Active immunization is achieved by the administration of the pertussis vaccine, usually given in combination with diphtheria and tetanus toxoids (DPT). The vaccine contains killed B. pertussis. The initial dose is given at 2 months, with 2 more doses at 4 week intervals. The first booster is given 1 year later and the next one at school entry.

WHOOPING COUGH – PERTUSSIS – Definition, Pathology, Clinical Manifestations, Diagnosis, Treatment and Prevention
WHOOPING COUGH – PERTUSSIS – Definition, Pathology, Clinical Manifestations, Diagnosis, Treatment and Prevention

WATER SOLUBLE VITAMINS – THIAMINE

WATER SOLUBLE VITAMINS – THIAMINE

THIAMINE (VITAMIN B1 – ANEURINE)

Thiamine plays an essential part in the metabolism of carbohydrates by acting as a coenzyme required for the decarboxylation of pyruvate to acetyl coenzyme A. It also takes part in other steps of the Kreb’s tricarboxylic acid cycle. Cereals contain the vitamin, which is maximal subjacent to the bran. Thiamine content of rice is lost during milling and polishing. Parboiling allows the vitamin to penetrate the grain and conserves it to some extent. Other good sources of the vitamin are sprouting pulses, green leafy vegetables, liver, pork, and legumes. Part of the vitamin is lost by washing or discarding the water used for cooking. The daily requirement is 0.4 mg/1000 kcal, i.e. 1.2 mg/day. Requirement is partially influenced by the intake of carbohydrates.

Deficiency States

Pathology of deficiency

In thiamine deficiency the cells cannot utilize glucose aerobically. Nervous system is affected first. Pyruvic and lactic acids accumulate and this leads to vasodilation. The myocardium shows loss of striation, vacuolation of fibers, fragmentation and edema. Cardiomyopathy, encephalopathy and peripheral neuropathy may develop. Sensory, motor and autonomic nerves show demyelination and degeneration.

Clinical features

Cardiovascular involvement results in ‘wet beriberi’ and nervous system involvement results in ‘dry beriberi’. Cardiovascular system Peripheral vasodilation leads to high output circulatory state, myocardial failure and retention of sodium and water leading to edema. The pulse is of high volume. The extremities are warm owing to vasodilation and tender owing to neuropathy. Acute fulminant cardiac failure may be rapidly fatal. Wet beriberi may occur in breastfed infants aged 2-8 months. The child presents with edema, oliguria and an aphonic cry. If not clinically suspected, this condition may be missed. Sudden death may occur.

Neurological involvement

This manifests as symmetrical sensori-motor polyneuropathy with muscle wasting. Foot-drop and wrist-drop are common. Deep hyperaesthesia occurs and it manifests as calf tenderness.

Wernicke’s encephalopathy

This is an acute neurological manifestation which is more common in alcoholics. Pathological changes occur in the upper part of the midbrain, hypothalamus and the walls of the third ventricle which show congestion and petechial hemorrhages, most marked in the mammillary bodies. The onset is sudden with vomiting, confusion, bilateral ophthalmoplegia, loss of consciousness, nystagmus, ataxia and psychological disturbances. Confusion proceeds to coma and death. Korsakoff’s syndrome is characterized by retrograde amnesia, impaired ability to learn and confabulation. Wernicke’s encephalopathy is associated with high mortality. Prompt administration of thiamine rapidly restores normalcy.

Diagnosis of thiamine deficiency

The condition has to be suspected clinically. It can be confirmed by demonstrating raised levels of blood pyruvate. Normal blood pyruvate is 62.5 to 125 mmol/liter and it may rise to 375 mmol/liter (3.3 mg/L). Measurement of erythrocyte transketolase activity, before and after the addition of thiamine pyrophosphate gives the most reliable diagnostic test.

Treatment:

When beriberi is suspected or diagnosed, 50 mg thiamine should be given intramuscularly daily for several days. After controlling the acute symptoms 2.5-5 mg should be given orally as maintenance. Wet beriberi and Wernicke’s encephalopathy have to be treated as medical emergencies. A dose of 25-100 mg of thiamine should be given intravenously to save life. Dramatic recovery with diuresis occurring within hours of injection confirms the diagnosis.

Infants with beriberi should be given 10 mg thiamine intramuscularly followed by oral doses. The mother also should be treated with oral doses of 10 mg twice daily for several days. Since polyneuropathy and Korsakoff’s psychosis are more resistant to treatment, the vitamin has to be given for prolonged periods. Once neuropathy is established, residual paralysis persists even after therapy. Adverse side effects to thiamine include sensitization and anaphylactic shock.

WATER SOLUBLE VITAMINS – THIAMINE
WATER SOLUBLE VITAMINS – THIAMINE

VITAMIN E AND K

VITAMIN E AND K (Fat Soluble Vitamin) – Dietary Sources, Clinical Features, Treatment and Prevention

VITAMIN E (ANTI-STERILITY VITAMIN)

Vitamin E is a tocopherol. Among the tocopherols alpha tocopherol is the most easily absorbed and biologically most active compound. All vegetable oils, wheat-germ, cotton seeds, egg yolk, butter and peas contain this vitamin and the average Indian diet contains the daily requirement which is 15 IU or 5 mg. Vitamin E which is a strong antioxidant prevents the peroxidation of cellular and subcellular membrane phospholipids. It is probably involved in preserving the integrity of cell membranes.

In cattle and poultry, vitamin E deficiency may lead to infertility. Nutritional deficiency of vitamin E is rare. Excess of free fatty acids in the diet increases the requirement for vitamin E. In premature infants fed on artificial diets containing iron and high concentrations of fatty acids, conditioned deficiency may develop, leading to the production of hemolytic anemia.

In doses of 400-800 mg, vitamin E acts as an effective antioxidant, thereby retarding the development of atheromatous changes in arteries.

VITAMIN K (COAGULATION VITAMIN)

This vitamin which is chemically a substituted naphthoquinone is present in adequate amounts in vegetable oils and green leafy vegetables as vitamin K1 (phytomenadione). Vitamin K comprises of several molecular forms that have a common 2-methyl-l, 4-naphthoquinone ring, but different side chains at the 3-position. In green leafy vegetables and legumes and vegetable oils such as rapeseed oil and soyabean oil vitamin K occurs as phylloquinone (old name K1).

Bacteria synthesize vitamin K which is named menaquinone (MK-n) which occurs in several molecular forms. Milk is a poor source. The colonic bacteria synthesize this vitamin (Vitamin K2) and this supplements the dietary source. Naturally occurring vitamin K is fat soluble. The synthetic form of this vitamin is vitamin K3 which is water-soluble. This can be given intramuscularly or intravenously, unlike the oily preparations which can be given only intramuscularly. Daily requirement is not clearly known, but is probably 1 μg/kg body weight. Body sources are limited and, therefore, signs of deficiency develop within 3 to 4 weeks of dietary deprivation. Oxidative phosphorylation processes which take place in cellular mitochondria require the presence of vitamin K. Vitamin K occurs in large amounts in liver and bone. In the liver it takes part in the synthesis of precursors for coagulation factors, protein C and protein S. Vitamin Kdependent coagulation factors (factors II, VII, IX and X) are produced in the inactive form by the liver, and vitamin K is required for their biological activation. The inhibitors of coagulation—Protein C and Protein S are also produced in the liver and these are also vitamin K dependent. Coumarins inhibit the enzyme vitamin K epoxide reductase and thereby inhibit further actions of Vitamin K.

Prothrombin (factor II) is synthesized in the liver as an inert precursor, termed protein induced by vitamin K absence (PIVKA). This is carboxylated to form prothrombin by the vitamin K dependent enzyme—gamma carboxylase. In the absence of vitamin K or after

administration of vitamin K antagonists such as coumarin PIVKA appears in the plasma.

Vitamin K is needed for the formation of several proteins concerned with calcium homeostasis. Vitamin K promotes the conversion of protein-bound glutamate residues to gamma-carboxy glutamate (Gla). Proteins containing Gla are present in several tissues such as bone, kidneys, placenta, pancreas, spleen and lungs.

Vitamin K also takes part in bone metabolism—both bone formation and resorption. Two of the important Vitamin K dependent proteins are osteocalcin and matrix Gla protein.

Vitamin K Deficiency

Vitamin K deficiency occurs in conditions associated with malabsorption of fat such as obstructive jaundice and malabsorption states. Prolonged treatment with broad spectrum antibiotics destroys the colonic bacteria which synthesize this vitamin. Deficiency manifests as mild or severe bleeding tendency occurring from injection sites, mucous membranes, and skin. Injections of vitamin K in doses of 5-10 mg corrects the defect, if hepatic parenchymal function is normal. In the presence of hepatic failure, vitamin K may not be effective.

HEMORRHAGIC DISEASE OF THE NEWBORN

Hemorrhage may develop in newborn infants occasionally. Prematurity predisposes to this condition. Vitamin K deficiency in the mother and anticoagulant medication aggravate this disorder. Hemorrhagic  tendency develops on the second or third day of delivery. This is due to exaggeration of the physiological hypoprothrombinemia which develops before the colon is colonized by bacteria.

A dose of 1 mg of vitamin K1 given intramuscularly to the baby brings about relief. Synthetic vitamin K is also effective. Larger doses have to be avoided since these lead to hemolysis. Administration of 5-10 mg vitamin K to the mother in late pregnancy abolishes this risk in the newborn.

Anticoagulant therapy Use of coumarin drugs or warfarin leads to alteration in the synthesis of coagulation factors. As a result proteins antigenically similar to factors II, VII, IX and X are produced but they lack the procoagulant properties. Excess of anticoagulants leads to hemorrhagic tendency.

Bleeding occurs from injection sites, urinary tract, gastrointestinal tract and uterus. Intramuscular injection of 10 mg vitamin K is usually effective. When the bleeding tendency is severe, large intravenous doses (50-75 mg) may be required. For severe cases transfusion of fresh blood or vitamin K-dependent coagulation factors may also be necessary.

VITAMIN E AND K (Fat Soluble Vitamin) – Dietary Sources, Clinical Features, Treatment and Prevention
VITAMIN E AND K (Fat Soluble Vitamin) – Dietary Sources, Clinical Features, Treatment and Prevention

VITAMIN – D

VITAMIN – D – Biological Actions, Daily Requirements, Rickets, Clinical Features, Diagnosis, Treatment and Prevention

Vitamin D is required for normal metabolism of calcium and phosphorus and for bone formation. It enhances the absorption of these minerals from the gut, their mobilization from bone and the reabsorption of phosphorus by the kidney. Vitamin D1 is the essential precursor for 1-25 alpha dihydroxy vitamin D1 which is the steroid hormone required for the development of bone, growth in children, maintenance of bone mass in adults and also for the retardation of osteoporosis and prevention of fractures in the elderly.

The two different forms of vitamin D active in man are vitamin D (calciferol) obtained by ultraviolet irradiation of ergosterol (also called ergocalciferol or provitamin D2) which is of plant origin, and vitamin D3 (cholecalciferol) which is formed by activation of 7-dehydrocholesterol present in the epidermal cells of human skin as a provitamin D2. This activation is effected by the ultraviolet rays ranging in wavelength from 296 to 310 A obtained from sunlight naturally. Exposure to sunlight for 20-30 minutes daily ensures adequate supply of Vitamin D. Excessive exposure does not lead to overdose of the vitamin. Skin damaged by burns will not be capable of producing Vitamin D on exposure to sunlight.

Vitamin D2 is obtained from the diet and vitamin D3 is formed endogenously. On an average the endogenous source supplies about 80% and diet about 20% of the total requirement. Vitamin D2 and D3 which are identical in potency, differ only in the configuration of the side chain. Vitamin D3, though formed in the skin is also absorbed through the small intestine. Further metabolism of vitamin D2 and D3 is identical and these together are referred to as vitamin D.

Biological actions of vitamin D metabolites:

1. Increase the absorption of calcium and phosphate from the small intestine by promoting active transport.

2. Increase mobilization of calcium from bone by promoting osteoclastic activity.

3. Stimulation of reabsorption of calcium and phosphate at the renal tubules.

The overall result of all these processes is to increase serum calcium and phosphate. Deficiency of vitamin D results in impairment of mineralization of bone leading to nutritional rickets in children and osteomalacia in adults.

Dietary sources of vitamin D are milk, butter, cheese, egg yolk and fish liver oils. This vitamin is heat stable. One international unit (IU) is equivalent to 0.025 μg. The daily requirement varies depending on the age.

DAILY REQUIREMENTS

Infant and children – 400 IU

Age 19-50 years – 200 IU

51-70 years – 400 IU

71 and above years – 600 IU

RICKETS

Prevalence Rickets is prevalent in India, more so in the north than in the south. Premature babies are more vulnerable. The disease is more florid during winter months when exposure to sunlight is minimal. Prevalence is more among the poor and illiterate classes. Indians who have emigrated to affluent countries still show a higher prevalence of rickets. Osteomalacia is more common in multiparous women who have nursed their babies repeatedly. Rickets has been ranked among the most frequent childhood diseases affecting children in the developing world. There is evidence that dietary deficiency of calcium may also lead to rickets.

In rickets, the arrangement and normal regenerative processes of cartilage are abnormal. Subsequent calcification of the cartilaginous matrix and osteoid do not proceed normally. The osteoid and cartilage which remain uncalcified are deposited irregularly. These give rise to a wide irregular frayed zone of non-calcified cartilage and osteoid termed rachitic metaphysis. These in turn account for many of the skeletal deformities. In the subperiosteal region also, while resorption of cortical bone continues normally, new bone is not laid down, resulting in softening and rarefaction of the bone shaft. In vitamin D deficiency, since absorption of calcium and, phosphorus from the gut is defective, serum calcium and phosphorus levels fall. Lowered level of serum calcium stimulates the secretion of parathyroid hormone which in turn, leads to mobilization of calcium from the bone. Thus, the serum calcium is usually maintained normal for considerable periods, tetany developing only rarely. Since parathyroid hormone (PTH) decreases reabsorption of phosphorus by the renal tubule, the serum phosphorus falls. The serum alkaline-phosphatase is elevated due to increased osteoblastic activity.

CLINICAL FEATURES

Florid rickets manifests by the age of 1-2 years. Early manifestations These include irritability, flabbiness of muscles, prominence of abdomen and delay in the appearance of milestones, except speech. Skeletal manifestations These are the most characteristic features. They develop several months after the deficiency is established. The bones which have the maximum rate of growth at the time of onset of the deficiency show gross abnormalities.

In children below the age of 1 year the lesion is craniotabes, characterized by abnormal softening of the skull in the occipital region. In children aged 2 years or more epiphyses of the wrists and ankles are widened and costochondral junctions are enlarged and beaded. In advanced rickets, deformities of bones are aggravated because of muscular action, gravity and weight bearing.

Head

Craniotabes disappears by 1 year of age, but the excess of osteoid and non-calcified cartilage gives rise to frontal and parietal bossing giving the skull a ‘hot cross bun’ appearance. Due to softening of the skull bones the calvarium is asymmetric. The head may be larger in size and closure of the anterior fontanelle may be delayed. The teeth erupt late; show defective enamel, and are more susceptible to develop caries. Permanent teeth also show grooving, pitting and hypoplastic enamel.

Rib-cage

Costochondral junctions are thickened (rachitic rosary) and the sternum projects forwards (pigeon chest deformity). A horizontal groove (Harrison’s sulcus) develops along the diaphragmatic attachment due to

muscular pull of the diaphragm on the softened bone.

Spine

This shows kyphosis and scoliosis when the baby starts sitting and later lordosis in the erect posture.

Pelvis

In lordotic subjects the pelvis shows a corresponding deformity. The pelvis is small and deformed (triradiate pelvis), and in female subjects the obstruction caused to the pelvic outlet gives rise to dystocia during parturition.

Extremities

The femur, tibia and fibula bend producing deformities like knock knees, coxa vara, etc. The thickened epiphyseal ends may be more prominent. Deformities of upper limbs develop if rickets sets in when the infant is crawling. Long bones may develop green stick fractures and pseudofractures. The sum total of bony deformities of the spine, pelvis, and legs leads to rachitic dwarfism.

Other general manifestations include hepatosplenomegaly, tetany, laryngysmus stridulus, convulsions and frequent respiratory infections.

Diagnosis

Rickets should be suspected in any child showing deformities of skull, long bones and ribs and in those with apathy, flabbiness, delayed milestones of development, laryngysmus stridulus or convulsions.

The clinical diagnosis is supported by the history of inadequate vitamin D in the diet or chronic diarrhea interfering with absorption of vitamin D, and it is confirmed by radiological investigations and biochemical tests. X-ray findings in active rickets Routine skiagrams of the wrists give clues in diagnosis and are helpful for following the progress. The distal ends of radius and ulna appear concave (cupping), widened (flaring) and irregular (fraying). The distance between the distal ends of the ulna and the radius and the metacarpal bones is apparently increased since the uncalcified rachitic metaphyses is translucent to X-ray. Shafts of long bones show decreased density and prominent trabeculations. Subperiosteal osteoid may give a double contour to the shaft.

With treatment, the lesions tend to heal. A line of preparatory calcification (LPC) appears. This is separated from the distal end of the shaft by a zone of translucency caused by the uncalcified osteoid. As healing progresses, the osteoid becomes calcified and shaft apparently grows towards the LPC and unites with it.

Measurement of serum 25 hydroxy vitamin D gives a reliable indication of the adequacy of the nutritional status. Normal values are above 15 ng/mL. Values below 8 mg/mL indicate severe deficiency.

Biochemical changes

In florid cases the serum phosphorus is low (1.5-3.5 mg/dL) Serum calcium may usually be normal, but in advanced cases it is reduced especially in cases with tetany. Serum alkaline phosphatase is raised to 20-60 KA units/dL (Normal 5-15). With correction of the lesion alkaline phosphatase level falls and serum phosphorus level goes up. Normal serum vitamin D levels range from 35 ± 3.5 ng/mL (80 nmol/L) and 1,25 (OH)2 D is 35 ± 3 pg/mL.

In active rickets these levels are lowered.

Prognosis for growth and cosmetic recovery is excellent if the condition is recognized early and treated before deformities develop. Intercurrent infections make the prognosis worse. If treatment is started after the bony deformities are established and the epiphyses are ossified, the deformities tend to persist.

Treatment

Oral administration of vitamin D in doses of 1500-5000 IU daily brings about rapid improvement in the vast majority of cases. Radiological improvement will be demonstrable in 2-4 weeks. A single dose of 600,000 units is preferable for advanced cases. The dose may be given orally or as in intramuscular injection. An oily preparation is available for intramuscular injection which is effective for 3 months. Three to four injections are given at intervals of two weeks. Parenteral administration is mandatory in cases showing malabsorption. If there is no improvement even after two parenteral doses of vitamin D, the case is considered to be resistant to vitamin D.

After complete healing of the lesion vitamin D should be given in doses of 400 units daily for preventing recurrence. Children should be encouraged to get exposure to sun for 20-30 minutes daily. Early bone lesions will be corrected with simple medical treatment. If treatment is started late and deformities are permanent, orthopedic correction is indicated.

Vitamin D-resistant rickets

This may be acquired, as in chronic renal failure or inherited as in congenital enzyme defects.

In chronic renal failure conversion of 25-OH D3 into the active metabolite 1,25(OH)2D3 becomes defective due to the progressive deficiency of the enzyme in the renal tubules. Such patients develop features of rickets (renal rickets) forming part of renal bone diseases.

Inherited forms of rickets

Pseudo-vitamin D deficiency: Two types are known. Rickets develop early in life. Hypotonia, weakness, seizures and growth failure develop.

Vitamin D dependent rickets type I

This is an autosomal recessive trait in which the gene for expressing the renal enzyme 25 hydroxy vit D3 1-alpha hydroxylase is defective, and so this enzyme level is low or absent. Plasma levels of 25(OH)D3 are normal, but 1,25 (OH)2D3 are low. The gene is located on chromosomes X 12 q 13.3.

Vitamin D dependent rickets type II

Two forms exist. In one form, the gene for vitamin D receptor is mutated. Hypocalcemic rickets develops. In the second form, also known as X-linked hypophosphatemic vitamin D resistant rickets the phosphate regulating gene (PEX gene) with homology to endopeptidoses on the X chromosome is defective. All these forms respond to 1,25(OH)2 vitamin D.

HYPERVITAMINOSIS D

Prolonged administration of massive doses of vitamin D results in vitamin D intoxication. This causes hypercalcemia. Symptoms include nausea, vomiting, constipation, drowsiness, and signs of renal impairment. Metastatic calcification occurs in several tissues including

the kidneys, lungs, gastric mucosa and blood vessels. Renal function may deteriorate before other signs of toxicity are manifest. Subjects receiving high doses of vitamin D should have regular monitoring of serum calcium and if it is above 2.6 mmol/liter (10.5 mg/dL), the intake of the vitamin should be stopped.

VITAMIN – D – Biological Actions, Daily Requirements, Rickets, Clinical Features, Diagnosis, Treatment and Prevention
VITAMIN – D – Biological Actions, Daily Requirements, Rickets, Clinical Features, Diagnosis, Treatment and Prevention

UNARMED TAPEWORM

UNARMED TAPEWORM (Taeniasis saginata) (Beef Tapeworm) – General Characteristics, Life Cycle, Clinical Features, Diagnosis, Treatment and Prevention

GENERAL CHARACTERISTICS

Taeniasis saginata is infection caused by Taenia saginata. This is the commonest among the large tapeworms found in man and is distributed worldwide. Prevalence is highest in areas where beef is a major source of meat. The adult worm grows to a length of 10 meters and may consist of over 2000 segments. It lies free in the jejunum and ileum, the head being attached to the mucosa. The scolex is 2 mm in diameter and bears no hooklets, but has four suckers. The gravid segments are actively motile and they come out in chains along with feces or wriggle out singly due to their intrinsic muscular action. The uterus has about 20 lateral branches.

The eggs are spherical measuring 30-45 μ in diameter and the egg shell is thick, striated and bile-stained. The embryo or onchosphere bears six hooklets and it remains viable for 4-8 weeks. The adult worm may live for 10-25 years.

Life Cycle

Man is the definitive host and cattle and llamas form the intermediate hosts. Eggs passed in feces contaminate soil. These are ingested by grazing cattle. The onchospheres are liberated in the intestine and they penetrate the mucosa, enter the blood stream, and reach various muscles, mainly those of the heart, tongue, shoulder, neck and loins. On reaching these sites the onchospheres lose their hooks and grow into the cystic stage known as cysticercus bovis in 60-70 days. The cysticercus is ovoid, measures 8 × 5 mm and contains a single sprouting scolex. Cysticercus remains viable for 1-3 years within the muscles. Heavily infected meat is easy to distinguish by the presence of numerous cysts.

On ingesting undercooked meat, the cyst wall is digested and the head attaches itself to the intestinal mucosa and rapidly grows to reach the adult size in 6-8 weeks. A host usually harbors only one or two worms.

Clinical Features

Majority is asymptomatic, though vague symptoms such as abdominal pain, diarrhea and increased appetite may occur in a few. The motile segments emerging out of the anus may cause pruritus and anxiety to the host. Appendicitis and biliary obstruction have been reported rarely.

Diagnosis

History of passing segments and seeing the segments in feces confirm the diagnosis. The species can be identified by observing the number of lateral branches of the uterus. An easy method is to press the segment between two glass slides and to hold it against light. Taenia saginata segment has more than 15 lateral branches, whereas Taenia solium has only less than 13. Eggs can be demonstrated by microscopic examination of the feces or by examining perianal scotch tape swab. The eggs of T. saginata, T. solium and T. echinococcus cannot be differentiated from each other

Treatment

Both niclosamide (Yomesan) and praziquantel are effective against T. saginata. Niclosamide kills the scolex and segments on contact. Four tablets, each of 0.5 g, are given as a single dose to be thoroughly chewed in the morning with a gulp of water. The worm is passed partially digested 24-36 h later. If the whole worm including the scolex is not passed, the worm re-grows and segments reappear in stools within 3 months. In this case the drug is repeated in the same dose. Praziquantel in a dose of 10-15 mg/kg body weight given as a single dose orally is adequate to dislodge the intestinal adult worm in almost all cases. The drug is generally safe. Side effects include dizziness, headache, vomiting and allergy. It is available as tablets of 500 mg and 600 mg.

Prevention

Taenia saginata infection can be prevented by avoiding infected beef, inspection of slaughterhouses and proper disposal of excreta.

UNARMED TAPEWORM (Taeniasis saginata) (Beef Tapeworm) – General Characteristics, Life Cycle, Clinical Features, Diagnosis, Treatment and Prevention
UNARMED TAPEWORM (Taeniasis saginata) (Beef Tapeworm) – General Characteristics, Life Cycle, Clinical Features, Diagnosis, Treatment and Prevention