Vitamin D detailed information
and diseases associated with vitamin D deficiency and toxicity
covering about rickets and osteomalacia, information from Harrison's internal medicine and online resources like uptodate
Excessive vitamin D intake can lead to vitamin D toxicity. The 25-OH metabolite plays a key role in vitamin D intoxication by competing for intracellular receptors, inducing responses normally caused by 1,25-(OH)2-D3. This leads to hypercalcemia through increased calcium absorption and bone resorption, decreasing PTH and kidney function and disrupting calcium homeostasis. Long-term effects include calcinosis, the deposition of calcium and phosphorus in soft tissues like the heart and kidneys. Risk depends on calcium and phosphorus intake in addition to vitamin D exposure.
Rickets and osteomalacia are diseases caused by a lack of calcium and phosphorus that prevents bone mineralization. Rickets occurs in children before growth plate closure, while osteomalacia occurs in adults. The most common causes are vitamin D deficiency from inadequate intake or absorption and phosphate deficiency. Treatment involves replacing the deficient nutrient, usually with vitamin D, calcium, and phosphate supplements. Monitoring treatment involves checking serum and urine calcium levels until they normalize and x-rays show bone healing.
This document provides an overview of rickets presented by Lyudmyla Olexandrivna Rakovska from the Department of Pediatrics at V.N. Karazin Kharkiv National University. The 10-point plan discusses the definition, etiology, pathogenesis, classification, clinical manifestations, laboratory/radiological findings, differential diagnosis, treatment and prevention of rickets. Key points include that rickets is caused by vitamin D deficiency impairing bone mineralization, especially in children under 2 years old. Symptoms involve soft, deformed bones and skeletal abnormalities. Treatment focuses on vitamin D supplementation through either low daily doses or high single doses.
This document summarizes various causes of rickets, including calcium deficiency, phosphorus deficiency, rickets of prematurity, and several genetic disorders. Calcium deficiency can result from low dietary intake or malabsorption and presents with signs of rickets in infancy. Phosphorus deficiency is usually due to inadequate intake or antacid use. Rickets of prematurity occurs in very low birth weight infants and is prevented by mineral supplementation. The document also describes several genetic causes of rickets, including X-linked hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, and Fanconi syndrome. Treatment involves calcium, vitamin D, and phosphorus supplementation tailored to the specific deficiency.
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. Symptoms include bowed legs, knock-knees, frontal bossing of the skull, and chest deformities like pigeon chest. Laboratory findings often include low calcium, phosphorus, and vitamin D levels as well as elevated alkaline phosphatase and parathyroid hormone levels. Radiographs show widened growth plates and fraying and cupping of the bone metaphysis. The condition is treated by supplementing with vitamin D and calcium.
Rickets and osteomalacia are diseases caused by inadequate bone mineralization due to vitamin D deficiency or impaired mineral metabolism. Rickets primarily affects children as it involves the growth plates, while osteomalacia affects adults. Symptoms include bone pain, deformities, and fractures. Diagnosis involves blood tests showing low calcium and phosphate levels and high alkaline phosphatase. X-rays show abnormalities in bone structure and density. Treatment focuses on correcting the underlying causes through vitamin D and calcium supplementation, with surgical intervention for severe deformities.
The document discusses the causes and presentation of rickets. The main causes are vitamin D disorders, calcium deficiency, phosphorus deficiency, renal losses, and distal renal tubular acidosis. Clinical features include bone deformities, softening of the skull, and leg pain. Diagnosis involves physical exam, x-rays showing bone changes, and lab tests showing abnormalities in calcium, phosphorus, vitamin D, and parathyroid hormone levels. Nutritional vitamin D deficiency is the most common cause globally. Treatment involves vitamin D, calcium, and phosphorus supplementation.
This document discusses vitamin D deficiency in India. It provides the following key points:
1. More than 80% of adults in India do not get enough vitamin D, despite India's sunny climate, due to factors like skin pigmentation and low dietary intake.
2. The most common disorders caused by vitamin D deficiency in India are osteomalacia and rickets, which are bone diseases characterized by softening of the bones.
3. Good food sources of vitamin D include cod liver oil, fatty fish like salmon and tuna, and fortified foods like milk, cereal and orange juice. However, dietary intake of vitamin D is still low for most Indians.
Excessive vitamin D intake can lead to vitamin D toxicity. The 25-OH metabolite plays a key role in vitamin D intoxication by competing for intracellular receptors, inducing responses normally caused by 1,25-(OH)2-D3. This leads to hypercalcemia through increased calcium absorption and bone resorption, decreasing PTH and kidney function and disrupting calcium homeostasis. Long-term effects include calcinosis, the deposition of calcium and phosphorus in soft tissues like the heart and kidneys. Risk depends on calcium and phosphorus intake in addition to vitamin D exposure.
Rickets and osteomalacia are diseases caused by a lack of calcium and phosphorus that prevents bone mineralization. Rickets occurs in children before growth plate closure, while osteomalacia occurs in adults. The most common causes are vitamin D deficiency from inadequate intake or absorption and phosphate deficiency. Treatment involves replacing the deficient nutrient, usually with vitamin D, calcium, and phosphate supplements. Monitoring treatment involves checking serum and urine calcium levels until they normalize and x-rays show bone healing.
This document provides an overview of rickets presented by Lyudmyla Olexandrivna Rakovska from the Department of Pediatrics at V.N. Karazin Kharkiv National University. The 10-point plan discusses the definition, etiology, pathogenesis, classification, clinical manifestations, laboratory/radiological findings, differential diagnosis, treatment and prevention of rickets. Key points include that rickets is caused by vitamin D deficiency impairing bone mineralization, especially in children under 2 years old. Symptoms involve soft, deformed bones and skeletal abnormalities. Treatment focuses on vitamin D supplementation through either low daily doses or high single doses.
This document summarizes various causes of rickets, including calcium deficiency, phosphorus deficiency, rickets of prematurity, and several genetic disorders. Calcium deficiency can result from low dietary intake or malabsorption and presents with signs of rickets in infancy. Phosphorus deficiency is usually due to inadequate intake or antacid use. Rickets of prematurity occurs in very low birth weight infants and is prevented by mineral supplementation. The document also describes several genetic causes of rickets, including X-linked hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, and Fanconi syndrome. Treatment involves calcium, vitamin D, and phosphorus supplementation tailored to the specific deficiency.
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. Symptoms include bowed legs, knock-knees, frontal bossing of the skull, and chest deformities like pigeon chest. Laboratory findings often include low calcium, phosphorus, and vitamin D levels as well as elevated alkaline phosphatase and parathyroid hormone levels. Radiographs show widened growth plates and fraying and cupping of the bone metaphysis. The condition is treated by supplementing with vitamin D and calcium.
Rickets and osteomalacia are diseases caused by inadequate bone mineralization due to vitamin D deficiency or impaired mineral metabolism. Rickets primarily affects children as it involves the growth plates, while osteomalacia affects adults. Symptoms include bone pain, deformities, and fractures. Diagnosis involves blood tests showing low calcium and phosphate levels and high alkaline phosphatase. X-rays show abnormalities in bone structure and density. Treatment focuses on correcting the underlying causes through vitamin D and calcium supplementation, with surgical intervention for severe deformities.
The document discusses the causes and presentation of rickets. The main causes are vitamin D disorders, calcium deficiency, phosphorus deficiency, renal losses, and distal renal tubular acidosis. Clinical features include bone deformities, softening of the skull, and leg pain. Diagnosis involves physical exam, x-rays showing bone changes, and lab tests showing abnormalities in calcium, phosphorus, vitamin D, and parathyroid hormone levels. Nutritional vitamin D deficiency is the most common cause globally. Treatment involves vitamin D, calcium, and phosphorus supplementation.
This document discusses vitamin D deficiency in India. It provides the following key points:
1. More than 80% of adults in India do not get enough vitamin D, despite India's sunny climate, due to factors like skin pigmentation and low dietary intake.
2. The most common disorders caused by vitamin D deficiency in India are osteomalacia and rickets, which are bone diseases characterized by softening of the bones.
3. Good food sources of vitamin D include cod liver oil, fatty fish like salmon and tuna, and fortified foods like milk, cereal and orange juice. However, dietary intake of vitamin D is still low for most Indians.
This document discusses rickets, a disease caused by vitamin D deficiency or impaired mineralization that affects growing bones in children. It defines rickets and outlines various types including nutritional, vitamin D dependent, and vitamin D resistant rickets. Clinical features like softening of bones and skeletal deformities are described. Laboratory findings of low calcium and phosphorus and high alkaline phosphatase are also summarized. The document outlines prevention through diet, supplementation, and sunlight exposure as well as treatment with high dose vitamin D or calcium therapy.
This document provides information on rickets, a metabolic bone disease caused by vitamin D deficiency or impaired mineralization. It discusses the following key points:
- Rickets mainly affects children under 2 years old and causes soft, weak bones and skeletal deformities from imperfect bone mineralization.
- It is most commonly caused by nutritional deficiencies, especially of vitamin D, but can also be caused by genetic or other medical conditions.
- Symptoms include bone pain, softening of the skull and ribs, bowed legs, fractures, and delayed growth. Radiographs show widened growth plates and fraying of the metaphysis.
- Treatment involves high-dose vitamin D and calcium supplementation to promote bone mineralization and
This document defines and discusses rickets and osteomalacia. It notes that rickets occurs in childhood prior to epiphyseal closure, while osteomalacia occurs in adulthood after closure. Bone formation requires mineralization of collagen fibers; in rickets and osteomalacia, mineralization does not occur properly, leaving bones soft and prone to bending or cracking. Causes include vitamin D deficiency, mineralization defects, and phosphate deficiency. Diagnosis involves blood tests, imaging of pseudofractures and bone biopsy showing increased osteoid levels. Treatment depends on the underlying cause but often involves vitamin D, calcium, and phosphate supplements.
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. The disease develops when vitamin D levels are too low to absorb calcium and phosphate from the intestines, causing these minerals to be lost from the bones. Symptoms include bowed legs, soft skull, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels and high alkaline phosphatase. X-rays show widened growth plates and fraying and cupping of the bone. Treatment involves high dose vitamin D and calcium supplementation to strengthen the bones.
This document discusses rickets and osteomalacia. It defines them as metabolic bone diseases where rickets occurs in growing children and is caused by defective mineralization of bone and cartilage. Osteomalacia occurs in adults and is caused by inadequate or delayed mineralization of new bone. Common causes include vitamin D deficiency, malabsorption, and renal problems. Clinical features include bone pain, deformities, fractures, and muscle weakness. Diagnosis involves lab tests showing low calcium and imaging showing bone abnormalities. Treatment focuses on vitamin D, calcium, and phosphate supplementation.
This document discusses rickets, a disease characterized by soft, weak, and deformed bones in children caused by vitamin D deficiency or disorders of vitamin D and phosphate metabolism. It defines rickets as occurring in growing children before bone growth plate closure, while osteomalacia occurs after closure in adults. The key roles and mechanisms of vitamin D in calcium and phosphate homeostasis are described. Causes, signs and symptoms, diagnosis using biochemical markers and radiology, treatment using large vitamin D doses, and prevention through diet and sunlight exposure are summarized. Other types of rickets including genetic and renal forms are also outlined.
In chronic renal failure, the inability to produce calcitriol (1,25-dihydroxyvitamin D) leads to renal osteodystrophy. Calcitriol deficiency results in low calcium and high phosphate levels in the blood, stimulating parathyroid hormone secretion and causing demineralization of bones. To treat this, vitamin D must be accompanied by phosphate reduction through a low-phosphate diet and phosphate binders, as high phosphate levels can lead to soft tissue calcification when combined with low calcium levels.
Ppt Approach to Rickets and it's Management Shinjan Patra
Rickets is a disease characterized by defective mineralization of bone. It is caused by vitamin D deficiency or disorders that impair bone mineralization, resulting in skeletal abnormalities and defects in growth. The document discusses the pathogenesis, clinical manifestations, diagnostic evaluation and management of rickets and osteomalacia. Key points include that rickets affects bone formation in children while osteomalacia affects mineralization of mature bone, and both are usually caused by vitamin D deficiency but can also be caused by genetic disorders. Symptoms include bone pain, muscle weakness, and skeletal deformities. Diagnosis is based on biochemical abnormalities and imaging features showing unmineralized or abnormally mineralized bone. Treatment involves vitamin D, calcium, and sometimes calc
Vitamin D deficiency can result from inadequate sunlight exposure, low dietary intake, or impairments in vitamin D metabolism. It causes rickets in children as their bones fail to properly mineralize, while in adults it causes osteomalacia marked by bone pain and fractures. Risk factors include liver or digestive diseases, certain drugs, and genetic mutations impacting vitamin D metabolism. Osteoporosis involves low bone density and increased fracture risk related to aging and declining estrogen levels along with impaired vitamin D function.
1. Vitamin D is a fat-soluble vitamin that functions like a hormone in the body.
2. Vitamin D3 is synthesized in the skin upon exposure to sunlight, while the biologically active form calcitriol is produced in the kidney.
3. Calcitriol regulates calcium and phosphate levels in the blood by increasing their absorption in the intestine and reabsorption in the kidney while also increasing calcium mobilization from bone. This helps maintain appropriate calcium homeostasis.
This document discusses a case of a 2-year old child who is unable to stand or walk. On examination, the child has signs consistent with rickets including an open fontanel, wide wrists, and prominent costochondral junctions. The diagnosis is nutritional rickets due to vitamin D deficiency. Treatment involves high dose vitamin D supplementation to correct the deficiency and allow for proper bone mineralization and healing of rickets. Unresponsive cases may be due to other underlying causes. Prevention involves routine vitamin D supplementation of children.
Rickets - Bony manifestation of altered Vit. D, Calcium, and phosphorus metabolism
- Rickets – child;
- Osteomalacia – adult form
there is an inability to mineralize chondroid and osteoid
- lack of available calcium or phosphorus (or both) for mineralization of newly formed osteoid
- osseous changes in both adults and children
--- Definition - a defect in mineralization of osteoid matrix caused by inadequate calcium and phosphate deposition prior to closure of physis.
- Clinical features arise from un-mineralized matrix at the growth plate.
- less mineralized bone per unit volume of bone
- classic changes of rickets will typically occur in children younger than 6-7 years of age
-- Pathophysiology of Rickets
- Vitamin D => increase the absorption of calcium from intestine
PTH => mobilizes calcium from bone and increases urinary excretion of phosphate
Calcitonin => inhibits bone resorption
CLINICAL FEATURES
Head:
Craniotabes — softening of cranial bones. also seen in osteogenesis imperfect, hydrocephalus and syphilis
Frontal bossing
Delayed dentition and tooth caries
Delayed closure of fontanel
Craniosynostosis.
Chest
Rachitic rosary — widening of osteochondral junction
Harrison’s groove — occurs due to pulling of softened ribs in inspiration by diaphragm. Softened ribs also predispose to atelectasis and pneumonia because of decreased air entry
Pectus carinatum (pigeon breast)
Spine
Scoliosis (uncommon)
Kyphosis (rachitic cat back)
Accentuation of lumbar lordosis
Limbs and Joints
Bone pain and tenderness
Coxa vara
Genu valgum or varum
Windswept deformity
Bowing of tibia, femur, radius and ulna
Widening of wrist, elbow, knee and ankle because of enlargement of ends of long bones
Rachitic saber shins
Sausage like enlargement of ends of phalanges and metacarpals, with regular constrictions corresponding of the joints string of pearls deformity
Double malleoli sign
General
Failure to thrive
Protuberant abdomen
Apathy, listlessness and irritability
Proximal muscle weakness
Ligament laxity
Symptoms of hypocalcemia—tetany, seizures and stridor due to laryngeal spasm
Bilateral lamellar cataract (Vitamin D deficiency in early infancy).
RADIOLOGICAL SIGNS
Generalized osteopenia
Bowing deformities of the long bones, femur and tibia
Widening of the growth plate
Cupping or flaring of the metaphysis
Radiographic findings in vitamin D resistant rickets
similar to those in infantile rickets
Bowing deformities and shortening of the long bones => more pronounced in early rickets
More common in distal ends of radius and ulna (more so in ulna)
Changes in the shaft appear a few weeks later than metaphysis.
The epiphysis is cloudy and indistinct and periosteum is thick.
The shaft shows diffuse rarefaction, thin cortices with coarse texture of spongiosa.
Umbau zones (Looser’s zones) => sharply defined radiolucent transverse zones
-- Findings of healing rickets:
Earliest finding => reappearance of the provisional zone of calcification, which gradually thickens
This document summarizes rickets and osteomalacia. It discusses the pathophysiology, causes, clinical presentation, diagnosis and treatment of both conditions. Rickets occurs in children and is caused by impaired mineralization of the growth plate. Osteomalacia occurs in adults and results from impaired mineralization of osteoid. Causes include vitamin D deficiency, calcium deficiency, hypophosphatemia, and factors that inhibit mineralization. Clinical features depend on age and include bone deformities, weakness, and fractures. Diagnosis involves clinical, biochemical, and radiographic evaluation. Treatment focuses on correcting the underlying cause and managing symptoms.
Osteogenesis imperfecta, or brittle bone disease, is caused by mutations in collagen genes COL1A1 and COL1A2 that result in abnormal bone formation and fragility. It is characterized by bones that break easily from minor trauma, along with other connective tissue problems like blue sclera and joint laxity. Treatment focuses on preventing fractures through braces and limiting activity, as well as bisphosphonates and surgery to insert rods for stabilization. The disease ranges in severity from mild cases with normal life expectancy to lethal prenatal forms.
This document discusses metabolic bone diseases, including their composition, calcium and phosphate metabolism, and specific diseases. It provides details on osteoporosis, rickets/osteomalacia, Paget's disease, and renal osteodystrophy. The composition of bone includes collagen, proteoglycans, and hydroxyapatite. Calcium and vitamin D intake recommendations are outlined for different populations. PTH, calcitonin, vitamin D, and alkaline phosphatase roles in calcium regulation are summarized. Osteoporosis risk factors and management strategies are highlighted.
This document summarizes rickets, a childhood bone disease caused by vitamin D deficiency or impaired vitamin D metabolism. It discusses the pathology of rickets, which involves abnormal cartilage cell maturation and failed bone mineralization. This leads to bone deformities and fractures. The document outlines various causes of rickets, including nutritional deficiencies, malabsorption, and genetic disorders affecting vitamin D and phosphate metabolism. Diagnosis involves x-rays showing characteristic bone changes. Treatment involves vitamin D, calcium, phosphate supplementation as needed, and sometimes surgery to correct deformities once the disease is resolved.
The document discusses the principles of managing compound fractures of the lower limb. It defines compound fractures as fractures where the broken bone communicates with an external wound. It describes the Gustillo classification system for open fractures based on wound size and soft tissue damage. Grade I fractures have a wound less than 1 cm while Grade III fractures have extensive soft tissue stripping. The key priorities in emergency management are resuscitation of the patient, assessment of limb vascularity and compartment syndrome, thorough wound debridement and splinting without reduction, and use of broad spectrum antibiotics. Surgical management involves thorough debridement of all devitalized soft tissues and temporary stabilization using external fixation to allow wound healing before definitive fixation.
The document discusses renal osteodystrophy, which refers to bone diseases that occur in patients with impaired kidney function. It outlines several types of renal osteodystrophy, including osteitis fibrosa, adynamic bone disease, and osteomalacia. It describes the pathogenesis of secondary hyperparathyroidism in kidney disease and the effects of parathyroid hormone and vitamin D on bone and mineral metabolism. Treatment goals are to control parathyroid hormone levels, calcium, phosphorus, and vitamin D to prevent bone complications in renal patients.
Vitamin D deficiency is common in critically ill neonates. A study found serum 25-OH vitamin D levels were significantly lower in critically ill neonates compared to healthy newborns, with no correlation to disease severity except in pneumonia cases. The study recommended measuring 25-OH vitamin D levels in critically ill neonates and ensuring adequate maternal vitamin D intake during pregnancy and lactation, as well as vitamin D supplementation for breastfed infants. Guidelines for treating vitamin D deficiency in children include daily or weekly high dose vitamin D supplementation for 4-8 weeks, followed by maintenance doses, while insufficiency is managed with biweekly or monthly lower dose supplementation.
Vitamin D deficiency is common, affecting approximately 66% of the global population. It is defined as a serum 25-hydroxyvitamin D level below 20 ng/mL. Symptoms include bone and muscle pain. At-risk groups include those with dark skin, obesity, or malabsorption issues. Screening is recommended for high-risk individuals. Treatment involves oral vitamin D supplements of 50,000 IU weekly or 6000 IU daily to raise levels above 30 ng/mL. Maintenance doses of 800-1000 IU daily are used thereafter to prevent recurrence.
This document discusses rickets, a disease caused by vitamin D deficiency or impaired mineralization that affects growing bones in children. It defines rickets and outlines various types including nutritional, vitamin D dependent, and vitamin D resistant rickets. Clinical features like softening of bones and skeletal deformities are described. Laboratory findings of low calcium and phosphorus and high alkaline phosphatase are also summarized. The document outlines prevention through diet, supplementation, and sunlight exposure as well as treatment with high dose vitamin D or calcium therapy.
This document provides information on rickets, a metabolic bone disease caused by vitamin D deficiency or impaired mineralization. It discusses the following key points:
- Rickets mainly affects children under 2 years old and causes soft, weak bones and skeletal deformities from imperfect bone mineralization.
- It is most commonly caused by nutritional deficiencies, especially of vitamin D, but can also be caused by genetic or other medical conditions.
- Symptoms include bone pain, softening of the skull and ribs, bowed legs, fractures, and delayed growth. Radiographs show widened growth plates and fraying of the metaphysis.
- Treatment involves high-dose vitamin D and calcium supplementation to promote bone mineralization and
This document defines and discusses rickets and osteomalacia. It notes that rickets occurs in childhood prior to epiphyseal closure, while osteomalacia occurs in adulthood after closure. Bone formation requires mineralization of collagen fibers; in rickets and osteomalacia, mineralization does not occur properly, leaving bones soft and prone to bending or cracking. Causes include vitamin D deficiency, mineralization defects, and phosphate deficiency. Diagnosis involves blood tests, imaging of pseudofractures and bone biopsy showing increased osteoid levels. Treatment depends on the underlying cause but often involves vitamin D, calcium, and phosphate supplements.
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. The disease develops when vitamin D levels are too low to absorb calcium and phosphate from the intestines, causing these minerals to be lost from the bones. Symptoms include bowed legs, soft skull, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels and high alkaline phosphatase. X-rays show widened growth plates and fraying and cupping of the bone. Treatment involves high dose vitamin D and calcium supplementation to strengthen the bones.
This document discusses rickets and osteomalacia. It defines them as metabolic bone diseases where rickets occurs in growing children and is caused by defective mineralization of bone and cartilage. Osteomalacia occurs in adults and is caused by inadequate or delayed mineralization of new bone. Common causes include vitamin D deficiency, malabsorption, and renal problems. Clinical features include bone pain, deformities, fractures, and muscle weakness. Diagnosis involves lab tests showing low calcium and imaging showing bone abnormalities. Treatment focuses on vitamin D, calcium, and phosphate supplementation.
This document discusses rickets, a disease characterized by soft, weak, and deformed bones in children caused by vitamin D deficiency or disorders of vitamin D and phosphate metabolism. It defines rickets as occurring in growing children before bone growth plate closure, while osteomalacia occurs after closure in adults. The key roles and mechanisms of vitamin D in calcium and phosphate homeostasis are described. Causes, signs and symptoms, diagnosis using biochemical markers and radiology, treatment using large vitamin D doses, and prevention through diet and sunlight exposure are summarized. Other types of rickets including genetic and renal forms are also outlined.
In chronic renal failure, the inability to produce calcitriol (1,25-dihydroxyvitamin D) leads to renal osteodystrophy. Calcitriol deficiency results in low calcium and high phosphate levels in the blood, stimulating parathyroid hormone secretion and causing demineralization of bones. To treat this, vitamin D must be accompanied by phosphate reduction through a low-phosphate diet and phosphate binders, as high phosphate levels can lead to soft tissue calcification when combined with low calcium levels.
Ppt Approach to Rickets and it's Management Shinjan Patra
Rickets is a disease characterized by defective mineralization of bone. It is caused by vitamin D deficiency or disorders that impair bone mineralization, resulting in skeletal abnormalities and defects in growth. The document discusses the pathogenesis, clinical manifestations, diagnostic evaluation and management of rickets and osteomalacia. Key points include that rickets affects bone formation in children while osteomalacia affects mineralization of mature bone, and both are usually caused by vitamin D deficiency but can also be caused by genetic disorders. Symptoms include bone pain, muscle weakness, and skeletal deformities. Diagnosis is based on biochemical abnormalities and imaging features showing unmineralized or abnormally mineralized bone. Treatment involves vitamin D, calcium, and sometimes calc
Vitamin D deficiency can result from inadequate sunlight exposure, low dietary intake, or impairments in vitamin D metabolism. It causes rickets in children as their bones fail to properly mineralize, while in adults it causes osteomalacia marked by bone pain and fractures. Risk factors include liver or digestive diseases, certain drugs, and genetic mutations impacting vitamin D metabolism. Osteoporosis involves low bone density and increased fracture risk related to aging and declining estrogen levels along with impaired vitamin D function.
1. Vitamin D is a fat-soluble vitamin that functions like a hormone in the body.
2. Vitamin D3 is synthesized in the skin upon exposure to sunlight, while the biologically active form calcitriol is produced in the kidney.
3. Calcitriol regulates calcium and phosphate levels in the blood by increasing their absorption in the intestine and reabsorption in the kidney while also increasing calcium mobilization from bone. This helps maintain appropriate calcium homeostasis.
This document discusses a case of a 2-year old child who is unable to stand or walk. On examination, the child has signs consistent with rickets including an open fontanel, wide wrists, and prominent costochondral junctions. The diagnosis is nutritional rickets due to vitamin D deficiency. Treatment involves high dose vitamin D supplementation to correct the deficiency and allow for proper bone mineralization and healing of rickets. Unresponsive cases may be due to other underlying causes. Prevention involves routine vitamin D supplementation of children.
Rickets - Bony manifestation of altered Vit. D, Calcium, and phosphorus metabolism
- Rickets – child;
- Osteomalacia – adult form
there is an inability to mineralize chondroid and osteoid
- lack of available calcium or phosphorus (or both) for mineralization of newly formed osteoid
- osseous changes in both adults and children
--- Definition - a defect in mineralization of osteoid matrix caused by inadequate calcium and phosphate deposition prior to closure of physis.
- Clinical features arise from un-mineralized matrix at the growth plate.
- less mineralized bone per unit volume of bone
- classic changes of rickets will typically occur in children younger than 6-7 years of age
-- Pathophysiology of Rickets
- Vitamin D => increase the absorption of calcium from intestine
PTH => mobilizes calcium from bone and increases urinary excretion of phosphate
Calcitonin => inhibits bone resorption
CLINICAL FEATURES
Head:
Craniotabes — softening of cranial bones. also seen in osteogenesis imperfect, hydrocephalus and syphilis
Frontal bossing
Delayed dentition and tooth caries
Delayed closure of fontanel
Craniosynostosis.
Chest
Rachitic rosary — widening of osteochondral junction
Harrison’s groove — occurs due to pulling of softened ribs in inspiration by diaphragm. Softened ribs also predispose to atelectasis and pneumonia because of decreased air entry
Pectus carinatum (pigeon breast)
Spine
Scoliosis (uncommon)
Kyphosis (rachitic cat back)
Accentuation of lumbar lordosis
Limbs and Joints
Bone pain and tenderness
Coxa vara
Genu valgum or varum
Windswept deformity
Bowing of tibia, femur, radius and ulna
Widening of wrist, elbow, knee and ankle because of enlargement of ends of long bones
Rachitic saber shins
Sausage like enlargement of ends of phalanges and metacarpals, with regular constrictions corresponding of the joints string of pearls deformity
Double malleoli sign
General
Failure to thrive
Protuberant abdomen
Apathy, listlessness and irritability
Proximal muscle weakness
Ligament laxity
Symptoms of hypocalcemia—tetany, seizures and stridor due to laryngeal spasm
Bilateral lamellar cataract (Vitamin D deficiency in early infancy).
RADIOLOGICAL SIGNS
Generalized osteopenia
Bowing deformities of the long bones, femur and tibia
Widening of the growth plate
Cupping or flaring of the metaphysis
Radiographic findings in vitamin D resistant rickets
similar to those in infantile rickets
Bowing deformities and shortening of the long bones => more pronounced in early rickets
More common in distal ends of radius and ulna (more so in ulna)
Changes in the shaft appear a few weeks later than metaphysis.
The epiphysis is cloudy and indistinct and periosteum is thick.
The shaft shows diffuse rarefaction, thin cortices with coarse texture of spongiosa.
Umbau zones (Looser’s zones) => sharply defined radiolucent transverse zones
-- Findings of healing rickets:
Earliest finding => reappearance of the provisional zone of calcification, which gradually thickens
This document summarizes rickets and osteomalacia. It discusses the pathophysiology, causes, clinical presentation, diagnosis and treatment of both conditions. Rickets occurs in children and is caused by impaired mineralization of the growth plate. Osteomalacia occurs in adults and results from impaired mineralization of osteoid. Causes include vitamin D deficiency, calcium deficiency, hypophosphatemia, and factors that inhibit mineralization. Clinical features depend on age and include bone deformities, weakness, and fractures. Diagnosis involves clinical, biochemical, and radiographic evaluation. Treatment focuses on correcting the underlying cause and managing symptoms.
Osteogenesis imperfecta, or brittle bone disease, is caused by mutations in collagen genes COL1A1 and COL1A2 that result in abnormal bone formation and fragility. It is characterized by bones that break easily from minor trauma, along with other connective tissue problems like blue sclera and joint laxity. Treatment focuses on preventing fractures through braces and limiting activity, as well as bisphosphonates and surgery to insert rods for stabilization. The disease ranges in severity from mild cases with normal life expectancy to lethal prenatal forms.
This document discusses metabolic bone diseases, including their composition, calcium and phosphate metabolism, and specific diseases. It provides details on osteoporosis, rickets/osteomalacia, Paget's disease, and renal osteodystrophy. The composition of bone includes collagen, proteoglycans, and hydroxyapatite. Calcium and vitamin D intake recommendations are outlined for different populations. PTH, calcitonin, vitamin D, and alkaline phosphatase roles in calcium regulation are summarized. Osteoporosis risk factors and management strategies are highlighted.
This document summarizes rickets, a childhood bone disease caused by vitamin D deficiency or impaired vitamin D metabolism. It discusses the pathology of rickets, which involves abnormal cartilage cell maturation and failed bone mineralization. This leads to bone deformities and fractures. The document outlines various causes of rickets, including nutritional deficiencies, malabsorption, and genetic disorders affecting vitamin D and phosphate metabolism. Diagnosis involves x-rays showing characteristic bone changes. Treatment involves vitamin D, calcium, phosphate supplementation as needed, and sometimes surgery to correct deformities once the disease is resolved.
The document discusses the principles of managing compound fractures of the lower limb. It defines compound fractures as fractures where the broken bone communicates with an external wound. It describes the Gustillo classification system for open fractures based on wound size and soft tissue damage. Grade I fractures have a wound less than 1 cm while Grade III fractures have extensive soft tissue stripping. The key priorities in emergency management are resuscitation of the patient, assessment of limb vascularity and compartment syndrome, thorough wound debridement and splinting without reduction, and use of broad spectrum antibiotics. Surgical management involves thorough debridement of all devitalized soft tissues and temporary stabilization using external fixation to allow wound healing before definitive fixation.
The document discusses renal osteodystrophy, which refers to bone diseases that occur in patients with impaired kidney function. It outlines several types of renal osteodystrophy, including osteitis fibrosa, adynamic bone disease, and osteomalacia. It describes the pathogenesis of secondary hyperparathyroidism in kidney disease and the effects of parathyroid hormone and vitamin D on bone and mineral metabolism. Treatment goals are to control parathyroid hormone levels, calcium, phosphorus, and vitamin D to prevent bone complications in renal patients.
Vitamin D deficiency is common in critically ill neonates. A study found serum 25-OH vitamin D levels were significantly lower in critically ill neonates compared to healthy newborns, with no correlation to disease severity except in pneumonia cases. The study recommended measuring 25-OH vitamin D levels in critically ill neonates and ensuring adequate maternal vitamin D intake during pregnancy and lactation, as well as vitamin D supplementation for breastfed infants. Guidelines for treating vitamin D deficiency in children include daily or weekly high dose vitamin D supplementation for 4-8 weeks, followed by maintenance doses, while insufficiency is managed with biweekly or monthly lower dose supplementation.
Vitamin D deficiency is common, affecting approximately 66% of the global population. It is defined as a serum 25-hydroxyvitamin D level below 20 ng/mL. Symptoms include bone and muscle pain. At-risk groups include those with dark skin, obesity, or malabsorption issues. Screening is recommended for high-risk individuals. Treatment involves oral vitamin D supplements of 50,000 IU weekly or 6000 IU daily to raise levels above 30 ng/mL. Maintenance doses of 800-1000 IU daily are used thereafter to prevent recurrence.
Vitamin D deficiency is common worldwide. It is important to measure 25-hydroxyvitamin D levels to assess vitamin D status, with levels below 30 ng/mL considered deficient. For children and adults who are deficient, treatment with high dose vitamin D is recommended for 8 weeks, followed by maintenance therapy. Supplementation of at least 400 IU of vitamin D daily is recommended for pregnant women to prevent deficiency. While sunlight exposure produces vitamin D, excess sun exposure should be avoided due to skin cancer risks.
The document provides an overview of vitamin D, including its history, sources, functions, deficiency, testing, and effects on bones and teeth. Vitamin D is important for calcium absorption and bone mineralization, and deficiency can lead to conditions like rickets and osteomalacia, causing bone deformities and increased risk of fractures. The document discusses various forms of vitamin D, recommended intake levels, biomarkers used to indicate status, laboratory testing methods, and dental considerations related to vitamin D deficiency.
This document provides information on vitamin D, including its history, forms, sources, functions, deficiency, testing, and role in dental health. It discusses the key points that vitamin D is important for calcium absorption and bone mineralization, sources include exposure to sunlight and dietary intake of oily fish, eggs, and fortified foods. Vitamin D deficiency can lead to metabolic bone diseases like rickets in children and osteomalacia in adults, causing bone pain and deformities. Biomarkers and tests are used to diagnose and monitor vitamin D levels.
Vitamin D is a fat-soluble steroid hormone important for calcium absorption and bone health. It exists in two major forms, D2 and D3, which are obtained from plant and animal sources respectively. Both forms undergo hydroxylation in the liver to form 25-hydroxyvitamin D [25(OH)D], the storage form, and then in the kidneys to form the active 1,25-dihydroxyvitamin D [1,25(OH)2D]. While 1,25(OH)2D levels are tightly regulated, 25(OH)D levels best indicate vitamin D status since it has a longer half-life and is not as affected by short term changes. Insufficient vitamin D
This document discusses vitamin D, including its role, metabolism, clinical assessment, and relevance to various diseases. It covers how vitamin D is obtained from skin exposure to sunlight and diet, converted to its active form in the liver and kidneys, and acts through vitamin D receptors. Deficiency can cause bone diseases like rickets and osteomalacia or muscle weakness. Low vitamin D may also exacerbate autoimmune diseases and increase cancer and infection risks. Testing for vitamin D levels is important and supplementation can help treat deficiency. Further research is still needed on vitamin D's complex anti-inflammatory and immunoregulatory functions.
Rickets is a disease affecting bone mineralization in children. It causes skeletal deformities and stunted growth. The document discusses the different types of rickets including nutritional rickets due to vitamin D or calcium deficiency, renal rickets, and genetic forms. Symptoms, causes, treatments, and prevention strategies are covered for each type of rickets.
Vitamin d insufficiency and deficiency in children and adolescentsAzad Haleem
Vitamin D insufficiency and deficiency can occur in children and adolescents. The document discusses the forms and pathways of vitamin D in the body. Risk factors for deficiency include dark skin, limited sun exposure, exclusive breastfeeding, obesity, and genetic disorders. Deficiency can lead to rickets in children or osteomalacia. Diagnosis is made by measuring 25-hydroxyvitamin D levels in the blood. Treatment involves vitamin D supplementation, with dosage depending on age and severity of deficiency. Monitoring of vitamin D levels is important during and after treatment.
This document discusses rickets, a disease of growing bone caused by unmineralized bone matrix. It causes include vitamin D deficiency, calcium deficiency, phosphorus deficiency, and renal losses. Symptoms include softening of the skull, chest wall abnormalities, limb deformities, and spinal curvature. Treatment involves vitamin D, calcium, and phosphorus supplementation. Refractory rickets can be caused by defects in vitamin D metabolism or low phosphate disorders. Congenital and secondary vitamin D deficiencies as well as genetic disorders affecting vitamin D metabolism can also cause refractory rickets.
This document discusses vitamin D, including its sources, functions, deficiency, recommended intake levels, associated health conditions, investigations, and management. Key points:
- Vitamin D is important for calcium absorption and bone health but many people are deficient due to lack of sun exposure and inadequate dietary intake.
- Deficiency can lead to bone diseases like rickets and osteomalacia as well as increased risk of cancers, cardiovascular disease, autoimmune disorders, and falls in older adults.
- At risk groups include breastfed infants, older adults, those with limited sun exposure or darker skin, obese individuals, and pregnant/postmenopausal women.
- Testing vitamin D levels helps diagnose deficiency as insufficient levels below
This document discusses vitamin D, its natural sources, deficiency, and importance. It notes that vitamin D is a fat-soluble vitamin essential for bone and calcium health. While sunshine is the main natural source, few foods contain significant amounts. Vitamin D deficiency is very common worldwide and increases risk of bone abnormalities and other diseases. Deficiency can result from inadequate sun exposure, skin pigmentation, obesity, lack of nutritional intake, and other factors. At-risk groups include breastfed infants, older adults, those with limited sun exposure or dark skin, and the obese. Blood tests can identify deficiency which is treated through dietary sources and supplements.
Pharmacology of endocrine system calcitonin & vitamin dNursing
Calcitonin and vitamin D are hormones that regulate calcium levels. Calcitonin is produced by the thyroid and decreases blood calcium levels by inhibiting bone resorption and kidney reabsorption. Vitamin D promotes intestinal calcium absorption and is obtained through sun exposure, diet, and supplements. Both work antagonistically with parathyroid hormone to maintain appropriate calcium and phosphorus levels in the blood and bones.
Vitamin D plays an important role in regulating calcium levels and bone health. It is also involved in insulin regulation and may protect against cancer, cardiovascular disease, and infections. Vitamin D deficiency can lead to rickets in children and osteomalacia in adults as well as increased risk of falls in older adults. Supplementation is recommended for those with inadequate sunlight exposure or dietary intake, with dosage depending on age.
detailed vitamin d synthesis and mechanism explained. pathophysiology of rickets explained. appropriate latest treatment guidelines given from uptodate. very nice given in uptodate and source from internate. ppt prepared by Dr sachin wagh junior resident in pediatrics MGM medical college & hospital aurangabad maharashtra
1. The document discusses vitamin D functions, deficiency, testing, and treatment recommendations. It provides guidelines on screening for deficiency, preferred tests, dosing for deficiency treatment in different populations, and use of vitamin D supplements for non-skeletal benefits like immunity and cancer reduction.
2. Treatment of vitamin D deficiency requires supplementation, not just dietary changes, with recommendations to use cholecalciferol over ergocalciferol. Dosing depends on factors like age and compliance monitoring is advised.
3. Beyond bone health, evidence is mixed on other benefits of vitamin D supplementation though fall prevention is recommended. Judicious evaluation of other causes is advised when vitamin D replacement does not resolve symptoms.
Vitamin D is an essential vitamin that must be metabolized to become biologically active. It plays an important role in calcium homeostasis, bone and muscle health, immune function, and the regulation of cell growth. The best indicator of vitamin D status is the measurement of 25-hydroxyvitamin D in the blood, as it reflects vitamin D from dietary intake and sunlight exposure. Low vitamin D levels have been associated with increased risk of various chronic diseases. Vitamin D deficiency can lead to impaired bone mineralization and increased fracture risk.
Vitamin D deficiency causes rickets in children and osteomalacia in adults. The document discusses vitamin D metabolism, forms, measurement, defining sufficiency, causes of deficiency including lack of sunlight and certain medical conditions or medications, clinical manifestations like bone pain and deformities, management including high dose oral supplementation or injections to correct deficiency followed by maintenance doses. Treatment aims to restore vitamin D levels to the sufficient range and ensure adequate calcium intake, with dosing recommendations provided for different age groups and medical conditions.
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Vitamin D and disorders – hypo/ hypervitaminosis D
1. VITAMIN D AND DISORDERS –
HYPO/HYPERVITAMINOSIS D
DR SANGAM H B
2. SYNTHESIS AND METABOLISM
• 1,25 dihydroxyvitamin D [1,25(OH)2 D] major steroid hormone
involved in regulation of mineral ion homeostasis
• Plant source – vitamin D2(ergocalciferol), Animal source – vitamin D3
(cholecalciferal)
• Skin is a major source of vitamin D which is synthesized upon skin
exposure to UV-B radiation (290-320nm)
• Except for fish, food (unless fortified) contains only limited amounts of
vitamin D
3.
4. D 1-α hydroxylase
• PTH and hypophosphatemia are major inducers of this microsomal
enzyme in the kidney
• Calcium, FGF23, and 1,25(OH)2 D repress the enzyme
• Expressed in epidermal keratinocytes, trophoblastic layer of placenta,
produced by macrophages associated with granulomas and
lymphomas
• In pathologic states, enzyme induced by interferon ϒ and TNF α
5. ✓Major pathway for inactivation is additional hydroxylation by vitamin
D 24-hydroxylase
✓FGF 23 induces this enzyme thereby reduces 1,25(OH)2 D levels both
by inactivating and impairing synthesis
✓Mutation of the gene encoding this enzyme (CYP24 A1) can lead to
infantile hypercalcemia
• Polar metabolites of vitamin D is secreted into the bile and reabsorbed
via enterohepatic circulation. Impairment of this recirculation leads to
accelerated losses of vit D metabolites, seen with terminal ileal
diseases.
6. Actions of 1,25(OH)2 D
• 1,25(OH)2 D mediates its biologic effects by binding to nuclear
receptor subfamily, vitamin D receptor (VDR)
• VDR binds to target DNA sequences as heterodimer with the retenoid
X receptor, resulting in induction of target gene expression
• This hormone is a major inducer of calbindin 9K, calcium-binding
protein in intestine
• Major calcium transporters, TRPV5 and TRPV6 are also vitamin D
responsive
7. • VDR is expressed in osteoblasts and regulates the expression of genes
like bone matrix protein, osteocalcin and osteopontin
• Both 1,25(OH)2 D and PTH induce the expression of RANK ligand
which promotes osteoclast differentiation, by this mechanism
1,25(OH)2 D induces bone resorption
• The VDR is expressed in the parathyroid gland, and 1,25(OH)2 D has
shown to have antiproliferative effects on parathyroid cells and to
suppress transcription of the parathyroid hormone gene.
• 1,25(OH)2 D also has antiproliferative effect on keratinocytes, breast
cancer cells and prostate cancer cells
8. • Vitamin D is thought to be important for maintaining normal function
of many non skeletal tissues such as muscle (including heart muscle),
for immune function and for inflammation as well as for cell
proliferation and differentiation
• Studies have shown role of vitamin D in treatment of tuberculosis,
psoriasis, and multiple sclerosis or for the prevention of certain
cancers and also SARS CoV-19
• Insufficiency can increase risk of type 1 DM, cardiovascular disease
(insulin resistance, hypertension, low grade inflammation) or brain
dysfunction(depression)
9. Deficiency and resistance – impaired action
• Impaired availability of vitamin D, secondary to inadequate dietary
vitamin D, fat malabsorptive disorders and/or lack of sunlight
• Impaired hydroxylation by the liver to produce 25 hydroxyvitamin D
(liver disease, isoniazid, 25 hydroxylase mutation)
• Impaired hydroxylation by the kidney to produce 1,25
dihydroxyvitamin D (vitamin D dependent rickets type 1, chronic renal
insufficiency)
10. • End organ insensitivity to vitamin D metabolites (hereditary vitamin D
resistant rickets [HVDRR], vitamin D dependent rickets type 2)
• Glucocorticoids when used chronically in high doses, inhibit intestinal
vitamin D dependent calcium absorption, leads to osteoporosis and
fractures
• Drugs that induce cyt P 450 – barbiturates, phenytoin and rifampicin
11.
12. Vitamin d sufficiency
• Most specific screening test for vitamin D deficiency is a serum
25(OH)vitamin D level
• Categorization of vitamin D status in adults
✓Vitamin D sufficiency:- > 20 ng/ml
✓Vitamin D insufficiency :- 12 to 20 ng/ml
✓Vitamin D deficiency:- <12 ng/ml
✓Risk of vitamin D toxicity:- > or = 100ng/ml
14. Osteomalacia
• Osteomalacia refers to impaired mineralization of bone matrix
• Clinical features-
✓Bone pain and muscle weakness
✓Bone tenderness
✓Fracture
✓Difficulty walking and waddling gait in four
✓Muscle spasms, cramps
• Most accurate way to diagnose – tetracycline labelling and
histomorphometric assessment
15. Rickets
• Rickets refers to deficient mineralization at the growth plate, as well as
architectural disruption of this structure
• Skeletal findings include-
✓Delayed closure of the fontanelles
✓Parietal and frontal bossing
✓Craniotabes (soft skull bones)
✓Rachitic rosary – beading of costochondral junction
✓Formation of Harrison sulcus at the lower margin of thorax by inward
pull of diaphragmatic attachments
16.
17.
18. Vitamin D dependent rickets
• Type 1 – 1 alpha hydroxylase defect
• Type 2 – vitamin D receptor defect
• Autosomal recessive disorder presents with syndrome of vitamin D
deficiency in the first year of life
• Presents with growth retardation, rickets and hypocalcemic seizures
• Treatment with vitamin D metabolites calcitriol, doxercalciferol. These
don’t require activation from the enzyme. Lifelong theraphy is
required
19. Vitamin D resistant rickets
• X linked dominant disorder, involving PHEX gene mutation
• Due to which there is FGF-23 level elevation which is a inhibitor of
enzyme 1 alpha hydroxylase, reduces PTH and cause phosphaturia
• Treatment – along with vitamin D supplementation, phosphate also
needs to be given
20. Vitamin D and COVID 19
• In patients with COVID 19, vitamin D supplementation may be necessary
to meet the recommended intake. Doses exceeding upper level intake
are not recommended.
• Vit D is considered as a facilitator of the innate immune response during
SARS-CoV 2 infection
• In large cohort study from UK Biobank, there was no association
between 25(OH)D levels and risk of or mortality from COVID 19.
subsequent studies have found positive COVID 19 test was higher in
those who were likely vitamin D deficient (<20ng/ml)
• and fewer patients on vitamin D supplementation required oxygen
therapy and ICU admission compared to general population
21. Vitamin D replenishment
• Preparation available –
✓Supplementation with cholecalciferol is suggested than with
ergocalciferol
✓Vitamin D3(Cholecaliferol) available in 400, 800, 1000, 2000, 5000,
10000, 50000,60000 unit oral capsule, solution, sachets. And also
3,00,000 and 6,00,000 unit injectable formulation
✓Vitamin D2(Ergocalciferol) is available for oral use in 200,400 and
50000 unit capsules or in liquid form 8000 units
22. Dosing
• In patients with normal absorptive capacity for every 100 unit of vit
D3, serum 25(OH)D concentration increase by approx. 0.7 to 1.0
ng/ml. larger increments seen in patients with lower baseline 25(OH)D
• For patients with serum 25(OH)D <12ng/ml 50,000 IU of D3 or D2
orally once per week for six to eight weeks and then 800IU of D3 daily
thereafter
• 25(OH)D levels >12 and < 20 ng/ml initial supplementation with 800
to 1000 IU daily may be sufficient. Repeat serum 25(OH)D level after 3
months to see if therapeutic goal is achieved
23. • If 25(OH)D level is 20 to 30ng/ml, 600 to 800 units of D3 daily may be
sufficient to maintain target range
• In patients with malabsorption oral dosing and duration depend upon
the absorptive capacity. High doses of vitamin D 10,000 to 50,000 IU
daily may be necessary to treat patients of gastrectomy or
malabsorption
• Vitamin D should always be given in conjunction with calcium
supplementation
• Calcium supplementation should include 1.5-2 gm/day of elemental
calcium
24. • To monitor treatment and resolution of vitamin D deficiency serum
and urinary calcium measurements are seen
• In patients who are vitamin D replete and are taking adequate calcium
supplements, 24 hour urinary calcium excretion should be in the
range of 100-250 mg/24 hr
• > 250mg/24 hr predispose to nephrolithiasis and should lead to a
reduction in vitamin D dosage and/or calcium supplementation.
• Lower levels suggests problem with adherence or with absorption of
calcium or vitamin D supplements
25. Vitamin D intoxication
• Occurs generally after inappropriate use of vitamin D supplements
• May occur in patients who consume megadoses of supplements or in
patients who take vitamin D replacement for malabsorption, renal
osteodystrophy, osteoporosis, or psoriasis
• Prolonged exposure of the skin to sunlight does not produce toxic
amounts of vitamin D3
• Upper limit of intake – 4000 IU/day
26. • Symptoms -
✓ Acute intoxication - hypercalcemia and include confusion, polyuria,
polydipsia, anorexia, vomiting and muscle weakness
✓Chronic intoxication – nephrocalcinosis, bone demineralization and
pain
• Treatment –
✓ Discontinuation of vitamin D and calcium supplements
✓ Treatment of hypercalcemia