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HYPOCALCEMIA. Hasan AYDIN , MD Yeditepe University Medical Faculty Department of Endocrinology and Metabolism. Overview of Calcium Balance. Etiolog y. Decreased GI Absorption Poor dietary intake of calcium Impaired absorption of calcium Vitamin D deficiency

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hypocalcemia

HYPOCALCEMIA

Hasan AYDIN, MD

Yeditepe UniversityMedicalFaculty

Department of EndocrinologyandMetabolism

etiolog y
Etiology

Decreased GI Absorption

Poor dietary intake of calcium

Impaired absorption of calcium

Vitamin D deficiency

Poor dietary intake of vitamin D

Malabsorption syndromes

Decreased conversion of vit. D to calcitriol

Liver failure

Renal failure

Low PTH

Hyperphosphatemia

Decreased Bone Resorption/Increased Mineralization

Low PTH ( hypoparathyroidism)

PTH resistance ( pseudohypoparathyroidism)

Vitamin D deficiency / low calcitriol

Hungry bones syndrome

Osteoblastic metastases

Increased Urinary Excretion

Low PTH

Thyroidectomy

I131 treatment

Autoimmune hypoparathyroidism

PTH resistance

Vitamin D deficiency / low calcitriol

parathyroid related disorders
Parathyroid Related Disorders
  • Absence of the parathyroid glands or of PTH
    • Congenital
      • DiGeorge’s syndrome
      • X-linked or autosomally inherited hypoparathyroidism
      • Autoimmune polyglandular syndrome type I
      • PTH gene mutations
    • Postsurgical hypoparathyroidism
    • Infiltrative disorders
      • Hemachromatosis
      • Wilson’s disease
      • Metastases
    • Hypoparathyroidism following radioactive iodine thyroid ablation
  • Impaired secretion of PTH
    • Hypomagnesemia
    • Respiratory alkalosis
    • Activating mutations of the calcium sensor
  • Target organ resistance
    • Hypomagnesemia
    • Pseudohypoparathyroidism (Type I and II)
vitamin d related disorders
Vitamin D Related Disorders
  • Vitamin D deficiency
    • Dietary absence
    • Malabsorbtion
  • Accelerated loss
    • Impaired enterohepatic recirculation
    • Anticonvulsant medications
  • Impaired 25-hydroxylation
    • Liver disease
    • Isoniazid
  • Impaired 1α-hydroxylation
    • Renal failure
  • Vitamin D dependent rickets type I
  • Oncogenic osteomalcia
  • Target organ resistance
    • Vitamin D dependent rickets type II
    • Phenytoin
other causes
Other Causes
  • Excessive deposition in to the skeleton
    • Osteoblastic malignancies
    • Hungry bone syndrome
  • Chelation
    • Foscarnet
    • Phosphate infusion
    • Infusion of citrated blood products
    • Infusion of EDTA containing contrast agents
    • Fluoride
  • Neonatal hypocalcemia
    • Prematurity
    • Asphyxia
    • Diabetic mother
    • Hyperparathyroid mother
  • HIV infection
    • Drug therapy
    • Vitamin D deficiency
    • Impaired PTH responsiveness
  • Critical illness
    • Pancreatitis
    • Toxic shock syndrome
    • Intensive care unit patients
clinical features
Clinical Features
  • Signs and symptoms depend on
    • Level of serum calcium
    • Age at onset and duration
    • Level of serum magnesium and potassium
    • Accompanying disturbances in acid-base homeostasis
  • Sometimes only symptoms of underlying disorder
symptoms and signs
Symptoms and Signs
  • Systemic
    • Confusion
    • Weakness
    • Mental retardation
    • Behavioral changes
symptoms and signs1
Symptoms and Signs
  • Neuromuscular
    • Parestesias
    • Psychosis
    • Seizure
    • Carpopedal spasm
    • Chvostek’s and Trousseau’s signs
    • Depression
    • Muscle cramps
    • Parkinsonism
    • Irritability
    • Basal ganglia calcifications
syptoms and signs
Syptoms and Signs
  • Cardiac
    • Prolonged QT interval
    • T wave changes
    • Congestive heart failure
  • Ocular
    • Cataracts
syptoms and signs1
Syptoms and Signs
  • Dental
    • Enamel hypoplasia of teeth
    • Defective root formation
    • Failure of adult tooth to erupt
  • Respiratory
    • Laryngospasm
    • Bronchspasm
    • Stridor
chvostek s s ign
Chvostek’s Sign
  • Elicited by tapping over facial nerve causing twitching of ipsilateral facial muscles
trousseau s s ign
Trousseau’s Sign
  • Carpal spasm in response to inflation of BP cuff to 20 mm Hg above SBP for 3 min
evaluation of h ypocalcemia
Evaluation of Hypocalcemia
  • History:
    • Paresthesias/ cramping
    • Tetany
    • Carpopedal spasm
    • Laryngospasm
    • Seizures
physical e xamination
PhysicalExamination
  • Signs of hypocalcemia:
      • Chvostek sign
      • Trousseau sign
      • Hyper-reflexia
  • Dysmorphism (Di George Syndrome, PHP)
  • Dental abnormalities
  • Chronic mucocutaneous candidiasis
  • Rickets
investigations
Investigations
  • Serum calcium (ionic), phosphate, magnesium
    • Ionized Ca is physiologically active
      • 0.1 increase in pH increases iCa by 3-8%
      • 10 g/L decrease in albumin increases iCa by 0.2
  • iPTH
  • Serum urea and creatinine levels
  • Vitamin D levels (if available)
  • Genetic studies (if necessary)
approach to low serum calcium
Approach to low serum calcium

PTH Level

Low

High

Mg level

Phosphate

Low

High

High

Low

Hypo

magnesemia

Hypo

parathyroid

Creatinine

25 OH Vit D

High

Normal

Low

Normal

Renal

Failure

PHP

1,25 OH Vit D

Nutrition

Malabsorption

Liver disease

Vit D

Dep Rickets

Vit D

Res Rickets

treatment
Treatment
  • Symptomatic:
    • Parenteral Ca
      • 10% CaCl2: 10 cc ampoules contains 360 mg of elemental Ca
      • 10% Ca gluconate: 10 cc ampoules contains 93 mg of elemental Ca
    • Recommended dose: 100-300 mg of elemental Ca over 10-20 min followed by an infusion of 0.5-2 mg/kg/h
treatment1
Treatment
  • Side effects:
    • Nausea
    • Vomiting
    • Flushing
    • Hypertension
    • Bradycardia, heart block (patients should be monitored)
treatment2
Treatment
  • Asymptomatic
    • Oral Ca supplementation
      • 1-4 g/day in divided doses
      • If patient has concurrent hypomagnesemia, Careplacement alone will not correct hypocalcemia unless Mg is also replaced (2-4 g IV for symptomatic patients)
acute management of hypocalcemia
Acute Management Of Hypocalcemia
  • Frank Tetany
    • 10-20 ml calcium gluconate (93 mgf elemental Ca/10 ml) for 10 min.
  • Ongoing severe hypercalcemia
    • 10 ampul of 10 ml calcium gluconate infused over 8-10 hours (in saline or dextrose)
  • When due to hypomagnesemia
    • 1-2 gram of magnesium sulfate (8-16 mEq) q6h, for several days
developmental abnormalities
DevelopmentalAbnormalities
  • DiGeorge Syndrome
    • Parathyroid dysplasia, thymic hypoplasia, immune deficiency, cardiac defects, craniofacial malformations, mental retardation
    • Deletion on long arm of chromosome 22
  • Kenny Caffey Syndrome
    • Parathyroid aplasia, medullary stenosis of long bones, growth retardation
  • Barakat syndrome
    • Hypoparathyroidism, nerve deafness, renal dysplasia
disorders of 25 oh d metabolism
Disorders of 25-OH D Metabolism
  • Hepatic and hepatobiliary disease
    • Impairement of synthesis
    • Particularly in biliary cirrhosis
  • Gastrointestinal disorders
    • Malabsorption and disruption of enterohepatic circulation of vitamin D
  • Protein wasting syndrome
  • Drugs
    • Increased conversion of 25 OH D to inactive metabolites
disorders of 1 25 oh d metabolism
Disorders of 1,25-OH D Metabolism
  • Vitamin D dependent rickets type I
  • Vitamin D dependent rickets type II
  • Vitamin D resistant rickets and osteomalacia
  • Hypercalciuric hypophosphatemic rickets
  • Tumor induced osteomalacia
vitamin d dependent rickets type i
Vitamin D Dependent Rickets Type I
  • Autosomal recessive
  • Inactivating mutations on chromosome 12
  • Circulating levels of 1,25 (OH) D are low
  • Treatment with calcitriol 0,5-3 mcg/day
vitamin d dependent rickets type ii
Vitamin D Dependent Rickets Type II
  • Target organ resistance to calcitriol
  • Markedly elevated plasma levels of 1,25 (OH) D
  • Sporadic and autosomal recessive
  • Alopecia, epidermal cysts, oligodentia
  • Low 24,25 (OH)2D3 and 24 (OH)-25-hydroxylase
  • Treatment with massive doses of vitamin D (10-20 mg/day) or 1,25 (OH)D (6 mcg/kg/day)
vitamin d resistant rickets and osteomalacia
Vitamin D Resistant Rickets and Osteomalacia
  • Sporadic or familial
  • X-linked hypophosphatemic VDRR
  • Hypophosphatemia, normocalcemia, normal PTH, hyperphophaturia
  • 25 (OH)D normal, 1,25 (OH)D low/normal
  • Treatment with administration of phosphorus supplements and vitamin D
tumor induced osteomalacia
Tumor Induced Osteomalacia
  • Release of humoral factors affecting renal phosphate reabsorption, and formation of 1,25 (OH)2D
  • Bone pain, muscle weakness, recurrent pathological fractures, pseudofractures
  • Hypophosphatemia, hypocalcemia, elevated ALP, PTH vary
  • Surgery of tumor
  • Treatment with phosphorus + vitamin D
hypoparathyroidism
Hypoparathyroidism
  • Clinically
    • Symptomsof neuromuscular hyperactivity
  • Biochemically
    • hypocalcemia,
    • hyperphosphatemia,
    • diminished to absent circulating iPTH.
etiology
Etiology
  • Surgical hypoparathyroidism(most common)
  • Familial hypoparathyroidism
  • Idiopathichypoparathyroidism
  • Functionalhypoparathyroidism
functional h ypoparathyroidism
Functional Hypoparathyroidism
  • long periods of hypomagnesemia
    • selective gastrointestinal magnesium absorption defects
    • generalized gastrointestinal malabsorption
    • alcoholism.
  • Serum PTH low
  • Hypocalcemia
  • Mg is required for PTH release
  • Mgis probably also required for the peripheral action of PTH
classification
Classification
  • 5 categories based primarily on the concentration of serum calcium.
    • Grades 1  with no hypocalcemia,
    • Grades 2 inconstant hypocalcemia
    • Grades 3  serum calcium is below 8.5 mg/dl
    • Grades 4  serum calcium is below 7.5 mg/dl
    • Grades 5 serum calcium is below 6.5 mg/dl
  • Clinical manifestations of hypoparathyroidism depend upon the severity and chronicity of the hypocalcemia.
treatment3
Treatment
  • Physiologic replacement of PTH.
  • Pharmacologic doses of vitamin D
    • (ergocalciferol or its more potent analog dihydrotachysterol, in combination with oral calcium administration)
  • Diets low in phosphate (restriction of dairy products and meat) and oral aluminum hydroxide gels
etiology of pseudohypoparathyroidism
Etiology of Pseudohypoparathyroidism
  • abnormal target tissue responses
    • receptor binding of the hormone
    • final expression of the cellular actions of PTH
  • resistance to several other hormones (vasopressin, glucagon).
  • secretion of a biologically inert form of PTH,
  • circulating inhibitors of PTH action,
  • an intrinsic abnormality of PTH receptors,
  • autoantibodies to the PTH receptor, 
pseudohypoparathyroidism
Pseudohypoparathyroidism
  • Rare familial disorder
  • Target tissue resistance to PTH,
  • Hypocalcemia, hyperphosphatemia
  • Increased parathyroid gland function,
  • Short stature and short metacarpal and metatarsal bones.
pshp type ia albright syndrome
PsHP Type Ia (Albright Syndrome)
  • Hypoparatrhyroidism, short stature, round facies, obesity, brachydactily, neck webbing, sc calcifications
  • Defect in the function of Gs protein
  • TSH, Glucagon, Gonadotropin resintance
  • Autosomal dominant
  • Intermittant hypocalcemia, elevated PTH, low urine Ca
p s eudopseudohypoparathyroidism
Pseudopseudohypoparathyroidism
  • developmental defects
  • without the biochemical abnormalities of pseudohypoparathyroidism.
  • lack evidence of PTH resistance
  • 50% reduction in Gs alpha function
  • Autosomal dominant
pseudoidiopathic hypoparathyroidism
Pseudoidiopathic hypoparathyroidism
  • Structurally abnormal form of PTH present
  • Fail to respond to own PTH
  • Normal response to exogenous PTH