This document summarizes key information about calcium balance and drugs that affect it. It discusses the physiological roles of calcium, how plasma calcium levels are regulated by parathyroid hormone (PTH), calcitonin, and calcitriol. It describes calcium absorption and excretion, preparations of calcium supplements, and uses of calcium supplements and drugs like PTH, calcitonin, and calcitriol to treat conditions like tetany, osteoporosis, and hypercalcemia. The actions, pharmacokinetics, and clinical uses of PTH, calcitonin, and calcitriol are also summarized.

1. Drugs Affecting
CalciumBalance
Dr. CHANDANE R. D.
Associate Professor
Dept. Of Pharmacology
Lady Hardinge Medical
College New Delhi

2. Calcium
Physiological role:
• Excitability of nerves and muscles, regulates
permeability and integrity of cell membranes and cell
adhesion
• Excitation-contraction coupling of all types of muscles
• Excitation and secretion of endocrine and exocrine
glands, neurotransmitters release from nerve endings
• Intracellular messenger for hormones, autacoids and
transmitters
• Impulse generation and conduction in heart
• Coagulation of Blood
• Structural function of Bone and Teeth - hydroxyapatite

3. Plasma Calcium Level
• Regulated by 3 hormones Parathormone,
calcitonin and Calcitriol (active vit. D)
• Normal plasma level = 9-11 mg/dl
• Hypoalbuminemia – no decrease in conc. Of
Ca++
• Acidosis – favours ionization
• Alkalosis – disfavours ionization
– hyperventilation precipitates tetany and
laryngospasm in Calcium deficiency

4. 40-41% is bound to plasma protein – albumin,
9-10% - citrate, carbonate and phosphate and
50% is free ionized and important form-Responsible
for calcium function and Can be directly
measured

5. Absorption and Excretion
• Absorbed from entire small intestine including
duodenum – carrier mediated active transport under
the influence of Vit.D
• Phytates, phosphates, oxalates and tetracycline, also
Glucocorticoides and Phenytoin reduces absorption
• Filtered through glomerulus but mostly reabsorbed
• Vit. D increases and Calcitonin decreases reabsorption
in proximal tubule
• PTH -increases distal tubular reabsorption -thiazide
• 300 mg is excreted daily in urine and faeces
• Daily requirement: 800 -1500 mg per day (1/3rd
absorbed)

6. Preparations of calcium
S.No Preparation Characteristic
1 Calcium
chloride
27 % calcium , highly irritant , not for IM
use. Orally also irritable
2 Calcium
gluconate
9 % calcium , non irritating Sense of
warmth produced on injection
3 Calcium
lactate
13 % calcium, orally well tolerated , non
irritating
4 Calcium
dibasic
phosphate
23 % calcium , used as antacid and calcium
supplement
5 Calcium
carbonate
40 % calcium , tasteless, non irritating ,
used as antacid and calcium supplement

7. USES
1. Tetany: Severe cases Calcium gluconate 10 to 20 ml IV
over 10 minutes followed by 50 to 100 ml of Ca
gluconate solution over 6 Hrs
• Oxygen inhalation, IV fluids then oral therapy
2. Dietary supplement: growing children, pregnant,
lactating and meopausal etc. In men and women reduce
the bone loss
3. Osteoporosis: Prevention ant treatment of osteoporosis
with HRT/raloxifene/Alendronate – to ensure Ca++
deficiency does not occur
• Calcium and Vit. D3 used as adjuvant

8. Uses….
4. Empirically in dermatoses, parathesia and
weakness
5. Antacids
6. Hyperkalemia: Calcium gluconate iv life
saving and reduce cardiotoxic effects
7. Black widow spider envenomation: iv
8. Magnesium toxicity, cardiac arrest and
Hyperphosphataemia(CRF)

9. Treatment of hypercalcemia
• Hydration & dietary calcium restriction < 400 mg/day
• Sodium chloride: Saline administration will cause renal
elimination of calcium
• Furosemide 20 -40 mg every 2-4 hrs
• Glucocorticoids: reduce intestinal absorption & tubular
reabsorption of calcium
• Calcitonin: 4 IU/kg SC OR IM twice or once daily can be
increased to 8 IU/kg IM 6 hrly
• Mithramycin (Plicamycin) : decrease bone resorption low
dose 10 μg/kg IV
• Inorganic phosphate: phosphosoda 5 ml TDS
- Biphosphonate

10. PARATHYROID HORMONE
(Parathormone)
• Location : Posterior to thyroid gland , 4 in nos
Secreted by principal cells
• Preproparathyroid hormone → proparathyroid
hormone → PTH(84 AA polypeptide)
• Plasma Ca2+ is the major factor regulating
PTH secretion. Hypocalcemia stimulates PTH
secretion whereas hypercalcemia inhibits it.
• Calcium inhibits PTH secretion by stimulating
calcium sensing receptor on parathyroid cells.

11. Mechanism of action
• PTH receptor - G protein coupled receptor on
activation increases cAMP formation & intracellular
Ca++ in target cells, in bone target cells are osteoblast
• induces a factor ‘Receptor for activation of nuclear
factor-κB-ligand’ (RANKL) which diffuses and
combines with RANK on osteoclast precursors and
transforms them into osteoclasts as well as activates
osteoclasts

12. • Increase formation of the remodeling pit is f/b
osteoblastic deposition of new bone into it.
• PTH enhances proliferation and differentiation of
preosteoblasts and deposition of osteoid as well.
• ↑ Bone resorption with high conc of PTH
continuously, but intermittent exposure to low conc
↑bone formation.

14. • Rapidly metabolised in liver & kidney
• T1/2 is 2-5 min
Actions
• Bone: Resorption of calcium from bone
increasing the number of bone remodeling units
and activating osteoclasts
• Kidney: increases calcium reabsorption in the
distal tubule also promote phosphate excretion
• Intestine:increase absorption indirectly by
increases circulating calcitriol by two
mechanisms 1) Directly by stimulating 1α
hydroxylase in kidney and 2) indirectly by
decreasing serum phosphate.
• Decrease ca level in milk saliva and ocular lens.

15. rParathyroid hormone [rPTH(1-34),
teriparatide]
• Mechanism of action: Stimulates new bone formation
on trabecular and cortical bone surfaces by preferential
stimulation of osteoblastic activity over osteoclastic
activity.
• Daily SC injections of 40mcg of rPTH for 12-18
months , increased BMD by 9-13% and decreased risk
of vertebral fractures by 65 to 69 % T1/2-1hr, costly
• Use: severe osteoporosis with multiple risk of fracture
• Diagnostic use: teriparatide i.v.: if plasma calcium
level fails to rise, then it is pseudohypoparathyroidism.
• S/E:headache, nausea, dizziness and leg cramps
• C/I: Pagets disease and hypercalcaemia

16. Hyperparathyroidism
• Hypercalcaemia, decalcification of bone—deformities
and fractures, metastatic calcification, renal stones,
constipation
T/T: 1) surgical removal of the parathyroid tumour
2) low calcium, high phosphate diet with plenty of fluids
is advised.
3) Cinacalcet: It activates the Ca2+ sensing receptor
(CaSR) in the parathyroids and blocks PTH secretion.
Use: secondary hyperparathyroidism due to renal
disease and in parathyroid tumour.

17. Calcitonin
• Calcitonin, 32-amino acid peptide hormone
(Mol Wt 3600) secreted by the thyroid
gland, tends to decrease plasma Ca conc and
has effects opposite to those of PTH
• Parafollicular cells, or C cells, lying in the
interstitial fluid between the follicles of the
thyroid gland
• rise in plasma Ca2+ increases, while fall in
plasma Ca2+ decreases calcitonin release.

18. Actions:
• Inhibit bone resorption by direct action on
Osteoclasts- decrease their ruffled surface
• inhibits the proximal tubular reabsorption of
calcium and phosphate by direct action on
kidney. But hypocalcemic action reduce
calcium glom filtration so reduce urinary ca
• Action is mediated through G- protein coupled
calcitonin receptor & increased cAMP
formation but target cells are different from
that of PTH

19. Calcitonin : Preparations: SC/IM routes
• Porcine (Natural) calcitonin: Antigenic
• Synthetic salmon calcitonin: More potent
due to slower metabolism. also as nasal spray
• Synthetic human calcitonin:
• 1 IU = 4 μg of std preparation
S/E: Nausea, flushing and tingling of fingers
Bad taste, flu-like symptoms, allergic reactions
and joint pain

20. Uses:
1) Hypercalcemia states: Hyperparathyroidism,
hypervitaminosis D, osteolytic bony metastasis and
hypercalcaemia of malignancy; used only to
supplement BPNs as weak hypocalcemic
2) Pagets disease of bone:Bisphosphonates are preferred
calcitonin 2nd line
3) Postmenopausal osteoporosis & corticosteroid
induced osteoporosis: It is less effective than
BPNs/HRT. Salmon calcitonin as nasal spray along
with Vit D supplements 200 IU /day increase bone
mineral density in menopausal women and to reduce
vertebral, but not nonvertebral, fractures.
4) Diagnosis of medullary carcinoma of thyroid:

21. Vitamin D
• Mainly D3 (cholecalciferol) and D2
(calciferol)
• Both are equally active in human
• Calcitriol (active form of D3) is more
important physiologically
• Released from liver in blood and binds to
specific vit D binding globulin

22. vit D should be considered a hormone because:
(a) It is synthesized in the body (skin); under
ideal conditions it is not required in the diet.
(b) It is transported by blood, activated and then
acts on specific receptors in the target tissues.
(c) Feedback regulation of vit D activation
occurs by plasma Ca2+ level and by the active
form of vit D itself.

24. Actions of calcitriol
1) Enhancement of absorption of Ca and PO4
from intestine
• By increasing the synthesis of calcium channels
and a carrier “calcium binding protein (CaBP)” or
calbindin
• Analogous to stroid hormones – binds to
cytoplasmic vit D receptor (VDR)-translocation-
increased synthesis of mRNA-regulation of
protein synthesis
• But, why quick? - Activation of VDR also
promotes endocytotic capture of Calcium and
transport across the duodenal mucosa

25. 2) Calcitriol also enhances recruitment and differentiation of
osteoclast precursor for remodelling – resorption of
Calcium and PO4 from bone
• Mature osteoclasts lack VDR, induces “receptor for
acivaton of nuclear factor-kB-ligand (RAANKL)” in
osteoblasts and activates osteoclasts indirectly
• Laying down and mineralization of osteoids
3) enhances tubular reabsorption of Calcium and phosphate
4) Apart from effects on Ca2+ and phosphate–, calcitriol also
affects maturation and differentiation of mononuclear
cells (possibility of use in cancers), inhibits epidermal
proliferation and promotes epidermal differentiation
(potential t/t of psoriasis ).

26. Pharmacokinetics
A) Absorbed from intestine in presence of Bile
salts mainly by lymphatics D3 is better
absorbed than D2
D) Binds to alpha-globulin and stored in fatty
tissues for many months
M) It is hydroxylated in the liver to active and
inactive metabolites
E) Half life varies from 1 – 18 days. Metabolites
of vit D are excreted mainly in bile

27. Unitage and preparation
• 1mcg of Cholecalciferol = 40 IU of vit.D
• Calciferol (D2): oily solutions in gelatin capsules –
25000/50000 IU caps
• Cholecalciferol (D3): oral and IM injections – given
3 to 4 weeks intervals
• Calcitriol: 0.25 to 1 mcg orally on altenate days
• Alfacalcidol: Prodrug – rapidly hydrolysed to
calcitriol in liver. Equally active to calitriol on long
term use. Dose – 1-2 mcg/day
• Dihydrotachysterol: Vit D2 analogue HypoPTH and
Renal bone disease

28. Vit D - Uses
1) Prophylaxis (400 IU/day ) and treatment(3000 -4000
IU/day) of rickets & osteomalacia : alternatively
Oral/IM injection 3-6 lac IU every 2-6 month interval
2) Metabolic Rickets
a)Vit D resistant rickets: PO4 with high doses of
calcitriol
b)Vit D dependent rickets:deficiency of renal
hydoxylating mechanism which converts 25-OHD3
into calcitriol. T/T: calcitriol or alfacalcidol
c) Renal rickets: Calcitriol/alfacalcidol or
dihydrotachysterol
3) Senile or postmenopausal osteoporosis:

29. 4) Hypoparathyroidism: calcitriol/alfacalcitriol
dihydrotachysterol
5) Doxercalciferol and Paricalcitol have been approved
for treatment of secondary hyperparathyroidism in
patients with chronic renal disease. These are less likely
to cause hypercalcemia than calcitriol
6) Fanconi like syndrome: can raise lowered phosphate
7) Calcipotriol : Vitamin D analog used topically in
psoriasis. slightly more effective than glucocorticoids.
Systemically tried for skin cancer and immunological
disorder

30. Drug Interactions:
1. Cholestyramine and chronic use of liquid
paraffine can reduce vit D absorption.
2. Phenytoin and phenobarbitone reduce the
responsiveness of target tissues to calcitriol;
their prolonged use (for epilepsy) can cause
rickets/ osteomalacia. It was believed earlier
that these drugs enhance degradation of vit D.
level of calcitriol is normal, but its effect on
intestine and bone is diminished.

31. Vitamin D deficiency
Rickets in small children
1. Osseous changes:
a) Head: craniotabes, frontal bossing, box like skull,
delayed closure of anterior fontanelle
b) Teeth: delayed eruption, with abnormal order
c) Chest: rachitic rosary, pigeon chest, funnel-shaped
chest
d) Spinal column: scoliosis,kyphosis, and lordosis
e) Extremities: bowlegs
f) Rachitic dwarfism
2. Muscular system: potbelly, late in standing and walking
3. Motor development: delayed
4. Other nervous and mental symptoms

33. Treatment
1. Food and nursing care
2. Prevention of complications
3. Special therapy
Vitamin D therapy
A. General daily Vitamin D 2000-4000IU/day for
2-4 weeks, then change to preventive dosage
(400IU).
B. A single large dose: For severe case, or Rickets
with complication, or those who can’t bear oral
therapy. Vitamin D3 3 LAC -6 LAC IU, im,
• preventive dosage can be used after 2-6 months.

34. Prevention
1. pregnant and lactating women should take adequate
amount of vitamin D.
2. Advocate sunbathing
3.Advocate breast feeding, give supplementary food on
time
4. Vitamin D supplementation:
• In prematures, twins & weak babies: 800 IU/day
• For term babies and infants : 400 IU per day,
• For those babies who can’t maintain a daily
supplementation: Vitamin D3 1-2L IU IM.
5. Calcium supplementation:

35. Vitamin D - Sources
• Sunlight is the most important source
• Not found naturally in many foods
• Synthesized in body
• Plants (ergosterol) – Sun-cured forages
• Fluid milk products are fortified with vitamin D
• Oily fish & Fish liver oil
• Egg yolk
• Butter
• Liver
• Difficult for vegetarians

36. Hypervitaminosis D
• chronic ingestion of large doses (~50,000 IU/day) or
due to increased sensitivity of tissues to vit D.
• causes hypercalcemia, which manifest as:
Nausea & vomiting • Excessive thirst , polyuria &
anorexia • Severe itching • Joint & muscle pains •
Disorientation & coma. • Calcification of soft tissue–
Lungs, heart, blood vessels ,
• Hypercalcemia - formation in renal stone
• Treatment: withholding the vitamin, low calcium diet,
plenty of fluids and corticosteroids

37. Calcium Homeostasis
• Calcium and phosphate homeostasis is
maintained by the action of vitamin D (active
form is calcitriol), parathyroid hormone
(PTH), and FGF-23 (Fibroblast growth
factor-23).
• Secondary regulators of Ca2+ homeostasis
include calcitonin, glucocorticoids and
estrogens.

40. Introduction
• Non-hormonal agent in Ca++ homeostasis
• Recently in attention due to Prevention of
osteoporosis, useful in metabolic bone diseases
and hypercalcaemia
• Most effective “antiresorptive” drug at present
• BPNs are analogous of pyrophosphates –
Carbon atom replacing “P-O-P skeleton”

41. Classification – BPNs
Classified in generations (chronological):
BPNs Relative Potency
First generation: Simpler side chain
Etidronate
Tiludronate
1
10
2nd generation: amino or nitrogenous
side chain
Pamidronate
Alendronate
Ibadronate
100
100-500
500-1000
3rd generation: nitrogen atom within a
heterocyclic ring
Risedronate
Zoledronate
1000
5000

42. MECHANISM OF ACTION
• BPNs have selective affinity for Calcium
phosphate – so calcified tissues
• 2 main component of Bone – Bone matrix and
Solid mineral phase (hydroxyapatite)
• Normally, The non-mineralized osteoid covers the
mineralized bone matrix preventing its resorption
by osteoclasts
• For resorption – osteoids must get dissolved or
mineralized (solubilized) such that osteoclasts can
attach to the mineralized matrix

43. • In resorptive pits – acidic zone is created at ruffled
boarders of osteoclasts followed by resorption of matrix
by acid hydrolases
• BPNs localize in the acidic zone due to high affinity for
Ca++ ions
• Ca++ ions released from bone surface due to high acidity
BPNs also released – internalized into osteoclasts by
endocytosis
• Results in:
A) Accelerated apoptosis of osteoclasts reducing their no.
B) Disruption of the cytoskeleton of the ruffled boarder of
osteoclasts
C) Also affect osteoclast precursors and inhibit their
differentiation by suppressing IL-6.

44. Osteoclastic membrane domains.
1) When an osteoclast is not resorbing bone, it shows no signs of
polarized membrane domains.
2) Once the osteoclast starts the resorbing, it quickly polarizes its
membrane into distinct domains. Ruffled border (RB) is a
membrane domain facing the bone surface, where the actual
resorption takes place. Sealing zone (SZ) forms a tight contact to
the bone, sealing the proteolytic enzymes and acid into the forming
resorption lacuna. Basolateral membrane (BL) faces towards the
bone marrow.
3) When the osteoclast is actively resorbing bone, a fourth domain
arises into the basolateral membrane, the functional secretory
domain (FSD), which acts as a route of osteoclasts to exocytose
the resorbed material.

45. • Reduction in cholesterol synthesis via inhibition of
farnesyl pyrophosphate synthase by bisphosphonates
• BPN esp 2nd and 3rd generation : Metabolic effects in
the mevalonate pathway for isoprenoid lipid synthesis.
They inhibit prenylation of certain GTP-binding
proteins involved in cytoskeletal organization,
membrane ruffling and vesicle movement. The net
result is inactivation of osteoclasts, impaired vesicle
fusion and enhanced apoptosis.
• Interference with mevalonate pathway may also impart
antitumor action on bony metastasis

46. Pharmacokinetics
• Highly polar so less poorly absorbed through
GIT
• Part of absorbed drug is incorporated into bone
& remains for long periods years to months
• The free drug is excreted unchanged in urine

47. USES
1. Osteoporosis: Alendronate>HRT or raloxifene
I. Prevention and treatment of post-manaupasal
osteoporosis
II. Both Men and Women – age related, steroid
induced and idiopathic osteoporosis
• Oestrogen prevents only vertebral fracture, BNPs >
effective than calcitonin 5 years protection on cont use.
t½ of alendronate in bone is ~ 10 years, treatment
beyond 5 years is considered unnecessary.
• first choice drugs now for osteoporosis.
2. Osteolytic Bone Metastasis: Parenteral
pamidronate/zoledronate

48. 3. Pagets disease: abnormal osteoclast function -
Honeycomb like bone architecture – arrest osteolytic
lesions, reduce bone pain and improve secondary
symptoms. Alendronate, Risedronate, Pami and Zole
are used. Calcitonin combination better.
4. Hypercalcaemia of Malignancy: Medical emergency
with altered consciousness – Pamidronate 60-90 mg IV
2-4 hours or Zoledronate 4 mg IV 15 minutes.
Supplement with calcitonin IM 6-12 Hrly for 2 days,
i.v. hydration, furosemide, Corticosteroids.
5. Breast Prostate cancer and multiple myeloma:
zolendronate anticancer effect and prevent bony
metastasis
6. Philadelphia-chromosome positive CML:
Zolendronate as adjunctive

49. Adverse effects
• Oral bisphosphonates causes Gastrointestinal
complications such as gastritis or esophagitis,
abdominal pain, nausea, vomiting, diarrhea, and
constipation.
• Bisphosphonate-related osteonecrosis of the jaw-
Phossy jaw so regular dental care and avoid dental
extraction.
• Zoledronate - associated with renal toxicity and first
generation bisphosphonates - osteomalacia.
• Long-term bisphosphonates -increases the risk of
atypical ‘chalkstick’ fracture of femur (subtrochantric
or shaft). Risk increases with concurrent high dose
steroid therapy.
• increase the risk of esophageal cancer.
Contraindication: renal dysfunction, esophageal motility
disorders and peptic ulcer

51. Individual Drugs
1. Etidronate: Not used anymore
2. Pamidronate: Only IV 60-90 mg for 2-4 Hrs, weekly
or monthly in Pagets disease and hypercalcaemia
3. Alendronate: Available in oral form 5, 10, 35, 70 mg
tabs. Prevention of osteoporosis in man and woman.
a. In empty stomach with glass of water
b. Do not allow to lie down or eat till 30 minutes –
oesophagitis; Tea, coffee, mineral water, Juice,
NSAIDs
c. ADRs: Gastric errosion, retrosternal pain, flatulence
d. Bioavailability 1%, 50% goes to Bone, terminal
elimination halflife 10.5 years

52. 4. Risedronate: Similar to Alendronate, but more
potent • Used in osteoporosis and Paget`s disease
5. Zolendronate: Parenterally effective, highly
potent
• Suppression of osteoclastic activity and additional
antitumor effect (mevalonate pathway)
• Proliferation of bony metastasis of Prostate and
breast cancer cells are suppressed
• Can be infused in 15 minutes
• ADR: Flu-like symptoms due to cytokine release

53. Osteoporosis
A systemic skeletal disease characterized by low
bone mass & micro-architectural deterioration
of bone tissue, with a consequent increase in
bone fragility and susceptibility to fracture

54. Primary osteoporosis
• Postmenopausal:↓ estrogen results in ↑ osteoclastic activity
without ↑osteoblastic activity
Bone loss – 2-3% per year of total bone mass
Most common fx: vertebral, distal forearm
• Age related – 3rd decade of life starts slow decline in bone
mass at rate of 0.5-1% per year
Most common types of fx: hip and radius, F>M
Secondary Osteoporosis
Acromegaly, Addison’s disease, Amyloidosis, Anorexia, COPD,
Hemochromatosis, Hyperparathyroidism, Lymphoma and
leukemia, Malabsorption states, Multiple myeloma, Multiple
sclerosis, Rheumatoid arthritis, Sarcoidosis, Severe liver dz,
esp. PBC, Thalessemia, Thyrotoxicosis

55. Drugs causing osteoporosis
• Aluminum
• Anticonvulsants
• Excessive thyroxine
• Glucocorticoids
• GnRH agonists
• Heparin
• Lithium

56. Drugs used in osteoporosis
• Other: Androgen, Androgenic progestin,
thiazide diuretics

57. Selective Estrogen Receptor Modulators
(SERM) & Estrogen
• Estrogens inhibit bone resorption directly by inhibiting
osteoclasts activity,
• Acts on osteoblast to ↓ pro-resorptive [IL-1, IL-6, TNF-
α and osteocalcin] and ↑ anti-resorptive [IGF-1 and
TGF-β]
• Raloxifene is a selective estrogen receptor modulator
with estrogen agonistic action on bone and antagonistic
action on breast and endometrium(Carcinoma risk↓) . So
preferred drug for the treatment and prevention of post-
menopausal osteoporosis.
Risk of thromboembolism.

58. Denosumab
• monoclonal antibody against RANK-L
• Osteoclasts express a receptor called receptor for
activated nuclear factor k B (RANK) When this
receptor is stimulated by RANK-L, bone resorption
results due to activation of osteoclasts
• Treatment and Prevention of osteoporosis.
• Also used for unresectable giant cell tumor of bone
• decrease serum calcium therefore avoided in
patients with hypocalcemia

59. Strontium ranelate
• It has a novel mechanism of action as it
inhibits bone resorption as well as stimulates
bone formation.
• Blocks osteoclastic differentiation and promote
their apoptosis so inhibit bone resorption.
• Strontium is incorporated into hydroxyapatite,
replacing calcium.
• Small increased risk of venous thrombosis,
seizures and abnormal cognition

60. • Gallium nitrate: inhibits bone resorption and is
useful in the management of Paget’s disease and
hypercalcemia of malignancy but nephrotoxicity
limits its use
• Fluorides are used to prevent dental caries,
osteoporosis?
• Thiazides inhibit the renal excretion of Ca2+ so
used in osteoporosis ( use in recurrent calcium stones
due to hypercalciurea).
• Romosozumab is an investigational bone-forming
agent that is designed to work by inhibiting the
protein sclerostin, thereby increasing bone formation
and decreasing bone breakdown.

61. Relative efficacy of drugs on BMD of
lumbar spine
• Most to least effective
Teriparatide 40mcg
PTH 25mcg+ estradiol
Allendronate 10mg
Estradiol 0.625mg
Raloxifene 120mg
Calcitonin 200IU