Source : https://www.nature.com/articles/tpj201052

• Regimen:

  • 60 mg orally once daily (with or without food).

• MOA (easy):

  • Acts like estrogen on bones → slows down bone loss.

  • Blocks estrogen in breast/womb → lowers cancer risk there.

• Side Effects:

  • Hot flushes, leg cramps.

  • ↑ Risk of venous thromboembolism (VTE: DVT/PE).

  • Mild flu-like symptoms.

• NOTES:

  • Works mainly for vertebral fractures, not hip.

  • Good option in postmenopausal women at breast cancer risk.

  • Avoid in history of VTE, stroke, or severe liver disease.

  • Encourage mobility (prolonged immobility raises clot risk).

https://www.mims.com/malaysia/drug/info/raloxifene?mtype=generic

2) Teriparatide (Parathyroid Hormone analogue, anabolic agent)

• Regimen:

  • 20 µg subcutaneous injection once daily (thigh or abdomen).

  • Maximum 2 years lifetime use (osteosarcoma risk in animals).

  • After stopping → must use anti-resorptive (e.g. bisphosphonate/denosumab) to maintain bone density.

• MOA (easy):

  • Small daily dose of “PTH copy” → activates bone-building cells (osteoblasts) → new bone formed.

• Side Effects:

  • Hypercalcemia, hypercalciuria.

  • Dizziness, nausea, headache.

  • Leg cramps.

  • Rare: osteosarcoma (very rare in humans).

• NOTES:

  • For severe osteoporosis (T-score ≤ –3.0 or multiple fragility fractures).

  • Avoid in bone cancers, Paget’s disease, hypercalcemia, or ↑ ALP.

  • Monitor calcium (blood and urine).

  • Expensive, reserved for very high-risk patients.

https://www.mims.com/malaysia/drug/info/teriparatide?mtype=generic

3) Strontium Ranelate (restricted use now)

• Regimen:

  • 2 g orally once daily (granules mixed in water, at bedtime, away from calcium-rich food/supplements).

• MOA (easy):

  • Two jobs in one:

    • Helps bone-building cells (osteoblasts) → more bone made.

    • Slows bone-breaking cells (osteoclasts) → less bone lost.

• Side Effects:

  • Nausea, diarrhea.

  • ↑ Risk of venous thromboembolism (VTE).

  • ↑ Cardiovascular risk (MI, stroke).

  • Rare: severe skin reactions (DRESS).

• NOTES:

  • Dual action (formation ↑ + resorption ↓).

  • Only if other drugs unsuitable (due to CV risk).

  • Avoid in past/current VTE, ischemic heart disease, uncontrolled hypertension.

  • Must take calcium + vitamin D if diet is lacking.

https://pmc.ncbi.nlm.nih.gov/articles/PMC4125318/

Definition (MOH CPG):

“Osteoporosis is defined as a skeletal disorder characterised by compromised bone strength predisposing a person to an increased risk of fracture. Bone strength reflects the integration of bone density and bone quality. Bone density (g/cm² or g/cm³) is determined by peak bone mass and amount of bone loss. Bone quality refers to the architecture, turnover, damage accumulation, and mineralisation of the bone.”

This definition highlights that fracture risk is not only about ‘how much bone’ (density) but also ‘how good the bone is’ (quality).”

The most common sites of fractures are spine, wrist and hip, and that hip fractures carry high morbidity and mortality (up to ~20 % mortality in first year) in Malaysia.

• Osteopenia refers to low bone mass, with a T-score between –1.0 and –2.5 (i.e. not yet low enough for osteoporosis).

• Osteoporosis is diagnosed when the T-score ≤ –2.5 (or via clinical diagnosis if fragility fracture present).

  
  

In other words, osteopenia is an intermediate stage — a “risk state” of lower than normal bone mass but not yet reaching the threshold for osteoporosis. People with osteopenia may progress to osteoporosis if bone loss continues, especially if other risk factors are present.

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Rheumatology/221115_MOS_CPG-Management_of_Osteoporosis-ed3_PREVIEW.pdf

• Vasomotor symptoms (VMS): hot flushes, night sweats, palpitations

• Genitourinary Syndrome of Menopause (GSM): vaginal dryness, irritation, itching, dyspareunia, recurrent UTIs, urinary urgency.

• Psychological/Neurocognitive: irritability, low mood, anxiety, depression, sleep disturbance, forgetfulness, reduced concentration.

• Somatic & Musculoskeletal: Joint pain, stiffness, fatigue, headaches, weight gain, changes in skin and hair (dryness, thinning).

• Long-term risks (from estrogen deficiency): osteoporosis, cardiovascular disease, cognitive decline/dementia, urogenital prolapse.

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Women%20Health/CPG_Management_of_Menopause_2022_e-version-1.pdf

https://pmc.ncbi.nlm.nih.gov/articles/PMC4890704/

1. Primary Osteoporosis

   • Type I (Postmenopausal osteoporosis):

     • Occurs within 15–20 years after menopause.

     • Due to estrogen deficiency → increased osteoclast activity, accelerated trabecular bone loss.

     • More common in women, leads to vertebral & wrist fractures.
       

   • Type II (Senile osteoporosis):

     • Occurs after ~70 years of age.

     • Due to aging, reduced osteoblast function, calcium/vitamin D deficiency.

     • Affects both cortical and trabecular bone, common fractures = hip, pelvis.

       
       

2. Secondary Osteoporosis

   • Due to underlying conditions or medications.

   • Examples:

     • Endocrine: hyperthyroidism, hyperparathyroidism, diabetes.

     • GI/malabsorption: celiac disease, inflammatory bowel disease.

     • Drugs: glucocorticoids (prednisolone), proton pump inhibitors (omeprazole), anticonvulsants.

     • Lifestyle: smoking, alcohol excess, immobility.

       
       

Secondary osteoporosis should always be ruled out in younger patients or when risk factors are present.

Case relevance (GR, 53 y/o, fragility fracture, T-score –2.6)

• GR fits Primary Type I (Postmenopausal osteoporosis) because she is ~1 year post-menopause, with fragility fracture and low BMD.
  

• She also has secondary contributors → previous prednisolone therapy, smoking, vegetarian diet (possible calcium/vitamin D deficiency), and chronic PPI (omeprazole) use.
  

So GR’s osteoporosis is a mixed case: postmenopausal (primary) with secondary risk factors.

• Osteoporosis = systemic skeletal disease

• Characterized by low bone mass + microarchitectural deterioration

• Osteoclasts: bone resorption

• Osteoblasts: bone formation

• Osteocytes: key regulators (signal balance)

• Controlled by hormones, cytokines, and mechanical loading

  
  

1. Pathophysiological Imbalance

• Osteoporosis occurs when:

  • Bone resorption > bone formation

• Results: net bone loss, weak trabecular bone, fractures

  
  

2. Cellular & Molecular Mechanisms

(A) Osteoclast Activation (Bone Resorption ↑)

• RANKL–RANK–OPG axis

  • ↑ RANKL / ↓ OPG → ↑ osteoclast differentiation

• Key pathways: NF-κB, MAPK, PI3K/Akt, NFATc1

• Cytokines: IL-1, TNF-α enhance osteoclastogenesis

• MALT1: boosts osteoclast activation

  
  

(B) Osteoblast Suppression (Bone Formation ↓)

• Osteoblast differentiation impaired from MSCs

• Pathways involved:

  • Wnt/β-catenin → inhibited by sclerostin

  • BMP/Smad → needed for Runx2 & osterix

  • Hedgehog → directs MSCs to osteoblasts

  • Notch → context dependent, can suppress osteoblasts

• Osteocytes secrete sclerostin → blocks Wnt signaling

  
  

  3. Systemic Regulators

Hormones

• Estrogen (Postmenopausal osteoporosis)

  • Normally: Estrogen suppresses osteoclasts by ↑ OPG and ↓ RANKL

  • Loss of estrogen → unchecked RANKL activity → excessive osteoclastogenesis

  • Leads to rapid bone loss, especially in trabecular bone

• Testosterone & aromatization also important in men

• PTH ↑ → stimulates bone resorption

• Calcitonin → inhibits osteoclasts

• Vitamin D → regulates Ca²⁺ absorption + bone metabolism

Nutrients & Cytokines

• Ca²⁺ deficiency → bone loss

• IL-6, TGF-β modulate bone turnover

  
  

4. Emerging Factors

• Non-coding RNAs (miRNA, lncRNA, circRNA): regulate osteoblast/osteoclast gene expression

• Bone marrow MSCs: shift from osteogenesis → adipogenesis

• Bone marrow adipocytes: secrete SFRP-1, inhibit Wnt signaling

• Bone vasculature: angiogenesis coupled with osteogenesis (HIF-1α, SLIT3)

• Bone innervation: neural signals regulate bone cells

• Gut microbiota: influence Ca²⁺ absorption, immune signaling, bone metabolism

https://cmbl.biomedcentral.com/articles/10.1186/s11658-022-00371-3

https://www.ncbi.nlm.nih.gov/books/NBK441901/

https://pmc.ncbi.nlm.nih.gov/articles/PMC7415937/

Haemoglobin

Check to identify if there is anaemia in the patient. Studies showed that postmenopausal women with anaemia are at a higher risk of bone fractures. The reduced blood volume would increase the proliferation of haematopoietic cells, such as osteoclasts. Proliferated osteoclasts would increase bone resorption. Although osteoblast is also stimulated, the resorption in bone would affect the bone remodelling. Hypoxemia in anaemia patients would also cause osteoporosis. Severe hypoxia would increase the oxidative stress and acidify the extracellular bone matrix, impairing the bone metabolism. The osteoblast formation would decrease. Hypoxia would reduce the bone mineral density in human.

Reference:

Bone Density Loss Is Associated with Blood Cell Counts - PMC

Association between Osteoporosis and Low Hemoglobin Levels: A Nested Case–Control Study Using a National Health Screening Cohort

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Rheumatology/221115_MOS_CPG-Management_of_Osteoporosis-ed3_PREVIEW.pdf

Types of MHT

1) Systemic Estrogen-only therapy (ET)

• Forms: oral tablets (conjugated estrogens, estradiol), transdermal patches, gels, sprays.

• Use: most effective for vasomotor symptoms and helps prevent bone loss. Only for women who have had a hysterectomy (no uterus)
  

2) Combined Estrogen + Progestogen Therapy (EPT / combined MHT)

• Forms: systemic estrogen (oral/transdermal) + oral progestogen (medroxyprogesterone acetate, micronized progesterone, norethisterone) OR intrauterine levonorgestrel system (LNG-IUS) for endometrial protection.

• Use: for women with an intact uterus who need systemic estrogen for vasomotor symptoms or bone protection. Progestogen prevents endometrial hyperplasia/cancer. Choice of progestogen and route (oral vs LNG-IUS) is individualized.
  

3) Tibolone

• Form: oral synthetic steroid with estrogenic, progestogenic and androgenic activity.

• Use: relief of vasomotor symptoms, GSM, and bone protection in some cases; often considered when conventional MHT not tolerated or not desired. Caution around vascular risks in older or high-risk women.
  

4) Local (vaginal) estrogen therapy

• Forms: creams, tablets, rings, low-dose local preparations.

• Use: genitourinary syndrome of menopause (vaginal dryness, dyspareunia, recurrent urinary symptoms). Minimal systemic absorption — can be used when systemic therapy is not indicated or when only GSM is present.
  

5) Tissue-selective approaches / SERMs / Combination (e.g., bazedoxifene + conjugated estrogen)

• Use: alternative for those who need symptom control with different risk profile (e.g., bazedoxifene + estrogen combo to avoid progestogen).

Relating options to GR’s case

Key facts: Age 53 (<60), within 10 years post-menopause, osteoporosis (fragility fracture), smoker, unclear uterus status.

Offer MHT as an option. Prefer a transdermal estradiol regimen combined with endometrial protection if uterus intact — e.g.:
Transdermal estradiol (low dose patch/gel) + levonorgestrel IUS (LNG-IUS) — preferred option if LNG-IUS acceptable/available.

Rationale: GR is within the favorable window for MHT (age/timing), has symptomatic menopause potential and bone benefit. Because she smokes, transdermal route reduces VTE risk versus oral estrogen. If uterus is present, LNG-IUS provides endometrial protection with minimal systemic progestin exposure

If MHT contraindicated or declined: use non-hormonal options for vasomotor symptoms (SSRI/SNRI, gabapentin) and continue targeted osteoporosis therapy (bisphosphonate/denosumab/teriparatide as appropriate). MHT is not a substitute for anti-osteoporotic drugs for established osteoporosis.

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Women%20Health/CPG_Management_of_Menopause_2022_e-version-1.pdf

1. Mobile apps & digital reminders

• Medication reminder apps (e.g. Medisafe, MyTherapy, MediSafe Pill Reminder):

  • These send push notifications when it’s time for her alendronate, inhaler, or calcium.

  • They allow tracking missed doses so she can see adherence over time.

  • Some apps even let you log supplements (like calcium & vitamin D) and generate a simple report for her doctor or pharmacist.

    
    

    https://multiculturalcaregiving.com/medisafe-pill-reminder-medication-tracker-app-review-can-medisafe-help-seniors-and-caregivers/#google_vignette

    
    

• Smart pillboxes / alarms: Devices that beep or flash if she forgets a dose — helpful if she struggles with routine.
  

• Wearables (smartwatch reminders): If she uses a smartwatch/fitness tracker, alarms can sync to remind her of medications or even prompt exercise.
  

2. Nutrition tracking (important since she’s vegetarian)

• Apps like MyFitnessPal or CalorieKing allow logging calcium and protein intake from food.
  

• Lighting: Ensure hallways, stairs, and bathrooms are well lit (motion sensor lights at night).

• Floor safety: Remove loose rugs/carpets, secure electrical cords, use anti-slip mats in bathroom/kitchen.

• Supportive fittings: Install grab bars near toilets, showers, and stairs; railings on both sides of staircases.

• Furniture placement: Arrange furniture so walkways are clear; avoid clutter that increases trip risk.

• Footwear: Encourage sturdy, non-slip shoes instead of slippers or heels.

• Emergency plan: Keep phone or alert system accessible in case of falls.

“Just like parents baby-proof a home for safety, we adult-proof GR’s home to reduce fall risk and protect her fragile bones.”

https://www.nia.nih.gov/health/aging-place/home-safety-tips-older-adults#:~:text=Install%20a%20ramp%20with%20handrails,surfaces%20that%20may%20get%20wet.

Reference:

A correlative studies between osteoporosis and blood cell composition: Implications for auxiliary diagnosis of osteoporosis - PMC

Reference:

The role of lipid metabolism in osteoporosis: Clinical implication and cellular mechanism - PMC

High Cholesterol Deteriorates Bone Health: New Insights into Molecular Mechanisms - PMC

Reference:

Lower Serum Creatinine Is Associated with Low Bone Mineral Density in Subjects without Overt Nephropathy - PMC

• Prevent fracture

• Increase bone mineral density

• Restore bone architecture

• Slow or stop bone loss

• Treat the cause of osteoporosis

• Improve lifestyle modification

Reference:

Goal-directed osteoporosis treatment: ASBMR/BHOF task force position statement 2024 - PubMed

Treatment of osteoporosis; treatment goals and duration of therapy | ECE2016 | 18th European Congress of Endocrinology | Endocrine Abstracts

Osteoporosis: Diagnosis, Treatment, and Steps to Take

https://www.ncbi.nlm.nih.gov/books/NBK441901/

Calcitriol

Dose:

Calcitriol 0.25 µg bd

MOA

• Calcitriol, the active form of vitamin D3 (cholecalciferol), binds to and activates the vitamin D receptors in the intestine, kidneys, parathyroid gland and bone, thus stimulating intestinal Ca transport and absorption. It also stimulates bone resorption and increases renal tubular reabsorption of Ca, thereby decreasing PTH levels and improving Ca-phosphate homeostasis.

• Calcitriol could increase the bone mineral density in postmenopausal osteoporosis.

SE:

Hypercalcaemia

Polyuria Polydipsia

Cardiac arrhythmias

Sensory disturbances

Apathy

Nephrocalcinosis

Urinary tract infections

Hypertension

Monitoring Parameter

Serum calcium should be monitored periodically, at minimum before starting therapy, and at 3 to 6 monthly intervals thereafter. In addition, measurement of 24 hour urinary calcium can be considered in those on calcitriol, especially in those with renal impairment.

Reference:

2022_CPG-ManagementofOsteoporosis-final.pdf

Calcitriol - StatPearls - NCBI Bookshelf

Calcitriol: Uses, Dosage, Side Effects and More | MIMS Malaysia

Inhaled corticosteroids improve the FEV1 better than systemic corticosteroids. The side effect of inhaled corticosteroids is less than systemic corticosteroid. Systemic corticosteroid is usually use for short term management, inhaled corticosteroid would be better option for long-term asthma management.

LABA (Salmeterol) better than SABA in improving exacerbation and hospitalisation.

Reference:

ROLE OF INHALED CORTICOSTEROIDS VERSUS SYSTEMIC CORTICOSTEROIDS IN THE MANAGEMENT OF ASTHMA | Journal of Population Therapeutics and Clinical Pharmacology

Caffeine increases faecal and urinary calcium excretion and may induce a negative calcium balance if dietary calcium intake is insufficient. High caffeine intake (>330 mg caffeine/day) has been associated with increased risk of fragility fracture.

Alcohol intake

Excessive alcohol intake (>2 units daily) should be avoided as it has been associated with increased rates of any fracture and osteoporotic fracture

Smoking

Smoking increases osteoporotic fracture risk. Current smokers have the highest risk, followed by ex-smokers, when compared to those who have never smoked.

Reference:

2022_CPG-ManagementofOsteoporosis-final.pdf

Diagnosis and Management of Osteoporosis | AAFP

• Bisphosphonates bind strongly to bone mineral

• When osteoclasts attempt to resorb bone, the drug is internalized → inhibits osteoclast activity → induces osteoclast apoptosis

• Serious side effects:

  - Atypical femoral shaft fractures

  -Osteonecrosis of the jaw (ONJ)

  -renal and kidney impairment

• Patients on oral bisphosphonates for 5 years or IV bisphosphonates for 3 years should have their fracture risk re-evaluated.

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Rheumatology/221115_MOS_CPG-Management_of_Osteoporosis-ed3_PREVIEW.pdf

• Reduce salt intake → high sodium increases urinary calcium loss.

• Limit soft drinks / carbonated beverages (esp. cola) → excess phosphates can worsen calcium balance.

• Adequate micronutrients: magnesium, zinc, vitamin K (esp. K2 in green leafy veg & fermented foods) support bone mineralisation.

• Soy isoflavones (plant estrogens) may benefit postmenopausal women.

• VCFs are the most common osteoporotic fracture, but ~⅔ go undiagnosed.

• Pain is often mistaken for muscle strain, general back pain, or normal aging.

Mechanism of Kyphosis in Osteoporosis

• Osteoporotic bones are brittle → fracture may occur with minimal stress (lifting, bending, coughing, sneezing, or even turning in bed).

• VCFs typically occur as wedge fractures → collapse of the vertebral front while the back remains intact.

• Multiple wedge fractures accumulate → forward curvature of the spine (kyphosis).

Progression of Kyphosis

• Dependent on cause.

• Untreated osteoporosis → continued bone loss → kyphosis worsens over time.

• Treated osteoporosis (e.g., medications to improve bone density) → may slow, halt, or prevent further kyphotic progression.

Clinical Impact

• Height loss and postural changes (kyphosis)

• Chronic back pain often overlooked as aging-related.

• Reduced mobility and quality of life.

• Severe kyphosis can lead to respiratory compromise due to restricted chest expansion.

Case Relevance (GR)

• May have had unnoticed vertebral fractures years earlier, leading to gradual kyphotic posture before formal osteoporosis diagnosis.

https://www.southeasttexasspine.com/blog/the-link-between-osteoporosis-and-kyphosis

https://www.hss.edu/health-library/conditions-and-treatments/list/kyphosis

https://www.hss.edu/health-library/conditions-and-treatments/list/kyphosis

In more serious case, minimally invasive interventions

• Vertebroplasty → bone cement injected into fractured vertebra → hardens, supports spine.

• Kyphoplasty → balloon inserted to expand compressed bone → cement injected into expanded area.

• Benefits: pain relief, height restoration, reduced spinal deformity.

https://jasonlowensteinmd.com/understanding-osteoporosis-degenerative-kyphosis/

https://www.southeasttexasspine.com/blog/the-link-between-osteoporosis-and-kyphosis

https://my.clevelandclinic.org/health/treatments/25168-spinal-fusion

http://southeasttexasspine.com/blog/the-link-between-osteoporosis-and-kyphosis

https://www.niams.nih.gov/health-topics/osteoporosis

• A low-trauma fracture:

- After a fall from standing height or less.

- Fractures occurring at the site of a typical osteoporotic fracture, i.e. at the hip, spine, forearm, humerus, ribs, tibia (excluding ankle), pelvis and other femoral fractures.

• Historical height loss of >4cm (>1.5 inches).

• Acute back pain following seemingly innocuous activities, e.g. bending, lifting objects, coughing or sneezing.

Bone mineral density (BMD) measurement:

BMD measurement via dual-energy x-ray absorptiometry (DXA) at the femoral neck, total hip or lumbar spine remains the gold standard recommendation for the diagnosis of osteoporosis. All patients should have BMD at the lumbar spine (L1-L4, posteroanterior) and hip (to include the femoral neck or total hip) measured. Forearm BMD (1/3rd radius of the non-dominant forearm) should be measured when the hip and/or spine cannot be measured or interpreted, in patients with hyperparathyroidism, and/ or in very obese patients (over the weight limit for the DXA table). BMD measurement is also used for determining fracture risk and treatment decisions.

BMD is reported as a T-score or Z-score, both of which are units of standard deviation (SD).

T-score

The T-score represents the number of SDs by which an individual’s BMD diverges from the mean value of young female adults. The recommended reference range* for determining the T-score is the United States of America Centres for Disease Control and Prevention’s National Health and Nutrition Examination Survey (US CDC NHANES) III database for femoral neck measurements in women aged 20-29 years. This classification does not apply to premenopausal women, men <50 years old, and children.

 Z-score

The Z-score describes the number of SDs by which the BMD in an individual differs from the mean value expected for age and sex. The Z-score should be used for premenopausal women, men <50 years old and children.

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Rheumatology/221115_MOS_CPG-Management_of_Osteoporosis-ed3_PREVIEW.pdf

-       1200 mg of calcium (a combination of dietary sources and supplements) is recommended daily for its positive effect on bone mineral density and fracture risk reduction.

-       Adequate Vitamin D supplementation to achieve Vitamin D levels of more than 50 ng/mL is advised in order to maintain skeletal health and reduce the risk of fractures and falls.

• Cognitive Behavioural Therapy:

Women experiencing menopausal symptoms may consider alternative therapy such as hypnotherapy, cognitive behavioural therapy, relaxation techniques, sleep hygiene and enforcing positive attitudes to help ease anxiety, sleep and vasomotor symptoms.

https://www.moh.gov.my/moh/resources/Penerbitan/CPG/Women%20Health/CPG_Management_of_Menopause_2022_e-version-1.pdf

1. PPIs act mainly toward suppressing gastric acid secretion. The presence of gastric acid and an acidic proximal duodenum are required to free ingested calcium from foodstuffs for absorption to occur in the small intestine.

Lack of sufficient amounts of gastric acid can lead to

• secondary hyperparathyroidism

• increased rates of osteoclastic bone resorption

• skeletal turnover

• subsequent reduction in bone mass.

https://www.gastrojournal.org/article/S0016-5085(13)00095-4/fulltext

2. PPI users taking calcium supplements were more likely to have hyperparathyroidism compared to non-users.

• Hyperparathyroidism was defined as a parathyroid hormone (PTH) > 65 pg/ml.

• Parathyroid hormone (PTH) plays a pivotal role in calcium homeostasis and bone metabolism. PTH maintains serum calcium concentration by releasing calcium from the skeleton through bone resorption, renal tubular calcium reabsorption, and activating vitamin D. PTH has major effects on bone turnover and remodelling. Hyperparathyroidism causes excessive bone remodelling, with bone resorption outpacing formation leading to lower BMD, altered microarchitecture and increased fracture risk

• Calcium carbonate is the most commonly used calcium supplement, and reduction of its absorption due to PPI-induced hypochlorhydria is well-described

https://doi.org/10.1007/s00198-023-06867-8

3. chronic use of PPIs is associated with potential adverse drug events, such as hypomagnesaemia, interstitial nephritis, and iron and vitamin B12 malabsorption

https://onlinelibrary.wiley.com/doi/10.1155/2021/8902367

• Ranitidine treatment resulted in insignificant changes in tested parameters.

• Pantoprazole given alone, significantly decreased serum calcium and increased serum BSALP.

Alendronate significantly improved BSALP level, serum calcium, BMD, cortical thickness and histopathological score.

• This improvement was not affected by combining ranitidine with alendronate.

• pantoprazole with alendronate caused a significant deterioration of tested parameters.

Ranitidine proved safer than pantoprazole for patients with high risk of osteoporosis and in alendronate-treated patients.

https://www.sciencedirect.com/science/article/pii/S1110116417300960

https://www.nogg.org.uk/full-guideline/section-5-non-pharmacological-management-osteoporosis

This is an inhibitor that helps slow down bone loss and is approved to treat osteoporosis in:

• Postmenopausal women or men with osteoporosis who are at high risk for fracture.

• Men who have bone loss and are being treated for prostate cancer with medications that cause bone loss.

• Women who have bone loss and are being treated for breast cancer with medications that cause bone loss.

• Men and women who do not respond to other types of osteoporosis treatment.

https://www.niams.nih.gov/health-topics/osteoporosis/diagnosis-treatment-and-steps-to-take

Indications and Dosage: Subcutaneous

Adult: 60 mg every 6 mth. Co-administer oral Ca 1,000 mg and vit D >= 400 IU

daily.

• Calcium citrate is better absorbed with low gastric acid; consider switch if persistent low Ca levels.

https://pmc.ncbi.nlm.nih.gov/articles/PMC4851231/