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Rheumatism with hormones, bones are mothed by "sugar"

 Last Update: 2022-10-20
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glucocorticoid osteoporosis, collect this article to understand

introduction

Glucocorticoids have powerful anti-inflammatory and immunosuppressive effects [1], and are used by about ¹% of adults worldwide for long-term treatment of a series of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus ^[2].

On the one hand, glucocorticoids are a powerful "weapon" for rheumatologists; On the other hand, glucocorticoids cause a catastrophic adverse reaction, glucocorticoid-induced osteoporosis (GIOP), characterized by loss of bone density and bone mass and increased risk of fracture ^[2].

Because the pain of osteoporosis is often masked by rheumatic pain, it is often difficult for patients to perceive that the bones have been "hollowed out"; When the course of the disease continues to progress, it is often too late for fractures of the vertebral body, ribs, and hips due to minor falls or daily activities [^3].

A large-scale epidemiological survey in China found that the incidence of osteopenia and osteoporosis in rheumatoid patients treated with glucocorticoids was as high as 90%, of which the incidence of osteoporosis was 41.
4%.

In stark contrast to the high prevalence, up to one-third of patients have never received any canonical approach to osteoporosis ^[3].

Internal and external difficulties - rheumatism patients

Concomitant osteoporosis is associated with a variety of factors

Why is the proportion of rheumatologists with osteoporosis so high? There are three main reasons:

Internal cause: inflammatory reaction in rheumatism

The normal metabolism of bone depends on the dynamic balance
of bone formation and bone resorption.
During the active phase of rheumatism, macrophage colony-stimulating factor, tumor necrosis factor-α (TNF-α), IL-1, IL-6, IL-17 and a large number of pro-inflammatory cytokines lead to active osteoclasts and inhibition of osteoblasts, disrupting the balance between bone formation and bone resorption, and causing bone loss ^{[3, 4].}

External causes: glucocorticoid drug effects

Glucocorticoids promote osteoclast-mediated bone resorption, inhibit osteoblast-mediated bone formation, and induce osteocyte apoptosis; This, in turn, affects tubular circulation and reduces bone mass ^{[3, 4].}

Other: decreased exercise + insufficient intake of calcium and vitamin D

musculoskeletal damage caused by rheumatism, foot deformities; Long-term glucocorticoid therapy leads to muscle atrophy, decreased balance ability, and increased risk of falls, which will lead to reduced outdoor activities, insufficient sun exposure, and decreased vitamin D synthesis; Glucocorticoids inhibit intestinal and renal calcium absorption and reabsorption, and calcium deficiency can further exacerbate bone loss ^[3,4].

Accumulation – GIOP degree

Closely related to glucocorticoid use

Compared with primary osteoporosis, which is mainly inversely associated with estrogen levels, GIOP severity tends to be positively correlated
with glucocorticoid use.

The effect of glucocorticoids on bone mineral density is positively correlated with the duration of use ^[3].

GIOP
can occur at the beginning of glucocorticoid use.
In the first year of treatment, bone mass loss is most pronounced, which can be as high as 12% to 20%; About 3%
is lost each year thereafter.
This "two-step" model suggests that GIOP progresses rapidly in the early stage and develops slowly but continuously in the later stages, so the intervention should be persisted ^[5].

The effect of glucocorticoids on bone mineral density is positively correlated with dose [^3].

The higher the glucocorticoid dose, the greater the bone loss; Large daily or cumulative doses increase fracture risk; There is no safety threshold for glucocorticoids, and small doses can lead to bone loss*
.
*The dose is equivalent to the equivalent dose of glucocorticisone≤ 2.
5 mg/day is a small dose; < 7.
5mg/day is a moderate dose; ≥ 7.
5mg/d is a large dose; ≥ 30 mg/day or a cumulative dose of 5 g over 1 year> is an extra-large dose
.

Only partial recovery of bone mass is achieved after cessation of glucocorticoids ^[3].

After 6 months of glucocorticoid discontinuation, bone mass can be partially recovered and the risk of fracture is reduced
.
Once more than 10% is lost, bone mass cannot be fully restored, and vertebral deformation and low back pain will persist
for a long time.

There is no linear relationship between fracture risk and bone mineral density ^[3].

Corticosteroids not only affect bone density, but also lead to a decrease
in bone mass.
Therefore, fragile fractures
may occur in GIOP patients when osteoporosis has not yet occurred in bone density testing.

Seeing the fire ——

Patients with GIOP are regularly assessed for fracture risk ^[3].

In order to more accurately grasp the degree of osteoporosis of patients, different response plans are adopted in a targeted manner; In the process of glucocorticoid treatment, bone density testing, FRAX and other methods should be used regularly to assess and stratify
the fracture risk of patients.
Dual-energy x-ray (DXA) is currently the most commonly used bone densitometry method in clinical practice, and the main sites are 1-4 lumbar vertebrae and proximal femur ^[3].
The World Health Organization's recommended FRAX ( is a simple and GIOP-friendly online assessment tool
.
Fig.
1: The FRAX assessment tool
calculates the fracture incidence rate of GIOP patients within 10 years calculated by FRAX, combined with the patient's age and fracture history, and can divide their fracture risk into low, moderate and high, as shown in Figure 2: Fracture risk stratification in patients treated with glucocorticoids ^[3]

Rock solid –

Calcium and vitamin D are the cornerstone of GIOP treatment

Glucocorticoids have been shown to increase renal calcium excretion, reduce intestinal calcium reabsorption, and produce a negative calcium balance in the body ^[4].
Therefore, calcium is recognized as a primary preventive measure
for GIOP.
When calcium and vitamin D are combined, the effect of reducing bone loss in the lumbar spine is better than calcium alone ^[6].
The American Rheumatology Association (ACR) Guidelines for the Prevention and Treatment of Glucocorticoidal Osteoporosis (hereinafter referred to as the ARC Guidelines) state that calcium and vitamin D are prioritized over bisphosphonates, teriparatide, and denosumab, and significantly higher than raloxifene in people over 40 years of age assessed as at low risk of fracture based on the benefits, costs, and potential risks of anti-fracture ^[7].
The ACR guidelines and the Chinese Expert Consensus on the Prevention and Treatment of Glucocorticoidal Osteoporosis 2020 (hereinafter referred to as the China Consensus) unanimously recommend that all GIOP patients should optimize their calcium intake to 1000-1200mg/day and vitamin D to 600-800IU/day, regardless of fracture risk ^{[3, 7].}
In the initial treatment of GIOP, those assessed as at low risk of fracture are advised to modify their lifestyle and supplement calcium and vitamin D; Those assessed as at moderate or high risk of fracture can choose bisphosphonates, teriparatide, denosumab, raloxifene (limited to postmenopause), calcitonin (limited to 3 months), etc.
in addition to calcium and vitamin D supplementation and lifestyle modifications[^3].

Good Beginning and Good Finish ——

Anti-osteoporosis therapy should be started early and ended late

Start early

The effect of glucocorticoids on bone remodeling is most pronounced
in the initial period of use.
Therefore, early and standardized calcium and vitamin D supplementation and standardized anti-osteoporosis treatment can effectively prevent or reduce bone loss and prevent the occurrence of osteoporotic fractures ^[3].

Late end

Although the effect of glucocorticoids on bone is reversible, bone mass recovery is very slow and only partially recovered
after discontinuation.
The Chinese consensus recommends: "Adult patients who have stopped glucocorticoid therapy should be assessed for fracture risk
every 12 months.
" Reassess for low-grade fracture risk and discontinue anti-osteoporosis medications, but calcium and vitamin D supplementation should continue; Assessed as moderate risk of fracture, continued use of anti-osteoporosis drugs in addition to calcium and vitamin D is recommended; The addition of antiosteoporosis agents to calcium and vitamin D is highly recommended for assessment of high fracture risk ^[3].
”

The adverse effects of glucocorticoids on bone mass in patients with rheumatism are rapid in the early stage, slow and persistent, and there is no safety threshold
.

Caught off guard, the bones have been "hollowed out"
.

Start osteoporosis as early as possible and plan ahead; Adhere to long-term treatment of bone looseness, prevent budding and gradually
.

References[1]Application of glucocorticoids in the treatment of rheumatism and treatment of its complications[J].
Shanghai Medical Journal,2012,(19):25-31.
) [2]Status of Glucocorticoid-Induced Osteoporosis Preventive Care in Korea: A Retrospective Cohort Study on the Korean National Health Insurance Service Database.
Medicina (Kaunas).
2022 Feb 21; 58(2):324.
[3] Rheumatology and Immunology Branch of Chinese Medical Doctor Association, Rheumatology Branch of Chinese Medical Association, Osteoporosis and Bone Mineral Salt Disease Branch of Chinese Medical Association, etc.
2020 edition of Chinese expert consensus on the prevention and treatment of glucocorticoid osteoporosis[J].
Chinese Journal of Internal Medicine,2021,60(1):9.
) [4] Research progress of rheumatic diseases complicated by osteoporosis[J].
Journal of Pediatric Pharmacy,2016, 22(10):5.
) [5] Interpretation of the 2017 ACR Guidelines for the Prevention and Treatment of Glucocorticoid Osteoporosis[J].
Chinese Journal of General Practice,2018,21(6):6 [6]Understanding and Managing Corticosteroid-Induced Osteoporosis.
Open Access Rheumatol.
2021 Jul 2; 13:177-190.
[7]2017 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis.
Arthritis Rheumatol.
2017 Aug; 69(8):1521-1537.

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