Knee Hurt

Category: Knee Arthritis

  • Real-world treatment patterns of rheumatoid arthritis in Brazil: analysis of DATASUS national administrative claims data for pharmacoepidemiological studies (2010-2020)

     

    Study design and database

    This was a descriptive, retrospective claims database study using the DATASUS database. The study identified patients with RA who sought care within SUS between January 1, 2010 and December 31, 2020.

    The administrative claims data in DATASUS is presented as procedure codes from billing data and includes demographic information, all procedures (inpatient and outpatient), costs, and additional information23. Hospital admission (SIH [Sistema de Informações Hospitalares])24 and outpatient (SIA [Sistema de Informações Ambulatoriais])11 data exists separately and is linked at the patient level through multiple steps with different combinations of individual level information (date of birth, gender, city and zip code) for a probabilistic linkage approach. This Brazilian Healthcare Record Linkage (BRHC-RLK) methodology has been used in previous studies to enable a more comprehensive recording of each patient’s health record and thus allow a more complete evaluation of their journey through the SUS system.25. The method is based on multiple steps with different combinations of patient information from both databases, making it possible to identify or link patient data in both systems, while maintaining the anonymized nature of the database.

    Patient-level data within DATASUS is anonymized and encrypted before being made available to researchers. DATASUS is publicly available and does not require further approval from ethics committees, according to Brazilian Ethics Resolution No. 510/2016.

    Study population

    The study population included patients with at least one claim of RA (according to the International Classification of Disease, 10th edition). [ICD-10] codes: M05.0, M05.3, M05.8, M06.0, M06.8, or M08.0) and ≥ 2 claims for disease-modifying antirheumatic drugs (DMARDs) ≥ 1 month apart in the 2010 survey– 2020 period. This study examined a treated population where the index date was the first DMARD claim and followed until the end of the study period (December 31, 2020) or the last available information. Detailed DMARD definitions can be found in Supplementary Table S1.

    To capture initial treatment and address the potential for misclassification common in claims data, patients with a DMARD claim without an RA ICD-10 code 12 months prior to the index date were excluded. The index date was defined as the date of the first RA ICD-10 and DMARD prescription in the public health system during the study period. Patients with RA with less than six months of follow-up were excluded, in an effort to reduce the number of individuals with a false diagnosis or lack of follow-up in the database.

    Because SUS is a healthcare system with universal coverage, patients with additional private health insurance can also receive medications (such as expensive drugs) covered by SUS at no out-of-pocket cost. This is often observed in other therapeutic areas26. For this reason, we stratified the results across the following cohorts: Cohort 1 is the entire study population, Cohort 2 is SUS-exclusive (i.e., dependent on SUS for all healthcare-related encounters, procedures, and treatments), and Cohort 3 represents SUS + private patients ( i.e. depending only on SUS for prescription drug coverage)26.

    Measurements of DMARD treatment

    DMARD treatments measured using procedure codes (see Supplementary Table S1) were grouped into the following categories: csDMARD for conventional synthetics and/or immunosuppressants (ciclosporin, cyclophosphamide, chloroquine, hydroxychloroquine, leflunomide, methotrexate, azathioprine and sulfasalazine), bDMARD for biological drugs (adalimumab, abatacept, etanercept, infliximab, rituximab, tocilizumab, golimumab, certolizumab) and tsDMARD for a synthetic, oral target therapy [Janus kinase (JAK) inhibitor, tofacitinib].

    Treatment patterns were evaluated by specific drug (independently of monotherapy or in combination) as provided for RA treatment and the order of available treatments in SUS, by line of therapy (LOT), time point of each drug, previous and subsequent DMARD treatments in SUS. The first treatment was the first therapy from the admission according to RA ICD-10 code. LOT was defined as at least three claims (dispensation) of the same drug (b/tsDMARD) in a row. A new series of at least three claims (dispensation) of the same drug in the correct order was considered a new line of treatment. Thus, the switch to a treatment was identified as at least three claims for drugs other than the previous one, which are not included in the definition of drugs used in combination. Gaps were allowed regardless of time and did not constitute a new LOT. First-line (LOT1) refers to initial treatment, first b/tsDMARD claim of RA during the study period. Second-line (LOT2) refers to the second b/tsDMARD used for RA treatment, when the first b/tsDMARD was stopped. Third line (LOT3) refers to the third b/tsDMARD, when the previous b/tsDMARD was terminated. csDMARDs used before b/tsDMARD were also assessed. Switching treatment was defined as at least three claims for drugs different from the previous one (new LOT), and not part of drugs used in combination.

    static analysis

    Derived variables included age and distance to the clinic. Age was defined as the age at the first claim of an ICD-10 code for RA in the database. Distance was calculated as the Euclidean distance (km) between two zip codes: the patient’s place of residence and the health care facility or tomography or antiangiogenic treatment facility, as applicable. Treatment switch, discontinuation and end of follow-up were the main outcomes of censoring events of interest, also relevant in defining LOT and creating Sankey diagrams.

    Continuous variables (e.g., age) are summarized by central tendency (means, medians) and dispersion (variance, range); and for categorical variables (e.g. gender) based on absolute number and percentage. Stratifications and/or sensitivity analyzes were performed to evaluate differences in gender, age groups, patient region of residence, drug use, treatment line, and others.

    Stratified analyzes for mainstream and new users were prespecified, and for SUS-exclusive and SUS+ private cohorts. Frequent users were patients with RA who were currently receiving bDMARD treatment, and new users were patients with RA who were starting a new bDMARD treatment (i.e., their first prescription). To describe the use and sequential patterns of RA bDMARD treatments, patients were stratified by treatment type, LOT-specific drug, and SUS-exclusive status.

    In multivariable logistic regression analyses, age, SUS-exclusive status, distance to clinic (160+ km), and pre-index cs/imsDMARD and other independent predictors were included to evaluate initiated therapy (LOT1) with b/tsDMARD (JAKi). Multivariable analyzes were performed using Cox regression models evaluating predictors by time to switch to tsDMARD (JAKi) compared to bDMARD (LOT2+), applying the same independent predictors from multivariable logistic regression analyzes (age, SUS-exclusive status , distance to clinic, pre-index cs/imsDMARD, other), plus the number of previously used bDMARDs. Sankey diagrams were used for visualizations of treatment patterns. Sankey diagrams quantitatively illustrate the sequence of treatment (and/or duration of treatment) and allow stratification by subpopulations of interest with censoring based on different treatment, discontinuation, or end of follow-up. Kaplan Meier survival analyzes and plots were generated for time to switch from LOT1 to LOT2, among those treated with b/tsDMARD, analyzed by drug type and by SUS-exclusive status.

    The visual representation of the time-to-event of the switch from LOT1 to LOT2 in patients receiving b/tsDMARD therapies was presented in Kaplan-Meier curves. The last available patient information or end of study period was considered censored for patients who did not switch from LOT1 to LOT2.

    All analyzes were performed using Python version 3.6.9 and statistical significance was set at p < 0.05.

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  • New treatment option for hand osteoarthritis identified

    New treatment option for hand osteoarthritis identified

    Osteoarthritis

    Relief could be on the way for people with painful hand osteoarthritis after a Monash University and Alfred Health-led study found that an affordable existing drug could help. Until now, no effective treatment existed.

    Published in The Lancetthe article examined methotrexate, a cheap, effective treatment for inflammatory joint diseases such as rheumatoid arthritis and psoriatic arthritis. It has been widely used in Australia and worldwide since the early 1980s.

    Researchers found that methotrexate reduced symptoms in people with hand osteoarthritis (OA). A weekly oral dose of 20 mg for six months had a moderate effect on reducing pain and stiffness in patients with symptomatic hand osteoarthritis.

    Hand osteoarthritis is a debilitating condition that causes pain and affects function, interfering with daily activities such as dressing and eating. It can significantly reduce the quality of life. About one in two women and one in four men will experience symptoms of hand osteoarthritis by the time they turn 85.

    About half have inflamed joints, which cause pain and are associated with significant joint damage. Despite the high prevalence and burden of disease, no effective medications exist.

    Senior author Professor Flavia Cicuttini, head of Monash University’s Musculoskeletal Unit and head of rheumatology at The Alfred, said the study identified the role of inflammation in hand osteoarthritis and the potential benefit of targeting patients experiencing painful hand osteoarthritis.

    “In our study, as in most osteoarthritis studies, pain improved in both the placebo and methotrexate groups in the first month or so,” Professor Cicuttini said.

    “However, pain levels remained the same in the placebo group but continued to decrease in the methotrexate group at three and six months, while still decreasing. The pain improvement in the methotrexate group was twice as much as in the placebo group.

    “Based on these results, the use of methotrexate may be considered in the treatment of hand osteoarthritis with an inflammatory pattern. This provides physicians with a treatment option for this group, which tends to sustain more joint damage.”

    Professor Cicuttini said that in patients with hand osteoarthritis and inflammation, the effects of methotrexate were visible after about three months and it was very clear after six months whether it was working.

    At that point, patients and their doctors can decide whether to continue or stop. This is very similar to what we are currently doing with other forms of inflammatory arthritis.”

    Professor Flavia Cicuttini, Monash University

    The NHMRC-funded randomized, double-blind, placebo-controlled trial of 97 people assessed whether methotrexate 20 mg weekly reduced pain and improved function compared to placebo in patients with symptomatic hand osteoarthritis and synovitis (inflammation) for six months.

    Participants with hand osteoarthritis and MRI-detected inflammation were recruited from Melbourne, Hobart, Adelaide and Perth.

    Professor Cicuttini said the results could provide relief for people with hand osteoarthritis, which was particularly common in women during the menopause.

    “Further studies are needed to determine whether the effect of methotrexate lasts longer than six months, how long we should treat patients and whether methotrexate reduces joint damage in patients with hand osteoarthritis and associated inflammation,” she said.

    Professor Cicuttini now plans to conduct a follow-up study to answer these questions, specifically whether women who develop hand osteoarthritis around menopause and often have severe pain and joint damage can benefit.

    Source:

    Magazine reference:

    Wang, Y., et al. (2023) Methotrexate for the treatment of hand osteoarthritis with synovitis (METHODS): an Australian, multisite, parallel group, double-blind, randomized, placebo-controlled trial. The Lancet. doi.org/10.1016/S0140-6736(23)01572-6.

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  • “If you’re trying to get pregnant, you should actually have sex”

    “If you’re trying to get pregnant, you should actually have sex”

     

    Screen Shot 2021 03 14 at 2.19.43 PM

    When I first started thinking about getting pregnant after being diagnosed with rheumatoid arthritis, I was eager to hear from other women who had succeeded in this goal. At the time there wasn’t much social media, but I did find a great book called Arthritis, Pregnancy and the Path to Parenthood. It contained quotes and advice from real women, and I found it invaluable.

    But I also discovered a problem: the book started by talking about the possibility of changing some of your medications before getting pregnant, and then skipped straight to being pregnant. But wait! If I stop taking my meds, won’t I flare up? And if I’m in pain, how can I ever get pregnant? Is there a chapter missing from this book about trying to get pregnant while living with arthritis?

    That’s the question I asked Iris Zink, a rheumatology nurse who recently wrote a book with Jenny Thorn Palter about intimacy and chronic illness. (The book is called “Sex – Interrupted” and you can read my review of it here!) Their book recommends many alternatives to intercourse – which I think is generally good advice for maintaining intimacy in a relationship while dealing with a chronic illness! But what if you want to start a family? If you’re trying to get pregnant, you actually have to have sex!

    Iris and I decided to have a discussion about a topic we haven’t seen anyone else talk about: the challenges many women face when actually trying to conceive while living with a chronic illness. I share my personal experiences, and Iris shares her expert advice this video!

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  • Irma Jennings’ Bone Health Test Results (DXA) 2020

    Irma Jennings’ Bone Health Test Results (DXA) 2020

    DXA 2022

    My latest DXA and TBS report has arrived. As a reminder, in 2005 I was diagnosed with osteopenia and given a script for Fosamax. I refused. I was in my fifties. Now I’m in my seventies. My intention was to implement my 7 pillars of bone health for better results:

    1. Calcium and mineral rich foods
    2. Supplements (Cal Citrate, Vit. D., Vit K2 – Mk7, Dr. McCormick’s Collagen and Mineral Whey)
    3. Bioidentical hormones
    4. Weight-bearing exercise
    5. Stress reduction
    6. Sleep hygiene
    7. Brings joy to my daily life

    At that time, Fosamax was a long-term drug. I would have been a long-term user. I am grateful for the work of Dr. Schneider and who has revealed her terrible story below. Because of her work, Fosamax users are now taking a drug holiday.

    The story of Dr. Jennifer Schneider

    Dr. Jennifer Schneider was standing on a subway in New York City when the train jolted and Schneider felt a kink in her right leg. It was her femur, the strongest bone in the body.

    “I shifted to the right to keep my balance and felt a large crack. I felt it in my thigh. There was no doubt that I had broken my femur,” says Schneider, a semi-retired internist from Tucson, whose The fracture was in the upper third of her thigh.

    “It’s extremely unusual to break that part of the femur,” she said. “It just doesn’t happen that way.”

    Schneider’s femur fracture occurred in October 2001, but it wasn’t until 2005 that she began to suspect the cause of the strange injury: long-term use of the drug Fosamax, which ironically is prescribed to treat and prevent the bone-thinning disease osteoporosis.

    Schneider had been taking the drug since 1995, when she was diagnosed with osteopenia, a condition considered by many doctors to be a precursor to osteoporosis.

    “The drug suppresses bone loss and in some people, who knows, it may be doing its job too well. It suppresses too much,” Schneider said.

    Fosamax drugs from New Jersey-based Merck say there is no evidence of a link between the drug and femur fractures. But in the interest of patient safety, Merck says it voluntarily amended the Fosamax label in July 2009 to include “low-energy femoral shaft and subtrochanteric fractures” in the side effects section of the label. [1]

    IMPORTANT:

    In June 2023 I will open my:

    Pilot program: Strong Bones – Healthy You
    A comprehensive bone health program – the whole body approach.

    Click HERE to schedule a free 30 minute session.

    This conversation will determine if my program is right for you.

    DXA from IRMA

    My ninety-minute pilgrimage to the University of Pennsylvania hospital yielded an excellent DXA.

    Below are my results

    Great results for my hips and spine – everything is moving in the right direction over time.

    Not so much my forearm.

    Note the colors in the report. We are looking for green.

    VEGETABLE

    The color chart below will help you understand the ranges.

    T-score less than -1 = Normal | COLOR GREEN

    T-score between -1 to -2.5 = osteopenia | COLOR YELLOW

    T-score greater than -2.5 = Osteoporosis | COLOR RED

    DXA AND TBS

    TBS L1-L4 = 1.393 (normal is 1.35 and higher)

    Below you will find the Trabecular Bone Score or TBS report of my spine. Simply put, the TBS measures the inner bones, while DXA measures the outer bones. Color falls into the vegetable normal area. My inner bones look good.

    Trabecular bone score

    DXA spine – Normal range L1-L4 = T-score 0.0

    Below is my DXA for my spine. It also falls into the vegetable (normal) part.

    DXA Spine 2022
    Measurement of the spine at DXA 2022

    DXA hip –

    Femoral neck -1.8 Total left hip -1.1

    YELLOW – Osteopenia

    Also measures in the normal yellow range. Note the DOT in the yellow section.

    DXA to measure bone density of the hip

    Forearm

    RED – Osteoporosis

    Radius 33% = -2.7

    Radius 33% is the size used for the forearm.

    DXA Forearm 2022

    Irma’s tracking schedule

    Click on the image for a better view.

    For my readers who like to track their DXA, below is my tracking chart. The diagram shows the type of machine used. Each machine has a serial number. When looking at a DXA comparison, it is essential to know the DXA machine and its serial number. That serial number can usually be found in the lower right corner of your DXA report. All my tests were on GE Lunar Prodigy with the same serial number.

    DXA Spreadsheet 2022 page 1
    DXA 2022 spreadsheet pg 2

    How to get a good DXA

    Hips

    The legs are turned inward, allowing a good DXA measurement.

    Hip rotation

    Spine

    The box places my back flat on the table

    Spine Position DXA small

    Forearm

    Forearm DXA 1

    Next steps

    My annual CMP (Comprehensive Metabolic Panel) blood test next year. This test measures the calcium levels that I monitor.

    Dr. McCormick uses blood tests to delve deeper into bone health.

    Also, my friend, Dr. Lani Simpson, DC, CCD, who has been in the osteoporosis trenches for decades, before I would get and follow bone markers:

    • CTX (full name Carboxyterminal cross-linking telopeptide or bone collagen) is a bone resorption marker.
    • My CTx was:
    • 346 (27-10-22 – Lab Corp)
    • 304 (2/22/22) Quest Labs (within the range offered in my Bone Marker presentation
    • P1NP (full name Procollagen type 1 N propeptide) measures bone formation. If my doctor does not write a script for this test, I will receive the script through Evexia or Life Extension.
    • My previous P1NP was 34
    • Vitamin D: I test twice a year – after summer and after winter
    • My last test showed 44.9 ng/ml

    Dr. Lani Simpson suggested an x-ray of my spine because arthritis makes a DXA look better than it is. My x-ray was taken by Dr. Kim Zambito, who reported mild arthritis in my spine and wrist.

    It takes a community.

    Forearm

    Why is the non-dominant forearm added to the DXA/TBS report?

    The spine and hip may have arthritis, but the DXA shows stronger results. The forearm can be a possible indication of problems with the parathyroid gland.

    Your forearm consists of 80 to 100% cortical bone. When a person has hyperparathyroidism, too much parathyroid hormone is pumped out. What does that degrade?

    That degrades cortical bone more than trabecular bone. And that’s why when you look at someone with hyperparathyroidism, their forearms often have low bone density.

    • “Primary hyperparathyroidism: Although this is a systemic disease that affects the entire skeleton, the lowest BMD is often the forearm, which may be the only site where the BMD is less than -2.5. In this case, the result should influence the decision regarding the surgical treatment of primary hyperparathyroidism (PHPT).” [i]

    Tests show negative for hyperparathyroidism. Bones are complicated.

    We are all different

    Several members of my Bones Tribe are on medication because it was deemed necessary based on a complete and comprehensive intake and blood work reviewed by their bone doctor. My Bones Tribe members seek other opinions before making a decision about medication based on knowledge versus fear of a decision.

    TIPS

    My DXA/TBS score was run on:

    The Hospital of the University of Pennsylvania

    3400 Civic Center Blvd. – Ground floor

    Philadelphia, PA

    phone: 215-662-3000 to book a DXA (ask for radiology to book your DXA).

    My script reads:

    • DXA bone density, axial CPT 77080
    • DXA bone density/peripheral CPT: 77081
    • Includes TBS and peripheral forearm.

    I asked for one full colored copy of my reports Before I left.

    I have a good feeling about the results.

    MEMORY:

    I open my:

    Pilot program: Stronger bones – Healthy you

    My 8-week Comprehensive Bone Health Program – The Whole Body Approach promises to educate you on every aspect of bone health. From DXA/TBS, bone markers, blood tests, calcium rich foods, exercise. You gain knowledge, a deep understanding of the terminology and move on to empowerment.

    Click HERE for a free 30 minute consultation to confirm that my program is right for you.

    I hope my shared experience is helpful to you and your beautiful bones.

    From my loving bones to yours,

    Irma Jennings, INHC, holistic bone coach

    e-mail: [email protected]

    [1] https://www.drug-injury.com/drug_injury/2010/09/doctor-files-suit-says-bone-drug-leads-to-breaks.html

    Let me support your bones

    Receive an in-depth, tailor-made private session

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  • The histone acetyltransferases CBP and p300 regulate stress response pathways in synovial fibroblasts at transcriptional and functional levels

     

    Hypoxia, the formation of reactive oxygen species (ROS) and subsequent oxidative stress in synovial tissues are key events in the pathogenesis of RA1. We provide evidence here that CBP and p300 are critical regulators of the adaptive response of SF that integrate the transcriptional and functional regulation of stress response pathways throughout the cell.

    CBP and p300 are HATs and H3K27ac mark writers, which activate post-translational histone modifications present in enhancers and promoters20. Among the CBP/p300 target proteins are several non-histone proteins in addition to histones, including many transcription factors and signaling effectors16.21. Despite their high protein sequence homology, CBP and p300 have distinct individual functions identified by our own and other studies12,13,14.

    In SF, persistent H3K27ac in inflammatory gene promoters was associated with long-lasting and persistent expression of the corresponding genes22. We recently demonstrated that p300 is the major HAT in SF that exerts a pro- and anti-inflammatory role. This is in contrast to CBP, which exerted anti-inflammatory effects upon silencing, and specifically regulated TNF-induced interferon signature gene expression14. Although we have ruled out that silencing p300 additionally reduced CBP and vice versa, we cannot completely rule out other potential off-target effects after our silencing approach. Krosel etc already. have shown that inhibitors targeting the HAT or bromodomain of CBP/p300 closely resemble the effects of p300 silencing, including increased expression of TNF-induced proinflammatory gene expression14.

    Our RNAseq data provide evidence that the number of p300-regulated target genes is greater than that of CBP-regulated target genes, also in terms of stress response. While the cellular response to oxidative stress and autophagy was co-regulated by CBP and p300, genes associated with response to oxygen levels, hypoxia, and pathways associated with proteasome regulation and function were specifically enriched upon knockdown of p300. In pathways co-regulated by CBP and p300, we identified several genes that were regulated in opposite directions. These results point to individual functions of the two enzymes at the level of target genes, similar to what we have already observed for many inflammatory genes14. Furthermore, a small number of measured CBP and p300 target genes, namely BCL2, SOD3 and HDAC6, could be regulated in a joint-specific manner, as indicated by our Real-time PCR results in a limited number of samples for each joint site. Frank-Bertoncelj et al. have previously shown that H3K27ac is one of the mechanisms controlling the joint-specific expression of homeobox (HOX) transcription factors in SF from different locations7. To draw a definitive conclusion whether stress-associated target genes are regulated in a joint-specific manner, larger numbers of SF from different joints would be needed, together with H3K27ac ChIPseq data in unstimulated and TNF-stimulated SF from different joints.

    In addition to the differential roles of CBP and p300 in regulating target gene expression, we showed here a differential regulation of CBP and p300 by stimulating SF with 4-HNE and TNF (Fig. 6). These factors are present in the synovial microenvironment in RA and mimic the oxidative stress and inflammation, respectively. While 4-HNE and TNF, similar to H2O2suppressed the expression of p300, CBP was not affected. 4-HNE is a lipid peroxidation product generated at elevated levels of ROS. Levels of 4-HNE are elevated in serum, synovial fluids, and synovial tissues of RA patients, and serum levels of 4-HNE correlate with structural damage such as erosions in the early stage of RA23,24. As mimicked by our silencing approach, the TNF- and 4-HNE-mediated suppression of p300 expression in the synovial RA microenvironment has fundamental consequences for SF behavior. Our datasets from the previous one14 and the present study indicates that reduced expression of p300 was associated with increased expression of many inflammatory cytokines, chemokines matrix metalloproteinases and stress response genes in SF. Among these genes were HK2, a marker indicating the metabolic switch from SF to glycolysis, and VEGF, a pro-angiogenic factor secreted to overcome hypoxia.1.

    Figure 6
    figure 6

    Summary of CBP- and p300-regulated pathways in SF. The expression of p300 but not CBP is down-regulated in synovial fibroblasts after exposure to TNF and oxidative stress. The effects of p300 and CBP silencing are demonstrated based on findings from this and a previous study14. Downward arrows indicate suppressed expression or function, upward arrows indicate increased expression or function. The figure was created by BioRender.com.

    TNF stimulation of SF markers of endoplasmic reticulum (ER) was shown to induce stress and autophagy25. Our data suggest that CBP and p300 regulate autophagy at the transcriptional level and influence autophagic flux. The assessment of autophagy in the presence of the lysosomal inhibitor bafilomycin A1 indicated that CBP and p300 regulate autophagy function at different stages within the autophagic process. CBP silencing affected autophagosome synthesis. In contrast, knockdown of p300 induced autophagy in unstimulated SF, and induced a late-stage block of autophagy in TNF-stimulated SF, a condition in which polyubiquitinated proteins in SF accumulated. Accordingly, knocking down p300 only increased cell death in the presence of TNF, as previously indicated14. Kato etc already. have previously shown that autophagy induction partially compensated for reduced clearance of polyubiquitinated proteins in SF after blocking proteasome function, indicating a protective effect of autophagy induction in SF under such conditions5. Here we observed a similar compensatory mechanism after p300 knockdown, which was associated with a suppression of proteasome enzymatic activities and an induction of autophagy. This finding is consistent with a previous study in HeLa cells in which p300 knockdown was associated with reduced acetylation of autophagy-related proteins and increased levels of autophagy.26.

    Acetylation and deacetylation of components of the autophagy machinery control all steps of this catabolic process, from autophagosome initiation to LC3 conjugation, cargo assembly, and autophagosome-lysosome fusion27,28. Several classes of acetyltransferases, including CBP and p300, and deacetylases, including sirtuin1, HDAC4 and HDAC6 are involved in the regulation of autophagy27.29. Furthermore, the function of autophagy-related transcription factors, such as transcription factor EB (TFEB), Foxo1 and Foxo3, is regulated by deacetylation28.30. Recently, the increased translation of FOXO3 mRNA has been described to facilitate the initiation of autophagy31. We showed here that in unstimulated SF, FOXO3 mRNA increased after p300 knockdown, a condition in which autophagic flux increased. HDAC6 binds to polyubiquitinated proteins in SF29and promotes autophagy by facilitating autophagosome-lysosome fusion27. On the other hand, HDAC6 was also shown to suppress autophagy by deacetylating TFEB and Foxo130. This could explain the inverse regulation of HDAC6 and ATG5 and ATG16L1 in SF.

    A global analysis of the CBP/p300-dependent acetylome in mouse embryonic fibroblasts (MEF) suggested that proteasome functions might also be regulated by these enzymes.21. The majority of proteasome machinery components showed numerous CBP/p300-dependent acetylation sites in regulatory and enzymatic subunits in MEF (http://p300db.choudharylab.org). Furthermore, ATG5 and ATG16L1, two proteins essential for autophagosome assembly, showed CBP/p300-dependent acetylation sites21. Whether proteasome and autophagy components are acetylated in a CBP- and p300-dependent manner in SF remains to be functionally evaluated21. Because CBP/p300-dependent acetylation sites in MEF were analyzed after a combinatorial knockout of both enzymes, it is not clear which of them is the key enzyme in regulating the post-translational acetylation of proteins involved in the regulation of autophagy and proteasome activities.

    In summary, we have identified CBP and p300 in particular as critical regulators of stress response pathways in SF, with overlapping and distinct functions within specific pathways. The downregulation of p300 by TNF and oxidative stress provides a mechanism underlying SF activation in the synovial microenvironment.

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  • My Personal Journey to Osteoporosis Care and Awareness in Underserved Communities – Bone Talk

    My Personal Journey to Osteoporosis Care and Awareness in Underserved Communities – Bone Talk

    IMG 20230830 WA0029

    My personal journey to osteoporosis care and awareness in underserved communities
    By Dr. Tasneem Hassan

    My name is Dr. Tasneem Hassan and I work as a general practitioner in Nairobi, Kenya. After graduating in 2019, I started working in a public hospital in Nairobi.

    Later I started working at Rayhaan Healthcare, where I met Dr. Mustafa Bhaiji, a consultant radiologist with a special interest in osteoporosis. I also learned about the DXA technology, which further sparked my interest in osteoporosis. As I learned more about my family’s history and observed many people with poor bone mass, I started to pay more attention to it.

    This is the story of my grandmother, who fell a few years ago and broke her hip, needing hip replacement surgery and leaving her bedridden for a while. All these difficulties contributed to her death. For starters, we know she had low bone mass, but the lack of a bone DXA scan in Mombasa, Kenya delayed early diagnosis and treatment. She also had dementia and her recovery was difficult. In addition, there is a lack of awareness in our system about osteopenia and osteoporosis, which hinders early diagnosis and prevention. If our thinking about osteoporosis had advanced significantly earlier at the time, she might not have died from the comorbidities associated with the fracture.

    Another interaction I had was with my mother, who had already suffered a fracture. She is currently going through menopause and a few months ago she broke her foot as a result of a fall. This could be a stress fracture. But given her age and menopause, higher risk of falls, and history of two fractures, I wouldn’t be shocked if she has poor bone mass, and thus osteopenia. Individualizing care is simple; we do it all the time. We shouldn’t allow people to walk around with untreated osteoporosis because they will eventually stop walking. It’s no longer the 1900s.

    Osteoporosis is a disease that roughly causes 8.9 million fractures per yearculminating in one osteoporosis fracture every 3 seconds. One in three women and one in five men those aged 50 and over will experience an osteoporotic fracture. Osteoporosis causes bones to become weak and brittle, causing them to break easily even after a minor fall, bump, sneeze, or quick movement. I have seen people who have fractures that damage them not only physically, but emotionally as well. It reduces their overall quality of life, sometimes resulting in despair and isolation as people reduce social connection or are no longer able to do the activities they used to do. The prolonged loss of freedom and freedom of movement has caused physical, emotional and financial hardship to patients as well as their relatives and friends.

    80% of it who have had at least one osteoporotic fracture are not diagnosed or treated for osteoporosis.

    As a GP, I tried to read as much as I could after recovering from my pity party, which I felt was tragically avoidable. Over the past few weeks I have been focusing on a study of the prevalence of osteoporosis in our organization, particularly as it relates to ethnicity, age, menopause and risk factors.

    Many women experience decreased bone mass after menopause and aging. I am very interested in following up on this group of patients and referring them to the best available care. We also conduct research based on the few DXA scans we have completed to help future generations.

    It is also overlooked as a health problem in Africa for several reasons, including:

    Overburdened by communicable diseases such as tuberculosis (TB) and human immunodeficiency virus (HIV).

    Not long ago there was a widespread belief that osteoporosis and resulting fragility fractures were uncommon among black Africans, but this is no longer the case.

    We have come across many people of all races affected by osteopenia. However, the problem remains that there is no African research. This brings the FRAX scoring guideline into conflict because it does not take African race into account.

    In our region, healthcare professionals also lack insights about osteoporosis.

    Despite advances in scientific research and available therapies and diagnostic techniques, osteoporosis remains a global health problem with potentially disastrous consequences for patients and enormous costs to healthcare systems.

    In this context, we can probably all agree that we need to improve osteoporosis treatment and raise awareness in underserved communities.

    My goal is for more physicians to be informed about this topic and for this disease to be prioritized alongside other chronic conditions.

    This story is part of a support initiative called Voices of Osteoporosis: Stories of Hope and Inspiration. If you have experienced osteoporosis as a patient or caregiver, we invite you to share your story. Your story can inspire others to learn how to protect their ability to live their best life and stay strong. click here learn more.

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  • Medicare enrollees can now switch coverage. Here’s what’s new and what you should keep in mind.

    Medicare enrollees can now switch coverage. Here’s what’s new and what you should keep in mind.

     

    Consumers know it’s fall when stores start offering Halloween candy and flu shots — and the airwaves and mailboxes fill with ads for Medicare options.

    It’s annual open enrollment time again for the 65 million Americans covered by Medicare, the federal health program for the elderly and some people with disabilities.

    From October 15 to December 7, participants in the traditional program or Medicare Advantage plans, which are offered by private insurers, can change their coverage. (First-time enrollees typically sign up within a few months of their 65th birthday, whether during open enrollment season or not.)

    There are a few new features for 2024, including a lower out-of-pocket limit for some patients on expensive medications.

    Whatever happens, experts say, it’s a good idea for beneficiaries to examine their current coverage, because health and drug plans may have made changes, including to the pharmacies or medical providers in their networks and how much prescriptions cost.

    “The advice is to check, check and check again,” says Bonnie Burns, a consultant with California Health Advocates, a nonprofit Medicare advocacy program.

    But as anyone in the program or who helps friends or family members with coverage decisions knows, it’s complicated.

    Here are a few things to keep in mind.

    Know the Basics: Medicare vs. Medicare Advantage

    People in traditional Medicare can see any participating doctor or hospital (and most do participate), while those in Medicare Advantage must choose from an itemized list of providers – a network – that is unique to that plan. Some Advantage plans offer a broader network than others. Always check whether your preferred doctors, hospitals and pharmacies are covered.

    Because traditional Medicare does not cover prescriptions, members should also consider signing up for Part D, the optional drug benefit, which includes a separate premium.

    Conversely, most Medicare Advantage plans include drug coverage, but be sure to check before you enroll because some do not. These private plans are heavily advertised, often touting that they offer “extras” not available in traditional Medicare, such as dental or vision coverage. Read the fine print to see what restrictions, if any, are placed on such benefits.

    Those age 65 and older who are new to traditional Medicare can purchase a supplemental or “Medigap” policy, which covers many out-of-pocket costs, such as deductibles and copays, which can be significant. Generally, beneficiaries have six months after enrolling in Medicare Part B to purchase a Medigap policy.

    So switching from Medicare Advantage to traditional Medicare during open enrollment could pose problems for those who want to purchase a supplemental Medigap policy. That’s because private insurers offering Medigap plans, with some exceptions, can turn away applicants with health problems, or increase premiums or limit coverage of pre-existing conditions.

    Some states offer beneficiaries more guarantees that they can switch Medigap plans without answering health questions, although the rules vary.

    To make all this even more confusing, there is a second open enrollment period each year, but it is only for those with a Medicare Advantage plan. They can change their plans or return to traditional Medicare from January 1 to March 31.

    Drug coverage has changed – for the better

    Beneficiaries who have enrolled in a Part D drug plan or receive drug coverage through their Medicare Advantage plan know that there are many copays and deductibles. But by 2024, some of these expenses will disappear for those who need a lot of expensive medicines.

    President Joe Biden’s Inflation Reduction Act places a new annual cap on Medicare beneficiaries’ out-of-pocket costs for medications.

    “That policy is going to help people who are taking very expensive medications for conditions like cancer, rheumatoid arthritis and hepatitis,” said Tricia Neuman, senior vice president and head of KFF’s Medicare policy program.

    The cap will greatly help beneficiaries who fall into Medicare’s “catastrophic” coverage — an estimated 1.5 million Americans in 2019, according to KFF.

    Here’s how it works: The cap is triggered after patients and their drug plans together spend about $8,000 on medications. KFF estimates that this means about $3,300 in out-of-pocket expenses for many patients.

    Some people could reach the limit within one month, given the high prices of many drugs for serious conditions. After the limit is reached, beneficiaries will not have to pay anything out of pocket for their medications that year, saving them thousands of dollars annually.

    It is important to note that this new limit will not apply to medications administered to patients, usually in doctor’s offices, such as many cancer chemotherapeutics. These drugs are covered by Medicare Part B, which pays for doctor visits and other outpatient services.

    According to the Medicare Rights Center, next year Medicare will also expand opportunities for some low-income beneficiaries to qualify for low- or zero-premium drug coverage with no deductibles and lower copayments.

    Insurers offering Part D and Advantage plans may also have made other changes to drug coverage, Burns said.

    Beneficiaries should consult their plan’s “formulary,” a list of covered medications, and how much they will have to pay for the medications. Be sure to note whether prescriptions require a co-pay, which is a fixed dollar amount, or coinsurance, which is a percentage of the drug cost. In general, copayments mean lower out-of-pocket costs than coinsurance, Burns said.

    Help is available

    In many parts of the country, consumers can choose from more than 40 Medicare Advantage plans. That can be overwhelming.

    Medicare’s online plan finder provides details on the Advantage and Part D drug plans available by zip code. Allows users to view details about each plan’s benefits, costs, and healthcare provider network.

    Insurers are expected to keep their supplier directories up to date. But experts say enrollees should contact directly the doctors and hospitals they would most like to confirm that they are participating in a particular Advantage plan. People concerned about drug costs should “check to see if their pharmacy is a ‘preferred pharmacy’ and if it is in network” under their Advantage or Part D plan, Neuman said.

    “There can be a significant difference in out-of-pocket expenses between one pharmacy and another, even in the same plan,” she said.

    To get the most complete picture of estimated drug costs, Medicare beneficiaries should look up their prescriptions, dosages and their pharmacies, says Emily Whicheloe, education director at the Medicare Rights Center.

    “For people with specific drug needs, it’s also a good idea to contact the plan and say, ‘Hey, will you still cover this drug next year?’ If not, change to a plan,” she said.

    Additional enrollment assistance can be obtained for free through the State Health Insurance Assistance Program, which operates in all states.

    Beneficiaries can also ask questions through a toll-free Medicare hotline: 1-800-633-4227 or 1-800-MEDICARE.

    Insurance brokers can also help, but with a caveat. “Working with a broker can be fun for that personal touch, but know that they may not represent all plans in their state,” says Whicheloe.

    Whatever you do, avoid telemarketers, Burns said. In addition to TV and mail ads, many Medicare beneficiaries are inundated with phone calls promoting private plans.

    “Hang up,” Burns said.

     

    Kaiser health newsThis article was adapted from khn.org, a national newsroom that produces in-depth journalism on health issues and is one of the core operating programs at KFF – the independent source for health policy research, polling and journalism.

     

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  • Chronic pain and movement and why I went to my physiotherapist for help

    Chronic pain and movement and why I went to my physiotherapist for help

     

    woman lifting dumbbell
    Photo by Leon Ardho on Pexels.com

    Okay, so I wanted to get back into doing more resistance training. Currently my resistance training involves my dogs pulling on the leash when we go for walks. While that certainly gives me a solid upper body workout, it is neither consistent nor conducive to gradually building strength and capacity.

    I also do archery, which is also a great upper body workout. I usually shoot about 4 times a week with a recurve bow. It’s also a lot of fun. My bow weighs about 36 pounds, so I’m fairly strong. Possibly, more accurately, “fairly strong for someone living with multiple chronic illnesses.”

    Although I get tired quickly. Part of the reason I want to do a good resistance training program is to get stronger for archery so I can shoot longer and have longer archery sessions. To build my endurance and increase my strength. If it’s easier to pull back a 36-pound bow, I can do it longer. Maybe I can even go every day.

    So that was the idea.

    I started two weeks ago and created a very simple program for myself.

    This is what I did.

    Upper body exercises

    All exercises consist of 3 sets of 10 repetitions.

    Bench press – 15kg

    Curved dumbbell rows – 8 kg

    Seated shoulder press – 3 kg

    Biceps curls – 5 kg

    Overhead Triceps Extension – 5kg Plate

    Lateral raises – 3 kg

    Lower body exercises

    Goblet squats body weight to sitting level and stands up

    Dumbbell lunges bodyweight

    Romanian deadlifts 20kg

    Calf increases body weight

    Dumbbell increases body weight

    My upper body was fine. I hardly had any pain anymore. But it’s a very easy, lightweight start. That’s what I was aiming for, and I got it right for my upper body.

    Now my lower body was something completely different.

    I woke up that night around 1am in terrible pain. And I mean *terrible*. It was an electric, diffuse, terrible pain through my legs. I’ve heard others call it an “electric storm in my muscles” and that’s a good description. A painful electrical storm.

    I had no control over my legs, they wouldn’t do what I wanted. Or they would…eventually. The response was slow. Talk about ‘delay’. Standing was almost impossible and walking was almost impossible used to be impossible, until I discovered that my legs were responding, just very slowly.

    I sat on the steps and lowered myself onto my butt. I didn’t feel safe walking down. I scooted on my butt, but it was the slowest scoot you’ve ever seen! It was more of a painful, slow lowering of my body, step by step, with most of my weight on my arms.

    Thank the gods you still have good upper body strength!

    This was all a big shock to me. I didn’t expect to react this way…I guess this is what happens when you do it too much when you have CIDP. I know how inflammatory arthritis responds to exercise, and too much exercise. But this neuropathic pain? This is new. A surprise. And not a nice one. But it’s all a learning experience, right?

    I took my usual painkillers, opioids, and the pain subsided a bit. But it was still unbearable. I took another dose.

    Long story short, I was in pain all day and couldn’t do anything. The next day things got better, but I still spent most of the day lying down. I couldn’t work or deliver my orders. It was the first time that I received NO orders within 24 hours. I pride myself on getting my orders FAST, so that was a big hit for me. I will NOT do that again!

    Day 3 my legs started to feel more normal. I walked normally; my legs responded in the normal time. Previously I felt like my upper body was leaning forward and my legs were catching up, way back. Very strange sensation and very unpleasant. Now I felt like I was walking normally, albeit a little slower.

    Please note, this is NOT muscle pain due to overdoing it, due to a heavy training. I’ve been a gym junkie my entire adult life. I know what sore muscles in the gym feel like. I’ve had DOMs and the cliche ‘can’t lower yourself onto the toilet because it hurts too much’. I know what it feels like when you’ve been working hard in the gym and overtraining your muscles.

    This was NOT that.

    This was something completely different. Something I’ve never felt before.

    And it took three days for me to feel vaguely normal.

    Those three statements were incredibly painful, and I was completely disabled for most of that time. It was a wake-up call.

    I made a big mistake.

    So.

    Solution? Lighten the weight. Reduce the reps. And try again.

    I’ve tried. I have failed. I felt terrible. I felt depressed.

    So.

    I went to my physio because I need support with this. The whole experience was very disappointing, disturbing even. Frustrating too. And even though I knew what to do, I knew how to do it, I didn’t do it right.

    I realized I needed some advice, with a dose of support and encouragement. Quality advice. I knew my physio would give me all that.

    He gave me two options: do it the easy way. Return it immediately to a small load. Try to do 5 reps, one set of everything. And only increased once every two weeks. And then increase the tax by 10%.

    Or do it the hard way. Start with 5 reps, but do 2 sets. If that goes well, increase by 10-20% every week. Whatever makes sense with the weights I use. If things aren’t going well, reduce the weight. And look what happens.

    Option one has the advantage that it causes absolutely NO pain. Because I can certainly do very light loads. I know it won’t leave me on the couch for two to three days, it won’t disable me and it won’t hurt. But the downside is that it will be very slow. Working slowly to find my baseline could take weeks from now. Many weeks.

    As we know, I am a very impatient person.

    Option 2 can cause pain. It might be too much. It may mean that you have to lie on the couch again for a day or two. While this would be very disappointing, my natural optimism (and perhaps my habit of overestimating my abilities) tells me I want to do it this way. If it’s too much, I wait until the pain goes away and reduce it by 20%. And try again.

    So today I’m starting over.

    I’m going to do the same upper body. It was fine. I might even increase it a bit.

    However, the lower body will be much, much less. There will be 2 sets of each.

    Squats – 5 reps

    Lunges – 5 reps per leg

    Romanian deadlifts – 10 kg

    Calf raises – 5 reps

    Step-ups – 5 per leg

    And then I’ll see how I can handle it. This is about a quarter of what I was doing before, even less. So I hope this doesn’t cause me any severe pain. A little pain is fine. And to be expected. Maybe even appreciated as a sign of progress.

    But we’ll see.

    I keep notes on what’s happening and how I’m going. It should be interesting.

    Above all, I will be honest. This is a challenge, and I’ve messed up before. And now I’m trying again, with the support of my physiotherapist.

    I don’t want people to think this is a walk in the park, it’s not. It’s a serious undertaking and I hope it will help me maintain muscle strength in my arms and legs. It will take a lot of energy, it will reduce my upright hours, hours of which I currently have too little. And it may not help. But in the worst case even if it doesn’t help. At least I’ll feel like I did everything I could to avoid muscle wasting and further disability.

    In four weeks I will go back to the physio to see how I am doing. I will also post progress reports here.

    I don’t want people to think this is easy. It’s not. But it IS feasible. And it IS worth it.

    Buy me a coffee

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  • Osteoarthritis: what you need to know

    Osteoarthritis: what you need to know

     

    By means of Jordan Brocker PT, DPT, CSSS | Foothills of Queen Creek

    Osteoarthritis is a normal physical condition caused by wear and tear on the body, leading to deterioration of the articular cartilage. This leaves the bones unprotected and eventually the deterioration of the joint can become so extreme that the bone rubs against the bone. The synovial fluid that helps lubricate the joint for normal, smooth function also deteriorates, leading to resistance to movement and often audible noises during movement. Both factors play a role in the pain and limitation of the affected joints.

    Unfortunately, there are no means to completely reverse arthritis that has already developed. But, and more importantly, there is something you can do about it. Research and my professional experience have shown that physiotherapy can help relieve the pain and discomfort caused by osteoarthritis, so that your recovery is more than adequate and you can continue to do the activities you enjoy.

    Osteoarthritis: important factors to address

    • Weakness and flexibility in muscles related to affected joints
    • Stability of associated joints
    • Specific joint movement and mobility
    • Body mechanics affected by different joints
    • Balance and proprioception for the joints of the lower extremities
    • Muscle endurance

    Patient with osteoarthritis is stretched by physiotherapist.

    How physiotherapy can treat osteoarthritis

    Physical therapy reduces the limitations caused by a person’s arthritis by addressing each of the above factors appropriately and uniquely for each individual. Everyone will have different causative factors that change how their arthritis is experienced and how it progresses. Your physical therapist should address these issues appropriately so that you can get the greatest benefit from treatment. Physiotherapy will allow optimal function of the arthritic joint to prevent further deterioration and promote its current integrity.

    For example, a widely arthritic joint is the knee. Often, degeneration of the lateral (outer) aspect of the knee can occur at a higher level than the medial (inner) joint due to more force being placed on the outside of the knee during weight-bearing activities. The knee position that causes this is known as genu valum and is seen when the knee is positioned towards the center of the body, not towards the hip. The culprits responsible for this positioning are often weak hip and ankle muscles. Therefore, targeting the weaknesses in these muscle groups and incorporating them into activities (such as walking or bending/squatting) could help reduce abnormal forces on the knee, reducing irritation.

    Physiotherapist helps patient build strength with osteoarthritis.

    Tailor-made exercise program for the treatment of osteoarthritis

    As physiotherapists, we observe local joints and the entire body to assess possible areas of disability and then improve an individual’s body mechanics. Based on our evaluation process, we create a program of specific exercises to best meet each person’s needs. We work to create independence with a home exercise program that allows them to continue the exercises. With a good understanding of the concepts behind the exercises for continued rehabilitation.

    Many factors can determine the effectiveness of osteoarthritis treatment. Such as the severity of the problem, current or previous level of function, joint deformity or other bone diseases. If these factors are present, it does not mean that a person cannot do anything about their arthritis. However, it can affect the amount of improvement that can occur and how long it takes to improve. Ultimately, doing something about osteoarthritis will be much more helpful than sitting still and allowing the process to continue. The amount of improvement you can achieve could change your life if you take action!

    Foothills Sports Medicine Physical Therapy is committed to providing hands-on, individualized care to people of all ages with numerous conditions. Our physiotherapists are committed to your complete recovery. Schedule a free assessment with highly trained staff, or contact one of our many locations throughout the valley.

    The post Osteoarthritis: What You Need to Know appeared first on Foothills Physical Therapy & Sports Medicine – Phoenix Metro.

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  • Do I have lupus? [Quiz] – AOTC Jax





    Lupus can be difficult to diagnose and even harder to live with. However, with the right treatments, you don’t have to suffer. At Arthritis and Osteoporosis Treatment Center, we are here to give you all the information you need to manage your pain and get back to doing the things you love. Take the quiz below and learn more about lupus so you can start treatment right away.

    What is lupus?

    Lupus is an autoimmune disease that causes the body to mistake healthy tissue for harmful viruses or bacteria. As a result, the body produces antibodies that attack, damage and destroy healthy tissue. This results in chronic pain and inflammation for patients suffering from the disease.

    Can men get lupus?

    Anyone can be diagnosed with lupus at any time, but the average age of those diagnosed is between 15 and 44 years. About 90 percent of patients currently living with lupus are women. Because of this, there is a myth that men do not get the disease. Men can get lupus, and research shows that their symptoms can be even more severe.

    What are the symptoms of lupus?

    Symptoms of lupus can be difficult to distinguish from those of other autoimmune diseases. Patients with the disease typically suffer from joint or muscle pain, stiffness, or swelling. It can also cause recurring fever, increased fatigue, and painful breathing.

    There are also several physical indicators of lupus, including hair loss. Patients often experience a red, flaky rash on their nose, cheeks, or other parts of the body. Additionally, lupus can result in dry mouth or recurring sores.

    How Long Do Lupus Flares Last?

    Patients suffering from lupus experience worsened symptoms during periods known as flare-ups. These flare-ups can occur at any time and last one to three weeks. Symptoms can be mild or severe, and these episodes are often caused by sun exposure and physical or emotional stress.

    Treatment options for lupus

    Although there is currently no cure for lupus, there are many treatment options and effective lifestyle changes that minimize painful symptoms and prevent flare-ups. Hydroxychloroquine is the mainstay of therapy for preventing disease progression and organ involvement. Other disease-modifying antirheumatic agents are also used to treat various disease manifestations. The advent of biologics such as Benlysta and now Saphnelo have been game changers in managing lupus.

    It is also recommended that lupus patients exercise regularly and avoid prolonged sun exposure to prevent flare-ups. Visit your rheumatologist often and follow an anti-inflammatory diet consisting of fruits, vegetables, whole grains, and oily fish to reduce painful symptoms.

    Schedule an appointment at our Orange Park office in Jacksonville, Florida

    If you are having trouble managing your lupus symptoms, make an appointment with one of our experienced lupus doctors. At AOTC we ensure that you receive the specialist care you deserve. Schedule an appointment with our rheumatologists in Jacksonville, FL today.

    Lupus Self-Assessment Quiz

    Still not sure if an appointment with an arthritis doctor is right for you? Answer these questions to find out if it’s time to discuss your symptoms and treatment options with a rheumatologist.


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