Moon face question

Posted , 20 users are following.

For those of you on low doses of Prednisone (under 10 mg?), how long did it take for your moon face to go away? Or, does it hang on? 

I'm currently on 14 mg and mine just keeps getting fuller, especially on my chin and neck area.  I feel like I have balloons under my chin.  Blah!

I was not overweight before taking Prednisone , but have now packed on 20 extra pounds, which I'm sure doesn't help.  I have so many different sizes of clothes in my closet, I could open up a thrift shop. Blah, again.

Have a good day, everyone!

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  • Posted

    Hi Pam

    I started prednisone September 2015 just now finishing a taper to 14mg. Im the rare slow moving turtle. I was on a low carb diet which kept the weight of but within 3 months I developed the moon face as well a fat deposits on shoulders just recently and the fat around the midrif. My face changes daily and can change within the day. I don't even look like the same person.

    I took a trip to visit family in Quebec Canada and ate way to many carbs and wine as the french do and gained then Christmas came and that didn't help so I have to get back into an exercise routine and be strict on carbs and hopefully I can loose it. I've never been so fat, I know how you feel it's depressing.

    Chin up, I thank god for these posts.

    Mariane

  • Posted

    I have lived with PMR for over 5 years now and was originally given 15 mgs of Prednisolone which made me feel wonderful.  Sadly, having glaucoma, the dose had to be lowered as my occular pressures rose dangerously and have been on 7mgs since then.  I was not happy to notice my face get rounder and my neck more chubby.  I have always had a round face so other than thinking that I had put on a bit of weight, my friends did not notice.  I think we are all different as I know of two people who have not developed a round face when on steroids.

    Mind you, I would rather have a round face than all the pain of life with PMR and no steroids. 

    Best regards

    • Posted

      Sorry to hear that - does the 7mgs actually do much? Were you not given drops or did they not work?
  • Posted

     My husband is down to 12 mg and still has the moon face. For reasons we still don't understand ( but believe me we will ) he is being put in an injectable medication, Enbrel. 

    And then taken off steroids and thst worries me. He just started steroids recently, soon after diagnosis. I didn't think they would discontinue them so soon. But Envrel is supposed to halt any weight gain

    • Posted

      I would be insisting on a good answer. Enbrel is an anti-TNF biologic and that group of drugs is explicitly mentioned in the most recent recommendations for the management of PMR:

      "Recommendation 8: (PICOs 10–11) The panel strongly recommends against the use of TNFa blocking agents for the treatment of PMR. The group agreed strongly against the use of TNFa blocking agents in PMR at this time since there is no evidence for benefit, but there is a considerable risk of potential harm and high resource use (55). No recommendation can be made for other biologic agents as no prospective trials have been published so far. There is one ongoing randomized study on the Box 2. Research agenda The group agreed that future studies in polymyalgia rheumatica (PMR) should be multicenter and properly powered using an agreed, validated core outcome set and a robust trial design that would maximize the power of studies, facilitate regulatory approvals and allow future meta-analysis. Specific research questions: 1. Which outcome measures including patient-related outcomes, and response, remission and relapse criteria should be used in PMR? What is the value of a composite score? What are the most relevant treatment targets in PMR? 2. What is the efficacy and safety of different routes of glucocorticoid (GC) administration (oral, intramuscular, intra-articular), different initial GC doses, various GC tapering regimens, and different GC flare doses? 3. What is the efficacy and safety of DMARDs (non-TNFa biologic, conventional synthetic and conventional targeted) in PMR? What is the optimal strategy for using DMARDs in PMR: monotherapy versus combination therapy, early versus late introduction, and (particularly for biologics) use with or without GCs? . What is the minimal/optimal duration of therapy and which strategies for withdrawing GCs and/or DMARDs yield the best efficacy/safety profile? 5. What is the optimal strategy for shared primary and specialty care including recommendations for specialist referral? How can patients be better involved in treatment decisions, and are there any decision aids? What is the role of self-management? 6. What is the value of tight control (ie, treat to target) versus conventional management strategies in PMR? 7. How should patients with long-standing disease and long-term low-dose GC therapy be managed?. What is the cost utility and effectiveness of DMARD use in PMR (versus GC use alone)?. What is the value of non-pharmacological therapies in PMR? Particularly, it is assumed but not yet demonstrated that physiotherapy may support preservation of function and reduce the risk of adverse events related to GC use. Patients may benefit from exercise by maintaining muscle mass and function as well as by fall prevention especially in the frail. What is the role of diet in PMR and nutrition supplements (eg, fish oil) related to outcomes?. What is the efficacy and safety of herbal preparations in PMR?. What is the role of imaging (particularly ultrasound) for the assessment and monitoring of PMR, identification of overlap with other diseases (eg, large vessel vasculitis or inflammatory arthritis) alongside clinical and patient reported outcomes?. Which biomarkers may be useful in PMR? Why do some patients do better than others? How can we identify these groups and what is the biological mechanism behind it? Should different drugs be applied to different PMR subgroups?. What is the morbidity and mortality of PMR patients (with a particular focus on cardiovascular risk) in long-term observational studies?. What is the etiopathogenesis of PMR? Which targeted therapies could be developed based on new knowledge of disease mechanisms? Bolded points indicate the top 5 items of the research agenda according to the opinion of the guideline panel. 2576 DEJACO ET AL use of tocilizumab (clinicaltrials.gov NCT01396317) and another three-arm trial comparing secukinumab, canakinumab and GCs (clinicaltrials.gov NCT01364389) in PMR. The results of these studies may lead to a modification of this recommendation."

      It is used for ankylosing spondylitis - and that CAN  present very similarly to PMR. 

      The link to the recommendations can be found here:

      https://patient.info/forums/discuss/pmr-gca-website-addresses-and-resources-35316

      If he has PMR then the biologic to be considered would be tocilizumab/Atemra.

    • Posted

      I don't get why my reply was moderated - I thought the only link I out in was for within the site.

      Anyway - what I said was I would certainly want to know WHY Enbrel is the intention. If the diagnosis is definitely PMR, the anti-TNF drugs are specifically mentioned in the 2015 Recommendations for the management of PMR as being of no benefit but associated with considerable risks. One study using an anti-TNF agent had to be discontinued because of adverse effects and no benefit being seen.

      There is one condition in particular where anti-TNF medications are used that can present very similarly to PMR but typically tends to cause night-time pain which improves with exercise. But I would expect to be TOLD that that was the suspicion.

      If they want to use a biologic instead of pred, the only one for which there is any suggestion it will help is tocilizumab (Actemra) and it has been through Phase 3 clinical trials for GCA with some considerable success. GCA and PMR are almost certainly closely related so a drug which works there could be useful in PMR. But it is very expensive.

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