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Fibromyalgia and inflammatory conditions


Recognition and treatment of inflammatory conditions is an integral part of rheumatology practice. However, recognition of alternative sources of pain is crucial for avoiding over-treatment of such patients. Patients presenting with joint pain are frequently conferred with a diagnosis of ‘chronic widespread pain’ or fibromyalgia, which pose their own treatment challenges.

Here we present the case of a young woman recently diagnosed with a spondyloarthropathy on a background of inflammatory bowel disease, whose pain presentation evolved over time. She has now progressed to a pattern of widespread pain. The latter predominates over her inflammatory pain and is so far refractory to a broad spectrum of analgesics. Her case highlights the importance of recognition of the pattern of fibromyalgia (FM) in patients with concomitant inflammatory conditions, and the challenge this presents for clinicians.


FM is a disorder of chronic, widespread pain and is a common cause of non-inflammatory pain in patients with underlying arthropathies. It affects 25 per cent of patients with rheumatoid arthritis, ankylosing spondylitis (AS) and systemic lupus erythematosus. Its prevalence is 3-4 per cent, predominantly Caucasian (90 per cent) females (70-90 per cent). It presents with a long history (over six months) of diffuse tenderness at discrete sites above and below the pelvis.

The ACR criteria are met when 11 of 18 trigger points test positive. Trigger-point testing in FM requires 4kg/cm2 — enough to blanch the distal thumbnail. In clinical assessment, pain amplification reduces the sensitivity of the tender joint score, so reliance is instead made upon swelling, range of movement and inflammatory blood markers.

FM is a contentious diagnosis; a recent Canadian study showed that 36 per cent of family physicians expressed doubt about their ability to diagnose FM and 23 per cent believed that FM patients were malingerers. A compromise is to consider FM as either a comorbidity (in this case of irritable bowel disease and AS), or a continuous phenotypic spectrum associated with variations in central pain processing.

In general, expressing doubt about diagnosis validity is not helpful in dealing with patients presenting with symptoms suggestive of FM. A model of chronic, non-malignant pain developed by Howell suggested that constant invalidation may become a barrier to effective pain management.

Studies of FM patients and their interaction with medical services (typically higher than the general population) show that having less invalidating experiences is associated with higher quality of life scores and that patients with greater trust in their physician had less pain.

Patients exhibit allodynia, hypothesised to be due to central sensitisation and amplification phenomenon. The pathophysiology of FM is also contentious, but speculated to be due to three interlocking pathways. Peripheral sensitisation occurs when non-noxious stimuli are perceived as noxious by pain receptors. Wind-up occurs when neurons become secondarily hyperexcitable due to peripheral sensitisation. Neuroplasticity results from expanded brain receptive fields for pain stimuli seen on functional MRI, predominantly in the insula, anterior cingulate cortex and somatosensory cortex. Cerebrospinal fluid studies have shown reduced levels of serotonin, noradrenaline and dopamine, all of which have antinociceptive properties. In addition, increased CSF opioid levels may account for the ineffectiveness of narcotics in this condition.

Intervening early in the course of a pain condition may help prevent the vicious cycle of long-term physical and psychological suffering. Patients who have had FM for an extended period have ingrained, maladaptive patterns of pain-coping and illness behaviours that are resistant to treatment. Finally, early intervention has the potential to reduce or prevent disability in patients with chronic pain, which in turn will reduce societal and medical costs.

When discussing analgesic regimes, it is important to determine if the patient has reached the maximal non-toxic dose of the agents trialled and to question the frequency of use to see if this has been fully exploited. Many patients will assume a drug has ‘failed’, when in fact it has worn-off over time. In this case, explaining analgesic half-life and the concomitant on-off effect may improve patient understanding, as might the use of slow-release formations to avoid this effect.

Low-impact exercise such as Pilates is recommended, along with pacing of activities, in conjunction with CBT. Multi-method CBT typically consists of a combination of various therapeutic elements, such as cognitive restructuring, pain-coping skills, problem-solving techniques, goal-setting, increasing activity levels, activity pacing, stress management and adjustment of pain-related medication. Studies on exercise programmes indicate that exercise may be useful in reducing disability but is less effective in decreasing pain and distress. Trials show that the fear that exercising will exacerbate pain is not justified.

From a pharmacological standpoint, NSAIDs and corticosteroids are not effective. The tricyclic antidepressant amitriptyline 10-50mg OD has been shown to be of benefit, especially in combination with tramadol. Tramadol is the best analgesic, as it has a weak SNRI effect.

High-dose venlafaxine is useful, but low dose is not. Where depressive symptoms predominate, duloxetine 20-30mg (or venlafaxine) is helpful. Where fatigue and unrefreshing sleep are of higher concern, pregabalin 50-150mg may prove beneficial. SSRIs such as fluoxetine may ameliorate depressive symptoms but are not effective for pain, fatigue or poor sleep. In some selected cases where a specific trigger point is particularly troublesome, injection with lignocaine and steroid may be used, but this is not routine. Less-common treatments are modafinil for fatigue and trazodone for sleep disturbance.

The American Pain Society and the Association of Scientific Medical Societies in Germany strongly recommend a pharmacological intervention in the form of amitriptyline and several non-pharmacological treatments (aerobic exercise, CBT, and multicomponent therapy.

Conversely, the European League Against Rheumatism (EULAR) has given only a strong recommendation for a variety of pharmacological therapies (TCAs, SNRIs, SSRIs, GABA analogues) but weak recommendations for non-pharmacological therapies. The EULAR recommendations are based on expert opinion and changes in pain assessed by VAS and function assessed by the FIQ in clinical trials. In general the trials and studies are of low quality.

In terms of complementary therapy, acupuncture has no proven benefit, while hydrotherapy and thalassotherapy may provide a temporary benefit, which is not sustained beyond 12 months.

In summation, while the treatment of inflammatory conditions such as sacroiliitis and ulcerative colitis in themselves is straightforward, the development of coexisting somatoform disorders such as IBS and FM complicates the picture substantially. The use of opioids is not the answer, but poor access to community psychotherapy and a reluctance on the part of practitioners at all levels to engage with psychosocial disorders often puts the treatment of last resort closer to the first. A holistic and empathic approach is imperative in meeting the care needs of this complex patient cohort.

Case report

LM is a 29-year-old lady who was diagnosed with ulcerative colitis in 2002 at the age of 16. She presented at that time with a two-week history of bloody diarrhoea and abdominal pain. She had a early response to steroids and was discharged on prednisolone 30mg and asacolon 800mg TDS. Repeat colonoscopy in 2003 showed active disease and she was becoming Cushingoid due to repeated courses of steroids. She was started on 6-mercaptopurine (6-MP) for symptom control. Since that time her bowel symptoms have been in remission for the most part.

In 2011 she presented to the rheumatology service in CUH with back pain and stiffness ongoing since 2003. At the time she was tender over her SI joints bilaterally and had a plain film of her pelvis, demonstrating sacroiliac erosions. She was diagnosed with secondary ankylosing spondylitis on foot of this and was encouraged to start adalimumab. However, she was both attempting and succeeding (in 2013) in becoming pregnant from the time of diagnosis and as yet is not keen to start anti-TNF therapy.

Unfortunately, her back pain progressed and she now experiences extensive paraspinal as well as rectal spasm, diagnosed as proctalgia fugax (a form of IBS) by gastroenterology. Her GP has found this pain hard to manage, requiring numerous courses of diazepam as well as various combinations of paracetamol, Solpadeine, Solpadol, Ixprim, pregabalin, tramadol, OxyNorm/OxyContin, and diclofenac. The opioid side-effect of constipation has become detrimental to her IBD. The GP described LM’s frustration at not having a definite cause for her back pain.

By 2014, her opioid requirement was 60mg OxyContin daily and she underwent injection by the pain services of her SI joints, nuchal line and paraspinally at T8 and T10. Follow-up by the pain service MDT showed mild mechanical allodynia of the paraspinal muscles between C5-T1, T5-T12 and L3-1 bilaterally.

She was trialled on amitriptyline and tramadol at this stage in an attempt to wean her off OxyContin, but this has been unsuccessful. Her current medications are Asacolon, Solpadol TDS, OxyNorm 5mg TDS, OxyContin 10mg BD, diazepam 10mg TDS, Calcichew D3F, folic acid, Galfer, 6-MP and a salbutamol inhaler. She is now attending the surgical services due to ongoing rectal spasm and haemorrhoids.

In summation, LM has three distinct entities of pain: Her IBD (controlled, and outside the scope of this article); sacroiliitis; and her diffuse, opioid-requiring back pain, part of a broader pattern of chronic widespread pain.


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