What is the Difference Between Inflammatory Arthritis and Fibromyalgia ?

Certain types of inflammatory arthritis and fibromyalgia are often confused because their symptoms mimic one another in early stages.

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While fibromyalgia is considered an arthritis-related condition, it is not a true form of arthritis because it does not cause tissue inflammation nor does it damage joints or muscles. However some consider it a rheumatic condition because it can make the joints and surrounding tissues painful and sore to use. In general people with fibromyalgia have normal looking X-ray and blood tests results, and family and friends drive them mad by telling them they look fine. A person with arthritis will have abnormal test results and they may also be in visible pain, with swollen or deformed joints.

Distinguishing between the two to yield a proper diagnosis is important to ensure proper treatment. Both are chronic disorders earmarked by long-lasting pain.

Inflammatory Arthritis

There are several types of inflammatory arthritis which include:

Inflammatory arthritis leads to inflammation of the joints and surrounding tissues. Long-standing inflammatory arthritis can result in joint deformation and disability.

Typical Signs of Rheumatoid Arthritis/Osteoarthritis  Osteoarthritis

• Pain in affected joints, particularly after repetitive use.
• Stiffness, you may feel creaky first thing in the morning.
• Creaking joint noises, cracking and crunching sounds.

Rheumatoid Arthritis

• Reduced appetite.
• Feeling generally unwell.
• Fatigue.
• Swollen glands.
• General feeling of weakness.

Fibromyalgia

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Fibromyalgia affects not only joints, but muscles, tendons, and other soft tissues in the elbows, hips, chest, knees, lower back, neck, and shoulders. Fibromyalgia can develop alone or with inflammatory arthritis.

Common Shared Symptoms

Both fibromyalgia and inflammatory arthritis sufferers have pain and stiffness in the morning. Other common symptoms shared by the two conditions include:

  • fatigue
  • sleep disturbances
  • limited range of motion
  • numbness or tingling

Typical Signs of Fibromyalgia

• Pain in specific points of the body called the fibromyalgia tender points.
• Flu like pain, primarily in the neck and shoulders.
Depression/anger.
• Feeling anxious.
• Constant extreme fatigue.
• Chronic back pain.
• Bouts of constipation or diarrhea.
• Jaw or facial tenderness (90 percent experience this symptom).
• Headaches and migraines (up to 50 percent of cases).

Diagnosing Symptoms

Tests to distinguish fibromyalgia and inflammatory arthritis include X-rays, blood tests, and ultrasound. Besides inflammatory arthritis, fibromyalgia also shares common symptoms with several other conditions.

  • chronic fatigue syndrome
  • cancer
  • depression
  • HIV infection
  • hyperthyroidism
  • irritable bowel syndrome
  • Lyme disease

Acetaminophen Mechanism of action

Paracetamol (acetaminophen) is generally considered to be a weak inhibitor of the synthesis of prostaglandins (PGs). However, the in vivo effects of paracetamol are similar to those of the selective cyclooxygenase-2 (COX-2) inhibitors.

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Paracetamol also decreases PG concentrations in vivo, but, unlike the selective COX-2 inhibitors, paracetamol does not suppress the inflammation of rheumatoid arthritis. It does, however, decrease swelling after oral surgery in humans and suppresses inflammation in rats and mice.

Paracetamol is a weak inhibitor of PG synthesis of COX-1 and COX-2 in broken cell systems, but, by contrast, therapeutic concentrations of paracetamol inhibit PG synthesis in intact cells in vitro when the levels of the substrate arachidonic acid are low (less than about 5 mumol/L). When the levels of arachidonic acid are low, PGs are synthesized largely by COX-2 in cells that contain both COX-1 and COX-2.

Thus, the apparent selectivity of paracetamol may be due to inhibition of COX-2-dependent pathways that are proceeding at low rates. This hypothesis is consistent with the similar pharmacological effects of paracetamol and the selective COX-2 inhibitors. COX-3, a splice variant of COX-1, has been suggested to be the site of action of paracetamol, but genomic and kinetic analysis indicates that this selective interaction is unlikely to be clinically relevant.

There is considerable evidence that the analgesic effect of paracetamol is central and is due to activation of descending serotonergic pathways, but its primary site of action may still be inhibition of PG synthesis. The action of paracetamol at a molecular level is unclear but could be related to the production of reactive metabolites by the peroxidase function of COX-2, which could deplete glutathione, a cofactor of enzymes such as PGE synthase.

Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects.

While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme’s active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2.

This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation.

Acetaminophen Drug Interactions (5)

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