Unusual co‐incidence of Heberden's and Bouchard's osteoarthritis, rheumatoid arthritis and haemochromatosis (2022)

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September 2003

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J. Schedel,

J. Schedel

Department of Internal Medicine I, Division of Rheumatology and Clinical Immunology, University Hospital of Regensburg, D‐93042 Regensburg, Germany

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A. Wimmer,

A. Wimmer

Department of Internal Medicine I, Division of Rheumatology and Clinical Immunology, University Hospital of Regensburg, D‐93042 Regensburg, Germany

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A. Friedrich,

A. Friedrich

Department of Internal Medicine I, Division of Rheumatology and Clinical Immunology, University Hospital of Regensburg, D‐93042 Regensburg, Germany

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R. Büttner,

R. Büttner

Department of Internal Medicine I, Division of Rheumatology and Clinical Immunology, University Hospital of Regensburg, D‐93042 Regensburg, Germany

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J. Schölmerich,

J. Schölmerich

Department of Internal Medicine I, Division of Rheumatology and Clinical Immunology, University Hospital of Regensburg, D‐93042 Regensburg, Germany

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U. Müller‐Ladner

U. Müller‐Ladner

Department of Internal Medicine I, Division of Rheumatology and Clinical Immunology, University Hospital of Regensburg, D‐93042 Regensburg, Germany

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Rheumatology, Volume 42, Issue 9, September 2003, Pages 1109–1111, https://doi.org/10.1093/rheumatology/keg272

Published:

01 September 2003

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Accepted:

08 January 2003

Published:

01 September 2003

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    J. Schedel, A. Wimmer, A. Friedrich, R. Büttner, J. Schölmerich, U. Müller‐Ladner, Unusual co‐incidence of Heberden's and Bouchard's osteoarthritis, rheumatoid arthritis and haemochromatosis, Rheumatology, Volume 42, Issue 9, September 2003, Pages 1109–1111, https://doi.org/10.1093/rheumatology/keg272

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Sir, We report a 49‐yr‐old female patient presenting with symmetrical polyarthritides involving proximal interphalangelal (PIP) joints, metacarpophalangeal (MCP) joints, wrists, ankles and metatarsophalangeal (MTP) joints. The patient had been diagnosed with Heberden's and Bouchard's disease 5 years previously. At the time of first visit, the patient presented in reduced condition, with impressive swelling of all PIPs and all distal interphalangeal (DIP) joints, and less swelling of MCPs II and III. Laboratory results revealed an ESR of 15/22, a CRP of 17.1 mg/l (normal <5 mg/l) and an RF of 421 U/ml. HLA‐DR4 was positive. X‐rays of hand and finger joints showed joint narrowing of all PIPs and DIPs with minor erosions in PIPs III and IV. A skeletal scintigraphy revealed tracer accumulation in all DIPs, PIPs, MCPs and the left wrist. Based on the ACR criteria for rheumatoid arthritis (RA) [1], the diagnosis of RA in addition to Heberden's and Bouchard's disease was made. Initial therapy consisted of 50 mg prednisolone/day and 75 mg diclofenac b.i.d. for pain relief.

One month later, during tapering prednisolone, joint pain and swelling had increased again, and a standard DMARD therapy with oral methotrexate (MTX) 15 mg/week was initiated.

(Video) Understanding Osteoarthritis

After 2 months, articular pains had decreased considerably, and clinical examination showed swelling of all PIPs including PIP I. Owing to chest pain, the patient was hospitalized and the following laboratory results were found (normal values in parentheses): ESR 8/30 mm, CRP 14 mg/l, haemoglobin 16.3 g/dl (11.7–15.7 g/dl), LDH 319 U/l (120–240 U/l), AST 19 U/l (<15 U/l), ALT 52 U/l (<17 U/l) gamma‐GT 26 U/l (4–18 U/l), iron 184 µg/dl (60–150 µg/dl), ferritin 1140 ng/ml (10–120 ng/ml), transferrin 179 mg/dl (200–360 mg/dl) and transferrin saturation 73% (16–45%). Duplex ultrasound of the lower extremity veins revealed a partial thrombosis of the left superficial vein. To further clarify the origin of the polyglobulinemia, a liver biopsy was performed and showed fatty changes and discrete parenchymal and mesenchymal siderosis, but not the classical picture of haemochromatosis. Quantitatively, however, liver iron was highly increased, at 1599 µg/g (<900 µg/g). Genetic analysis revealed a HLA‐H Cyst‐282→Tyr mutation (HLA‐H His 63 Asp wt/wt), the diagnosis of familiar haemochromatosis could then be established and MTX was discontinued.

Three months later, the patient still complained of joint swelling of PIPs and articular pain in wrists, MCPs, ankles and MTPs, and leflunomide (20 mg/day) in combination with rofecoxib was started. Of interest, the recommended phlebotomies had not been performed for 3 months. Subsequently, laboratory results showed a reduced inflammatory activity (ESR 9/29, CRP 6.5 mg/l), but increasing iron metabolism parameters (iron 173 µg/dl, ferritin 932 ng/ml, transferrin 168 mg/dl, transferrin saturation 58%).

Nine months later, the patient again complained about pain and swelling in PIPs, the right MCP I and the left wrist. Two weeks earlier, she had discontinued leflunomide due to chest pain. Laboratory results showed a slightly increased disease activity (ESR 20/45, CRP 19 mg/l). Whereas the iron value had increased again [136 µg/dl (60–150 µg/dl)], ferritin levels continued to decrease [199 ng/ml (10–120 ng/ml)] due to regular phlebotomies. As the clinical symptoms still persisted and the inflammatory disease activity had increased again, a DMARD therapy with etanercept was started, and was followed by a decrease in clinical and serologic activity of RA.

This report describes the unusual co‐incidence of Heberden's and Bouchard's osteoarthritis, RA and familiar haemochromatosis in a 49‐yr‐old female patient within a short period of time. Joints affected predominantly by RA are MCPs and PIPs, whereas the predilection sites of finger osteoarthritis are DIPs (Heberden's disease) and PIPs (Bouchard's disease) [2]. Application of the respective classification criteria showed the presence of both diseases in our patient. Familiar haemochromatosis as the most common autosomal recessive hereditary disease, with a prevalence of ∼1:400 in Europe, is frequently underestimated as a cause of arthropathies [3]. It is caused by a homocygeous mutation of the HFE gene on chromosome 6 [4].

Radiologically, the typical signs of Heberden's and Bouchard's osteoarthritis could be documented in our patient at the DIP and PIP joints. In addition, the marginal erosions in the PIPs could have also been an initial sign of RA. When evaluating bone scintigraphy, discrete tracer accumulations were seen in some of the MCP/MTP joints, supporting the diagnosis of RA [1].

Articular symptoms are frequent manifestations of hereditary haemochromatosis (30% of the patients), sometimes even constituting the first symptoms of the disease [3]. Typically, MCP joints II and III are involved radiologically, often presenting as an osteoarthritis‐like picture [3]. In our case, these articular alterations could not be seen. Even though there have been reports on patients in which hereditary haemochromatosis was masquerading as RA [5], in our patient, these two entities could be well differentiated due to the following reasons: first, RA was diagnosed according to the established criteria; secondly, development of pathological laboratory values of iron metabolism occurred definitely after the diagnosis of RA; thirdly, RA as chronic inflammatory disease is usually characterized by a normocytic, normochromic anaemia associated with reduced serum iron and transferrin saturation; fourthly, symptoms of RA improved during therapy with corticosteroids and MTX and worsened after discontinuation of MTX; and finally, even though phlebotomy as therapy for haemochromatosis was unfortunately not started until 6 months after its diagnosis, there was no correlation between the degree of articular symptoms and the concentration of iron and ferritin (see Fig. 1). Thus, it can be concluded that in this patient clinically active RA (plus Heberden's and Bouchard's osteoarthritis) was associated with haemochromatosis.

HFE gene mutations have been described in patients with RA: the prevalence of the H63D mutation was shown to be significantly higher in a RA population when compared with healthy subjects; the prevalence of the Cyst‐282→Tyr mutation, the one found in our patient, however, was not increased in this population [6].

Nevertheless, the possibility that high iron values may have modulated the inflammatory activity of RA can not be ruled out as long as these values were not lowered to a therapeutic level (ferritin <50 ng/ml) [7]. In line with this hypothesis, it has long been known that disease‐modifying drugs such as MTX or ciclosporine are capable of increasing serum iron levels in arthritis [8]. Iron, in turn, is known to catalyse oxidative radical reactions with subsequent formation of hydroxyl radicals and lipid peroxidation, which both can cause inflammatory tissue damage [9]. Moreover, iron has been demonstrated to stimulate DNA synthesis of synovial cells and to exhibit an additive effect on synovial cell proliferation, together with cytokines such as interleukin‐1β or TNF‐α, underlining the role of iron itself in the modulation of disease activity of RA [10]. The hypothesis, therefore, would be that treatment of RA with MTX resulted in an increase of serum iron values that demasqued an underlying so far ‘latent’ haemochromatosis, and led to its manifestation (see Fig. 2).

In summary, as our case appears to be the first report on the unusual co‐incidence of Heberden's and Bouchard's osteoarthritis, RA and hereditary haemochromatosis, we recommend screening each RA or osteoarthritis patient with unusually high levels of iron, ferritin or transferrin saturation for the presence of familiar haemochromatosis. The differentiation between RA and haemochromatosis arthropathy is essential since the latter does not improve when using DMARDs but rather by rapid initiation of phlebotomies, and in addition requires genetic counseling of the patient's family. Moreover, an early diagnosis of haemochromatosis would offer the chance of identifying patients in precirrhotic stages.

Fig. 1.

Unusual co‐incidence of Heberden's and Bouchard's osteoarthritis, rheumatoid arthritis and haemochromatosis (3)

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Inflammatory activity (CRP), haemoglobin and serum values of iron metabolism (ferritin, transferrin saturation) are shown over time. There is no obvious correlation between inflammatory activity and ferritin values, suggesting that the inflammatory activity most likely caused by RA was not influenced significantly by haemochromatosis.

Fig. 2.

Unusual co‐incidence of Heberden's and Bouchard's osteoarthritis, rheumatoid arthritis and haemochromatosis (4)

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Schematic illustration of the hypothesis that in this patient treatment of RA with MTX may have lead to an increased serum iron concentration which, in turn, triggered the manifestation of a so far ‘latent’ haemochromatosis. Conversely, increased levels of iron per se are able to modulate the disease activity of RA via the production of hydroxyl and oxygen radicals and the activation of synovial cell proliferation (also see text).

References

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Ines LS, da Silva JA, Malcata AB, Porto AL. Arthropathy of genetic hemochromatosis: a major and distinctive manifestation of the disease.

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Philpott CC. Molecular aspects of iron absorption: Insights into the role of HFE in hemochromatosis.

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(Video) Osteoarthritis (Arthritis of Hands, Knees) | Causes, Risk Factors, Symptoms, Diagnosis, Treatment

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Lonardo A, Neri P, Mascia MT, Pietrangelo A. Hereditary hemochromatosis masquerading as rheumatoid arthritis.

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Connolly KM, Stecher VJ, Danis E, Pruden DJ, LaBrie T. Alteration of interleukin‐1 production and the acute phase response following medication of adjuvant arthritic rats with cyclosporin‐A or methotrexate.

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(Video) Looking Inside the Arthritic Joint: Lessons from RA and OA Synovium

Rheumatology 42 ©British Society for Rheumatology 2003; all rights reserved

Rheumatology 42 ©British Society for Rheumatology 2003; all rights reserved

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FAQs

Can you have rheumatoid arthritis and hemochromatosis? ›

Infrequently the distribution can be polyarticular, symmetrical, and severe, mimicking rheumatoid arthritis. Hydroxyapatite and calcium pyrophosphate crystal deposition are commonly associated with hemochromatosis and often happen concomitantly. This likely accounts for the acute flares.

What joints affect hemochromatosis? ›

Most patients with symptomatic arthropathy of hemochromatosis present with chronic, indolent pain and joint stiffness; bony enlargement; and minimal signs of inflammation. Hemochromatosis may involve the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints, wrists, knees, hips, feet, and shoulders.

What does heterozygous for the H63D mutation mean? ›

H63D carrier (also known as “H63D heterozygous”)

If you are a “H63d carrier” it means that you have inherited a single copy of the H63d variant from one of your parents. This is sometimes called a heterozygous carrier. Carriers are not usually at risk of iron loading.

Are heberden's nodes hereditary? ›

They commonly affect single joints as a result of injury but we are interested in idiopathic Heberden's nodes arising spontaneously near the time of the menopause. They are definitely hereditary, depending upon a single autosomal factor, sex influenced to be dominant in women and recessive in men.

What are warning signs of hemochromatosis? ›

Symptoms of hemochromatosis include:
  • Pain in your joints, especially your knuckles.
  • Feeling tired.
  • Unexplained weight loss.
  • Skin that has a bronze or gray color.
  • Pain in your belly.
  • Loss of sex drive.
  • Loss of body hair.
  • Heart flutter.
Dec 7, 2020

What does hemochromatosis joint pain feel like? ›

Joint damage from haemochromatosis does not tend to disappear – it's degenerative, even if iron levels return to normal with treatment. People with joint damage often have ongoing pain, stiffness and difficulties using their joints – it is very similar to a typical osteoarthritis (OA) presentation.

Can hemochromatosis cause eye problems? ›

Ocular manifestations of hemochromatosis may cause visual changes such as diminished visual acuity due to pathological changes in the cornea and retina.

Can hemochromatosis affect mood? ›

Emotional Issues and Support

Living with hemochromatosis may cause fear, anxiety, depression, and stress.

Does hemochromatosis cause back pain? ›

Inability to Relax Muscles, Back Pain. Headache, Dizziness. Skin conditions- including rash and itching. Digestive Disturbances- Nausea, abdominal pain, constipation, or diarrhea may also be attributable to iron overload.

Can you have hemochromatosis with only one gene mutation? ›

If you inherit 1 abnormal gene, you're unlikely to develop hemochromatosis. However, you are considered a gene mutation carrier and can pass the mutation on to your children. But your children wouldn't develop the disease unless they also inherited another abnormal gene from the other parent.

What triggers hemochromatosis? ›

Haemochromatosis is caused by a faulty gene that can be passed on to a child by their parents. Most cases are linked to a fault in a gene called HFE, which affects your ability to absorb iron from food. Normally, your body maintains a steady level of iron.

Is H63D a hemochromatosis? ›

The homozygous H63D variant is an indicator of the iron metabolism disorder hemochromatosis, which may increase the risk of developing a fatty liver. In patients with a cirrhotic liver, the mutation can increase the rate of liver cancer.

How do you get rid of arthritis nodules on your fingers? ›

Rest your hand. Wear a splint or orthotic device (orthosis) to help support your finger joints. Use heat, such as paraffin wax or warm compresses on your hand. You can alternate heat therapy with cold therapy to ease pain, or use heat before activity and ice after activity.

How do you get rid of heberden's finger nodes? ›

Treatment. You can treat pain and swelling with rest, splints, ice, physical therapy, and pain medicines like nonsteroidal anti-inflammatory drugs (NSAIDs). In rare cases, your doctor might suggest surgery to remove the nodes, or replace or fuse one of the joints in your fingers.

How do you stop the progression of heberden's nodes? ›

Can You Prevent Heberden's Nodes?
  1. Exercising regularly, including stretching exercises such as yoga or tai chi (at least 30 minutes every day)
  2. Eating a non-inflammatory diet (avoiding sugar, and processed and refined foods) and drinking plenty of water.
  3. Maintaining a healthy weight.

What are the 3 types of hemochromatosis? ›

Type 1 hemochromatosis results from mutations in the HFE gene, and type 2 hemochromatosis results from mutations in either the HJV or HAMP gene. Mutations in the TFR2 gene cause type 3 hemochromatosis, and mutations in the SLC40A1 gene cause type 4 hemochromatosis.

What foods to avoid if you have hemochromatosis? ›

6 foods to avoid in a hemochromatosis diet
  • Vitamin C-rich foods. Dr. ...
  • Red meat in excess. Nutritionist Best says animal sources of protein, like beef, contain heme iron, which is more easily absorbed by the body. ...
  • Raw fish and shellfish. ...
  • Alcoholic beverages. ...
  • Sugar. ...
  • Iron-fortified foods.
Jun 28, 2021

Does hemochromatosis affect your fingernails? ›

Fingernails: Possible problems

Often, spoon nails are a sign of iron deficiency anemia or a liver condition known as hemochromatosis, in which your body absorbs too much iron from the food you eat. Spoon nails can also be associated with heart disease and hypothyroidism.

Does hemochromatosis affect sleep? ›

Many patients also have periodic limb movements in sleep (PLMS), and they may complain of insomnia and/or hypersomnia. Hereditary haemochromatosis is an autosomal recessive disease of iron metabolism in which increased intestinal absorption of iron leads to iron deposition in multiple organs.

Can hemochromatosis cause memory loss? ›

Cognitive impact of untreated haemochromatosis

Case reports have described patients with extrapyramidal or cognitive dysfunction,7 confusion and psychomotor retardation,8 fatigue and impaired short-term memory.

Can hemochromatosis affect your feet? ›

joint pain, and possibly joint swelling. This occurs most commonly in the joints of the fingers and hands. The wrists, elbows, hips, knees, ankles and joints in the feet can also be affected.

Can rheumatoid arthritis cause high iron levels? ›

The chronic inflammation in RA leads to secretion of proinflammatory cytokines that influence iron metabolism. The parameters that are most affected are plasma iron levels and the production of transferrin, ferritin, and hepcidin.

Can hemochromatosis cause autoimmune disease? ›

This disorder is caused by mutations in the hemojuvelin or hepcidin genes. Neonatal hemochromatosis. In this severe disorder, iron builds up rapidly in the liver of the developing baby in the womb. It is thought to be an autoimmune disease, in which the body attacks itself.

Can rheumatoid arthritis cause high ferritin levels? ›

Ferritin is an acute phase reactant and a marker of acute and chronic inflammation. It is elevated in a wide range of inflammatory conditions, including chronic kidney disease, rheumatoid arthritis, and other autoimmune disorders, acute infections, and cancer [1, 2].

What autoimmune diseases cause high ferritin levels? ›

Hyperferritinemia is associated with inflammation, infections, and malignancies. While elevated levels of ferritin are characteristic of adult-onset Still's disease and hemophagocytic syndrome, both associated with inflammation, it has scantly been evaluated in other autoimmune diseases.

When do symptoms of hemochromatosis appear? ›

Symptoms of haemochromatosis usually begin between the ages of 30 and 60, although they can occur earlier. The symptoms tend to develop earlier in men than in women. Women often do not experience problems until after the menopause. Sometimes there are no symptoms and the condition is only found during a blood test.

What foods to avoid if you have hemochromatosis? ›

6 foods to avoid in a hemochromatosis diet
  • Vitamin C-rich foods. Dr. ...
  • Red meat in excess. Nutritionist Best says animal sources of protein, like beef, contain heme iron, which is more easily absorbed by the body. ...
  • Raw fish and shellfish. ...
  • Alcoholic beverages. ...
  • Sugar. ...
  • Iron-fortified foods.
Jun 28, 2021

Does stress affect hemochromatosis? ›

In particular, stress-impaired iron metabolism is closely associated with the stress responsive sentinels which are involved in the susceptibility to the hemochromatosis and other chronic distress. Some mutations in the sentinel-linked genes contribute to primary hemochromatosis.

What are the 3 types of hemochromatosis? ›

Type 1 hemochromatosis results from mutations in the HFE gene, and type 2 hemochromatosis results from mutations in either the HJV or HAMP gene. Mutations in the TFR2 gene cause type 3 hemochromatosis, and mutations in the SLC40A1 gene cause type 4 hemochromatosis.

What is the life expectancy of a person with hemochromatosis? ›

Most people with hemochromatosis have a normal life expectancy. Survival may be shortened in people who are not treated and develop cirrhosis or diabetes mellitus.

Is hemochromatosis a disability? ›

Genetic haemochromatosis qualifies as a disability under the Equality Act 2010. Under the Act, genetic haemochromatosis represents a protected characteristic - a “physical or mental impairment” which has “a substantial and long-term adverse effect” on someone's “ability to carry out normal day-to-day activities”.

What helps joint pain from hemochromatosis? ›

Treatments for arthritis vary depending on which joints are affected and can include:
  1. pain relief, using medicines such as paracetamol.
  2. non-steroidal anti-inflammatory drugs (NSAIDs), including topical creams and ointments.
  3. an exercise program tailored to your needs and ability.
  4. a weight loss program, if you are overweight.

Can I exercise with hemochromatosis? ›

There is evidence that even properly treated hemochromatosis may cause a reduced exercise capacity in sufferers. This is probably due to reduced oxygen uptake as studies have shown no change in left ventricular function. Phlebotomy appears to have no effect on exercise capacity.

How do you treat hemochromatosis? ›

Lifestyle and home remedies
  1. Avoid iron supplements and multivitamins containing iron. These can increase your iron levels even more.
  2. Avoid vitamin C supplements. Vitamin C increases absorption of iron. ...
  3. Avoid alcohol. ...
  4. Avoid eating raw fish and shellfish.
Dec 30, 2020

How is hemochromatosis diagnosed? ›

Doctors usually order blood tests to check for the gene mutations link that cause hemochromatosis. Finding two copies of the HFE link gene with the C282Y mutation confirms the diagnosis of primary hemochromatosis. Doctors usually order blood tests to check for the gene mutations that cause hemochromatosis.

Can you have high iron levels and not have hemochromatosis? ›

Conclusion. In a patient with signs and symptoms of tissue iron overload and high serum ferritin levels, low or normal transferrin saturation should alert the physician to other - primary as well as secondary - causes of iron overload besides hemochromatosis.

What is hereditary hemochromatosis? ›

Hereditary hemochromatosis is a genetic disorder that can cause severe liver disease and other health problems. Early diagnosis and treatment is critical to prevent complications from the disorder. If you have a family health history of hemochromatosis, talk to your doctor about testing for hereditary hemochromatosis.

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