SLE and connections with Parvovirus.

[Neverforget]

Has anybody been found to have positive blood work for SLE with a positive blood test stating contact with parvovirus following severe initial flare of their illness? If so what was found to be your diagnosis if any?

Best wishes

x x x x

[MandieR]

thats interesting you know. My first puppy at the age of 20, I am now 51, died of parvo and for 4 or 5 days I looked after her at home until she passed.

Is there a link between the two?

I know years ago there was some link between canine distemper and MS

[Neverforget]

Hi MandieR thank you for your post. Human parvovirus is different to canine parvovirus. Human parvovirus is also known as slap cheek syndrome in children. I have looked ar medical journels and it appears that parvovirus may actually be a contrubuting factor in people who go on to be diagnosed with SLE. It would interesting to know peoples experiences. x x x x x

[Mimi1900 in reply to Neverforget]

I had parvovirus when my 10 year old had it. It is a known viral trigger for SLE in women with a genetic tendency for Lupus. I had significant arthritis symptoms for Parvo and at time my primary care/GP considered running a rheumatoid arthritis blood tests but in end decided not to. A year or too later as arthritis persisted I was diagnose with SLE

[Tigerlily4]

I had a dog when pregnant and began to develop lupus then but he was vaccinated against parvo. Neither did I have any of the associated symptoms nor was my son born anything other than healthy. Interesting link though and something to bear in mind!

[sunshine16]

how interesting ...years ago I worked in a school and caught the human parvo virus and was quite poorly...i then seemed to catch everything going including pleurisy and my Gp took blood tests where it showed my white cells were low and this continued for years until i became very poorly and few years ago was diagnosed with SLE with cardiac involvement...i wonder if there is a link?

BTW love you Les miserable pic...awesome musical!

[brave in reply to sunshine16]

can i ask what cardiac involvement you have ?

[sunshine16 in reply to brave]

Yes Brave i have pericarditis and mitral and aortic valve damage

[sunshine16 in reply to brave]

sorry first time clicked report tag instead of replying...having silly day again!!!

[Neverforget]

Hi Tigerlily4 thankyou for your response. My question was in respect of human parvovirus and not canine parvovirus both are completly different illnesses so contact with your dog would probably not affect you or your unborn child. x x x x

[Tigerlily4 in reply to Neverforget]

I had no idea there was such a thing as human parvovirus in fact - how odd!

[Neverforget]

Hi Italiana thank you for response. In 2004 I became ill very quickly and ended up in hospital. I felt like I had been hit by a bus and it was too painful to breath. Whilst in hospital I had difficulty straighting my hands. In outpaitients I was told that a number of my blood tests had come back positive. I had positive Ana, antiphospolids, c protein, sr and cpr were up and other tests were positive too. A blood test also showed that I had recently been in contact with human parvovirus. Although my blood tests were positive for Lupus the consultant at the time said they didnt want to label and stated that the virus could have caused false psitives. Since 2004 I have continued to experience joint pain, swelling, rash on arms, thighs and stomach, exhaustion, slight hair loss on occasions, weight gain, chest problems, miscarriage, migraines and stiffness on waking or sitting too long. I have noted in my research that a number of people who had the same blood results as I had in 2004 were automatically diagnosed as having SLE. Other people were not diagnosed with Lupus until years later. Some medical journels released over the last few years appear to show a connection between the two. Did they do ana and other blood tests Italiana when they tested you for parvovirus? I have been really unwell since March 2012. I saw a rheumy in August. I have been on plaquinel but I had a reaction and ended up in hospital. I was placed on methotrexate for three months and this appeared to help but due to weight gain and being sick for three days each time I took it I was placed on methophenolate. I was only on this for three days and was taken off it due to side effects. I began to flare at the beginning of January and hit crisis whilst waiting for my rheumy to prescribe medication. I am currently waiting diagnosis. My rheumy has informed my GP that she feels that my rash is a mild lupus rash she has also informed my GP that her diagnosis is connective tissue with possible overlap of SLE. I am being referred to another rhuemy for second opinion. x x x x

[sunshine16 in reply to Neverforget]

aw sorry to hear that...no the didn't do an ANA test just full blood count where they noticed my whites cell were very low..it took years to be diagnosed.

hope you fell better soon keep positive as hard as it sometimes is xx

[butterfly1000]

Hi Neverforget,

I was initially diagnosed with parvo and this then became an sle diagnosis that years later came a MCTD diagnosis.

would be interested in reading any related papers if you have a link.

hope you get a diagnosis soon - the label can be very helpful. I am on long-term steroids which have their issues but keep me functioning.

[Neverforget]

Hi Butterfly, Thank you for your response. I have been looking through various sites over the last few days looking for a connection. I have come across a number of people discussing this who have been in a similar situation as ourselves. I have down loaded some information on my phone. If I find out how to link a post on here then I will do. When you were diagnosed with parvo did you also have positive ana and positive anti-pospholipid etc too? Best wishes x x x x

[Neverforget]

Hi Butterfly, I found some interesting information on a site (Wiley Online Library) but I don't know how to do the link sorry.

Systemic lupus erythematosus associated with acute parvovirus B19 infection

F. Díaz, J. Collazos, F. Mendoza, J. M. De la Viuda, J. Cazallas, J. C. Urkijo, M. Flores

Article first published online: 21 MAR 2002

DOI: 10.1046/j.1198-743x.2001.00361.x

Issue

Clinical Microbiology and Infection

Volume 8, Issue 2, pages 115–117, February 2002

Acute parvovirus B19 infection has been implicated in the pathogenesis of several autoimmune conditions, including systemic lupus erythematosus. Viruses, including human parvovirus B19, may trigger bouts of systemic lupus erythematosus in genetically susceptible individuals. Herein, we report on two patients who developed systemic lupus erythematosus associated with acute parvovirus B19 infection and discuss the possible pathogenetic mechanisms implicated.

Case 1

An 18-year-old previously healthy man was admitted because of arthralgia involving hands, wrists, shoulders, knees and ankles of 1 month's duration. Physical examination was unremarkable. The leukocyte count was 3.5 × 109/L, and hemoglobin and platelet counts were within normal limits. The erythrocyte sedimentation rate (ESR) was 35 mm/h, serum creatinine was 1.5 mg/dL, and the serum albumin level was 3.03 g/dL. Urinalysis showed proteinuria of 14.3 g/day and microhematuria. The titer of antinuclear antibodies (ANAs) was >1/5120, with a speckled pattern, anti-dsDNA >1/160, anti-ribouscleoprotein 1/50, anticardiolipin IgM 13 MPL/mL (normal <12), and IgG antibodies 62 GPL/mL (normal <24). Rheumatoid factor, anti-Sm antigen, anti-Ro/La antigens, antineutrophil cytoplasmic antibodies and cryoglobulins were negative. Serum complement levels were decreased. Serologic tests for hepatitis B and C virus, cytomegalovirus, Epstein–Barr virus, HIV, syphilis, Yersinia and Brucella were negative. IgM antibodies against parvovirus B19, measured by ELISA (Parvoscan-B19 IgM, Euro-Diagnostica AB Ideon, Malmö, Sweden) were positive. Radiographs of the chest and involved joints and abdominal ultrasonogram were normal. A renal biopsy showed diffuse proliferative glomerulonephritis with deposits of IgM, IgG, IgA and complement in mesangial, subepithelial and subendothelial locations. With a diagnosis of WHO class IV lupus nephritis, the patient was treated with prednisone, 1 mg/kg per day, and cyclophosphamide, 6-month intravenous pulses followed by 3-month pulses, with improvement. Four months later, proteinuria, serum creatinine and complement levels were normal. One year after the first determination, IgM antibodies against pB19 were negative. Currently, ANA and anti-dsDNA titer continue to be positive, and serum complement levels are normal.

Case 2

A 27-year-old previously healthy woman reported high fever and lumbar pain for 4 days before admission. A presumptive diagnosis of acute pyelonephritis was made, and ciprofloxacin, 1 g/day, was started. However, the patient's condition deteriorated on the following day, and she developed oral ulcers and a macular eruption involving face and trunk. Physical examination was unremarkable, apart from fever and the mucocutaneous lesions. The leukocyte count was 2.2 × 109/L, hemoglobin was 10.8 g/dL, platelet count was 57 × 109/L, and ESR was 103 mm/h. Serum creatinine was normal. Urinalysis revealed many red and white blood cells without proteinuria. ANA at a titer of 1/640, anti-dsDNA 1/80, anti-Sm >1/200, anti-RNP >1/200 and anticardiolipin antibodies IgG 24 GPL/mL were positive. Complement levels were decreased. Direct Coomb, test was positive for IgG and negative for complement. Abdominal computed tomography revealed only homogeneous hepatosplenomegaly. Chest radiographs were unremarkable. Blood and urine cultures were negative. Serologic tests against hepatitis B and C virus, HIV, cytomegalovirus, Epstein–Barr virus and syphilis were negative. IgM antibodies to pB19 were positive. A skin biopsy showed a chronic inflammatory perivascular infiltrate without vasculitis. Immunofluorescence was negative. Bone marrow biopsy revealed erythroid hypoplasia. The patient was treated with antibiotics, with slow improvement. However, 1 month after discharge, the patient still had oral ulcers and complained of loss of scalp hair. ANA, anti-dsDNA, anti-Sm, anti-RNP and direct Coombs' test continued to be positive. The leukocyte count was 3.9 × 109/L, hemoglobin was 10.8 g/dL, platelet count was 257 × 109/L, and ESR was 30 mm/h. Prednisone, 1 mg/kg per day, was started. The symptoms rapidly disappeared, and blood cell counts became normal. Two months later, IgM antibodies against pB19 were negative. Prednisone was tapered and finally stopped 10 months after its onset. Fourteen months after presentation, the patient is asymptomatic, although anti-dsDNA antibodies are still positive and complement levels are decreased.

Discussion

Autoimmunity results from an immune response against autoantigens and represents a failure of immunologic tolerance. The mechanisms underlying the onset of the autoimmune response are undetermined. However, viral infections have long been associated with the development of autoimmune disorders [6]. Several mechanisms have been proposed to explain how a viral infection can induce these disorders. Infection may overcome immunologic tolerance by exposure of cryptic epitopes of autoantigens to the immune system and then activation of resting autoreactive T-cells [7]. Another alternative mechanism, that of molecular mimicry, consists of the induction of an immune response against antigenic determinants shared by the host and virus, which would result in tissue injury [6].

Some authors [4,8] have suggested that pB19 is able to induce a transient or chronic autoimmune response. In addition, it is recognized that pB19 infection may trigger some clinical syndromes with immunologic pathogenetic mechanisms [9]. Our two cases, as well as other reported cases of pB19-induced SLE [3–5], suggest that this virus may trigger mechanisms leading to an autoimmune response in the form of SLE. In addition, our patients had anticardiolipin antibodies, and a remarkable similarity in specificity of anticardiolipin antibodies has been found between pB19-infected patients and SLE patients [10].

Although pB19 may trigger the development of SLE, some authors have not found an increased prevalence of pB19 infection in SLE patients in relation to the general population [11]. However, in another study [12], the presence of pB19 DNA was detected in 24% of patients with SLE but in none of those with other systemic rheumatic diseases, and the prevalence of antibodies against pB19 in SLE patients with detectable pB19 DNA was lower than that of patients without pB19 DNA, suggesting that certain individuals with chronic SLE are unable to mount an antibody response to the virus. Clearance of the virus may be impaired in these immunosuppressed patients, and viral DNA could integrate into the human chromosome, establishing latency [13], which could have clinical consequences. In fact, the association of immunocompromised patients and autoimmune phenomena is well known. Consequently, it could be speculated that treatment for pB19 in SLE patients with this infection might be useful to reduce flare-ups of such a serious disease, and administration of immunoglobulins could be helpful to control infection if discontinuation of the immunosuppressive therapy is not feasible.

We believe that the possibility of acute pB19 infection should be considered in patients presenting with SLE features, and that a systematic search for this infection in patients with new-onset SLE should be carried out to delineate the pathogenetic significance of pB19 in this condition.

References

1

Horwitz MS, Sarvetnick N. Viruses, host responses, and autoimmunity. Immunol Rev 1999; 169: 241–53.

Direct Link:

AbstractPDF(882K)ReferencesWeb of Science®

2

Woods VL Jr. Pathogenesis of systemic lupus erythematosus. In: KelleyWN, HarrisEDJrRuddyS, SledgeCB, eds. Textbook of Rheumatology. Philadelphia: WB Saunders, 1993: 999–1016.

3

Trapani S, Ermini M, Falcini F. Human parvovirus B19 infection: its relationship with systemic lupus erythematosus. Semin Arthritis Rheum 1999; 28: 319–25.

CrossRef,PubMed,CAS,Web of Science®

4

Vigeant P, Ménard HA, Boire G. Chronic modulation of the autoimmune response following parvovirus B19 infection. J Rheumatol 1994; 21: 1165–7.

PubMed,CAS,Web of Science®

5

Cope AP, Jones A, Brozovic M, Shafi MS, Maini RN. Possible induction of systemic lupus erythematosus by human parvovirus. Ann Rheum Dis 1992; 51: 803–4.

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6

Albert LJ, Inman RD. Molecular mimicry and autoimmunity. N Engl J Med 1999; 341: 2068–74.

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7

Mackay IR. Tolerance and autoimmunity. BMJ 2000; 321: 93–6.

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8

Lunardi C, Tiso M, Borgato L et al. Chronic parvovirus B19 infection induces the production of anti-virus antibodies with autoantigen binding properties. Eur J Immunol 1998; 28: 936–48.DOI: 10.1002/(sici)1521-4141(199803)28:03<936::aid-immu936>3.0.co;2-x

Direct Link:

AbstractPDF(227K)ReferencesWeb of Science®

9

Soloninka CA, Anderson MJ, Laskin CA. Anti-DNA and antilymphocyte antibodies during acute infection with human parvovirus B19. J Rheumatol 1989; 16: 777–81.

PubMed,CAS,Web of Science®

10

Loizou S, Cazabon JK, Walport MJ, Tait D, So AK. Similarities of specificity and cofactor dependence in serum antiphospholipid antibodies from patients with human parvovirus B19 infection and from those with systemic lupus erythematosus. Arthritis Rheum 1997; 40: 103–8.

Direct Link:

AbstractPDF(582K)ReferencesWeb of Science®

11

Bergtsson A, Widell A, Elmstahl S, Sturfelt G. No serological indications that systemic lupus erythematosus is linked with exposure to human parvovirus B19. Ann Rheum Dis 2000; 59: 64–6.

CrossRef,PubMed,Web of Science® Times Cited: 21

12

Hsu TC, Tsay GJ. Human parvovirus B19 infection in patients with systemic lupus erythematosus. Rheumatology 2001; 40: 152–7.

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13

Kerr JR. Pathogenesis of human parvovirus B19 in rheumatic disease. Ann Rheum Dis 2000; 59: 672–83.

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[butterfly1000]

thanks for that Neverforget. Am very interested to learn this - 10years later!! Makes me a wee bit wary of my little girl being in contact with slap cheek when its doing the rounds at school. I guess I have to assume she is "genetically susceptible", although both case studies were in adults. I am unsure of the measurements used for diagnosis. I dont think I have APS but unsure about my ANA. My rheumy is very good but Id like a good look at my notes so that I can better understand my diagnosis etc. It was 10 years ago and I just accepted what they told me.

thanks again

[Neverforget]

Your very welcome butterfly. I had all positive blood tests and symptoms for SLE when I was admitted into hospital. Due to bloods also showing recent contact with human parvovirus they said they didnt want to label me. Ive had various similar flares nut not as server over the past 9 years. Each time I have been tested for underactive thyroid or told thst I have gor a post viral syndrome, exhaustion due to over work or some sort of reacyive athritis. In August my Rheumy said that I have connevtibe tissue auto immune and gave probably had it since 2004. I am waiting to see Dr Bruce at Manchester for a further opinion and possible diagnosis. Best wishes x x x x

[Neverforget]

ps I apologies for typos but its difficult to type and see typos on my phone

I hope you can understand my message x x x

[sunshine16 in reply to Neverforget]

thanks for posting the link very interesting i wish you all the best

[Neverforget]

Thank you Italian all the very best to you too c x x x

[amandajayne]

Hi there I've just came across this my little girl took not well and got tests and they came back .S L E. At first but a week or too later we found out that she had Parva virus in her system so now we are fighting with the hospital as myself husband and family are not convinced it's S.L.E . I suggest if u rly think it's Parva virus and not lupus do loads of research and consult your rheumatology. Hope you find this useful xx