In my opinion, the ANA titres are not a good outcome parameter. They don´t follow the disease inflamatory activity or damage degree. So, I think they are not usually influenced by treatment.

Thank you very much Jose.

Just one more question, do you recommend any test in particular? Or the measurement of antinuclear antibodies, although they have a low sensitivity and specificity remains the election test?

Thank you.

Hi  Ricardo

The information I have, at least regarding human diagnosis is that, between the several antibodies involved (ANAs), the most reliable for clinical following is the anti-native DNA.

http://www.ncbi.nlm.nih.gov/pubmed/6334672

Thank you Luís Martins and Cristina Queiroga.

As clinical researchers, do you know any entity that makes the measurement of anti-DNA, or even anti-MS or anti-nucleus factor (ANF)?

I could not find any institution or european laboratory that performs these analyzes, which makes me think they're only performed for research purposes at certain universities.

Thank you very much for your precious help.

ANA is a diagnostic tool not a follow-up parameter.

The question is: if a patient comes with what suggests Lupus or another disease associated with positive ANA, and this patient has already been given steroids (before anyone ordered ANA testing),  can we still order ANA or its subsets or do steroids affect the results?

The answer is that steroids do affect the results.

ANA are antibodies and steroids decrease the ability of immune cells to synthesize antibodies. This has been studied in the context of the rare ANA-negative lupus. We must ask about previous treatment before labeling the patient as such: if steroids were already given, then a negative result is inconclusive. ANA could still be positive with a lower titer.

We must always ask for the history of previous treatment.

Thanks for you help Majda.

Thus, after corticosteroid therapy, which alternative laboratory parameters you suggest for the diagnosis of disease?

Is being really difficult to answer this question because most of the literature i found has more than 20 years.

And which monitoring laboratory parameters you recommend?

I need an alternative immune parameter to ANA to be realized for clinical purposes. I've contacted the major european laboratories and the answer they always gave me is that they only do the measurement of ANA, although not specific.

But no one can tell me what are the alternatives.

Thanks!

1.The diagnosis of Lupus requires 4 out 11 criteria set by the ACR (American College of Rheumatology).

7 of these criteria are clinical. ANA is one laboratory criterion.

Consequently: One can diagnose lupus without ANA.

2. Lupus is a systemic disease that affects different systems in different people.

A patient might spend a lifetime with only one problem: low platelets. I have one such patient. 

But a patient can develop any other complication any time.

Hence: while we monitor clinically for arthritis, cardio-pulmonary signs, neurologic signs..etc..

We also monitor for renal function, blood counts, liver functions with appropriate tests.

There is no one miracle test for monitoring: it depends on the manifestations in the individual case, and there are mandatory serial routine tests to unveil new hidden manifestations.

It was what i feared.

I know that there aren't miraculous tests for the diagnosis of SLE and the diagnosis is performed by the evaluation of clinical manifestations of the disease, but at least i expected to find an alternative immune parameter that has, at least, similar sensitivity and specificity than ANA tests.

It seems that the developments and research in this field changed very little over the past 20 years, most likely due to its rarity and its difficult diagnosis, and the reflection of this is the lack of scientific articles and solid bibliographic database.

Thank you very much for all the help.

It was what i feared.

I know that there aren't miraculous tests for the diagnosis of SLE and the diagnosis is performed by the evaluation of clinical manifestations of the disease, but at least i expected to find an alternative immune parameter that has, at least, similar sensitivity and specificity than ANA tests.

It seems that the developments and research in this field changed very little over the past 20 years, most likely due to its rarity and its difficult diagnosis, and the reflection of this is the lack of scientific articles and solid bibliographic database.

Thank you very much for all the help.

It was what i feared.

I know that there aren't miraculous tests for the diagnosis of SLE and the diagnosis is performed by the evaluation of clinical manifestations of the disease, but at least i expected to find an alternative immune parameter that has, at least, similar sensitivity and specificity than ANA tests.

It seems that the developments and research in this field changed very little over the past 20 years, most likely due to its rarity and its difficult diagnosis, and the reflection of this is the lack of scientific articles and solid bibliographic database.

Thank you very much for all the help.

It was what i feared.

I know that there aren't miraculous tests for the diagnosis of SLE and the diagnosis is performed by the evaluation of clinical manifestations of the disease, but at least i expected to find an alternative immune parameter that has, at least, similar sensitivity and specificity than ANA tests.

It seems that the developments and research in this field changed very little over the past 20 years, most likely due to its rarity and its difficult diagnosis, and the reflection of this is the lack of scientific articles and solid bibliographic database.

Thank you very much for all the help.

It was what i feared.

I know that there aren't miraculous tests for the diagnosis of SLE and the diagnosis is performed by the evaluation of clinical manifestations of the disease, but at least i expected to find an alternative immune parameter that has, at least, similar sensitivity and specificity than ANA tests.

It seems that the developments and research in this field changed very little over the past 20 years, most likely due to its rarity and its difficult diagnosis, and the reflection of this is the lack of scientific articles and solid bibliographic database.

Thank you very much for all the help.

Positivity ANA  does not make the diagnosis of SLE. Moreover, ANA  positivity increases  with the age and gender. Treatment with kortikoids leads to decrease of autoantibodies (not only ANA but  IgG too) - it is time and dose dependent. You can expect these effects after month . There is no correlation between titer of ANA and time and dose of kortikoids. Homogenous type of ANA, IgG subtypes  can help, anti dsDNA, Sm Ag, ENA pozitivity etc.    

Probably the most specific laboratory test which supports a diagnosis of SLE is anti-double stranded DNA (anti-ds-DNA). Anti-DNA is seen almost exclusively in patients with SLE. ANAs include anti-DNA and are observed as a 'ring' or 'rim' pattern in immunofluroscence tests for ANA, using a cell or tissue substrate. With treatment (corticosteroids or cytotoxics) ANA (even anti-DNA) may become undetectable in the patient's serum. Perhaps 10-20% of lupus patients in remission lose detectable antinuclear antibodies.

Some ANA are atubborn and will remain positive without reflecting clinical activity of SLE (e.g. anti: -SSA, -SSB, -U1 RNP); as oposite anti-nucleosome and anti-DNA fluctuate with clinical actiivity. Therefore succesfull corticoid therapy will be seen in ANA positivity if they are solely caused by these two specificities. This situation however is rather rare in SLE.

ANA titers should be done by immunofluorescence (IF) and usually do not change much by the lupus treatment. Anti-DNA titers correlate with nephritis and active lupus, and it can fluctuate over time. It can become negative by anti-inflammatory treatment with immunsuppressive agents, including corticosteroids. Incidentally, lupus is not a rare disease; it affects 1 in 2,500 individuals, usually young females. There is plenty of literature on SLE over the last few decades, and several active ongoing clinical trials looking at different potential newer therapeutic agents, e.g., atacicept, sifalimumab, etc. The prevalent thought now is that alpha interferon may well be the signtaure cytokine for the disease. BLYS-APRIL also represent newer potential targets as well as CD20 and CD22 on B cells, among others; all patients with lupus should be on hydroxychloroquine, or HCQ (Plaquenil), and vitamin D supplementation,