[CIS PIDD] [cis-pidd] pneumococcal vaccine strategy in adolescents & adults with immune deficiency

[Seppänen Mikko]

I would completely agree with Soheil.

Why? A lenghty explanation based on my experience and on available studies, at least how I interpret these two. Like we see in discussion there can be various interpretations.Let us hope we one day can consolidate these.

1) The lenght of the tolerizing effect of PCV13 is not yet known, and is probably not longer than a few years. There are studies on HAART HIV patients under way. I might be able to give them PCV13 later.

2) I always like a definite diagnosis better, if it is possible to achieve. Thus if the goal is to find out if the person has IgAD and SAD, we need to use PPV23. If the presentation is severe either due to asthma or due to LRTIs (which asthmatics get, without PID, with RR/OR 2-3x higher rate than normals), the more important it becomes.
If I find out that the person indeed has IgAD and SAD and bronchiectasis, they currently fulfill criteria in our hospital for IgGRT, if secondary ID seems unlikely. And we follow up LFTs very closely during a possible attempt and tell the patient this is a trial, not definite long term decision. But there is no proper data that would tell me just exactly how low the anti-PnP responses should be, if not completely missing and the avarage steroid dose  p.o. below 7.5 mg/d the previous 18-24 months .

3) When immune suppressed persons (e.g. long-term corticosteroids) are studied, there are absolutely no studies on PPV23 responsiveness using the present AAAI criteria, so at least I do not have a clue on how to interpret these with certainty. What I know is that if <0.35 in over 50% of serotypes (we use 10) there is a reasonable chance that there is a primary behind it, but there are patients in the literature which in the end still turn out to be secondary. How to then interpret PCV13... ????

4) If an asthmatic, and borderline or tough to interpret vaccine responses, I might do both some good (by getting frequent URTIs, occasional LRTIs prevented by IgGRT) but also a lot of harm (I also might make the asthma worse leading to an increased CS dose, this might kill, URTIs do not). High dose IgGRT in rodents leads to FcR-DCSIGN-mediated overproduction of IL33 that an asthmatic might produce too much anyway (the most significant asthma risk factor in GWASs is IL33 polymorphisms leading to IL-33 overproduction). And high dose IgGRT is to me clearly immunomodulatory.

5) Fraction of asthmatics tolerate IgGRT well, especially those with bronchiectasis this seems more common? Has not been studied properly, as far as I know, have tried in wane to find data.

6) But I've had asthmatics with undiagnosed B12-deficiency, with undiagnosed Vitamin A deficiency or with undiagnosed hypothyroidism who seemed to have SAD and got the to be frequent customers of ERs due to severe asthma, angioedema, severe dyspnoea due to vocal cord dysfunction after IgGRT...and when waned and retested after substiution of the true deficiency responded very strongly to PPV23... And had mild to moderate asthma ever since...These patients often respond very strongly to T-B antigens.
I test for B12-TC2, fS-A-vit, TSH, T4-free before anti-PnP testing - every time - nowadays.

7) And I have had asthmatics started with IgGRT by me /colleagues, who insidiously and slowly became to fare badly/very badly - though no URTIs - and a long-term steroid use below 7.5mg of Prednisone (or equivalent) p.o. before testing.
When waned off IgG, KCOc has occasionally popped up 10-20% and/or frequently spirometry results much better than in years (not to mention subjective wellbeing, though again URTIs frequently).The DBRCT by prof C Cunningham-Rundles has noted this phenomenon years ago. So nothing new. And my warmest regards to her!

Presently, I am very cautious in starting therapy blindly. Especially if an asthmatic, I definitely want to know how certain I am of PID diagnosis and if hesitant, and if T-dependent B responses strong to both diphtheria and tetanus, it usually does little good and very often insidiously something the patient does not benefit from.And they are often very labourious to get to take a break from therapy (but if they do agree, are usually not eager to test IgGRT again). And shownig the results of LFTs in a graph usually makes them very convinced... (we get these graphs automatically).

If I however meet a heavily immune-suppressed person with findings like CVID and typical clinical phenotype, I do start blindly, but they are typical and seem to fare much better than before. If RTX, I wait 18-24 mo before making any long term decisions.

Not a simple solution, mimicks life... At least I have found that if one tries too much to do good, one might do the opposite. Sadly.

Yours respectfully

Mikko Seppänen
MD, Finland, Helsinki


________________________________
Lähettäjä: Soheil Chegini [mailto:schegini at yahoo.com]
Lähetetty: 5. joulukuuta 2013 1:06
Vastaanottaja: CIS-PIDD
Aihe: Re: [cis-pidd] pneumococcal vaccine strategy in adolescents & adults with immune deficiency

Hello,

The right answer to that question very much depends on the objective of vaccination. You and all who commented so far would be perfectly right, if you only aim to provide immunity (therapeutic intent).

If you, however wish to use vaccination as a diagnostic tool to gain insight into her underlying immunodeficiency and assess her ability to produce specific anti-polysaccharide antibodies in addition to a prophylactic intent to induce immunity and reduce her frequency of pneumococcal infections, you will have to use pure polysaccharide antigens (Pneumovax) and conjugation with a potent protein immune stimulant (Prevnar) will obscure the diagnostic aspect of this intervention.

Best wishes,

Soheil Chegini, M.D.
Exton Allergy & Asthma Associates
656 West Lincoln Hwy.
Exton, PA 19341
Phone: (610) 269-3066
Fax: (610) 269-8615


On Wednesday, December 4, 2013 5:19 PM, "Verbsky, James" <jverbsky at mcw.edu> wrote:
Stan



For our patients in rheumatology on immunosuppression it is recommend to receive the PCV13 then the PPSV23.  We are doing this on all of our patients



Best

James



James Verbsky MD/PhD
Associate Professor of Pediatrics and Microbiology and Molecular Genetics
Medical College of Wisconsin
Milwaukee, WI  53226

________________________________
From: Stan Ress [stan.ress at uct.ac.za<mailto:stan.ress at uct.ac.za>]
Sent: Wednesday, December 04, 2013 3:04 PM
To: CIS-PIDD
Subject: [cis-pidd] pneumococcal vaccine strategy in adolescents & adults with immune deficiency

Hi all,

I have been referred a 15 year-old patient with extremely severe IgA deficiency, recurrent respiratory infections, & bronchiectasis on CT chest. Her baseline vaccine status revealed low IgG ELIZA antibodies against 4/5 antigens, including S. pneumonia & H. Influenza B. Our policy has been to vaccinate such patients with 23-valent pneumococcal polysaccharide vaccine. However, I saw a reference to ACIP recommendation that children & adults with immune compromising conditions or asplenia, should receive 13-valent conjugate vaccine 1st, followed 8 weeks later by unconjugated PPSV23.

Is this the general current practise?

Thanks.
--
Stanley Ress
Associate Professor of Medicine
Head: Division of Clinical Immunology
Department of Medicine
H47 Old Main Building-room 26
Groote Schuur Hospital and UCT
Observatory 7925
Cape Town
South Africa
TEL:INTERN. + 2721-4066201 or 4066197
FAX:  "    + 2721-(0)865173095
Cell: 0833115482
email: stan.ress at uct.ac.za<mailto:stan.ress at uct.ac.za><mailto:stan.ress at uct.ac.za<mailto:stan.ress at uct.ac.za>>

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