[CIS PIDD] [cis-pidd] ten year old with CVID and focal white matter demyelination

[Dr. Carsten Speckmann]

  I think one should be cautious when comparing adult CVID observations 
with "complicated hyogamma in children".
Patients with white matter changes and hypogamma should be thoroughly 
worked up i.e. for an underlying CID (e.g. Nakaoka, et al. (2012). 
Delayed onset adenosine deaminase deficiency associated with acute 
disseminated encephalomyelitis. International journal of hematology) and 
hyomorphic HLH (Rohr, J.,et al. (2010). Atypical familial hemophagocytic 
lymphohistiocytosis due to mutations in UNC13D and STXBP2 overlaps with 
primary immunodeficiency diseases. Haematologica, 95(12), 2080–2087).

Dr. med. Carsten Speckmann
Funktionsoberarzt/Consultant Immunologist
Zentrum fuer Kinderheilkunde und Jugendmedizin
Centrum fuer Chronische Immundefizienz - CCI
Universitaet Freiburg
Mathildenstr. 1
79106 Freiburg
Germany

phone: +49 (0)761-270 43010
mail: carsten.speckmann at uniklinik-freiburg.de
web: www.cci.uniklinik-freiburg.de



Am 19.09.13 14:56, schrieb Keller, Michael:

> Greetings all,

>

> Since the topic came up, I would mention about a year ago, a 22 year 

> old woman with CVID cared for at CHOP presented with severe headaches 

> and was found to have a MRI that looked like CNS lymphoma - but on 

> biopsy, was consistent only with a 'non-malignant lymphoproliferative 

> process'.   Though she gave us quite a scare, she dramatically 

> improved with steroid therapy.

>

> Perhaps these CNS complications of CVID would warrant a case series if 

> anyone was so inclined?

>

> Best,

> Mike

>

> -------------------------

>

> Michael D. Keller MD

>

> Division of Allergy / Immunology

>

> Children's National Medical Center

>

> 111 Michigan Ave NW, Room 1W-314B

>

> Ph: 202.476.5843

>

> Fax: 202.476.2280

>

> ------------------------------------------------------------------------

> *From:* Seppänen Mikko [Mikko.Seppanen at hus.fi]

> *Sent:* Thursday, September 19, 2013 1:14 AM

> *To:* CIS-PIDD

> *Subject:* VS: [cis-pidd] ten year old with CVID and focal white 

> matter demyelination

>

> Dear Javeed,

> The nicest of all alternatives, by far. Neuroradiologically this grave 

> and widespread ADEM is easy to pinpoint. If radiology is typical, You 

> have the diagnosis, no biopsy needed in my mind. Agree thus with John, 

> provided that both neurologist and neuroradiologist agree.

> I have had one borderline SAD patient with very chronic ADEM years 

> ago, and lesions resolved when experimental  IVIg was initiated by 

> neurologists and our unit jointly ("um etwas zu tun"). It was later 

> stopped and a.o.t. we checked vaccine responses, then due to only 

> borderline findings (if my memory serves me right?) he was kept off 

> IgG for a shortish while, lesions reappeared and became 

> symptomatic and after yet another treatment period --> SCIg high dose 

> substitution, lesions resolved.

> Then he was lost to my follow up, moved to another district. I do know 

> the doctor who further followed him up though, so digging his files up 

> are not entirely impossible, if a case series is needed, John, 

> Javeed and Dewton ;=) Ellie's case sounds truly like granulomas, 

> another patient group?

> According to what I have heard from my British colleagues, even brain 

> granulomas might occasionally resolve spontaneously (or maybe with IgG 

> dose adjustment?)? This however is second-hand information.

> Thus this might be a slight tip to treating this patient??? And keep 

> us posted on further developments?

> mikko

> Mikko Seppänen, HUCH, Finland

>

> ------------------------------------------------------------------------

> *Lähettäjä:* Akhter, Javeed [mailto:javeed.akhter at advocatehealth.com]

> *Lähetetty:* 18. syyskuuta 2013 20:42

> *Vastaanottaja:* CIS-PIDD

> *Aihe:* RE: [cis-pidd] ten year old with CVID and focal white matter 

> demyelination

>

> Drs Seppanen, Routes, Vasconcelos and Haddad

>

> Thank you all for taking the time to review and respond to this case.  

> Your input is extremely useful and highly appreciated

>

> I am pasting a bit more of the data on this child’s CSF.

>

> Our Neurologist’s diagnosis is ADEM

>

> I will be meeting with the patient and family soon and share your 

> thoughts and suggestions with them.  If it is OK I will share the 

> family’s response and the child’s progress with you all.

>

> Dr Routes I will be in touch with you and may be one of our residents 

> can help write up a case report in the future.

>

> Thanks again

>

> Javeed Akhter

>

> Advocate Children’s Hospital, Oak Lawn. IL

>

> JMF center

>

> CSF SYNTH PNL W ELEC [MSCSF] Final

>

> ALBUMIN, SERUM 3720 3430-4990 mg/dL

>

> IGG 2010 H 694-1618 mg/dL

>

> CSF PROTEIN 32 15-45 mg/dL

>

> CSF ALBUMIN 11 0-35 mg/dL

>

> CSF IgG 2.8 0.5-6.1 mg/dL

>

> CSF IgG INDEX 0.47 <0.77

>

> CSF IGG SYNTH.RATE 0.0 0.0-8.0 mg/24 hr

>

> Unit: mg/day

>

> IGG/ALB INDEX 0.25 0.09-0.25

>

> CSF ELECTROPHORESIS

>

> Negative for oligoclonal bands.

>

> LYME DISEASE by PCR

>

> NOT DETECTED

>

> CSF CULTURE [CSFCS] Final

>

> CSF CULTURE/SMEAR

>

> SPECIMEN DESCRIPTION: CEREBROSPINAL FLUID

>

> GRAM SMEAR: NO ORGANISMS SEEN

>

> GRAM SMEAR: POLYMORPHONUCLEAR CELLS PRESENT

>

> ENTERO VIRUS PCR NOT DETECTED NOTD

>

> HERPES SIMPLEX PROBE NOT DETECTED NOTD

>

> VARICELLA ZOSTER VIR NOT DETECTED NOTD

>

> CMV QUALITATIVE NOTD

>

> NOT DETECTED

>

> CSF VOLUME 4.0 mL

>

> NUMBER OF TUBES 3

>

> PERFORMED ON TUBE 3

>

> CSF APPEARANCE CLEAR COLORLESS

>

> CSF RBC 30 H 0 /mcL

>

> NUCLEATED CELL COUNT 89 H 0-10 /mcL

>

> SEG NOT APPLICABLE

>

> LYMPH 93 28-95 %

>

> MONO/MACROPHAGE 7 L 16-56 %

>

> EOS NOT APPLICABLE

>

> BASO NOT APPLICABLE

>

> GLUCOSE CSF [CSFGL] Final

>

> CSF PROTEIN 32 15-45 mg/dL

>

> *From:* Elie Haddad [mailto:elie.haddad at umontreal.ca]

> *Sent:* Wednesday, September 18, 2013 9:31 AM

> *To:* CIS-PIDD

> *Subject:* Re: [cis-pidd] ten year old with CVID and focal white 

> matter demyelination

>

> We also folowed a patient with CVID and GLILD. First we treated her 

> with steroids + antiTNF.

>

> After 1 year, she developped seizures and the brain biopsy showed "a 

> GLILD in the brain" as said our pathologist. He told us that the 

> lesions in the brain were a copy/paste of the lesions in the lungs. He 

> did not mention ADEM. Of course, all the infectious work-up was negative.

>

> We tried Rituximab (withour Imuran) and it worked well for a while but 

> then seizures relapsed. Therefore, we decided to transplant the patient.

>

> More than 2 years after double cord blood transplantation, she has no 

> relapse of GLILD (in lungs or in brain...), her immune system is very 

> slowly recovering, she has had some GvHD and recently she developed an 

> autoimmune hemolytic anelmia for which we had to give steroids and 

> rituximab. Not so perfect but so far, we "cured" the brain and the lung.

>

> All the best

>

> Elie

>

> Elie Haddad, MD, PhD,

>

> Professor of Pediatrics, University of Montreal,

>

> Head, Pediatric Immunology and Rheumatology Division,

>

> CHU Sainte-Justine, 3175 Cote Sainte-Catherine

>

> Montreal, QC, H3T 1C5, Canada

>

> Ph: 1 514 345 4713

>

> fax: 1 514 345 4897

>

> e-mail: elie.haddad at umontreal.ca <mailto:elie.haddad at umontreal.ca>

>

>

>

> Le 2013-09-18 à 10:18, Routes, John a écrit :

>

>

>

> Dear Javeed

> Well since Mikko broke the ice I will add my 2 cents

> I agree with the workup suggested below but doubt it will reveal 

> infection---

> We were referred an 18 you female with CVID and the w/u revealed GLILD 

> (had splenomegaly, diffuse adenopathy etc….)---she also had focal 

> demylelination of the CNS and after an extensive w/u was diagnosed 

> with ADEM

> She has been treated with rituximab and azathioprine, which induced a 

> remission of both the CNS disease and GLILD----interestingly, when we 

> DC'd immunosuppressive therapy, her ADEM recurred

> so we restarted Aza/RTX (recently substituted MMF due to nausea) and 

> her CNS disease is stable and pulmonary disease essentially gone

>

> if the dx turns out to be ADEM, let me know and we can write these 

> cases up

> Remember the adage----one patient is a case report, 2 is a series and 

> 3 is a career.

> good luck and let me know if i can be of any help

> Jack

>

>

> John M. Routes, MD

> Chief, Section of Allergy and Clinical Immunology

> Co-Director, Clinical and Translational Science Institute of Southeast 

> Wisconsin

> Professor of Pediatrics, Medicine, Microbiology and Molecular Genetics

> Department of Pediatrics

> Children's Hospital of Wisconsin

> Medical College of Wisconsin

> 9000 W. Wisconsin Ave.

> Milwaukee, WI  53226-4874

> Phone: Office 414-266-6840

> Fax: 414-456-6487 (Clinical)

> Fax: 414-456-6323 (Laboratory)

> Email: jroutes at mcw.edu <mailto:jroutes at mcw.edu><mailto:jroutes at mcw.edu>

>

>

>

>

>

> On Sep 18, 2013, at 4:45 AM, Seppänen Mikko <Mikko.Seppanen at hus.fi 

> <mailto:Mikko.Seppanen at hus.fi><mailto:Mikko.Seppanen at hus.fi>> wrote:

>

> Dear Javeed,

>

> Since no one seems eager to comment, a quick note:

>

> a)      Q: values of CSF-prot, leuk, ADA, LZM, IgG index, cytology, 

> CSF/S-oligoclonal bands? S-LD, thymidine kinase, IL2R??

>

> b)      Seems awfully widespread for “normal” infection. Due to immune 

> suppression, fungal and parasitic diseases are a possibility, as is 

> PMLE (!). Neuroradiologists would suspect PMLE,

> c)       …. and would recognize ADEM, in which waxing and waning as 

> well as relapses are rarely, but occasionally seen. Of nice dgs I 

> would seriously consider this.

> d)      TBC is rare in CVIDs, but needs to be excluded.

> e)      For CNS autoimmunity vs. SLE, MCTD, Sjogren, grey matter is 

> usually also affected.

> f)       For known autoimmune encephalitis forms the involvement is 

> too widespread, too radiologically active and symptoms too few, the 

> patient has cerebritis + rhombencephalitis (= cerbellitis and basal 

> encephalitis) /demyelination  and  this dg seems less likely. Of 

> course one does see peculiar AIE-like syndromes in CVIDs, I have 2 

> patients not conforming to any but whom I regard to suffer from such, 

> thus exclusion 100% might be impossible, peculiar, severe and fatal 

> cases are also in literature, at least 1 well-documented patient 

> series published

> g)      and I would sadly very actively search for CNS lymphoma, CNS 

> granulomas, PMLE, severe hard-to-treat opportunistic infections

> h)      biopsy seems to me both urgent and mandatory

>

> i)        BTW. You might want to consider WES for the whole family… AD 

> mode of inheritance? If interested in this, contact me?

> See also recent JACI letter:

> Neil Romberg et al “Gain-of-function STAT1 mutations are associated 

> with PD-L1 overexpression and a defect in B-cell survival”

>

> Hope this helps,

>

> mikko

> Mikko Seppänen, MD PhD, HUCH, Finland

>

>

>

> Lähettäjä: Akhter, Javeed 

> [mailto:javeed.akhter at advocatehealth.com<http://advocatehealth.com>]

> Lähetetty: 17. syyskuuta 2013 19:26

> Vastaanottaja: CIS-PIDD

> Aihe: [cis-pidd] ten year old with CVID and focal white matter 

> demyelination

>

> Hi colleagues

> I need help with this 10 yr old with CVID who is experiencing focal 

> demyelination of the white matter with headaches and two seizures. 

>  Infectious disease work up is negative.

>

> Here is a brief summary of this patient who I initially saw at 8 years 

> of age.  She had a diagnosis of Evan’s syndrome and was starting to 

> have sino-pulmonary infections.

> Her initial labs were

>

> IGG  374                              IGA 16 L               IGM 40 

>                 mg/dL

> Isohemagglutinins            Anti A 16       Anti B  16

>

> Tetanus antibody: 2.54

> PNEUMOCOCCAL antibodies: 2/23 were above 1.3

> Post immunization tiers: 7/23

>

> FLOW CYTOMETRY - THE PATIENT HAS INCREASED PERCENTAGES OF

> CD3+ T CELLS AT 80%, NORMAL RANGE EQ (54-79%) AND CD4+ T CELLS AT 61%,

> NORMAL RANGE EQ (28-49%).  THE ABSOLUTE NUMBERS OF CD4+ T CELLS WERE

> INCREASED.  THE PROPORTION OF T CELLS EXPRESSING HLA-DR IS ABOVE

> NORMAL AND CONSISTENT WITH RECENT IMMUNE ACTIVATION.  NO OTHER

> SIGNIFICANT ABNORMALITIES WERE OBSERVED IN ANY OF THE LYMPHOCYTE

>

> MEMORY B CELLS: APPROXIMATELY 23.1% (NORMAL RANGE: 5.6-33%)

> OF THE PATIENT'S B CELLS EXPRESS A MEMORY PHENOTYPE (I.E., CD27+).

> THE PATIENT HAS DECREASED PERCENTAGES OF THE MEMORY B CELLS

> EXPRESSING AN IMMUNOGLOBULIN "CLASS SWITCHED" EXPRESSION PROFILE AT

> 14.6% (NORMAL RANGE: 28.7-65.6%).

>

> As a part of the initial w/u a CT chest and abdomen were done.

>

> CT chest revealed mediastinal lymph nodes and small nodules in the 

> lung parenchyma

> There is thoracic lymphadenopathy. This includes lymphadenopathy in 

> both axilla as well as in both hila. There are also at least mildly 

> prominent nodes in the mediastinum. For reference purposes, one of the 

> larger axillary nodes is identified on the left measuring 

> approximately 2.5 x 1.4 cm. No pleural effusions are seen. There are 

> hazy ground glass opacities throughout both lung fields. Superimposed 

> upon this are innumerable patchy and nodular densities. These appear 

> more prominent in the lower lungs. While cavitary changes are 

> difficult to fully exclude, these are not clearly evident.

> CT abdomen revealed heapto spenomegaly and no abdominal lymph nodes

>

> A lung and lymph node biopsy revealed non-caseating granulomas that 

> are negative for infection

>

> A lymphoma w/u done by our hem/onc service is negative

>

> Because of the Granulomas in the lung and splenomegaly and persistent 

> thrombocytopenia she was started on long term oral steroids in a dose 

> of 1mg/kg initially once daily and then qod.  She was also give 4 

> doses of Rituximab

>

> Another interesting f/h is that her dad has CVID also.  He has had 

> only infections but no auto immune problems, non-caseating granuloms 

> or GI issues.  I have started taking care of him as well.  Father’s 

> brother I am told has CVID also but I have not seen him and do not 

> have access to his labs

>

> The patient responded very nicely to the therapy.  Her lung lesions 

> have cleared up and her spleen has shrunk.

>

> In August of 2012 she came in with a seizure. .MRI of the brain showed 

> the following:

> Poorly defined left temporal lobe lesion associated with mild mass 

> effect as describe above. Finding may represent encephalitis, possibly 

> viral in nature. Underlying mass lesion is not entirely excluded. MRI 

> of the brain is recommended for further evaluation. All of the 

> infectious disease w/u including PCR on the CSF were negative.

>

> She improved.  Was continued on the same therapy of IVIG and tapering 

> systemic steroids qod

> Her headaches returned and she had another seizure. The repeat MRI 

> (there have been four MRIs) reveled the following.

>

> Technique: Diffusion, T1 sagittal, T2 axial, SWI, axial FLAIR, T2 

> coronal, coronal FLAIR, T1 axial PRE and postcontrast, T1 coronal 

> fat-sat postcontrast, T1 sagittal postcontrast, Magnevist 10 mL

>

> There is redemonstration of the abnormal FLAIR hyperintensity 

> involving the left cerebellum, left temporal lobe, left posterior 

> basal ganglia, right posterior parietal occipital lobe as well right 

> medial parietal lobe. There is residual enhancement in these regions. 

> Some of the enhancement appears to be improved compared to prior exam. 

> However there also appears to be region of subtle increased 

> enhancement in the left cerebellum compared to the prior exam.

> There are also now a new regions of focal abnormal FLAIR 

> hyperintensity in the right subfrontal lobe, left medial parietal lobe 

> adjacent to the body and splenium of the corpus callosum as well as a 

> along the right posterior parietal convexity. There is corresponding 

> enhancement in these regions. This again may reflect immunodeficiency 

> post inflammatory or infectious etiology. Close interval followup 

> suggested.

> 1. New regions of abnormal FLAIR hyperintensity and enhancement in the 

> right subfrontal lobe, right posterior parietal lobe and along the 

> left medial parietal lobe as described above.

> 2. The previously descried regions of FLAIR hyperintensity and 

> enhancement are also again noted as described above.

>

> The lesions are strictly in the white matter.  New lesions are being seen.

>

> Repeat w/u including CSF analysis shows no evidence of infection in 

> particular enterovirus.

>

> Is this auto-immune process? (she is on steroids and has had rituximab)

> Is there another condition that I am missing?

> Should I suggest a brain biopsy?

> Is she a candidate for azathioprine?

>

> Any suggestions would be highly appreciated.

>

> Javeed Akhter, M.D.

> JMF Immunology Referal Center

>

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