[CIS PIDD] [cis-pidd] Asymptomatic CK of 25, 000 U/L in XLA - OTHER DX?

Sun Sep 10 02:23:29 EDT 2017

We've seen CK transiently around 18,000 in a teenager using "protein boosts" in relation to heavy gymnasium activity. We were assured he hadn't been using anabolic steroids.

From: cis-pidd at lyris.dundee.net [mailto:cis-pidd at lyris.dundee.net] On Behalf Of CIS-PIDD
Sent: Saturday, 9 September 2017 8:34 AM
To: CIS-PIDD
Subject: Re: [cis-pidd] Asymptomatic CK of 25,000 U/L in XLA - OTHER DX?

Doping drugs may induce CK.
Best, Bodo

Ugeskr Laeger.<https://www.ncbi.nlm.nih.gov/pubmed/7985283> 1994 Oct 3;156(40):5872-3.
[Side-effects and doping control of anabolic steroids].
[Article in Danish]
Jensen LK<https://www.ncbi.nlm.nih.gov/pubmed/?term=Jensen%20LK%5BAuthor%5D&cauthor=true&cauthor_uid=7985283>1.
Author information<https://www.ncbi.nlm.nih.gov/pubmed/7985283>
Abstract

We present a case of a 26 year-old male body-builder who had used the anabolic steroids (AS) trenbolone and stanozolol for 10 weeks. After four weeks creatine-kinase (CK) including CK-B (cardiac specific isoenzymes) levels were elevated five to ten times. He was without cardiac symptoms and electrocardiography was normal. Three weeks after he stopped using AS, CK and CK-B levels had normalized. One of the drugs, stanozolol could not be detected by the doping-control, maybe because of a fast excretion time. Sale, use and delivery of AS is prohibited in Denmark, but is used in spite of the prohibition. It is important to spread knowledge about the risks of AS among the users.

Von: <cis-pidd at lyris.dundee.net<mailto:cis-pidd at lyris.dundee.net>> on behalf of CIS-PIDD <cis-pidd at lists.clinimmsoc.org<mailto:cis-pidd at lists.clinimmsoc.org>>
Antworten an: CIS-PIDD <cis-pidd at lyris.dundee.net<mailto:cis-pidd at lyris.dundee.net>>
Datum: Friday 8 September 2017 23:47
An: CIS-PIDD <cis-pidd at lyris.dundee.net<mailto:cis-pidd at lyris.dundee.net>>
Betreff: RE: [cis-pidd] Asymptomatic CK of 25,000 U/L in XLA - OTHER DX?

Dr. Raasch:

Might there be any occupational risk factors for this patient to have a high CK?   Weight-lifting?  Running?  Construction worker who works a jackhammer? (Sorry ... couldn't resist)      ;-)

The sports science literature is rather rich.  E.g., Kanda et al., Exerc Immunol Rev 2014 -- apparently, 10 sets of 40 calf lifts is enough to raise serum CK to a maximum of 6000 +/- 6500 (SD) at 96 h.     Latham et al., J Fam Pract 2008 cite a paper that I can't find that suggests that 13% of exercise subjects would break 20,000 IU/L.

The "macro CK" in the review Dr. Sullivan cited sounds interesting.  I've never heard of that before.

       - Karl

Karl O. A. Yu, M.D., Ph.D., F.A.A.P.
Scientist II and Assistant Director, Center for Infectious Diseases and Immunology
RGH Research Institute | Rochester General Hospital | Rochester Regional Health
1425 Portland Ave., Room R-403, Rochester, NY   14621
Tel  585-922-3709  |  Fax  585-922-2415

From: cis-pidd at lyris.dundee.net<mailto:cis-pidd at lyris.dundee.net> [mailto:cis-pidd at lyris.dundee.net] On Behalf Of CIS-PIDD
Sent: Friday, September 08, 2017 5:36 PM
To: CIS-PIDD
Subject: Re: [cis-pidd] Asymptomatic CK of 25,000 U/L in XLA - OTHER DX?

Great discussion here

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871266/#!po=18.2927<https://urldefense.proofpoint.com/v2/url?u=https-3A__www.ncbi.nlm.nih.gov_pmc_articles_PMC4871266_-23-21po-3D18.2927&d=DwMFAg&c=ZcS_IThVDLRgSnibLQVJ9vwqRPpc3RkFqvJL1VfvJu0&r=SS5WX_zJKFGQt9gnWxXM2zj3mGuaCrOGfogIF4rsPm06T2ggGCIyqTpu8I8GvD7y&m=cmfKRU5PMXQnSXjVlSAR3OEn3yGE0DT-wo8P8pgMLnk&s=VPl0scrdzUt-vQiw6MJRwAn8XcxIVwz8Gwsth0tTnog&e=>
Kate Sullivan
Sent from my iPhone

On Sep 8, 2017, at 4:36 PM, CIS-PIDD <cis-pidd at lists.clinimmsoc.org<mailto:cis-pidd at lists.clinimmsoc.org>> wrote:

Hello everyone, thoughts about DRAMATICALLY ELEVATED CK in asymptomatic young man with XLA (other than the obvious myositis)?

19 year-old young man with XLA.  'Low flyer' until a few years ago  when noted creatine kinase (CK) of 25,000 U/L (REF. 24-200) about 4 years ago (modestly elevated transaminases led to this finding).  Interestingly then (and presently) he has had NO symptoms of fatigue, weakness, myalgia; exam has revealed NO evidence of muscle wasting or atrophy; skin and nail exam is unremarkable.

** MY QUESTION ** :  any other considerations outside myopathy (including lab error, interfering substances, etc.) that would result in persistently and (intermittently dramatically elevated) CK FOR SEVERAL YEARS in an asymptomatic young man??    CK 25K a few years ago; nadir of 3,000 U/L for several years and recent peak again to >25,000 U/L.

Only remarkable labs have been CK; modestly increased ALT/AST both hovering in 90s; aldolase  of 23 (and low 20s; ref. " < 14.5 U/L"); modest thrombocytosis

UNREMARKABLE(!) LABORATORY STUDIES: EKG; echo;  ESR; CRP; GGT; CBC; TSH/T4/T3; U/A; urine myoglobin; troponin; EBV/CMB/PARVO PCR; urine organic acids; serum amino acids; CBC; electrolytes.   Genetic testing for dystropin mutation unremarkable as was screening for
AGAT  and GAMT deficiency.

Consultants have include neuromuscular/metabolic specialists.  Family is consistently reluctant to schedule open muscle biopsy, primarily because he is asymptomatic.

An obvious next step in his workup is open muscle biopsy and associated studies as recommended by neurology/metabolics.  Just wondering if there is additional considerations or alternative explanations.

thank you!

-jason

jason raasch, md
Midwest Immunology Clinic
Plymouth, MN

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