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1 month after plasma exchange vitamin D levels reduced by 40 percent – Oct 2013

Plasma Exchange Induces Vitamin D Deficiency

QJM (2013) doi: 10.1093/qjmed/hct208
Thomas F Hiemstra 1,2,
Alina Casian 2,
Paul Boraks 3,
David R Jayne 2 and
Inez Schoenmakers 4
1 Divisions of Clinical Pharmacology and Nephrology, Department of Medicine, University of Cambridge; 2 Lupus and Vasculitis and 3 Apheresis units, Addenbrooke's Hospital, Cambridge; 4MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge.
To whom correspondence should be addressed: Thomas F Hiemstra, Divisions of Nephrology and Clinical Pharmacology, Department of Medicine, University of Cambridge, Box 118 Addenbrooke's Hospital, Hills Road, Cambridge, CB2 0QQ, tfh24 at cam.ac.uk, Phone: +44 1223 349844

Background: Plasma exchange is used in the treatment of diseases mediated by pathogenic circulating proteins, or for transplant desensitisation. Its non-targeted nature results in the depletion of physiologically important molecules, and it is often complicated by hypocalcaemia.

Aim: To determine the effects of plasma exchange on vitamin D binding protein and associated vitamin D metabolites.

Design: Single-centre prospective cohort study of 11 patients.

Methods:DBP and vitamin D metabolites were measured before and immediately after 5 plasma exchanges, and 7 and 28 days after discontinuation of plasma exchange.

Results:Plasma exchange reduced plasma

  • vitamin D binding protein concentration from 196.9 ± 53.2 to 98.5 ± 34 μg/mL (p = 0.0001),
  • 1,25-dihydroxyvitamin D from 103 ± 52 pmol/l to 42 ± 4pmol/l (p = 0.003), and
  • 25-hydroxyvitamin D from 49.7 ± 29 to 22 ± 9.4 nmol/l (p = 0.0017),

through their removal in effluent.
After 7 days, DBP and 1,25-dihydroxyvitamin D were not significantly different from baseline, but 25-hydroxyvitamin D remained significantly lower after

  • 7 days (26.4 ± 9.8 nmol/l, p = 0.02) and
  • 28 days (30.8 ± 15.5 nmol/l, p = 0.048).

Corrected calcium decreased from 2.23 ± 0.11 mmol/l to 1.98 ± 0.08 mmol/l(p=0.0007) immediately after 5 treatments. Plasma calcium was significantly associated with 1,25-dihydroxyvitamin D (r2 = 0.79, p < 0.0001).

Conclusions: Plasma exchange inducedan acute reversible decrease in plasma 1,25-dihydroxyvitamin D, DBP, calcium, and a sustained decrease in plasma 25-hydroxyvitamin D.

Figure 1 (Black bars = vitamin D)

Effect of plasma exchange on 25-hydroxyvitamin D and DBP.
Statistical comparisons are made with baseline values for each variable.
Plasma exchange significantly reduced DBP, although this had recovered to baseline after 7 days.
In contrast, 25-hydroxyvitamin D concentrations remained significantly lower than baseline after 7 and 28 days.

Serum level:

nmol ng %
Initially 50 20 100%
Exchange 23 946 %
7 days261052%
28 days3112 62%

PDF is attached at the bottom of this page

Plasmapheresis Wikipedia

  • Plasmapheresis is used as a therapy in particular diseases.
  • It is an uncommon treatment in the United States, but it is more common in Europe and particularly Japan

Guillain-Barré syndrome
Miller Fisher syndrome
Chronic inflammatory demyelinating polyneuropathy
Goodpasture's syndrome
Hyperviscosity syndromes: Cryoglobulinemia, Paraproteinemia, Waldenström macroglobulinemia
Myasthenia gravis
Thrombotic thrombocytopenic purpura (TTP)/hemolytic uremic syndrome
Wegener's granulomatosis
Lambert-Eaton Syndrome
Antiphospholipid Antibody Syndrome (APS or APLS)
Microscopic polyangiitis
Recurrent focal and segmental glomerulosclerosis in the transplanted kidney
HELLP syndrome
PANDAS syndrome
Refsum disease
Behcet syndrome
HIV-related neuropathy
Graves' disease in infants and neonates
Pemphigus vulgaris
Neuromyelitis optica
Multiple sclerosis
Toxic Epidermal Necrolysis (TEN)

Aetna Insurance (US) will pay from plasma exchange for

  • Acute, severe neurological deficits caused by multiple sclerosis that have a poor response to treatment with high-dose glucocorticoids;
  • Babesiosis if member has high-grade parasitemia (greater than or equal to 10 %), severe anemia (hemoglobin less than or equal to 10 g/dL), or hepatic, pulmonary, or renal compromise;
  • Chronic relapsing polyneuropathy (chronic inflammatory demyelinating polyneuropathy [CIDP]) with severe or life-threatening symptoms, in persons who have failed to respond to conventional therapy.
  • Essential thrombocythemia (when platelet count is greater than 1,000,000/mm3) (platelet pheresis);
  • Glomerulonephritis associated with antiglomerular basement membrane antibodies and advancing renal failure or pulmonary hemorrhage;
  • Goodpasture’s syndrome;
  • HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome of pregnancy, in persons who are not getting better within 5 days after delivery;
  • Hyperglobulinemias, including (but not limited to) multiple myelomas, cryoglobulinemia, primary (Waldenstrom's) macroglobulinemia, and hyperviscosity syndromes;
  • Last resort treatment of acute disseminated encephalomyelitis, where conventional treatment (including corticosteroids) has failed (i.e., severe neurological deficits have persisted after treatment with corticosteroids);
  • Last resort treatment of life-threatening rheumatoid vasculitis;
  • Last resort treatment of life-threatening systemic lupus erythematosus (SLE) when conventional therapy has failed to prevent clinical deterioration;
  • Leukemia (leukapheresis) (for acute debulking only);
  • Moderate to severe active rheumatoid arthritis in adults with longstanding disease who have failed or are intolerant of disease–modifying anti-rheumatic drugs (DMARDs);
  • Myasthenia gravis, in persons with any of the following: (i) acute, short-term benefit is critical because of a sudden worsening of symptoms (such as in impending respiratory crisis), (ii) needs rapid improvement of strength before surgery or irradiation, or (iii) requires chronic intermittent treatment because of failure to respond to all other treatments;
  • Pemphigus vulgaris that is resistant to standard therapy (dapsone, corticosteroids, immunosuppressants such as azathioprine or cyclosporine);
  • Pruritus from cholestatic liver disease (plasma perfusion of charcoal filters), last resort treatment in persons who have failed (unless contraindicated): bile acid resins (cholestyramine or cholestepol), rifampin, ursodeoxycholic acid (in primary biliary cirrhosis), and opioid antagonists (naltrexone, naloxone or nalmefene);
  • Refsum's disease;
  • Renal transplantation from live donor with ABO incompatibility or positive cross-match, where a suitable non-reactive live or cadaveric donor is unavailable;
  • Scleroderma and polymyositis, in persons who are unresponsive to conventional therapy;
  • Severe (grades 3 to 5) Guillain Barre' syndrome
  • Severe hypercholesterolemia in persons refractory to diet and maximum drug therapy who are homozygous for familial hypercholesterolemia (LDL apheresis, also known as heparin-induced extracorporeal LDL precipitation (HELP) or dextra sulfate adsorption) with LDL levels greater than 500 mg/dL, or persons heterozygous for familial hypercholesterolemia with LDL levels greater than 300 mg/dL or greater than 200 mg/dL with documented history of coronary artery disease.
  • Sickle cell disease (therapeutic cytopheresis);
  • Solid organ transplant from donor with positive cross-match, where a suitable non-reactive donor is unavailable;
  • Treatment of neuromyelitis optica (Devic's syndrome) that is refractory to glucocorticoids;
  • Treatment of thrombotic thrombocytopenic purpura (TTP) or microangiopathic hemolytic anemia
  • Treatment of transverse myelitis when corticosteroid treatment has failed.

Plasma Guidelines at attached at the bottom of this page

Vitamin D was not even mentioned by WikiPedia, Aetna, nor Plasma Guidelines (bottom of this page)

See also VitaminDWiki

See also web

Is a lot of vitamin D stored in the plasma?

Used to think that a lot of Vitamin D was stored in the Liver

Attached files

ID Name Comment Uploaded Size Downloads
3603 Plasma Exchange F1.jpg admin 08 Feb, 2014 12:21 30.54 Kb 1263
3602 Plasma Exchange.pdf PDF 2013 admin 08 Feb, 2014 12:17 210.34 Kb 972
3141 Hematology-2012-Winters-7-12.pdf PDF admin 16 Oct, 2013 10:42 94.89 Kb 933