Approach
Cryoglobulinemia may be asymptomatic or present acutely. Mixed cryoglobulinemia (MC) was first described as a triad of purpura, weakness, and arthralgia.[20] However, the clinical presentation of cryoglobulinemia varies from asymptomatic to a cryoglobulinemic syndrome consisting of purpura and leukocytoclastic vasculitis with multiple organ involvement.[4]
The pace and extent of evaluation depends on the presentation. Type I cryoglobulinemia is usually associated with lymphoproliferative disorders. MC is associated with infectious or autoimmune disorders, particularly chronic hepatitis C virus (HCV) infection.[1][2] If a patient is diagnosed with a hematologic malignancy while being evaluated for cryoglobulinemia, referral to a hematologist is imperative.
Clinical evaluation
Careful clinical evaluation may provide clues to the type of cryoglobulinemia and its complications:
The presence of acrocyanosis; Raynaud phenomenon; skin ulcers; gangrene; and, less frequently, purpura, renal disease, or neurologic disorder should raise the possibility of type I cryoglobulinemia.[1] This may be complicated by life-threatening hyperviscosity syndrome, which may present with bleeding, visual disturbances, diplopia, ataxia, headache, and confusion. Signs of retinal hemorrhage and retinal vein thrombosis may be seen.[21][22]
MC should be suspected in patients with symptoms and signs consistent with small- to medium-vessel vasculitis. These include the presence of purpura, mononeuritis multiplex, or glomerulonephritis.[23] It may suggest a more rapid workup with particular attention to multiple organ function.[24] Other manifestations may include arthralgia, sicca syndrome, weakness, or hypertension in those with renal involvement.[Figure caption and citation for the preceding image starts]: Lower extremity palpable purpuraFrom the personal collection of Dr GS Kaeley [Citation ends].
[Figure caption and citation for the preceding image starts]: Unusual case of hepatitis C-related cryoglobulin-induced digital gangreneAbdel-Gadir A, Patel, K, Dubrey SW. Cryoglobulinaemia induced digital gangrene in a case of hepatitis C. BMJ Case Reports. 2010. [Citation ends].
Isolation of cryoglobulins
The detection of serum cryoglobulins is necessary to classify the cryoglobulinemic syndrome. Because cryoglobulins precipitate below normal body temperature, the collection and processing of the sample is critical.
Blood sampling (10-20 mL of blood is required), clotting, and serum separation should be carried out at 98.6°F (37°C). The serum sample is then stored at 39.2°F (4°C) for 24-72 hours and observed for the formation of a white precipitate (cryoglobulins). An aliquot of the cryoprecipitate should be rewarmed to 98.6°F (37°C) for 24 hours to test for the reversibility of cryoprecipitation.
Initial investigations
The Ig cryoprecipitate is isolated and analyzed by immunoelectrophoresis or immunofixation. Cryoprecipitate measurement methods vary, and cryocrit levels do not correlate with disease activity.[1][4] However, a sudden decrease of cryoglobulin levels with increased levels of C4 may signal the evolution of a lymphoproliferative disorder.[25] This is thought to reflect the change of benign polyclonal B cells that produce antibodies to malignant B cells that no longer produce immunoglobulins.[4]
Other markers of activity are rheumatoid factor, complement C1q, C3, C4, CH50 (total complement activity), and acute-phase reactants (C-reactive protein and erythrocyte sedimentation rate [ESR]).[4][6][26] Findings may include IgM rheumatoid factor positive, elevated ESR, and normocytic normochromic anemia. Complement C1q and C4 may be low.
The evaluation for organ involvement should include a complete blood count, a comprehensive chemistry panel, and a urinalysis. An ECG and chest x-ray are indicated in patients with suspected multiorgan involvement.[4]
The etiology of vasculitis should be assessed by performing the following tests: antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies, extractable nuclear antigen antibody (ENA), dsDNA antibodies, complement assay, and specific biopsies (e.g., IgA deposits on skin or kidney are suggestive of Henoch-Schonlein purpura).
If a viral cause is suspected, testing for HCV antibody and hepatitis B is recommended.[4]
Further investigations
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