Cryoglobulins
Cryoglobulinemia
Paraproteinemias
Rheumatoid Factor
Complement Activating Enzymes
Antigen-Antibody Complex
Vasculitis, Leukocytoclastic, Cutaneous
Immunoglobulin G
Complement C1q
Complement C3
Complement C4
Immunoglobulin M
Antibodies, Anti-Idiotypic
Glomerulonephritis, Membranoproliferative
Hepatitis C, Chronic
Waldenstrom Macroglobulinemia
Immunodiffusion
Nephelometry and Turbidimetry
Lupus Erythematosus, Systemic
Antibodies, Antinuclear
Complement System Proteins
Hepatitis C
Complement receptor 1 (CD35) on human reticulocytes: normal expression in systemic lupus erythematosus and HIV-infected patients. (1/235)
The low levels of complement receptor 1 (CR1) on erythrocytes in autoimmune diseases and AIDS may be due to accelerated loss in the circulation, or to a diminished expression of CR1 on the red cell lineage. Therefore, we analyzed the expression of CR1 on reticulocytes (R) vs erythrocytes (E). Healthy subjects had a significant higher CR1 number per cell on R (919 +/- 99 CR1/cell) than on E (279 +/- 30 CR1/cell, n = 23), which corresponded to a 3. 5- +/- 1.3-fold loss of CR1. This intravascular loss was confirmed by FACS analysis, which showed that all R expressed CR1, whereas a large fraction of E was negative. The systemic lupus erythematosus (SLE), HIV-infected, and cold hemolytic Ab disease (CHAD) patients had a CR1 number on R identical to the healthy subjects, contrasting with a lower CR1 on their E. The data indicated a significantly higher loss of CR1 in the three diseases, i.e., 7.0- +/- 3.8-, 6.1- +/- 2.9-, and 9.6- +/- 5.6-fold, respectively. The intravascular loss was best exemplified in a patient with factor I deficiency whose CR1 dropped from 520 CR1/R to 28 CR1/E, i.e., 18.6-fold loss. In one SLE patient and in the factor I-deficient patient, the FACS data were consistent with a loss of CR1 already on some R. In conclusion, CR1 is lost progressively from normal E during in vivo aging so that old E are almost devoid of CR1. The low CR1 of RBC in autoimmune diseases and HIV-infection is due to a loss occurring in the circulation by an active process that remains to be defined. (+info)Serious hazards of transfusion (SHOT) initiative: analysis of the first two annual reports. (2/235)
OBJECTIVE: To receive and collate reports of death or major complications of transfusion of blood or components. DESIGN: Haematologists were invited confidentially to report deaths and major complications after blood transfusion during October 1996 to September 1998. SETTING: Hospitals in United Kingdom and Ireland. SUBJECTS: Patients who died or experienced serious complications, as defined below, associated with transfusion of red cells, platelets, fresh frozen plasma, or cryoprecipitate. MAIN OUTCOME MEASURES: Death, "wrong" blood transfused to patient, acute and delayed transfusion reactions, transfusion related acute lung injury, transfusion associated graft versus host disease, post-transfusion purpura, and infection transmitted by transfusion. Circumstances relating to these cases and relative frequency of complications. RESULTS: Over 24 months, 366 cases were reported, of which 191 (52%) were "wrong blood to patient" episodes. Analysis of these revealed multiple errors of identification, often beginning when blood was collected from the blood bank. There were 22 deaths from all causes, including three from ABO incompatibility. There were 12 infections: four bacterial (one fatal), seven viral, and one fatal case of malaria. During the second 12 months, 164/424 hospitals (39%) submitted a "nil to report" return. CONCLUSIONS: Transfusion is now extremely safe, but vigilance is needed to ensure correct identification of blood and patient. Staff education should include awareness of ABO incompatibility and bacterial contamination as causes of life threatening reactions to blood. (+info)Modulation of renal disease in MRL/lpr mice genetically deficient in the alternative complement pathway factor B. (3/235)
In systemic lupus erythematosus, the renal deposition of complement-containing immune complexes initiates an inflammatory cascade resulting in glomerulonephritis. Activation of the classical complement pathway with deposition of C3 is pathogenic in lupus nephritis. Although the alternative complement pathway is activated in lupus nephritis, its role in disease pathogenesis is unknown. To determine the role of the alternative pathway in lupus nephritis, complement factor B-deficient mice were backcrossed to MRL/lpr mice. MRL/lpr mice develop a spontaneous lupus-like disease characterized by immune complex glomerulonephritis. We derived complement factor B wild-type (B+/+), homozygous knockout (B-/-), and heterozygous (B+/-) MRL/lpr mice. Compared with B+/- or B+/+ mice, MRL/lpr B-/- mice developed significantly less proteinuria, less glomerular IgG deposition, and decreased renal scores as well as lower IgG3 cryoglobulin production and vasculitis. Serum C3 levels were normal in the B-/- mice compared with significantly decreased levels in the other two groups. These results suggest that: 1) factor B plays an important role in the pathogenesis of glomerulonephritis and vasculitis in MRL/lpr mice; and 2) activation of the alternative pathway, either by the amplification loop or by IgA immune complexes, has a prominent effect on serum C3 levels in this lupus model. (+info)Cytoplasmic inclusions in leukocytes. An unusual manifestation of cryoglobulinemia. (4/235)
Cryoglobulins are circulating immunoglobulins characterized by reversible, cold-induced precipitation. A variety of laboratory abnormalities, including hypocomplementemia, elevated erythrocyte sedimentation rate, rheumatoid factor activity, pseudoleukocytosis, and pseudothrombocytosis, are associated with cryoglobulinemia. Extracellular, faintly basophilic, amorphous deposits of cryoglobulins occasionally have been described in blood smears. In the present study, smears prepared from blood collected at room temperature from 6 patients with cryoglobulinemia exhibited neutrophil and, occasionally, monocyte inclusions containing clear, light pink, or faintly basophilic amorphous material. The inclusions were absent in smears from blood collected and maintained at 37 degrees C. Ultrastructural examination revealed that the material within the leukocyte inclusions was consistent with phagocytosed immunoglobulins. The identification of characteristic cytoplasmic inclusions in leukocytes may be an important clue in the early recognition of cryoglobulinemia. (+info)Correlation between tumor induction and the large external transformation sensitive protein on the cell surface. (5/235)
The distribution on the cell surface of the large external LETS protein that is transformation sensitive of normal, transformed and tumorigenic cells was examined by immunofluorescent staining. A correlation was established between the expression of fibril-like LETS protein and the oncogenic capabilities of a series of adenovirus-transformed cell lines. In cells expressing a transformed phenotype in vitro, LETS protein is only detected in cell-cell contact areas, wheras in "untransformed" cells LETS protein is distributed over the cell surface. Transformed cells capable of inducing invasive tumors, and the cells of established tumor lines, have low or undetectable levels of LETS protein, as measured by this method. The results indicate that LETS protein has a role in cell-cell adhesion and that reduced expression of this protein at the cell surface is related to the oncogenic phenotype. This relationship has been established for experimentally induced and spontaneous tumors. (+info)Complement fixation by rheumatoid factor. (6/235)
The capacity for fixation and activation of hemolytic complement by polyclonal IgM rheumatoid factors (RF) isolated from sera of patients with rheumatoid arthritis and monoclonal IgM-RF isolated from the cryoprecipitates of patients with IgM-IgG mixed cryoglobulinemia was examined. RF mixed with aggregated, reduced, and alkylated human IgG (Agg-R/A-IgG) in the fluid phase failed to significantly reduce the level of total hemolytic complement, CH50, or of individual complement components, C1, C2, C3, and C5. However, sheep erythrocytes (SRC) coated with Agg-R/A-IgG or with reduced and alkylated rabbit IgG anti-SRC antibody were hemolyzed by complement in the presence of polyclonal IgM-RF. Human and guinea pig complement worked equally well. The degree of hemolysis was in direct proportion to the hemagglutination titer of the RF against the same coated cells. Monoclonal IgM-RF, normal human IgM, and purified Waldenstrom macroglobulins without antiglobulin activity were all inert. Hemolysis of coated SRC by RF and complement was inhibited by prior treatment of the complement source with chelating agents, hydrazine, cobra venom factor, specific antisera to C1q, CR, C5, C6, or C8, or by heating at 56 degrees C for 30 min. Purified radiolabeled C4, C3, and C8 included in the complement source were bound to hemolysed SRC in direct proportion to the degree of hemolysis. These data indicate that polyclonal IgM-RF fix and activate complement via the classic pathway. The system described for assessing complement fixation by isolated RF is readily adaptable to use with whole human serum. (+info)Cryofibrinogenaemia: a study of 49 patients. (7/235)
The purpose of this study was to characterize the clinical features and components of 30 patients with isolated cryofibrinogen (CF) versus those of 19 patients with combined CF and cryoglobulins (CG). Secondary forms of cryofibrinogenaemia associated with collagen disorders, infectious or malignant diseases, were significantly more frequent in patients with combined CF and CG than those with isolated CF (79 versus 47%, P = 0.02). Both groups of CF patients presented predominantly cutaneous symptoms (77% in isolated CF; 58% in combined CF + CG), and less frequently venous and/or arterial thrombosis (13% in isolated CF; 3% in combined CF + CG). Patients with idiopathic forms of CF, and particularly those without CG, suffered essentially from recurrent painful skin ulcers, mainly triggered by cold exposure. Patients with isolated CF had higher mean plasma concentrations of CF than those with combined CF + CG (1. 61 +/- 1.26 versus 0.82 +/- 1.18 g/l, respectively; P = 0.004), but there was no correlation between the CF plasma level and either the severity of symptoms or the sensitivity to cold. In patients with isolated CF, fibronectin was suggested (by precipitation analysis) to be a major component of the cryoprecipitate, whereas immunoglobulins were rarely present (in only three out of 30 patients). By contrast, in the majority of patients (78%) with combined CF and CG, the CF consisted mainly of immunoglobulins of the same class as those characterizing the associated CG. Analysis of the CG precipitate revealed the presence of fibronectin but not fibrinogen, alpha1-antitrypsin and alpha2-macroglobulin. In conclusion, isolated and combined cryofibrinogenaemia are associated with different clinical signs requiring different clinical management, but there is no evidence as yet for a causal role of the cryoprecipitates in the differences observed. (+info)Specific concentration of polynucleotide immune complexes in the cryoprecipitates of patients with systemic lupus erythematosus. (8/235)
Although the association of cryoglobulinemia with hypocomplementemia and tissue injury in systemic lupus erythematosus is well recognized, composition of cryoprecipitates in terms of circulating antigens and antibodies in this disease is less clear. To clarify this question, cryoprecipitates from patients with SLE were examined with sensitive assay techniques for certain antipolynucleotide antibodies and DNA antigen. DNA antibodies were highly enriched relative to serum levels in the majority of cryoprecipitates. DNA antigen was also demonstrable. Antibody to ribonucleoprotein, although less frequently present, was similarly enriched in certain cryoprecipitates. In contrast, anti-double strand RNA, which was commonly detectable in relatively high titer in serum, was only minimally concentrated in a minority of cryoprecipitates. Absorption experiments using red blood cells heavily coated with polynucleotide antigen indicated that a major proportion of the IgG in certain cryoprecipitates was specific antibody. The data strongly suggest that the cryoprecipitates in systemic lupus erythematosus represent circulating immune complexes that are soluble at 37 degrees C and come out of solution in the cold. The marked concentration of immune complexes in the cryoglobulin offers a simple and direct method for determination of the nature of the complexes. The accumulated evidence obtained in the present study indicates that these complexes closely reflect, in their composition, the circulating immune complexes which are most significant pathogenetically in renal tissue injury. (+info)The exact cause of cryoglobulinemia is not known, but it is believed to be related to an autoimmune disorder or a viral infection. Treatment options for the condition include medications to reduce inflammation and improve blood flow, as well as plasmapheresis, a process that removes abnormal proteins from the blood. In some cases, a bone marrow transplant may be recommended.
Cryoglobulinemia is a rare disease, and it can be difficult to diagnose, as the symptoms are similar to those of other conditions such as rheumatoid arthritis or lupus. However, if cryoglobulinemia is suspected, a doctor may perform a range of tests to confirm the diagnosis, including blood tests to look for the presence of cryoglobulins and imaging studies to examine the blood vessels.
Overall, cryoglobulinemia is a rare and complex condition that can have a significant impact on a person's quality of life. While there is no cure for the disease, with proper treatment, many people with cryoglobulinemia are able to manage their symptoms and lead active lives.
There are several types of paraproteinemias, including:
1. Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow, leading to an overproduction of immunoglobulins.
2. Monoclonal gammopathy of undetermined significance (MGUS): This is a condition in which there is an abnormal increase in the level of immunoglobulins in the blood, but the cause cannot be determined.
3. Waldenström macroglobulinemia: This is a rare type of cancer that affects the plasma cells in the bone marrow and leads to an overproduction of immunoglobulins.
4. Primary amyloidosis: This is a condition in which abnormal proteins called amyloids accumulate in the organs, leading to damage and dysfunction.
5. Secondary amyloidosis: This is a condition in which abnormal proteins called amyloids accumulate in the organs due to another underlying condition, such as rheumatoid arthritis or systemic lupus erythematosus.
The symptoms of paraproteinemias can vary depending on the type and severity of the disorder. Common symptoms include fatigue, weakness, weight loss, infections, kidney damage, and bone pain. Treatment options for paraproteinemias depend on the specific type of disorder and may include chemotherapy, radiation therapy, or medications to reduce protein production.
LCV typically presents with palpable purpura (raised, red or purple spots on the skin), papules, pustules, or nodules. The lesions may be itchy or painful and can appear anywhere on the body, but are most common on the lower extremities.
The exact cause of LCV is not known, but it is believed to be an autoimmune disorder triggered by infections, medications, or other stimuli. Treatment typically involves corticosteroids and immunosuppressive drugs, as well as addressing any underlying conditions that may be contributing to the disease.
The condition is often difficult to diagnose, as the symptoms can be similar to other skin conditions such as urticaria or eczema. A biopsy of the affected skin is usually necessary to confirm the diagnosis and rule out other possibilities.
Overall, LCV is a relatively uncommon but potentially serious condition that can cause significant discomfort and disfigurement if left untreated. It is important for patients to seek medical attention if they experience any symptoms consistent with the condition.
Idiopathic membranous nephropathy (IMN) is an autoimmune disorder that causes GNM without any identifiable cause. Secondary membranous nephropathy, on the other hand, is caused by systemic diseases such as lupus or cancer.
The symptoms of GNM can vary depending on the severity of the disease and may include blood in the urine, proteinuria, edema, high blood pressure, and decreased kidney function. The diagnosis of GNM is based on a combination of clinical findings, laboratory tests, and renal biopsy.
Treatment for GNM is aimed at slowing the progression of the disease and managing symptoms. Medications such as corticosteroids, immunosuppressive drugs, and blood pressure-lowering drugs may be used to treat GNM. In some cases, kidney transplantation may be necessary.
The prognosis for GNM varies depending on the severity of the disease and the underlying cause. In general, the prognosis for IMN is better than for secondary membranous nephropathy. With proper treatment, some patients with GNM can experience a slowing or stabilization of the disease, while others may progress to end-stage renal disease (ESRD).
The cause of GNM is not fully understood, but it is believed to be an autoimmune disorder that leads to inflammation and damage to the glomerular membrane. Genetic factors and environmental triggers may also play a role in the development of GNM.
There are several risk factors for developing GNM, including family history, age (GMN is more common in adults), and certain medical conditions such as hypertension and diabetes.
The main complications of GNM include:
1. ESRD: Progression to ESRD is a common outcome of untreated GNM.
2. High blood pressure: GNM can lead to high blood pressure, which can further damage the kidneys.
3. Infections: GNM increases the risk of infections due to impaired immune function.
4. Kidney failure: GNM can cause chronic kidney failure, leading to the need for dialysis or a kidney transplant.
5. Cardiovascular disease: GNM is associated with an increased risk of cardiovascular disease, including heart attack and stroke.
6. Malnutrition: GNM can lead to malnutrition due to decreased appetite, nausea, and vomiting.
7. Bone disease: GNM can cause bone disease, including osteoporosis and bone pain.
8. Anemia: GNM can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
9. Increased risk of infections: GNM increases the risk of infections due to impaired immune function.
10. Decreased quality of life: GNM can significantly decrease a person's quality of life, leading to decreased mobility, pain, and discomfort.
It is important for individuals with GNM to receive early diagnosis and appropriate treatment to prevent or delay the progression of these complications.
The symptoms of chronic hepatitis C may be mild or absent, but some people experience fatigue, joint pain, muscle aches, nausea, loss of appetite, and jaundice (yellowing of the skin and eyes).
Chronic hepatitis C is usually diagnosed through blood tests that detect the presence of antibodies against HCV or the virus itself. Imaging tests such as ultrasound and liver biopsy may also be performed to assess the extent of liver damage.
Treatment for chronic hepatitis C typically involves a combination of medications, including interferon and ribavirin, which can help clear the virus from the body. In severe cases, a liver transplant may be necessary. Prevention of the spread of HCV includes avoiding sharing of needles or other sharp objects, practicing safe sex, and getting tested for the virus before donating blood or organs.
See also: Hepatitis C; Liver; Virus
The disease is named after the Swedish physician Jan G. Waldenström, who first described it in 1944. It is also known as lymphoplasmacytic lymphoma or IgM multoculullarity.
The exact cause of Waldenström macroglobulinemia is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. The condition usually affects older adults and is more common in males than females.
Symptoms of Waldenström macroglobulinemia can include:
* Fatigue
* Weight loss
* Enlargement of the liver and spleen
* Swelling in the legs, ankles, and hands
* Pain in the bones or joints
* Increased risk of infections
* Numbness or tingling in the hands and feet
The diagnosis of Waldenström macroglobulinemia is based on a combination of physical examination, blood tests, and imaging studies. Treatment options include chemotherapy, immunomodulatory drugs, and stem cell transplantation. The prognosis for the disease varies depending on the severity of the symptoms and the response to treatment.
Overall, Waldenström macroglobulinemia is a rare and complex condition that requires careful management by a team of healthcare professionals. With appropriate treatment, many patients with this condition can experience long-term remission and improved quality of life.
Nephritis is often diagnosed through a combination of physical examination, medical history, and laboratory tests such as urinalysis and blood tests. Treatment for nephritis depends on the underlying cause, but may include antibiotics, corticosteroids, and immunosuppressive medications. In severe cases, dialysis may be necessary to remove waste products from the blood.
Some common types of nephritis include:
1. Acute pyelonephritis: This is a type of bacterial infection that affects the kidneys and can cause sudden and severe symptoms.
2. Chronic pyelonephritis: This is a type of inflammation that occurs over a longer period of time, often as a result of recurrent infections or other underlying conditions.
3. Lupus nephritis: This is a type of inflammation that occurs in people with systemic lupus erythematosus (SLE), an autoimmune disorder that can affect multiple organs.
4. IgA nephropathy: This is a type of inflammation that occurs when an antibody called immunoglobulin A (IgA) deposits in the kidneys and causes damage.
5. Mesangial proliferative glomerulonephritis: This is a type of inflammation that affects the mesangium, a layer of tissue in the kidney that helps to filter waste products from the blood.
6. Minimal change disease: This is a type of nephrotic syndrome (a group of symptoms that include proteinuria, or excess protein in the urine) that is caused by inflammation and changes in the glomeruli, the tiny blood vessels in the kidneys that filter waste products from the blood.
7. Membranous nephropathy: This is a type of inflammation that occurs when there is an abnormal buildup of antibodies called immunoglobulin G (IgG) in the glomeruli, leading to damage to the kidneys.
8. Focal segmental glomerulosclerosis: This is a type of inflammation that affects one or more segments of the glomeruli, leading to scarring and loss of function.
9. Post-infectious glomerulonephritis: This is a type of inflammation that occurs after an infection, such as streptococcal infections, and can cause damage to the kidneys.
10. Acute tubular necrosis (ATN): This is a type of inflammation that occurs when there is a sudden loss of blood flow to the kidneys, causing damage to the tubules, which are tiny tubes in the kidneys that help to filter waste products from the blood.
The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.
There are several subtypes of LES, including:
1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.
There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.
It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.
There are several types of hepatitis C, including genotype 1, which is the most common and accounts for approximately 70% of cases in the United States. Other genotypes include 2, 3, 4, 5, and 6. The symptoms of hepatitis C can range from mild to severe and may include fatigue, fever, loss of appetite, nausea, vomiting, joint pain, jaundice (yellowing of the skin and eyes), dark urine, pale stools, and itching all over the body. Some people with hepatitis C may not experience any symptoms at all.
Hepatitis C is diagnosed through a combination of blood tests that detect the presence of antibodies against HCV or the virus itself. Treatment typically involves a combination of medications, including interferon and ribavirin, which can cure the infection but may have side effects such as fatigue, nausea, and depression. In recent years, new drugs known as direct-acting antivirals (DAAs) have become available, which can cure the infection with fewer side effects and in a shorter period of time.
Prevention measures for hepatitis C include avoiding sharing needles or other drug paraphernalia, using condoms to prevent sexual transmission, and ensuring that any tattoos or piercings are performed with sterilized equipment. Vaccines are also available for people who are at high risk of contracting the virus, such as healthcare workers and individuals who engage in high-risk behaviors.
Overall, hepatitis C is a serious and common liver disease that can lead to significant health complications if left untreated. Fortunately, with advances in medical technology and treatment options, it is possible to manage and cure the virus with proper care and attention.
Cold sensitive antibodies
Cryoglobulinemia
Haemophilia
Cryoprecipitate
Waldenström macroglobulinemia
CD5L
Cryoglobulinemic vasculitis
Rheumatoid factor
Shunt nephritis
July 1964
Nephrotic syndrome
Edward C. Franklin
List of MeSH codes (D12.776)
List of MeSH codes (D12.776.124)
Systemic vasculitis
Plasma cell dyscrasias
Thrombocythemia
Cryoglobulins: MedlinePlus Medical Encyclopedia
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DeCSMonoclonal4
- Vasculitis is related to vessel obstruction by monoclonal cryoglobulin aggregates in type I cryoglobulins and immune complex deposition in type II and III mixed cryoglobulins. (nih.gov)
- Evidence of circulating monoclonal cryoglobulins in patients with primary Sjögren's syndrome. (nih.gov)
- The cryoglobulins were tested by immunofixation, which detected monoclonal IgM and polyclonal IgG with only traces of IgA (i.e. type II mixed cryoglobulinaemia) ( Figure 1 ). (who.int)
- Blood investigations showed elevated rheumatoid factor and mixed polyclonal IgG and monoclonal IgM cryoglobulins. (bvsalud.org)
Cryoglobulinemia3
- Cryoglobulins come in three main types, but in most cases the cause of having cryoglobulins is hepatitis C . The disease in which cryoglobulins are found is called cryoglobulinemia . (medlineplus.gov)
- Cryoglobulins are associated with cryoglobulinemia. (medlineplus.gov)
- In patients with cryoglobulinemia associated with a lymphoproliferative disorder, treatment should focus on the underlying hematologic malignancy that is producing the cryoglobulin. (nephronpower.com)
Antibodies2
- Cryoglobulins are antibodies that become solid or gel-like at low temperatures in the laboratory. (medlineplus.gov)
- Serology for antineutrophil cytoplasmic antibodies, cryoglobulins, hepatitis and HIV was negative, as was serum protein electrophoresis. (clevelandclinic.org)
Immune complex deposition1
- The pathogenesis of cryoglobulin-induced injury involves two main mechanisms, hyperviscosity and immune complex deposition, that activate complement and induce vascular inflammation. (nephronpower.com)
Vasculitis1
- Cryoglobulins can cause inflammation in blood vessels, called vasculitis. (medlineplus.gov)
Clinical imp1
- Cryoglobulins - clinical imp. (rrml.ro)
Rheumatoid1
- In the laboratory record of his blood and those of others, the C-reactive protein, rheumatoid facror, anti-nuclear antibody, cryoglobulin and other blood chemistries were all negative except that the anti-streptolysin O titer was reactive and alkaline phosphatase was also increased. (koreamed.org)
Peripheral3
- This phenomenon is favored by low temperature, especially in skin, joints, and peripheral nerves, or increased cryoglobulin concentration in kidneys. (nih.gov)
- Here, we present the typical hemogram and peripheral smear findings of circulating cryoglobulins that led to the unraveling of the underlying lymphoproliferative disorder. (who.int)
- Karthika KV, Tripathi P, Pati H, Saxena R. A Peripheral Smear Finding Beyond Cells: Cryoglobulins in a Case of Lymphoplasmacytic Lymphoma. (who.int)
Complement1
- Serum cryoglobulin and complement assays may be useful. (medscape.com)
Laboratory2
- In the laboratory, cryoglobulins come out of solution in blood when the blood sample is cooled below 98.6°F (37°C). They dissolve again when the sample is warmed up. (medlineplus.gov)
- Cryoglobulins can thus cause a range of laboratory artefacts which need to be recognized, warranting further search for possible underlying etiologies. (who.int)
Arthritis1
- 1. [Cryoglobulins in arthritis]. (nih.gov)
Temperature1
- Because they are temperature sensitive, cryoglobulins are hard to accurately measure. (medlineplus.gov)
Symptoms1
- This test is most often done when a person has symptoms of a condition associated with cryoglobulins. (medlineplus.gov)
Patients1
- On EM, cryoglobulins may appear as paired, curved microtubules with a diameter of 20-30 nm), although it should be noted that this feature is observed in only a subset of patients. (nephronpower.com)
Found1
- We then analysed the IgG component of the cryoglobulins and found it to be almost entirely composed of anti-adult worm antigen (AWA) Schistosoma spp. (who.int)
Cold1
- Cryoglobulins are immunoglobulins precipitating in cold condition. (nih.gov)
Disease1
- Cryoglobulin characterization and quantification are important to identify the underlying disease. (nih.gov)
Immunoglobulins2
- Cryoglobulins are immunoglobulins precipitating in cold condition. (nih.gov)
- Cryoglobulins are single or mixed immunoglobulins that undergo reversible precipitation at low temperatures and that arise from B-cell lymphoproliferative disorders. (medscape.com)
Serum2
- Testing his serum for hepatitis C viral mRNA by PCR would be unrevealing because any hepatitis C virus that was consumed within the cryoglobulin would be contained within the clot and not within the serum. (medscape.com)
- [ 1 ] Serum cryoglobulins in most individuals are in low concentrations (100-300 mg/L) among the high concentrations (60,000-80,000 mg/L) of normal serum proteins. (medscape.com)
Hepatitis3
- This decision was based on a 1992 New England Journal of Medicine [ 1 ] article by Vincent Agnello and colleagues, who showed that the hepatitis C virus is concentrated 1000-fold within the cryoglobulin compared with the plasma. (medscape.com)
- We had the team obtain cryoglobulin, which was then prepared, washed, and sent to another laboratory for PCR testing to determine whether the cryoglobulin itself contained hepatitis C virus. (medscape.com)
- Presumably, because hepatitis C virus is a polyclonal activator of B cells, this virus is driving the patient's cryoglobulin production and, hence, its clinical manifestations. (medscape.com)
Immune1
- Following precipitation after exposure to lower temperatures, cryoglobulin-containing immune complexes form and trigger a systemic inflammatory response. (medscape.com)
Concentration1
- This phenomenon is favored by low temperature, especially in skin, joints, and peripheral nerves, or increased cryoglobulin concentration in kidneys. (nih.gov)
Type1
- At baseline, one patient was negative and two were positive for mixed-type cryoglobulins. (nih.gov)
Plasma1
- Las formas presentes en el plasma se ldenominan globulinas insolubles en frío. (bvsalud.org)
Important1
- Cryocrit is an important parameter used to quantify cryoglobulins. (medscape.com)
