Complement Activation
Complement C3
Complement System Proteins
Complement C4
Complement C5
Receptors, Complement
Complement C3b
Complement C1q
Complement Pathway, Alternative
Complement C9
Complement Pathway, Classical
Complement Membrane Attack Complex
Complement Inactivator Proteins
Complement C2
Complement Factor B
Complement Factor H
Complement Inactivating Agents
Complement C3a
Complement C5a
Complement C6
Receptors, Complement 3b
Complement C1
Complement C4b
Complement Activating Enzymes
Complement C3d
Complement C3-C5 Convertases
Complement Fixation Tests
Complement C7
Complement C8
Complement C3c
Receptors, Complement 3d
Complement Hemolytic Activity Assay
Complement C3b Inactivator Proteins
Complement C4a
Complement Factor D
Complement Factor I
Complement C4b-Binding Protein
Complement C1s
Complement C1r
Antigens, CD55
Antigens, CD59
Complement C1 Inactivator Proteins
Complement C5b
Complement Pathway, Mannose-Binding Lectin
Properdin
Cobra Venoms
Hemolysis
Complement C1 Inhibitor Protein
Anaphylatoxins
Complement C3 Convertase, Alternative Pathway
Antigens, CD46
Receptor, Anaphylatoxin C5a
Genetic Complementation Test
Antigen-Antibody Complex
Opsonin Proteins
Immunoglobulin G
Molecular Sequence Data
Phagocytosis
Blood Bactericidal Activity
Mannose-Binding Lectin
Amino Acid Sequence
Macrophage-1 Antigen
Erythrocytes
Mannose-Binding Protein-Associated Serine Proteases
Immunoglobulin M
Complement C5a, des-Arginine
Neutrophils
Protein Binding
Base Sequence
Mutation
Antibodies
Rabbits
Collectins
Macular Degeneration
Cloning, Molecular
Blood Proteins
Guinea Pigs
Immune Adherence Reaction
Enzyme-Linked Immunosorbent Assay
Escherichia coli
Immunoelectrophoresis
Fluorescent Antibody Technique
Glomerulonephritis
Hemoglobinuria, Paroxysmal
Immune Complex Diseases
Immunoglobulins
Cells, Cultured
Lupus Erythematosus, Systemic
Immunodiffusion
Binding Sites
Complement C2b
Cryoglobulins
Lectins
Mice, Knockout
Sequence Homology, Amino Acid
Immunity, Innate
Sheep
Cytotoxicity, Immunologic
Macrophages
Antigen-Antibody Reactions
Dose-Response Relationship, Immunologic
Species Specificity
Electrophoresis, Polyacrylamide Gel
Autoantibodies
Binding Sites, Antibody
Disease Models, Animal
Glycoproteins
Kidney Glomerulus
Serum
Rosette Formation
Phenotype
Peptide Fragments
RNA, Messenger
Protein Structure, Tertiary
Glomerulonephritis, Membranoproliferative
Antigens, CD
Antibody-Dependent Cell Cytotoxicity
gamma-Globulins
Complement C3 Convertase, Classical Pathway
Antigens, Surface
Cricetinae
Surface Plasmon Resonance
Flow Cytometry
Immunoglobulin Fc Fragments
Membrane Proteins
Carrier Proteins
Arthus Reaction
Sequence Alignment
Antibody Specificity
Plasmids
B-Lymphocytes
Monocytes
Saccharomyces cerevisiae
Edetic Acid
Receptors, IgG
Inflammation
Angioedema
Bacterial Outer Membrane Proteins
Lipopolysaccharides
DNA
Receptors, Fc
Cell Membrane
Antibody Formation
Models, Molecular
Leukocytes
Neutralization Tests
Blotting, Western
T-Lymphocytes
Microscopy, Electron
CHO Cells
Integrin alphaXbeta2
Clusterin
Serum Globulins
Streptococcus pneumoniae
Erythrocyte Membrane
Gene Expression Regulation
Gene Deletion
Sequence Analysis, DNA
Histocompatibility Antigens
Immunoglobulin A
Mice, Inbred Strains
Recombinant Fusion Proteins
Neisseria meningitidis
Immunization, Passive
Reperfusion Injury
Hemagglutination Tests
Chromium Isotopes
Immunohistochemistry
Kidney
Protein Conformation
Serine Endopeptidases
Chemotaxis, Leukocyte
Temperature
Snake Venoms
Rheumatoid Factor
Isoantibodies
Complement activity and pharmacological inhibition in cardiovascular disease. (1/54)
While complement is the most important component of humoral autoimmunity, and inflammation plays a key role in atherosclerosis, relatively few studies have looked at complement implications in atherosclerosis and its complications. C-reactive protein is a marker of inflammation and is also involved in atherosclerosis; it activates complement and colocalizes with activated complement proteins within the infarcting myocardium and the active atherosclerotic plaques. As new agents capable of modulating complement activity are being developed, new targets for the management of atherosclerosis are emerging that are related to autoimmunity and inflammation. The present paper reviews the putative roles of the various complement activation pathways in the development of atherosclerosis, in ST segment elevation and non-ST segment elevation acute coronary syndromes, and in coronary artery bypass graft surgery. It also provides a perspective on new therapeutic interventions being developed to modulate complement activity. These interventions include the C1 esterase inhibitor, which may be consumed in some inflammatory states resulting in the loss of one of the mechanisms inhibiting activation of the classical and lectin pathways; TP10, a recombinant protein of the soluble complement receptor type 1 (sCR1) which inhibits the C3 and C5 convertases of the common pathway by binding C3b and C4b; a truncated version of the soluble complement receptor type 1 CRI lacking the C4b binding site which selectively inhibits the alternative pathway; and pexelizumab, a monoclonal antibody selectively blocking C5 to prevent the activation of the terminal pathway that is involved in excessive inflammation and autoimmune responses. (+info)Therapeutic strategy with a membrane-localizing complement regulator to increase the number of usable donor organs after prolonged cold storage. (2/54)
A shortage of donor organs and increasing dependence on marginal grafts with prolonged ischemic times have meant that new methods are needed to prevent postischemic damage. Herein is reported a new strategy aimed to protect donor kidney from complement-mediated postischemic damage and therefore increase the number of successful transplants. Rat donor kidneys were perfused with a membrane-localizing complement regulator derived from human complement receptor type 1 (APT070) and then subjected to prolonged periods of cold storage (at 4 degrees C). A relationship was found between the duration of cold ischemia and the extent of complement-mediated tubule damage and loss of graft function. After 16 h of cold storage, APT070-treated kidneys that were transplanted into syngeneic recipients showed a significant increase in the number of surviving grafts, compared with control-treated grafts (63.6 versus 26.3%). Surviving grafts also displayed less acute tubular injury and better preservation of renal function. These results not only enhance the understanding of the mechanism by which prolonged cold ischemia reduces immediate graft survival but also provide essential information about the effectiveness of membrane-localizing complement regulator with prolonged cold storage. This could lead to more effective strategies for improving the use of severely ischemic donor organs. (+info)Relapsing fever spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H. (3/54)
Relapsing fever is a rapidly progressive and severe septic disease caused by certain Borrelia spirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused by Borrelia recurrentis and transmitted by lice, and the endemic form, caused by several Borrelia species, such as B. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that the Borrelia organisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogen B. recurrentis and an endemic relapsing fever pathogen, B. duttonii, are serum resistant, i.e., resistant to complement in vitro. They acquire the host alternative complement pathway regulator factor H on their surfaces in a similar way to that of the less serum-resistant Lyme disease pathogen, B. burgdorferi sensu stricto. More importantly, the relapsing fever spirochetes specifically bind host C4b-binding protein, a major regulator of the antibody-mediated classical complement pathway. Both complement regulators retained their functional activities when bound to the surfaces of the spirochetes. In conclusion, this is the first report of complement evasion by Borrelia recurrentis and B. duttonii and the first report showing capture of C4b-binding protein by spirochetes. (+info)A novel inhibitor of the alternative pathway of complement reverses inflammation and bone destruction in experimental arthritis. (4/54)
Complement is an important component of the innate and adaptive immune response, yet complement split products generated through activation of each of the three complement pathways (classical, alternative, and lectin) can cause inflammation and tissue destruction. Previous studies have shown that complement activation through the alternative, but not classical, pathway is required to initiate antibody-induced arthritis in mice, but it is unclear if the alternative pathway (AP) plays a role in established disease. Previously, we have shown that human complement receptor of the immunoglobulin superfamily (CRIg) is a selective inhibitor of the AP of complement. Here, we present the crystal structure of murine CRIg and, using mutants, provide evidence that the structural requirements for inhibition of the AP are conserved in human and mouse. A soluble form of CRIg reversed inflammation and bone loss in two experimental models of arthritis by inhibiting the AP of complement in the joint. Our data indicate that the AP of complement is not only required for disease induction, but also disease progression. The extracellular domain of CRIg thus provides a novel tool to study the effects of inhibiting the AP of complement in established disease and constitutes a promising therapeutic with selectivity for a single complement pathway. (+info)Characterization of Ehp, a secreted complement inhibitory protein from Staphylococcus aureus. (5/54)
We report here the discovery and characterization of Ehp, a new secreted Staphylococcus aureus protein that potently inhibits the alternative complement activation pathway. Ehp was identified through a genomic scan as an uncharacterized secreted protein from S. aureus, and immunoblotting of conditioned S. aureus culture medium revealed that the Ehp protein was secreted at the highest levels during log-phase bacterial growth. The mature Ehp polypeptide is composed of 80 residues and is 44% identical to the complement inhibitory domain of S. aureus Efb (extracellular fibrinogen-binding protein). We observed preferential binding by Ehp to native and hydrolyzed C3 relative to fully active C3b and found that Ehp formed a subnanomolar affinity complex with these various forms of C3 by binding to its thioester-containing C3d domain. Site-directed mutagenesis demonstrated that Arg(75) and Asn(82) are important in forming the Ehp.C3d complex, but loss of these side chains did not completely disrupt Ehp/C3d binding. This suggested the presence of a second C3d-binding site in Ehp, which was mapped to the proximity of Ehp Asn(63). Further molecular level details of the Ehp/C3d interaction were revealed by solving the 2.7-A crystal structure of an Ehp.C3d complex in which the low affinity site had been mutationally inactivated. Ehp potently inhibited C3b deposition onto sensitized surfaces by the alternative complement activation pathway. This inhibition was directly related to Ehp/C3d binding and was more potent than that seen for Efb-C. An altered conformation in Ehp-bound C3 was detected by monoclonal antibody C3-9, which is specific for a neoantigen exposed in activated forms of C3. Our results suggest that increased inhibitory potency of Ehp relative to Efb-C is derived from the second C3-binding site in this new protein. (+info)Effect of the complement inhibitor eculizumab on thromboembolism in patients with paroxysmal nocturnal hemoglobinuria. (6/54)
Hemolysis and hemoglobinemia contribute to serious clinical sequelae in hemolytic disorders. In paroxysmal nocturnal hemoglobinuria (PNH) patients, hemolysis can contribute to thromboembolism (TE), the most feared complication in PNH, and the leading cause of disease-related deaths. We evaluated whether long-term treatment with the complement inhibitor eculizumab reduces the rate of TE in patients with PNH. Clinical trial participants included all patients in the 3 eculizumab PNH clinical studies, which recruited patients between 2002 and 2005 (n = 195); patients from these studies continued treatment in the current multinational open-label extension study. Thromboembolism rate with eculizumab treatment was compared with the pretreatment rate in the same patients. The TE event rate with eculizumab treatment was 1.07 events/100 patient-years compared with 7.37 events/100 patient-years (P < .001) prior to eculizumab treatment (relative reduction, 85%; absolute reduction, 6.3 TE events/100 patient-years). With equalization of the duration of exposure before and during treatment for each patient, TE events were reduced from 39 events before eculizumab to 3 events during eculizumab (P < .001). The TE event rate in antithrombotic-treated patients (n = 103) was reduced from 10.61 to 0.62 events/100 patient-years with eculizumab treatment (P < .001). These results show that eculizumab treatment reduces the risk of clinical thromboembolism in patients with PNH. This study is registered at http://clinicaltrials.gov (study ID no. NCT00122317). (+info)Management of hereditary angioedema in pediatric patients. (7/54)
Hereditary angioneurotic edema is a rare disorder caused by the congenital deficiency of C1 inhibitor. Recurring angioedematous paroxysms that most commonly involve the subcutis (eg, extremities, face, trunk, and genitals) or the submucosa (eg, intestines and larynx) are the hallmarks of hereditary angioneurotic edema. Edema formation is related to reduction or dysfunction of C1 inhibitor, and conventional therapy with antihistamines and corticosteroids is ineffective. Manifestations occur during the initial 2 decades of life, but even today there is a long delay between the onset of initial symptoms and the diagnosis of hereditary angioneurotic edema. Although a variety of reviews have been published during the last 3 decades on the general management of hereditary angioneurotic edema, little has been published regarding management of pediatric hereditary angioneurotic edema. Thus, we review our experience and published data to provide an approach to hereditary angioneurotic edema in childhood. (+info)Association of reactive oxygen and nitrogen intermediate and complement levels with apoptosis of peripheral blood mononuclear cells in lupus patients. (8/54)
OBJECTIVE: Both increased production of reactive oxygen and nitrogen intermediates (RONI) and reduced levels of complement may play a role in the increased apoptosis and reduced clearance of apoptotic cells in systemic lupus erythematosus (SLE). The objective of this study was to evaluate both processes in a parallel, prospective, longitudinal manner. METHODS: Sixty-seven SLE patients were evaluated during multiple visits, and 31 healthy control subjects were evaluated once or twice. Clinical and laboratory features of SLE disease activity were determined, and blood was collected for measurement of serum nitrate plus nitrite (NOx) levels and for isolation of peripheral blood mononuclear cells (PBMCs). PBMCs were cultured with a nitric oxide (NO) donor and SLE or control plasma, with or without heat inactivation, cobra venom factor (CVF), or lipopolysaccharide plus interferon-gamma treatment. Cells were analyzed for apoptotic index (AI), cellular subsets, and RONI production. RESULTS: The PBMC AI was associated with SLE and was inversely associated with complement levels over time. Changes in the AI with addition of a NO donor was longitudinally associated with serum NOx levels, and stimulation of SLE PBMCs led to parallel increases in RONI production and apoptosis. Addition of SLE plasma resulted in a greater PBMC AI, an effect that was increased with heat inactivation and was corrected with CVF treatment. CONCLUSION: These data suggest that the greater AI observed in SLE PBMCs relates to increased PBMC RONI production and reduced complement levels. The longitudinal nature of these parallel associations within individuals suggests that these processes are dynamic and additive. (+info)There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
There are two main types of MD:
1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.
The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:
* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision
MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.
There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:
* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.
It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.
The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:
* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure
Glomerulonephritis can be caused by a variety of factors, including:
* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia
The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.
Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:
* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases
The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.
The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.
HP is classified into two types based on the severity of symptoms:
1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.
There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.
The term "immune complex disease" was first used in the 1960s to describe a group of conditions that were thought to be caused by the formation of immune complexes. These diseases include:
1. Systemic lupus erythematosus (SLE): an autoimmune disorder that can affect multiple organ systems and is characterized by the presence of anti-nuclear antibodies.
2. Rheumatoid arthritis (RA): an autoimmune disease that causes inflammation in the joints and can lead to joint damage.
3. Type III hypersensitivity reaction: a condition in which immune complexes are deposited in tissues, leading to inflammation and tissue damage.
4. Pemphigus: a group of autoimmune diseases that affect the skin and mucous membranes, characterized by the presence of autoantibodies against desmosomal antigens.
5. Bullous pemphigoid: an autoimmune disease that affects the skin and is characterized by the formation of large blisters.
6. Myasthenia gravis: an autoimmune disorder that affects the nervous system, causing muscle weakness and fatigue.
7. Goodpasture's syndrome: a rare autoimmune disease that affects the kidneys and lungs, characterized by the presence of immune complexes in the glomeruli of the kidneys.
8. Hemolytic uremic syndrome (HUS): a condition in which red blood cells are destroyed and waste products accumulate in the kidneys, leading to kidney failure.
Immune complex diseases can be caused by various factors, including genetic predisposition, environmental triggers, and exposure to certain drugs or toxins. Treatment options for these diseases include medications that suppress the immune system, such as corticosteroids and immunosuppressive drugs, and plasmapheresis, which is a process that removes harmful antibodies from the blood. In some cases, organ transplantation may be necessary.
In conclusion, immune complex diseases are a group of disorders that occur when the body's immune system mistakenly attacks its own tissues and organs, leading to inflammation and damage. These diseases can affect various parts of the body, including the skin, kidneys, lungs, and nervous system. Treatment options vary depending on the specific disease and its severity, but may include medications that suppress the immune system and plasmapheresis.
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.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
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 Arthus reaction is named after French physician Louis-Jean-Baptiste Arthus, who first described the phenomenon in 1890. It is commonly seen in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and other autoimmune disorders.
The reaction occurs when antibodies bind to antigens, such as proteins or cells, on the surface of tissues. The binding of antibodies to antigens can activate complement proteins, which are a group of proteins that work together to destroy pathogens. In the case of the Arthus reaction, the activation of complement proteins leads to the formation of a membrane attack complex (MAC), which is composed of various proteins and can cause damage to tissues.
The Arthus reaction can cause a range of symptoms, including joint pain, swelling, and warmth, as well as fever and fatigue. In severe cases, it can lead to permanent joint damage and disability. Treatment options for the Arthus reaction include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive medications.
In summary, the Arthus reaction is an allergic response that occurs when antibodies bind to antigens and form immune complexes, leading to inflammation and tissue damage. It is commonly seen in autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and can cause a range of symptoms including joint pain and swelling, fever, and fatigue. Treatment options include NSAIDs, corticosteroids, and immunosuppressive medications.
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.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
Acute angioedema is usually triggered by an allergic reaction or exposure to certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), blood pressure medications, or antibiotics. It can also be caused by infections, insect bites, and other environmental triggers.
Chronic angioedema, on the other hand, is a more persistent form of the condition that can last for weeks, months, or even years. It is often associated with conditions such as hereditary angioedema (HAE), which is caused by a genetic defect that affects the production of a protein called C1 esterase inhibitor.
The symptoms of angioedema can vary depending on the location and severity of the swelling, but they typically include:
* Swelling in the face, hands, feet, or other parts of the body
* Redness and warmth of the affected area
* Pain or discomfort
* Difficulty breathing or swallowing (in severe cases)
There is no cure for angioedema, but there are several treatments available to help manage the symptoms. These may include:
* Antihistamines or corticosteroids to reduce inflammation and relieve itching
* Ice packs or cool compresses to reduce swelling
* Compression stockings or bandages to prevent fluid buildup
* Pain relief medications, such as ibuprofen or acetaminophen, to manage discomfort
In severe cases of angioedema, hospitalization may be necessary to provide more intensive treatment and monitoring. In some cases, injectable medications such as epinephrine or corticosteroids may be administered to help reduce swelling and prevent complications.
Overall, angioedema is a serious condition that requires prompt medical attention to manage symptoms and prevent complications. If you suspect you or someone else may have angioedema, it is important to seek medical help right away.
The most common form of this disease is Meningococcal Group B (MenB). Symptoms often develop within hours or days after exposure, but can be nonspecific, such as fever, headache, and muscle aches.
Early signs that are more specific and suggestive of the diagnosis include neck stiffness, confusion, seizures, and rash. Diagnosis is by culture or PCR of a sterile site. Treatment consists of antibiotics that cover Neisseria meningitidis, which should be initiated promptly after recognition of the signs and symptoms.
Prevention with vaccines is recommended for infants at 2 months of age; boosters are given at 4 months, 6 months, and 12 to 15 months of age.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
The two main types of TMAs are:
1. Thrombotic thrombocytopenic purpura (TTP): This is a rare autoimmune disorder caused by the formation of antibodies against ADAMTS13, an enzyme involved in platelet function. TTP patients have low levels of ADAMTS13 and abnormal platelets that are prone to clotting.
2. Hemolytic uremic syndrome (HUS): This is a condition that occurs when red blood cells are destroyed and removed from the circulation, leading to anemia, low platelet count, and kidney failure. HUS can be caused by various factors, such as infections, certain medications, or genetic mutations.
Both TTP and HUS can lead to TMAs, which can cause severe morbidity and mortality if left untreated. Treatment options for TMAs include plasmapheresis, corticosteroids, and immunosuppressive drugs, as well as dialysis in cases of acute kidney injury. Early diagnosis and aggressive treatment are essential to prevent long-term complications and improve patient outcomes.
Here are some key points to define sepsis:
1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.
Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.
Examples of Immunologic Deficiency Syndromes include:
1. Primary Immunodeficiency Diseases (PIDDs): These are a group of genetic disorders that affect the immune system's ability to function properly. Examples include X-linked agammaglobulinemia, common variable immunodeficiency, and severe combined immunodeficiency.
2. Acquired Immunodeficiency Syndrome (AIDS): This is a condition that results from the human immunodeficiency virus (HIV) infection, which destroys CD4 cells, a type of immune cell that fights off infections.
3. Immune Thrombocytopenic Purpura (ITP): This is an autoimmune disorder that causes the immune system to attack and destroy platelets, which are blood cells that help the blood to clot.
4. Autoimmune Disorders: These are conditions in which the immune system mistakenly attacks and damages healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, and multiple sclerosis.
5. Immunosuppressive Therapy-induced Immunodeficiency: This is a condition that occurs as a side effect of medications used to prevent rejection in organ transplant patients. These medications can suppress the immune system, increasing the risk of infections.
Symptoms of Immunologic Deficiency Syndromes can vary depending on the specific disorder and the severity of the immune system dysfunction. Common symptoms include recurrent infections, fatigue, fever, and swollen lymph nodes. Treatment options for these syndromes range from medications to suppress the immune system to surgery or bone marrow transplantation.
In summary, Immunologic Deficiency Syndromes are a group of disorders that result from dysfunction of the immune system, leading to recurrent infections and other symptoms. There are many different types of these syndromes, each with its own set of symptoms and treatment options.
The term "serum sickness" was first used in the late 19th century to describe this condition, which was often seen in people who had received serum (a type of blood product) containing antibodies against diseases such as diphtheria or tetanus. Today, the term is still used to describe similar reactions to other substances, including medications and vaccines.
Serum sickness can be mild or severe, and in rare cases, it can lead to serious complications such as kidney failure or inflammation of the heart. Treatment typically involves stopping the use of the offending substance and providing supportive care to manage symptoms. In severe cases, corticosteroids or other medications may be used to reduce inflammation.
While serum sickness is a relatively rare condition, it is important for healthcare providers to be aware of it as a potential complication of medication and vaccine use. This knowledge can help them recognize and manage the condition effectively, reducing the risk of serious complications and improving outcomes for patients.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
1. Autoimmune diseases: These occur when the immune system mistakenly attacks healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, multiple sclerosis, and type 1 diabetes.
2. Allergies: An allergic reaction occurs when the immune system overreacts to a harmless substance, such as pollen, dust mites, or certain foods. Symptoms can range from mild hives to life-threatening anaphylaxis.
3. Immunodeficiency disorders: These are conditions that impair the immune system's ability to fight infections. Examples include HIV/AIDS and primary immunodeficiency diseases.
4. Infectious diseases: Certain infections, such as tuberculosis or bacterial meningitis, can cause immune system dysfunction.
5. Cancer: Some types of cancer, such as lymphoma, affect the immune system's ability to fight disease.
6. Immune thrombocytopenic purpura (ITP): This is a rare autoimmune disorder that causes the immune system to attack and destroy platelets, leading to bleeding and bruising.
7. Guillain-Barré syndrome: This is a rare autoimmune disorder that occurs when the immune system attacks the nerves, leading to muscle weakness and paralysis.
8. Chronic fatigue syndrome (CFS): This is a condition characterized by persistent fatigue, muscle pain, and joint pain, which is thought to be related to an immune system imbalance.
9. Fibromyalgia: This is a chronic condition characterized by widespread muscle pain, fatigue, and sleep disturbances, which may be linked to immune system dysfunction.
10. Autoimmune hepatitis: This is a condition in which the immune system attacks the liver, leading to inflammation and damage to the liver cells.
It's important to note that a weakened immune system can increase the risk of infections and other health problems, so it's important to work with your healthcare provider to identify any underlying causes and develop an appropriate treatment plan.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
Examples of autoimmune diseases include:
1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.
The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.
Membranous nephropathy is a specific type of glomerulonephritis that is characterized by the deposition of immune complexes in the glomerular basement membrane. This leads to inflammation and damage to the glomeruli, which can progress to end-stage renal disease if left untreated.
The exact cause of membranous nephropathy is not fully understood, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissue in the kidneys. Factors such as genetics, environmental triggers, and certain medical conditions may contribute to the development of the disease.
Symptoms of membranous nephropathy can include proteinuria, hematuria, high blood pressure, swelling, fatigue, and weight loss. The disease is typically diagnosed through a combination of physical examination, laboratory tests, and kidney biopsy.
Treatment for membranous nephropathy typically involves a combination of medications to control proteinuria, hematuria, and high blood pressure, as well as immunosuppressive drugs to suppress the immune system and prevent further damage to the kidneys. In severe cases, dialysis or kidney transplantation may be necessary.
People with agammaglobulinemia are more susceptible to infections, particularly those caused by encapsulated bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae type b. They may also experience recurrent sinopulmonary infections, ear infections, and gastrointestinal infections. The disorder can be managed with intravenous immunoglobulin (IVIG) therapy, which provides antibodies to help prevent infections. In severe cases, a bone marrow transplant may be necessary.
Agammaglobulinemia is an autosomal recessive disorder, meaning that a person must inherit two mutated copies of the BTK gene (one from each parent) to develop the condition. It is relatively rare, affecting approximately one in 1 million people worldwide. The disorder can be diagnosed through genetic testing and a complete blood count (CBC) that shows low levels of immunoglobulins.
Treatment for ag
There are two forms of trypanosomiasis, depending on the stage of the parasite:
1. Acute trypanosomiasis: This form of the disease occurs in the early stages of infection and is characterized by fever, headache, muscle pain, and joint swelling.
2. Chronic trypanosomiasis: This form of the disease occurs in the later stages of infection and is characterized by progressive neurological symptoms, including confusion, slurred speech, and difficulty walking.
If left untreated, trypanosomiasis can be fatal. Treatment typically involves the use of antiparasitic drugs, such as melarsoprol or eflornithine.
In addition to its medical significance, trypanosomiasis has also had significant social and economic impacts on affected communities, particularly in rural areas where the disease is more common. The stigma associated with the disease can lead to social isolation and marginalization of infected individuals and their families, while the financial burden of treatment can be a significant source of poverty.
Overall, trypanosomiasis is a serious and potentially deadly disease that requires prompt diagnosis and treatment to prevent complications and improve outcomes for affected individuals.
Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.
The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.
Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.
Examples of diseases with a known genetic predisposition:
1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.
Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."
Types of Pneumococcal Infections:
1. Pneumonia: This is an infection of the lungs that can cause fever, cough, chest pain, and difficulty breathing.
2. Meningitis: This is an infection of the membranes that cover the brain and spinal cord, which can cause fever, headache, stiff neck, and confusion.
3. Septicemia (bloodstream infection): This is an infection of the blood that can cause fever, chills, and low blood pressure.
4. Sinusitis: This is an infection of the sinuses, which can cause headache, facial pain, and difficulty breathing through the nose.
5. Otitis media (middle ear infection): This is an infection of the middle ear, which can cause ear pain, fever, and hearing loss.
Causes and Risk Factors:
Pneumococcal infections are caused by the bacteria Streptococcus pneumoniae. These bacteria can be spread through close contact with an infected person, such as touching or sharing food and drinks. People who are at high risk for developing pneumococcal infections include:
1. Children under the age of 5 and adults over the age of 65.
2. People with weakened immune systems, such as those with cancer, HIV/AIDS, or taking medications that suppress the immune system.
3. Smokers and people with chronic respiratory diseases, such as asthma or chronic obstructive pulmonary disease (COPD).
4. People who have recently had surgery or have a severe injury.
5. Those who live in long-term care facilities or have limited access to healthcare.
Prevention and Treatment:
Preventing pneumococcal infections is important, especially for high-risk individuals. Here are some ways to prevent and treat pneumococcal infections:
1. Vaccination: The pneumococcal conjugate vaccine (PCV) is recommended for children under the age of 5 and adults over the age of 65, as well as for people with certain medical conditions.
2. Hand washing: Frequent hand washing can help prevent the spread of pneumococcal bacteria.
3. Good hygiene: Avoiding close contact with people who are sick and regularly cleaning surfaces that may be contaminated with bacteria can also help prevent infection.
4. Antibiotics: Pneumococcal infections can be treated with antibiotics, but overuse of antibiotics can lead to the development of antibiotic-resistant bacteria. Therefore, antibiotics should only be used when necessary and under the guidance of a healthcare professional.
5. Supportive care: Those with severe pneumococcal infections may require hospitalization and supportive care, such as oxygen therapy or mechanical ventilation.
Conclusion:
Pneumococcal infections can be serious and even life-threatening, especially for high-risk individuals. Prevention and prompt treatment are key to reducing the risk of complications and improving outcomes. Vaccination, good hygiene practices, and appropriate antibiotic use are all important in preventing and treating pneumococcal infections. If you suspect that you or a loved one has a pneumococcal infection, it is essential to seek medical attention right away. With proper care and support, many people with pneumococcal infections can recover fully and resume their normal lives.
Symptoms of meningococcal meningitis typically develop within 3-7 days after exposure and may include fever, headache, stiff neck, confusion, nausea and vomiting, sensitivity to light, and seizures. In severe cases, the infection can lead to shock, organ failure, and death within hours of the onset of symptoms.
Diagnosis is typically made by a combination of physical examination, laboratory tests (such as blood cultures and PCR), and imaging studies (such as CT or MRI scans). Treatment typically involves antibiotics, intravenous fluids, and supportive care to manage fever, pain, and other symptoms. In severe cases, hospitalization in an intensive care unit may be necessary.
Prevention of meningococcal meningitis includes the use of vaccines, good hygiene practices (such as frequent handwashing), and avoidance of close contact with people who are sick. A vaccine is available for children and teens, and some colleges and universities require students to be vaccinated before moving into dorms.
Early diagnosis and treatment are crucial in preventing long-term complications and reducing the risk of death from meningococcal meningitis. If you suspect that you or someone else may have meningococcal meningitis, it is important to seek medical attention immediately.
Once infected, humans can experience a range of symptoms including fever, headache, muscle pain, and fatigue. In severe cases, the infection can spread to the bones and joints, causing swelling and pain. Brucellosis can also lead to complications such as endocarditis (inflammation of the heart valves) and meningitis (inflammation of the lining around the brain and spinal cord).
Brucellosis in cows is typically diagnosed through a combination of physical examination, laboratory tests, and blood samples. Treatment typically involves antibiotics, but it is important to detect and treat the infection early to prevent complications. Prevention measures include vaccination of animals, proper handling and disposal of animal products, and avoiding contact with infected animals or their products.
In addition to its medical significance, brucellosis has also been associated with significant economic losses in the livestock industry due to reduced milk production and fertility issues in infected animals.
There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:
* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.
Lupus Nephritis can cause a range of symptoms, including:
* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Fatigue
* Fever
* Joint pain
Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.
Types of Kidney Diseases:
1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.
Symptoms of Kidney Diseases:
1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss
Diagnosis of Kidney Diseases:
1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)
Treatment of Kidney Diseases:
1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)
Prevention of Kidney Diseases:
1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings
Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.
Symptoms of anaphylaxis include:
1. Swelling of the face, lips, tongue, and throat
2. Difficulty breathing or swallowing
3. Abdominal cramps
4. Nausea and vomiting
5. Rapid heartbeat
6. Feeling of impending doom or loss of consciousness
Anaphylaxis is diagnosed based on a combination of symptoms, medical history, and physical examination. Treatment for anaphylaxis typically involves administering epinephrine (adrenaline) via an auto-injector, such as an EpiPen or Auvi-Q. Additional treatments may include antihistamines, corticosteroids, and oxygen therapy.
Prevention of anaphylaxis involves avoiding known allergens and being prepared to treat a reaction if it occurs. If you have a history of anaphylaxis, it is important to carry an EpiPen or other emergency medication with you at all times. Wearing a medical alert bracelet or necklace can also help to notify others of your allergy and the need for emergency treatment.
In severe cases, anaphylaxis can lead to unconsciousness, seizures, and even death. Prompt treatment is essential to prevent these complications and ensure a full recovery.
There are several types of disease susceptibility, including:
1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.
Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.
In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.
Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.
In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.
Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.
In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.
There are several types of blood protein disorders, including:
1. Hemophilia A: a deficiency of factor VIII, which is necessary for blood clotting.
2. Hemophilia B: a deficiency of factor IX, also involved in blood clotting.
3. Von Willebrand disease: a deficiency of von Willebrand factor, which helps to platelets stick together and form blood clots.
4. Protein C deficiency: a lack of protein C, an anticoagulant protein that helps to prevent blood clots.
5. Protein S deficiency: a lack of protein S, another anticoagulant protein that helps to prevent blood clots.
6. Antithrombin III deficiency: a lack of antithrombin III, a protein that prevents the formation of blood clots.
7. Fibrinogen deficiency: a lack of fibrinogen, a protein that is essential for blood clotting.
8. Dysproteinemia: an abnormal amount or type of proteins in the blood, which can lead to various symptoms and complications.
Symptoms of blood protein disorders can vary depending on the specific condition and the severity of the deficiency. Common symptoms include easy bruising or bleeding, frequent nosebleeds, prolonged bleeding after injuries or surgery, and joint pain or swelling.
Treatment for blood protein disorders typically involves replacing the missing protein or managing symptoms with medication or lifestyle changes. In some cases, gene therapy may be an option to correct the underlying genetic defect.
It's important for individuals with blood protein disorders to work closely with their healthcare provider to manage their condition and prevent complications such as joint damage, infections, and bleeding episodes.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
This definition of 'Angioedemas, Hereditary' in the medical field is from the Medical Dictionary for the Health Professions and Nursing, provided by the Fortune Company.
BacMam
List of MeSH codes (D27)
39th Air Base Wing
Complementary DNA
Germinal center B-cell like diffuse large B-cell lymphoma
Kyasanur Forest disease
Infection
Daratumumab
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Proteins3
- PNH results from expansion of a clone of hematopoietic cells that, as a consequence of an inactivating mutation of the X-linked gene PIG-A, are deficient in glycosylphosphatidylinositol (GPI)-linked proteins: since these include the surface membrane complement-regulatory proteins CD55 and CD59, the red cells arising from this clone are exquisitely sensitive to lysis by activated complement. (aamds.org)
- Certain proteins in the blood potential points of entry and inside (such as proteins of the complement the body (see figure). (nih.gov)
- The T-antigen partners with two growth silencer proteins, p53 and the retinoblastoma protein pRb, and inactivates them. (eccscotland.com)
Inhibitor eculizumab1
- The complement inhibitor eculizumab has dramatically improved the outcome of atypical hemolytic uremic syndrome. (nih.gov)
Vaccines1
- Killed or inactivated vaccines do not represent a danger to immunocompromised persons and generally should be administered as recommended for healthy persons. (cdc.gov)
Eculizumab2
- Renal recovery under eculizumab was equally good in patients with and those without complement gene variants detected. (nih.gov)
- Since 2007, PNH has received renewed and much wider attention because a new form of treatment has become available, namely complement blockade through the anti-C5 monoclonal antibody eculizumab . (aamds.org)
Antiviral agents4
- Although treatment with antiviral agents has proven a very effective way to improve the health and survival of infected individuals, as we discuss here, the epidemic will continue to grow unless greatly improved prevention strategies can be developed and implemented. (jci.org)
- Whereas there were once no effective therapies for herpes zoster (shingles), the advent of oral antiviral agents has made the treatment of this condition possible. (medscape.com)
- Antiviral agents exert a direct antiviral effect on varicella-zoster virus (VZV). (medscape.com)
- Meanwhile, microscale thermophoresis (MST) indicated that compound 4l have strong binding capability to tobacco mosaic virus coat protein (TMV-CP) with dissociation constant (Kd) values of 0.34 μmol/L, which was better than ningnamycin (0.52 μmol/L). These results suggest that novel myricetin derivatives bearing ferulic acid amide scaffolds may be considered as an activator for antiviral agents. (preprints.org)
Protein2
- 13. Gedunin inactivates the co-chaperone p23 protein causing cancer cell death by apoptosis. (nih.gov)
- Oxytocin may specifically inactivate SARS-COV-2 spike protein and block viral entry into cells via angiotensin-converting enzyme 2 by suppressing serine protease and increasing interferon levels and number of T-lymphocytes. (frontiersin.org)
Serum1
- Human serum is used to culture human cells and is available as plasma-derived AB human serum, clotted whole blood AB human serum, heat inactivated preparations, and complement-depleted preparations. (sigmaaldrich.id)
Activation2
Antibodies4
- Antibodies, gamma globulin, agglutinins, complement, neutralizers] And the internal body defenses, the antibodies and other materials found in the body fluids and tissues. (nih.gov)
- Within days or and inactivate them in an intense for example, by lymphocytes of the weeks, the adaptive immune system chemical shower of reactive oxygen adaptive immune systems, and they manufactures antibodies tailored species cal ed the respiratory burst. (nih.gov)
- Acculturated antibodies or counter acting agent adaptation are intended to lessen immunogenicity reaction while keeping up with high explicitness. (eccscotland.com)
- Utilizing our restrictive innovations (broad immunizer information base, bioinformatics programming, extraordinary counter acting agent humanness score guidelines) and for quick creation of cell lines communicating full length recombinant antibodies, arrangements of the neutralizer variable spaces which decide its limiting explicitness are integrated into human contributor groupings, making a board of full length adapted antibodies for articulation. (eccscotland.com)
Chemicals1
- While chemicals are not disease-producing agents, they may cause injury to body tissues and increase susceptibility to infection. (nih.gov)
Viruses1
- Coccus, virus, spirochete] The nurse must know that plant-like agents including bacteria, fungi, molds, and yeasts can cause disease, as well as those without distinctive plant or animal characteristics such as the viruses and rickettsiae. (nih.gov)
Infection1
- Severe immunosuppression can be due to a variety of conditions, including congenital immunodeficiency, human immunodeficiency virus (HIV) infection, leukemia, lymphoma, generalized malignancy or therapy with alkylating agents, antimetabolites, radiation, or large amounts of corticosteroids. (cdc.gov)
Cells2
- Plant tissue culture reagents, including gelling agents, plant growth regulators, auxins, cytokinins, and other supplements for supporting the growth and development of plant cells and tissues in culture. (sigmaaldrich.id)
- The complement system, along with natural killer cells and dendritic cells, straddles both innate and adaptive immunity. (nih.gov)
Body2
- agents involve two interrelated systems: body. (nih.gov)
- In addition, oxytocin can promote parasympathetic outflow and the secretion of body fluids that could dilute and even inactivate SARS-CoV-2 on the surface of cornea, oral cavity and gastrointestinal tract. (frontiersin.org)
Virus2
- Mixtures of inactivated unidluted sera an tenfold dilutions of Sedlec virus were incuabted for 90 min. (cdc.gov)
- In particular, compound 4l possessed significant protection activity against tobacco mosaic virus (TMV), with an half maximal effective concentration (EC50) value of 196.11 μg/mL, which was better than commercial agent ningnamycin (447.92 μg/mL). (preprints.org)
Patients2
- Twenty-one patients (55%) carried novel or rare complement genes variants. (nih.gov)
- If patients ingest the agent, patients with a daily basis by appropriate laboratory studies are indicated in patients who are too large will cause distended neck veins, rales, abnormal heart and leads to bone marrow failure. (aaan.org)
Include1
- 1] Available chelation therapy agents include deferoxamine (parenterally administered) and deferiprone and deferasirox (both orally administered). (medscape.com)
Absorption1
- It also assist digestion, enhance absorption of other drugs and is a potential postoperatively agent that promote wound healing and reduce postsurgical discomfort and swelling. (scielo.br)
Entry1
- She must also be familiar with the portals of entry and exit of an infective agent. (nih.gov)
Risk1
- The risk appears to be related to the intensity and duration of immunosuppression rather than to the use of any specific agent. (astellascares.com)
Disease2
- She must know the various types of disease- producing agents. (nih.gov)
- Not only must the nurse know that agents can cause disease, she must also be familiar with the methods by which disease is produced, whether by direct invasion of tissue, as in streptococcal infections, or through the liberation of toxin, as in diphtheria. (nih.gov)
Response1
- These agents modify the body's immune response to diverse stimuli. (medscape.com)
Effective1
- Oak Biosciences have been conveyed counter acting agent acculturation administration beginning around 2008, and north of 300 effective undertakings have been finished. (eccscotland.com)
Inhibitors1
- Furthermore, VHL deficiency conferred increased sensitivity to PARP inhibitors, analogous to the synthetic lethality observed between hypoxia and these agents. (nih.gov)
Neutralization1
- IVIG may work via several mechanisms, including the blockage of macrophage receptors, the inhibition of antibody production, the inhibition of complement binding, and the neutralization of pathologic antibodies. (medscape.com)
Malignancy1
- Severe immunosuppression can be due to a variety of conditions, including congenital immunodeficiency, human immunodeficiency virus (HIV) infection, leukemia, lymphoma, generalized malignancy or therapy with alkylating agents, antimetabolites, radiation, or large amounts of corticosteroids. (cdc.gov)