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Issues of Concern – Acute or Chronic Inflammation Acute inflammation has a rapid onset of minutes or hours, usually resolves in a few days, has classic signs and symptoms, and has cellular infiltrate primarily composed of neutrophils. The erythema seen in acute inflammation results from increased blood flow to the affected area due to vasodilation.

Cryotherapy is often an effective treatment for the acute inflammation caused by musculoskeletal injury with decreased pain and more rapid “return-to-participation.” Chronic inflammation has a slow onset of days, a long duration of years, less prominent classical signs and symptoms, and cellular infiltrate primarily composed of monocytes/macrophages and lymphocytes.

Chronic exposure to toxic chemicals and environmental agents such as cigarette smoke can cause chronic inflammation. Mediators and Biomarkers of Inflammation The discovery of cellular and molecular inflammatory mediators and the development of sensitive biomarkers have rapidly advanced our understanding of inflammation and its role in pathology.

Reactive oxygen and reactive nitrogen oxide species (ROS and RNOS) Formation of DNA adducts Cytokines (e.g., IL-6 and TNF-alpha) and chemokines Acute-phase proteins (e.g., C-reactive protein or CRP) Prostaglandins Cyclooxygenase (COX)-related metabolites Inflammation-related growth factors and transcription factors (e.g., NF-kappaB) Major immune cell types

The specific immune cells and mediators at play are variable and dependent upon the injury, the onset/duration of the injury, and multiple genetic loci. CRP is a widely used clinical inflammatory biomarker present in two forms with distinct functions.

1. One form is a homopentamer termed native-CRP (nCRP), and the other is a monomer (mCRP).
2. There are two clinical assays for CRP, a standard assay and a high-sensitivity assay (hs-CRP).
3. Inflammation and Cardiovascular Disease Hs-CRP is often used to assess increased cardiovascular disease (CVD) risk.
4. Increased plasma hs-CRP levels are a CVD risk factor in addition to LDL-cholesterol and the degree of metabolic syndrome.

Some suggested that increased inflammation from any cause (e.g., periodontal disease and arthritis) has a damaging effect on vascular endothelium. Central obesity, a risk factor for type 2-diabetes and CVD, is also associated with increased hs-CRP in metabolic syndrome.

1. It is not yet certain whether CRP plays an active pro-atherogenic role in CVD or that lowering hs-CRP is a valid goal for the primary prevention of CVD.
2. In contrast, the 2018 CANTOS trial on tertiary prevention in patients with a history of myocardial infarction showed that reducing hs-CRP levels by use of canakinumab was effective in reducing (by 25%) a major CVD event but primarily in those patients where treatment lowered hs-CRP to less than 2 mg/ml.

Canakinumab is a monoclonal antibody that targets interleukin-1-beta and has no effect on plasma lipoprotein levels. It should be noted that most participants in the CANTOS trial were already on statin therapy. Statins, besides lowering LDL-C, also lower hs-CRP.

1. Nevertheless, a large-scale study found the effectiveness of simvastatin to lower a first major vascular event was unaffected by baseline CRP levels.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs) have analgesic, antipyretic, antiplatelet as well as anti-inflammatory effects.
3. They are among the world’s most used/prescribed medications.

The effects of NSAIDs on CRP levels are mixed and dependent upon the particular NSAID. In patients taking NSAIDs for rheumatoid arthritis, naproxen was associated with a decreased CRP; whereas, lumiracoxib was associated with an increased CRP. Lumiracoxib is a selective inhibitor of cyclooxygenase-2 (COX-2), the inducible form of COX, while naproxen is a nonselective COX inhibitor, inhibiting COX-2 as well as COX-1, the constitutively expressed form of COX.

1. The COX-2 selective inhibitors are collectively called coxibs.
2. The more selective an NSAID is for COX-2, the greater its effect on increasing CRP.
3. Due to the increased risk of severe CVD events, celecoxib is the only coxib available in the US market.
4. The CVD risks posed by NSAIDs is an area of active research and are an under-recognized issue.

Inflammation, Aging, and Cancer Inflammation is closely associated with an increased production of ROS and RNOS, which can damage DNA. Chronic inflammation is, therefore, an ongoing process that can increase mutations and increase cancer risk. Increased cellular or tumor micro-environmental ROS production is associated with diminished control of cell growth.

1. For example, activated macrophages are a major source of ROS, and these inflammatory cells are located in the tumor microenvironment of breast cancer tumors, where they promote growth and metastasis.
2. Chronic inflammation is associated with many types of cancer and all stages of cancer.
3. Obesity, which increases chronic inflammation, is now recognized as a major (and preventable) increased cancer risk factor.

Increasing evidence supports a strong positive association between CRP levels and cancer. For example, elevated CRP (at the time of diagnosis) is associated with breast cancer, breast cancer subtypes, and poor outcome. The risk of epithelial cancers such as liver, lung, colorectal, endometrial, breast, and ovarian cancer are all positively associated with elevated CRP levels.

CRP levels have proven to be a valuable prognostic biomarker in a wide variety of adult tumors. Elevated CRP is linked with a shorter survival time for most solid tumors. Aging is a major risk factor for cancer, and systemic, sterile (non-infection-caused), age-related chronic inflammation (termed inflamm-aging or inflammaging) is thought to be an underlying etiological connection.

CRP and other inflammatory biomarkers increase with age. Gut microbiota is thought to become more pro-inflammatory with aging and contribute to systemic chronic inflammation. Diet, Exercise, and Inflammation Levels Over the last decade, a fairly consistent view has emerged in the relationship between lifestyle and inflammation.

1. Individuals with high CRP levels of greater than 3.0 mg/L tend to be physically inactive, have higher plasma glucose levels, less likely to follow the Mediterranean diet, have a higher incidence of hypertension, have a lower HDL-cholesterol (anti-atherogenic), and increased abdominal obesity.
2. Adopting a Mediterranean diet combined with a medium level of physical activity markedly reduces the incidence of high CRP by 72%.

The dietary inflammatory index (DII) is a flexible tool for accessing the relationship between diet and inflammation (smartphone apps are available).

What are the steps of acute inflammation pathology?

Acute inflammation is the early (almost immediate) response of a tissue to injury. It is nonspecific and may be evoked by any injury short of one that is immediately lethal. Acute inflammation may be regarded as the first line of defense against injury and is characterized by changes in the microcirculation: exudation of fluid and emigration of leukocytes from blood vessels to the area of injury.

1. Acute inflammation is typically of short duration, occurring before the immune response becomes established, and it is aimed primarily at removing the injurious agent.
2. Until the late 18th century, acute inflammation was regarded as a disease.
3. John Hunter (1728–1793, London surgeon and anatomist) was the first to realize that acute inflammation was a response to injury that was generally beneficial to the host: “But if inflammation develops, regardless of the cause, still it is an effort whose purpose is to restore the parts to their natural functions.” Clinically, acute inflammation is characterized by 5 cardinal signs: rubor (redness), calor (increased heat), tumor (swelling), dolor (pain), and functio laesa (loss of function) ( Figure 3-1 ).

The first four were described by Celsus (ca 30 bc –38 ad ); the fifth was a later addition by Virchow in the nineteenth century. Redness and heat are due to increased blood flow to the inflamed area; swelling is due to accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings; and loss of function is due to a combination of factors.

These signs are manifested when acute inflammation occurs on the surface of the body, but not all of them will be apparent in acute inflammation of internal organs. Pain occurs only when there are appropriate sensory nerve endings in the inflamed site—for example, acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, where there are pain-sensitive nerve endings.

The increased heat of inflamed skin is due to the entry of a large amount of blood at body core temperature into the normally cooler skin. When inflammation occurs internally—where tissue is normally at body core temperature—no increase in heat is apparent.

What are the 4 stages of acute inflammation?

Inflammation | Definition, Symptoms, Treatment, & Facts Inflammation is a response triggered by damage to living, The inflammatory response is a defense mechanism that evolved in higher organisms to protect them from infection and, Its purpose is to localize and eliminate the injurious agent and to remove damaged tissue components so that the body can begin to heal.

• The response consists of changes in blood flow, an increase in permeability of blood vessels, and the migration of fluid, proteins, and white blood cells () from the circulation to the site of tissue damage.
• An inflammatory response that lasts only a few days is called acute inflammation, while a response of longer duration is referred to as chronic inflammation.

The four cardinal signs of inflammation are redness (Latin rubor ), heat ( calor ), swelling ( tumor ), and pain ( dolor ).

Redness is caused by the dilation of small blood vessels in the area of injury.Heat results from increased blood flow through the area and is experienced only in peripheral parts of the body such as the skin. is brought about by chemical mediators of inflammation and contributes to the rise in temperature at the injury.Swelling, called, is caused primarily by the accumulation of fluid outside the blood vessels.The pain associated with inflammation results in part from the distortion of tissues caused by edema, and it also is induced by certain chemical mediators of inflammation, such as bradykinin,, and the,

Inflammation serves as a defense mechanism against infection and injury, and localizing and eliminating injurious factors and removing damaged components allows the healing process to begin. During the healing process, damaged cells capable of proliferation regenerate.

1. Tissue repair, resulting in formation, may occur when normal tissue architecture cannot be regenerated successfully.
2. Failure to replicate the original framework of an organ can lead to disease.
3. Acute inflammation is usually beneficial but often causes unpleasant sensations, such as pain or itching.
4. In some instances inflammation can cause harm.

Tissue destruction can occur when the regulatory mechanisms of the inflammatory response are defective or the ability to clear damaged tissue and foreign substances is impaired. In other cases an inappropriate immune response may give rise to a prolonged and damaging inflammatory response.

In reactions, the body’s immune system attacks its own tissues, leading to long-term chronic inflammation. inflammation, a response triggered by damage to living, The inflammatory response is a that evolved in higher organisms to protect them from and, Its purpose is to localize and eliminate the injurious agent and to remove damaged tissue components so that the body can begin to heal.

The response consists of changes in flow, an increase in permeability of, and the migration of fluid,, and (leukocytes) from the to the site of tissue damage. An inflammatory response that lasts only a few days is called inflammation, while a response of longer duration is referred to as chronic inflammation.

Although acute inflammation is usually, it often causes unpleasant sensations, such as the of a or the of an, Discomfort is usually temporary and disappears when the inflammatory response has done its job. But in some instances inflammation can cause harm. Tissue destruction can occur when the regulatory mechanisms of the inflammatory response are defective or the ability to clear damaged tissue and foreign substances is impaired.

In other cases an inappropriate immune response may give rise to a prolonged and damaging inflammatory response. Examples include, or, reactions, in which an environmental agent such as, which normally poses no threat to the individual, inflammation, and, in which chronic inflammation is triggered by the body’s immune response against its own tissues.

The factors that can stimulate inflammation include microorganisms, physical agents, chemicals, inappropriate immunological responses, and tissue death. Infectious agents such as and are some of the most common stimuli of inflammation. Viruses give rise to inflammation by entering and destroying cells of the body; bacteria release substances called that can initiate inflammation.

Physical trauma,,, and can damage tissues and also bring about inflammation, as can corrosive chemicals such as acids, alkalis, and oxidizing agents. As mentioned above, malfunctioning immunological responses can incite an inappropriate and damaging inflammatory response.

• Inflammation can also result when tissues die from a lack of oxygen or nutrients, a situation that often is caused by loss of blood flow to the area.
• The four cardinal signs of inflammation—redness (Latin rubor ), ( calor ), swelling ( tumor ), and pain ( dolor )—were described in the 1st century ad by the Roman medical writer,

Redness is caused by the dilation of small blood vessels in the area of injury. Heat results from increased blood flow through the area and is experienced only in parts of the body such as the skin. Fever is brought about by chemical mediators of inflammation and contributes to the rise in temperature at the injury.

Swelling, called, is caused primarily by the accumulation of fluid outside the blood vessels. The pain associated with inflammation results in part from the distortion of tissues caused by edema, and it also is induced by certain chemical mediators of inflammation, such as bradykinin,, and the, A fifth consequence of inflammation is the loss of function of the inflamed area, a feature noted by German pathologist in the 19th century.

Loss of function may result from pain that mobility or from severe swelling that prevents movement in the area. When tissue is first injured, the small blood vessels in the damaged area constrict momentarily, a process called vasoconstriction. Following this event, which is believed to be of little importance to the inflammatory response, the blood vessels dilate ( ), increasing blood flow into the area.

1. Vasodilation may last from 15 minutes to several hours.
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3. Next, the walls of the blood vessels, which normally allow only water and salts to pass through easily, become more permeable.
4. Protein-rich fluid, called exudate, is now able to exit into the tissues.

Substances in the exudate include factors, which help prevent the spread of infectious agents throughout the body. Other proteins include antibodies that help destroy invading microorganisms. As fluid and other substances leak out of the blood, blood flow becomes more sluggish and begin to fall out of the axial stream in the centre of the vessel to flow nearer the vessel wall.

What is the pathogenesis of inflammation?

Abstract – The objective of this chapter is to understand the pathophysiology and pathogenesis of pain and inflammation. Inflammation is the most prevalent issue and also challenging to diagnose. To put it simply, pain and inflammation are complicated, encompassing psychological and behavioral components as well as the consequences of physical trauma, disease, or surgery.

When you undergo inflammation and its manifestations, you’ll have an uncomfortable feeling accompanied by a potentially harmful impact on tissue, or equal of such damage. Inflammation occurs when tissue injury and inflammation-inducing factors such as histamine, cytokines, and others lead to venular dilatation, increased vascular permeability, and entrance of inflammatory components.

The stress responses promote inflammation, which is an essential component of it. Once the problematic agent is removed, the mission can be ended and inflammation will be terminated. In this chapter we discuss the order of events and their accompanying mediators during the process of short-term inflammation as well as discuss the possible morphology patterns.

What are the types of acute inflammation?

1. What are the Types of Acute Inflammation? – Acute inflammation begins within seconds to minutes following injury to tissues. It is usually characterized by four key features, including redness, heat, swelling and pain. Redness results from secondary to vasodilatation and increased blood flow.

Heat is caused by localized increase in temperature, and also due to increased blood flow. Swelling results from increased vessel permeability and allows fluid loss into the interstitial space. Pain is caused by stimulation of the local nerve endings, from mechanical and chemical mediators. Due to the difference of inflammatory factors, the degree of tissue reaction and the different sites of inflammation, the pathological form of acute inflammation is also different.

According to the main components of exudate, acute inflammation is divided into four types, including serous inflammation, fibrinous inflammation, purulent inflammation and hemorrhagic inflammation. The differences of these four types of acute inflammation are shown as follows:

Type	Features	Prevalent disease or location
Serous inflammation	The main component of the serous exudation is serum; It can cause effusion in the chest cavity, pericardium, joints, and abdominal cavity; It is mild and easy to subside.	Mucosa, serosa, loose connective tissue
Fibrinous inflammation	It is dominated by fibrinogen exudation and the formation of cellulose in the inflammation focus; The blood vessel wall is severely damaged, and the vascular permeability is obviously increased.	Mucosa, serosa, Lung bacillary dysentery, fluffy heart
Purulent inflammation	It is characterized by neutrophil exudation, with different degrees of tissue necrosis and pus formation.	Appendices, skin, subcutaneous, muscle, internal organs, serous membrane, etc.
Hemorrhagic inflammation	It is characterized by severe blood vessel damage, and the exudate contains a large number of red blood cells	Epidemic hemorrhagic fever, leptospirosis, plague.

What is the difference between acute inflammation and chronic inflammation?

What is the difference between acute inflammation and chronic inflammation? – There are two types of inflammation:

Acute inflammation: The response to sudden body damage, such as cutting your finger. To heal the cut, your body sends inflammatory cells to the injury. These cells start the healing process. Chronic inflammation: Your body continues sending inflammatory cells even when there is no outside danger. For example, in rheumatoid arthritis inflammatory cells and substances attack joint tissues leading to an inflammation that comes and goes and can cause severe damage to joints with pain and deformities.

What are the 8 signs of inflammation in the body?

The 10 classic signs of inflammation in the body are heat, affected function of the infected body part, redness, swelling, pain, fatigue, joint pain, fever, chest and abdominal pain, and skin rash. For centuries, inflammation has been used as a metric of telling the extent of injury to your body.

When the word was first used, it was to describe the visual observation of an area of the body affected by reddening, swelling, pain, and heat. Today, when the doctor says you have inflammation, they’re most often summarizing the changes to any area of your body after it has been injured. However, for it to qualify as inflammation, the injury must have not been to such extent that you lose complete function of the affected body part.

Normally, inflammation happens as your body’s response to fight off an infection in an attempt to heal itself. With the right treatment and proper diet, you can manage and treat inflammation and relieve the body of any discomfort.

What is the difference between acute and chronic inflammation pathology?

General Concepts of Acute and Chronic Inflammation – Overview: The body must undergo changes locally through vasodilation and increased vascular permeability in the area of the agent inciting the inflammatory reaction to allow white blood cells to accumulate.

The white blood cells must then leave the blood vessel, cross the basement membrane, and be drawn to the area where they are needed. The process by which white blood cells are drawn to the area where they are needed is referred to as chemotaxis. Acute inflammation has a rapid onset, lasts for minutes to days, and is characterized by exudation of fluid and protein from vessels and emigration of neutrophils.

Acute inflammation is a protective process that is designed to rid the body of the inciting agent and set up the process of repair. Chronic inflammation has a longer time course (days to years) and involves different cell types than does acute inflammation (lymphocytes and macrophages versus neutrophils).

Also, in chronic inflammation, tissue repair coexists with tissue destruction. Cardinal signs of acute inflammation: Rubor (red discoloration), calor (heat), dolor (pain), tumor (mass effect), and loss of function. Causes of acute inflammation: Infection, trauma, physical and chemical agents, necrosis, foreign bodies, and immune reactions.

Stages of acute inflammation ( Table 2-1 )

1. Vasodilation (after a transient vasoconstriction)
   • How: Vasodilation occurs through release of mediators from cells. These mediators include histamine, prostacyclin (PGI 2 ), and nitric oxide (NO).
   • Why: Vasodilation increases the hydrostatic pressure by causing slowing (sludging) of blood flow. Sludging of blood also causes margination of leukocytes along the wall of the blood vessel.
2. Increased vascular permeability (increased leakiness of vessels)
   • How: Increased vascular permeability occurs through release of mediators from cells. These mediators include histamine and leukotrienes C 4, D 4, and E 4,
   • Why: Increased vascular permeability allows fluid to cross into the interstitial tissue, which increases protein levels in the interstitial tissue, thereby decreasing osmotic pressure in the,

What are the 2 events of acute inflammation?

Events In Acute Inflammation The two main events of the acute inflammation are:  Vascular events  Cellular events.

What are the stages of inflammation pathophysiology?

What are the Stages of Inflammation? – G4 Physiotherapy & Fitness

• Inflammation is a result of damage to body tissues and can be caused by a number of factors including trauma, repetitive use and those conditions affected by age such as Osteoarthritis.
• The are three main stages of inflammation which can each vary in intensity and duration:

1. Acute -swelling stage
2. Sub-acute – regenerative stage
3. Chronic – scar tissue maturation and remodelling stage

During the acute inflammatory stage, there is evident redness (erythema) and swelling due to vascular changes. Exudation of cells and chemicals cause swelling and pain. A haematoma may form if there is bleeding within the tissues. Secondarily, chemical irritants are neutralized and the area is sealed off from surrounding tissues and circulation is impaired.

There is early fibroblastic cell activity. Pain is normally present at rest over a diffuse area and can be aggravated by activity. Secondary muscle spasm and guarding normally restrict passive movement. During range of movement testing, pain is felt before the tissue resistance is reached. Injuries to deep structures or poorly vascularised areas can lead to surface swelling and oedema but may not be noticeable.

The sub-acute stage is the commencement of healing and repair. Noxious chemicals are further neutralized and new capillary beds growing into the damaged areas are supported by connective tissue growth (collagen fibres) and together form granulation buds.

Visible signs of inflammation start to subside and range of movement increases with pain felt at the point of tissue resistance. The chronic inflammatory stage is the period when tissue remodelling takes place. Signs of inflammation are absent and scar tissue is maturing. Pain is felt further into the range of movement after the tissue resistance has been reached.

Maturation refers to the growth of the fibroblasts to fibrocytes and remodelling refers to the organization of and shrinking of collagen fibres along the lines of stress. The skill of the physiotherapist is to identify the exact stage of the inflammation and then intervene to enhance the healing process with the most appropriate form of treatment.

What is the process of inflammation?

The immune response is how your body recognizes and defends itself against bacteria, viruses, and substances that appear foreign and harmful. The immune system protects the body from possibly harmful substances by recognizing and responding to antigens,

• Antigens are substances (usually proteins) on the surface of cells, viruses, fungi, or bacteria.
• Nonliving substances such as toxins, chemicals, drugs, and foreign particles (such as a splinter) can also be antigens.
• The immune system recognizes and destroys, or tries to destroy, substances that contain antigens.

Your body’s cells have proteins that are antigens. These include a group of antigens called HLA antigens, Your immune system learns to see these antigens as normal and usually does not react against them. INNATE IMMUNITY Innate, or nonspecific, immunity is the defense system with which you were born.

Cough reflexEnzymes in tears and skin oilsMucus, which traps bacteria and small particlesSkinStomach acid

Innate immunity also comes in a protein chemical form, called innate humoral immunity. Examples include the body’s complement system and substances called interferon and interleukin-1 (which causes fever). If an antigen gets past these barriers, it is attacked and destroyed by other parts of the immune system.

1. ACQUIRED IMMUNITY Acquired immunity is immunity that develops with exposure to various antigens.
2. Your immune system builds a defense against that specific antigen.
3. PASSIVE IMMUNITY Passive immunity is due to antibodies that are produced in a body other than your own.
4. Infants have passive immunity because they are born with antibodies that are transferred through the placenta from their mother.

These antibodies disappear between ages 6 and 12 months. Passive immunization may also be due to injection of antiserum, which contains antibodies that are formed by another person or animal. It provides immediate protection against an antigen, but does not provide long-lasting protection.

Immune serum globulin (given for hepatitis exposure) and tetanus antitoxin are examples of passive immunization. BLOOD COMPONENTS The immune system includes certain types of white blood cells. It also includes chemicals and proteins in the blood, such as antibodies, complement proteins, and interferon.

Some of these directly attack foreign substances in the body, and others work together to help the immune system cells. Lymphocytes are a type of white blood cell. There are B and T type lymphocytes.

B lymphocytes become cells that produce antibodies. Antibodies attach to a specific antigen and make it easier for the immune cells to destroy the antigen.T lymphocytes attack antigens directly and help control the immune response. They also release chemicals, known as cytokines, which control the entire immune response.

As lymphocytes develop, they normally learn to tell the difference between your own body tissues and substances that are not normally found in your body. Once B cells and T cells are formed, a few of those cells will multiply and provide “memory” for your immune system.

1. This allows your immune system to respond faster and more efficiently the next time you are exposed to the same antigen.
2. In many cases, it will prevent you from getting sick.
3. For example, a person who has had chickenpox or has been immunized against chickenpox is immune from getting chickenpox again.
4. INFLAMMATION The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause.

The damaged cells release chemicals including histamine, bradykinin, and prostaglandins. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling, This helps isolate the foreign substance from further contact with body tissues.

1. The chemicals also attract white blood cells called phagocytes that “eat” germs and dead or damaged cells.
2. This process is called phagocytosis.
3. Phagocytes eventually die.
4. Pus is formed from a collection of dead tissue, dead bacteria, and live and dead phagocytes.
5. IMMUNE SYSTEM DISORDERS AND ALLERGIES Immune system disorders occur when the immune response is directed against body tissue, is excessive, or is lacking.

Allergies involve an immune response to a substance that most people’s bodies perceive as harmless. IMMUNIZATION Vaccination ( immunization ) is a way to trigger the immune response. Small doses of an antigen, such as dead or weakened live viruses, are given to activate immune system “memory” (activated B cells and sensitized T cells).

• Memory allows your body to react quickly and efficiently to future exposures.
• COMPLICATIONS DUE TO AN ALTERED IMMUNE RESPONSE An efficient immune response protects against many diseases and disorders.
• An inefficient immune response allows diseases to develop.
• Too much, too little, or the wrong immune response causes immune system disorders.

An overactive immune response can lead to the development of autoimmune diseases, in which antibodies form against the body’s own tissues. Complications from altered immune responses include:

Allergy or hypersensitivity Anaphylaxis, a life-threatening allergic reactionAutoimmune disorders Graft versus host disease, a complication of a bone marrow transplantImmunodeficiency disorders Serum sickness Transplant rejection

Updated by: Stuart I. Henochowicz, MD, FACP, Clinical Professor of Medicine, Division of Allergy, Immunology, and Rheumatology, Georgetown University Medical School, Washington, DC. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.