Case Study AnalysisAfter review and examination of the provided

Case Study Analysis
After review and examination of the provided case study, the
patient presented with symptoms that are consistent with
Rhabdomyolysis. The findings in this case study that support a
diagnosis of Rhabdomyolysis include substance abuse,
prolonged lying down or immobility, and hyperkalemia
(Cleveland, 2022). In this case study the patient has a history of
substance abuse, and it is unknown if the patient used any type
of substance prior to becoming unresponsive. However, because
Naloxone was used by EMS upon arrival and the patient became
responsive, it can be presumed the patient had an opioid related
overdose. This is presumed because Naloxone is a medication
that rapidly reverses an opioid overdose and is classified as an
opioid antagonist (Substance, 2022). Opioid antagonists attach
to opioid receptors and reverse and block the effects of other
opioids (Substance, 2022). If an opioid overdose is suspected,
Naloxone can quickly restore normal breathing to a person if
their breathing has slowed or stopped because of an opioid
overdose (Substance, 2022). Recreational drug use with such
substances as opioids and their derivatives and amphetamines
can directly result in Rhabdomyolysis (Substance, 2022).
The patient was found lying down by the roommate for an
unknown amount of time. This prolonged period lying down
could have led to increased compartmental pressure of the
muscles in the left hip and forearm (Cleveland, 2022).
Compartmental pressure occurs when pressure rises in and
around the muscles (Cleveland, 2022). This can limit blood
flow, oxygen, and nutrients to muscles and nerves, resulting in
muscle ischemia, infarction, and necrosis by compartmental
tamponade which will also cause injury to the nerves
(Cleveland, 2022). Compartmental pressure begins to develop
when the tissue pressure exceeds the venous pressure and
impairs blood outflow (American, 2022). Lack of oxygenated

blood and the build up of waste products will result in pain and
decreased peripheral sensation secondary to nerve irritation
(American, 2022). This would explain the patients’ complaints
of the burning pain over his left hip and forearm due to muscle
necrosis.
Patient was hyperkalemic with a serum potassium level
of 6.9 mEq/L. Hyperkalemia has multiple causes, one of which
includes damage to muscles (American, 2022). Muscle damage
results in the release of intracellular potassium into circulation
resulting in elevated serum potassium levels (American, 2022).
Potassium plays a crucial role in electrical signal functioning of
the hearts middle thick layer called the myocardium (American,
2022). Increased potassium levels can interfere with proper
electrical signals in the myocardium which can lead to heart
arrythmias (American, 2022). As potassium levels increase, T-
waves peak, and PR intervals are prolonged due to action
potential duration (APD) shortening which causes more
synchronous repolarization across the ventricular wall (Scalco
et. al., 2015). In this case study the patients T-waves were
peaked, and PR intervals were prolonged due to increased serum
potassium levels.
Genetics and Rhabdomyolysis
Rhabdomyolysis is characterized by acute and often severe
skeletal muscle damage which results in the release of
intracellular muscle components into the blood stream resulting
in myoglobinuria (Scalco et. al., 2015). A common finding with
Rhabdomyolysis is increased intracellular free ionized calcium
which leads to muscle cell death through the activation of
harmful mechanisms such as enzymatic activation and
prolonged muscle fiber contraction (Scalco et. al., 2015). These
disorders include metabolic muscle disorders, mitochondrial
disorders, disorders of intramuscular calcium release and
excitation-contraction coupling, and muscular dystrophies
(Scalco et. al., 2015). Epigenetics is the study of how your
behaviors and environment can cause changes that affect the
way your genes work (Centers, 2022). Epigenetic changes do

not change your DNA sequence, but they do change how your
body reads a DNA sequence (Centers, 2022). Epigenetics
change as you age, as part of normal development and aging as
well as in response to your behaviors and environment (Centers,
2022). Epigenetics work through DNA methylation, histone
modifications, and non-coding RNA (Centers, 2022). Neurobio-
genetics use recent advances in genome sequencing to better
understand the cause of brain and nerve disorders (Yale, 2022).
Neurobio-genetics help pinpoint genetic factors of inherited
diseases and can help determine the extent to which their
genetic material plays a role in their condition (Yale, 2022).
Drug addiction can be woven into your DNA (Cleveland, 2022).
The genetic connection between individuals and addiction is
through inherited levels of dopamine which is a
neurotransmitter made in the brain that acts as a “feel good”
hormone (Cleveland, 2022). Because dopamine acts as a “feel
good” hormone it can power poor impulse control leading
individuals towards addictive type behaviors (Cleveland, 2022).
Genetics merely indicate a predisposition toward addictive
behaviors (Cleveland, 2022).
Specific Symptoms
The patient’s potassium is elevated due to muscle damage from
lying for a prolonged amount of time. The necrotic tissue was
the result of increased compartmental pressure around the
trochanter and forearm due to decreased blood flow, oxygen,
and nutrients to these muscles and nerves leading to necrosis of
the tissues. The EKG is showing prolonged PR intervals with
peaked T-waves due to the increased serum potassium affecting
the electrical conduction of the myocardium resulting in an
abnormal EKG.
Physiologic Response
Hyperkalemia is significant in this case study as it was
a direct result of the Rhabdomyolysis while it was also the
cause of decreased electrical conduction of the myocardium
resulting in prolonged PR intervals and peaked T-waves
indicating an abnormal EKG. Cardiotoxicity is heart damage

that arises from certain drugs (American, 2022). EKGs are
essential in a suspected drug overdose as they are cardiotoxic
drugs. Specific myocardial effects of cardiotoxic drugs have
well-described electrocardiographic manifestations making
EKGs a quick tool that can provide key pieces of information
prompting early interventions (American, 2022).
Cells Involved in Rhabdomyolysis
Rhabdomyolysis involves the muscle cells (American,
2022). When the muscle cells are damaged the myoglobin in the
muscle cells leak into the blood stream causing renal toxicity
(American, 2022). Due to the hyperkalemia and the effects it
has on the myocardium, cardiomyocytes or the cells that make
up the cardiac muscle are also involved (American, 2022).
Nerve cells are involved because of muscle ischemia causing
nerve damage (American, 2022). Neurons are involved in
overdose death by specific receptors in the neurons being
triggered that cause opioid-induced respiratory depression (The,
2021). The specific receptor is the mu opioid receptor, and
these are in the brainstems breathing modulation center and
these are the neurons responsible for opioid-induced respiratory
depression (The, 2021).
Change in Response Related to Characteristics
Regarding gender, it could change the response as
females are less prone to suffer from Rhabdomyolysis
(American, 2022). However, just because there is a lower
incidence does not indicate complete rule out of
Rhabdomyolysis in females (American, 2022). Genetics could
play a role in a change in the response. Certain genetic
disorders can increase the chances of developing
Rhabdomyolysis. These include muscle diseases such as
muscular dystrophy or certain metabolic or mitochondrial
disorders (Cleveland, 2022). However, this case study
presentation of Rhabdomyolysis occurred due to prolonged
immobility related to substance use.
References
American Academy of Family Physician. (2022).

Rhabdomyolysis.
https://www.aafp.org/pubs/afp/issues/2002/0301/p907.html
Centers for Disease Control and Prevention. (2019).
Rhabdomyolysis.
https://www.cdc.gov/niosh/topics/rhabdo/default.html
Cleveland Clinic. (2022).
Rhabdomyolysis.
https://my.clevelandclinic.org/health/diseases/21184-
rhabdomyolysis
Substance Abuse and Mental Health Services Administration.
(2022).
Naloxone.
https://www.samhsa.gov/medication-assisted-
treatment/medications-counseling-related-conditions/naloxone
The Salk Institute for Biological Studies. (2021).
Researchers identify neurons involved in
overdose deaths.https://www.salk.edu/news-release/researchers-
identify-neurons-involved-in-overdose-deaths/
Scalco, R. S., Gardiner, A. R., Pitceathly, R. D., Zanoteli, E.,
Becker, J., Holton, J. L., Houlden
H., Jungbluth, H., & Quinlivan, R. (2015). Rhabdomyolysis: a
genetic perspective.
Orphanet Journal of Rare Diseases,
10(51).https://doi.org/10.1186/s13023-015-0264-3
Yale Medicine. (2022).
Neurogenetics.
https://www.yalemedicine.org/conditions/neurogenetics
Cellular In this scenario, a 27-year-old patient with a substance
abuse history was found unresponsive after an unknown amount
of time by his roommate who called emergency medical services
(EMS). The EMS team used naloxone which revived the patient.
He started to complain about burning pain in his left forearm

and left hip. After arriving in the ER, it was discovered that he
had a large amount of necrotic tissue on the forearm and greater
trochanter. An electrocardiogram (EKG) showed peaked T
waves and prolonged PR waves which are indicative of
hyperkalemia. His serum potassium level 6.9mEq/L.
In breaking down the scenario to determine the
diagnosis, the substance abuse is opioid-related due to the
positive reaction from the naloxone. According to NIH,
naloxone has no effect on someone who does not have opioids
in their system. (National Institute of Health, 2022, para 1).
Opioid use alone causes damage to many cells. The patient's
necrotic areas on the forearm and greater trochanter, at some
point, were inflamed which progressed to necrosis. Knowing
there is a history of drug abuse, and with the roommate not
being constantly available, it is hard to determine how long he
was really laying there. The patient could have been drug-
induced for days lying on the left side to create that necrotic
tissue.
The process taken to create the necrosis begins at the
cellular level. The cell injury and death, in this case, were
caused by an outside factor of drug overdose and hypoxia. The
injury initially begins as a mast cell that is damaged and
releases histamine which swells capillaries (vasodilation), then
chemokines are release that act as a messenger to attract
phagocytes (leukocytes) to the area of inflammation to
immediately begin the healing process (Khan, 2010). Even
though the area is trying to heal itself the continuous damage
that affects adenosine triphosphate (ATP) depletion,
mitochondrial damage, DNA damage, altered calcium, and
accumulation of oxygen-derived free radicals, continue to injure
the cell and if not treated cause cell death (McCance, &
Huether, 2019, p. 51). The burning pain that the patient felt is
the response from the damaged cells, nerves, and tissue
surrounding the necrotic areas and he felt it due to the
immediate reversal from the naloxone treatment. The opioid

effect may have been how he did not notice the inflamed areas,
and when the opioid receptors are stimulated they suppress the
sensation of pain (Schiller, Goyal, & Mechanic, 2022, para 4).
Another factor that caused the necrotic area was the
hypoxic reaction from the pressure he placed on the forearm and
hip from the actual drug abuse. Hypoxia creates an immense
amount of cellular damage due to how a human will not
function well if at all without a sufficient supply of oxygen. The
cell reaction to hypoxia reduces cell respiration and energy by
decreasing mitochondrial phosphorylation (insufficient ATP
production) in which the calcium and sodium exchange fails to
force them back into the cell releasing potassium into the
extracellular fluid (ECF) (McCance & Huether, 2019, p.51). It
appears with this information the patient could have had several
hypoxic events over time that it continued to cause such an
extensive amount of damage over some time. The failure of the
sodium-potassium pump prevents the calcium-sodium exchange
that caused hyperkalemia. In the scenario, the patient's level of
potassium was high due to the large area of necrosis that caused
the potassium to leak into the cellular fluid. A sign of
hyperkalemia is peaked T waves and prolonged PR interval
(McCance & Huether, 2019, p. 118). The EKG is necessary
because it can show signs of electrolyte imbalance, heart
failure, significant arrhythmias, and ischemia, and has faster
results than the laboratory. A patient who has a drug overdose
can cause an imbalance with ion channels of potassium,
calcium, and sodium that causes cardio effect on the
myocardium membrane, in which an EKG will show significant
changes that could be life-threatening (Yates & Manini, 2012).
All cells in our system have an important role and
function. As seen in the small scenario, one misstep will cause
major damage and potential loss of life. The process of
discovering exactly what happened and how this person was
found would be questioning the roommate and speaking with the
patient.
References

Khan Academy (2010, February 24).
Inflammatory response | Human anatomy and
physiology | Health & medicine [Video file]. Retrieved from
https://www.youtube.com/watch?v=FXSuEIMrPQk
McCance, K. L. & Huether, S. E. (2019).
Pathophysiology: The biologic basis for disease in
adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Schiller, E.Y., Goyal, A., Mechanic, O.J. Opioid Overdose.
[Updated 2022 May 9]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2022 Jan-. Retrieved
from:
https://www.ncbi.nlm.nih.gov/books/NBK470415/
U.S. Department of Health & Human Services.(2022, January).
National Institute on Drug Abuse |Naloxone Drug Facts.
Retrieved from:
https://nida.nih.gov/publications/drugfacts/naloxone
Yates, C., & Manini, A. F. (2012). Utility of the
electrocardiogram in drug overdose and poisoning: theoretical
considerations and clinical implications.
Current cardiology reviews,
8(2), 137–151.
https://doi.org/10.2174/157340312801784961 Retrieved from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3406273/
Bottom of Form
PRAC 6665/6675 Clinical Skills
Self-Assessment Form
Desired Clinical Skills for Students to Achieve
Confident (Can complete independently)
Mostly confident (Can complete with supervision)

Beginning (Have performed with supervision or needs
supervision to feel confident)
New (Have never performed or does not apply)
Comprehensive psychiatric evaluation skills in:
Recognizing clinical signs and symptoms of psychiatric
illness across the lifespan
X
Differentiating between pathophysiological and
psychopathological conditions
X
Performing and interpreting a comprehensive and/or interval
history and physical examination (including laboratory and
diagnostic studies)
X
Performing and interpreting a mental status examination
X
Performing and interpreting a psychosocial assessment and
family psychiatric history
X

Performing and interpreting a functional assessment (activities
of daily living, occupational, social, leisure, educational).
X
Diagnostic reasoning skill in:
Developing and prioritizing a differential diagnoses list
X
Formulating diagnoses according to DSM 5-TR based on
assessment data
X
Differentiating between normal/abnormal age-related
physiological and psychological symptoms/changes
X
Pharmacotherapeutic skills in:
Selecting appropriate evidence based clinical practice
guidelines for medication plan (e.g., risk/benefit, patient
preference, developmental considerations, financial, the process
of informed consent, symptom management)
X
Evaluating patient response and modify plan as necessary

X
Documenting (e.g., adverse reaction, the patient response,
changes to the plan of care)
X
Psychotherapeutic Treatment Planning:
Recognizes concepts of therapeutic modalities across the
lifespan
X
Selecting appropriate evidence based clinical practice
guidelines for psychotherapeutic plan (e.g., risk/benefit, patient
preference, developmental considerations, financial, the process
of informed consent, symptom management, modality
appropriate for situation)
X
Applies age appropriate psychotherapeutic counseling
techniques with individuals and/or any caregivers
X
Develop an age appropriate individualized plan of care
X

Provide psychoeducation to individuals and/or any caregiver s
X
Promote health and disease prevention techniques
X
Self-assessment skill:
Develop SMART goals for practicum experiences
X
Evaluating outcomes of practicum goals and modify plan as
necessary
X
Documenting and reflecting on learning experiences
X
Professional skills:
Maintains professional boundaries and therapeutic relationship
with clients and staff
X
Collaborate with multi-disciplinary teams to improve clinical
practice in mental health settings

X
Identifies ethical and legal dilemmas with possible resolutions
X
Demonstrates non-judgmental practice approach and empathy
X
Practices within scope of practice
X
Selecting and implementing appropriate screening
instrument(s), interpreting results, and making
recommendations and referrals:
Demonstrates selecting the correct screening instrument
appropriate for the clinical situation
X
Implements the screening instrument efficiently and effectively
with the clients
X
Interprets results for screening instruments accurately

X
Develops an appropriate plan of care based upon screening
instruments response
XX
Identifies the need to refer to another specialty provider when
applicable
X
Accurately documents recommendations for psychiatric
consultations when applicable
X
Summary of strengths:
I have made a lot of progress in my career and profession as
nurse practitioner. I acknowledged the significance of self-
evaluation and ever since I have embodied the practice of
regular self-evaluation as an important component of my career
growth. Through my career profession I have master good
corporate communication with distinct report writing skills that
has enabled me to be one of the best nurses in the facilities I
have worked. I have also improved my interpersonal skills
significantly that has seen me take up advanced responsibilities
from my seniors. I have acquired good work ethics and
professionalism. As a nurse I have always maintained the need
for respect for patient needs and opinions. My immediate

supervisor once marveled at how I handled the case of a
Jehovah witness patient who had refused blood transfusion since
it was against the doctrines of her denomination. I obeyed her
position but requested her to attest to that in writing so I may
not be held culpable for negligence. My supervisor told me that
I employed wisdom at its echelons. I am also good in clinical
assessment and pharmacological support to my clients. I always
work day and night to improve my relationships with my
clients. A condition which yields better outcomes in patient
conditions when I handle them.
Opportunities for growth:
One of the opportunities in my career as a nurse practitioner is
diversity. I have always loved to diversify my knowledge and
understanding about different pharmacological practices. In this
sense, I have managed to improve my knowledge about
differential diagnosis. I have been expanding my knowledge
through continuous research about such topics which have
significantly honed my understanding. I also need to develop
good leadership and management practices. I believe with good
administrative skills there are a lot of opportunities for vertical
mobility. Effective administration calls for good knowledge and
better understanding. I need to develop sound knowledge in the
field of healthcare administration. I have also realized that good
understanding of effective pharmacotherapy support to patients.
I have had some slight challenges with prescriptions and
recommendations for effective medication. I feel this will
contribute to better medication to the patients under my care

Now, write three to four (3–4) possible goals and objectives for
this practicum experience. Ensure that they follow the SMART
Strategy, as described in the Learning Resources.
• Goal: To hone my corporate communication skills within the
next 10 weeks of my practicum cycle
• Objective: to improve my report writing skills for timely
delivery of reports
• Objective: to facilitate effective communication and
prescriptions to patients
• Objective: to enhance my negotiation and interaction with
colleagues an patients
• Goal: To expand my pharmacological knowledge through
advanced studies and research on diagnostic and
pharmacological processes
• Objective: to grasp the concept of differential diagnosis
• Objective: to improve personal experience with patients
• Objective: to reduce chances of error of wrong diagnosis on
patients
• Goal: To expand my knowledge about professional ethics of
healthcare practitioners including understanding their
application in real-life situation
• Objective: to avoid cases of litigation both to the institution
and to me as a practitioner
• Objective: to promote good work ethics in the institutions and
facilities where I will work.
• Objective: to promote good public image of nursing as a
profession by demonstrating exemplary behavior
• Goal: To continuously engage in educational learning through
research, regular training programs such as work study, short
courses, and exchange programs to expand my knowledge and
understanding of nursing as a profession.
• Objective: to continually nourish my knowledge and expertise
• Objective: to strategically position myself for vertical
mobility in the administrative ranks
• Objective: to improve my skills, knowledge and experience to
match the dynamic world of nursing.

Signature: Monica Castelao
Date:September 1, 2022
Course/Section: Practicum 6665
NCBI Bookshelf. A service of the National Library of Medicine,
National Institutes of Health.
StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2019 Jan-.
Immediate Hypersensitivity Reactions
Authors
Angel A. Justiz Vaillant; Patrick M. Zito1.
Affiliations
1 Walden University
Last Update: June 18, 2019.
Introduction
Hypersensitivity reactions (HR) are immune responses that are
exaggerated
or inappropriate against an antigen or allergen. Coombs and
Gell classified
hypersensitivity reactions into four forms. Type I, type II, and
type III
hypersensitivity reactions are known as immediate
hypersensitivity reactions

(IHR) because occur within 24 hours. Antibodies including IgE,
IgM, and
IgG mediate them.[1]
Type I or Anaphylactic Response
Anaphylactic Responseis mediated by IgE antibodies that are
produced by
the immune system in response to environmental proteins
(allergens) such as
pollens, animal danders or dust mites. These antibodies (IgE)
bind to mast
cells and basophils, which contain histamine granules that are
released in the
reaction and cause inflammation. Type I hypersensitivity
reactions can be
seen in bronchial asthma, allergic rhinitis, allergic dermatitis,
food allergy,
allergic conjunctivitis, and anaphylactic shock.[2][3]
Anaphylaxis
Anaphylaxis is a medical emergency because can lead to an
acute, life-
threatening respiratory failure. It is an IgE-mediated process. It
is the most
severe form of an allergic reaction, where mast cells suddenly
release a large
amount of histamine and later on leukotrienes. In severe cases
intense
bronchospasm, laryngeal edema, cyanosis, hypotension, and
shock are
present.[4]
https://www.ncbi.nlm.nih.gov/books/NBK513315/?report=printa
ble

ble
ble
ble
Allergic bronchial asthma
Allergic bronchial asthma is an atopic disease, characterized by
bronchospasm. It may also be a chronic inflammatory disease.
In its etiology,
and environmental factors along with a genetic background play
an important
role. The diagnosis is dependent on history and examination. In
allergic
bronchial asthma, IgE is elevated, and sputum eosinophilia is
common.
Epidemiologically, a positive skin prick test or specific IgE are
risk factors
for asthma.[5]
Allergic rhinitis
Allergic rhinitis is another atopic disease where histamine and
leukotrienes
are responsible for rhinorrhea, sneezing and nasal obstruction.
Allergens are
similar to those found in bronchial asthma. Nasal polyps may be
seen in
chronic rhinitis.[6]
Allergic conjunctivitis
Allergic conjunctivitis presents with rhinitis and is IgE-

mediated. Itching and
eye problems including watering, redness, and swelling always
occur.[7]
Food allergy
One must differentiate food allergy (IgE-mediated) from food
intolerance that
can be cause for a variety of etiology including malabsorption
and celiac
disease. It is more frequent in children as seen in cow's milk
allergy. Food
allergy symptoms mostly affect the respiratory tract, the skin,
and the gut.
Skin prick tests are helpful to test for food allergens that can
trigger severe
reactions, e.g., peanuts, eggs, fish, and milk.[3]
Atopic eczema
Atopic eczema is an IgE-mediated disease that affects the skin
and has an
immunopathogenesis very similar to that of allergic asthma and
allergic
rhinitis, which are present in more than half of the diseased.
Radioallergosorbent (RAST) may reveal the specificity of the
IgE antibody
involved but has little help in management.[8]
Drug allergy
Drugs may cause allergic reactions by any mechanism of
hypersensitivity.
For example, penicillin may cause anaphylaxis, which is IgE-
mediated but

ble
ble
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ble
ble
must responses be trivial. Penicillin cross-reacts with other
semisynthetic
penicillins including monobactams and carbapenems and may
also cross-
react with other antibiotics such as cephalosporins.[9]
Type II or Cytotoxic-Mediated Response
IgG and IgM mediate cytotoxic-mediated response against cell
surface and
extracellular matrix proteins. The immunoglobulins involved in
this type of
reaction damages cells by activating the complement system or
by
phagocytosis. Type II hypersensitivity reactions can be seen in
immune
thrombocytopenia, autoimmune hemolytic anemia, and
autoimmune
neutropenia.
Immune thrombocytopenia (ITP)
ITP is an autoimmune disorder that occurs at any age.
Phagocytes destroy

sensitized platelets in the peripheral blood. Clinically, it
manifests by
thrombocytopenia with shortened platelet survival and increased
marrow
megakaryocytes. Sudden onset of petechiae and bleeding from
the gums,
nose, bowel, and urinary tract occurs. Bleeding can accompany
infections,
drug reactions, malignancy and other autoimmune disorders
such as thyroid
disease and SLE.[10]
Autoimmune hemolytic anemia (AIHA)
There are two types of immune hemolytic anemia: IgG-mediated
(warm
AIHA) and IgM-mediated (cold AIHA). The warm type may be
idiopathic
autoimmune or secondary to other diseases such as malignancy
affecting the
lymphoid tissues. The cold type may be idiopathic or secondary
to infections
such as Epstein-Barr virus. The primary clinical sign of the two
is jaundice.
The laboratory diagnosis is made by a positive Coombs test,
which identifies
immunoglobulins and C3 on red blood cells.[11]
Autoimmune neutropenia
Autoimmune neutropenia may be present with bacterial and
fungal
infections, or it may occur alone or with autoimmune diseases
(SLE, RA,
autoimmune hepatitis), infections and lymphoma. Bone marrow
examination

is needed if neutropenia is severe. For associated autoimmune
disorders, an
autoimmune antibody panel is necessary (ANA, ENA, and
dsDNA).[12]
Hemolytic disease of the fetus and the newborn
(erythroblastosis fetalis)
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ble
The maternal immune system suffers an initial sensitization to
the fetal Rh+
red blood cells during birth, when the placenta tears away. The
first child
escapes disease but the mother, now sensitized, will be capable
of causing a
hemolytic reaction against a second Rh+ fetus, which develops
anemia and
jaundice once the maternal IgG crosses the placenta.[13]
[14]Myasthenia gravis is an autoimmune disorder caused by
antibodies to
post-synaptic acetylcholine receptors that interfere w ith the
neuromuscular
transmission. It is characterized by extreme muscular fatigue,
double vision,
bilateral ptosis, deconjugate eye movements, difficulty
swallowing, and

weakness in upper arms. Babies born to myasthenic mothers can
have
transient muscle weakness due to pathogenic IgG antibodies that
cross the
placenta.
Goodpasture syndrome
Goodpasture syndrome is a type II hypersensitivity reaction
characterized by
the presence of nephritis in association with lung hemorrhage.
In most
patients, it is caused by cross-reactive autoantigens that are
present in the
basement membranes of the lung and kidney. A number of
patients with this
problem exhibit antibodies to collagen type IV, which is an
important
component of basement membranes.[15]
Pemphigus
Pemphigus causes a severe blistering disease that affects the
skin and mucous
membranes. The sera of patients with pemphigus have
antibodies against
desmoglein-1 and desmoglein-3, which are components of
desmosomes,
which form junctions between epidermal cells. Pemphigus is
strongly linked
to HLA-DR4 (DRB1*0402), which is a molecule that presents
one of the
autoantigens involved in the immunopathogenesis of this
disease
(desmoglein-3).[16][17]

Type III or Immunocomplex Reactions
These are also mediated by IgM and IgG antibodies that react
with soluble
antigens forming antigen-antibody complexes. The complement
system
becomes activated and releases chemotactic agents that attract
neutrophils
and cause inflammation and tissue damage as seen in vasculitis
and
glomerulonephritis. Type III hypersensitivity reactions can
classically be seen
in serum sickness and Arthus reaction.
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ble
ble
Serum sickness
Serum sickness can be induced with massive injections of
foreign antigen.
Circulating immune complexes infiltrate the blood vessel walls
and tissues,
causing an increased vascular permeability and leading to
inflammatory
processes such as vasculitis and arthritis. It was a complicati on
of anti-serum

prepared in animals to which some individuals produced
antibodies to the
foreign protein. It was also experienced in the treatment with
antibiotics such
as penicillin.[18]
Arthus reaction
Arthus reaction is a local reaction seen when a small quantity of
antigens is
injected into the skin repeatedly until detectable levels of
antibodies (IgG) are
present. If the same antigen is inoculated, immune complexes
develop at the
mentioned local site and in the endothelium of small vessels.
This reaction is
characterized by the presence of marked edema and hemorrhage,
depending
on the administered dose of the foreign antigen.[19][20]
Etiology
Multiple causes of IHR depend on the type of antigen or
allergen that trigger
this inappropriate immune reactivity. In type I hypersensitivity
reactions, the
allergens are proteins with a molecular weight ranging from 10
to 40 kDa.
These include cats, dust mite, German cockroaches, grass, rats,
fungi, plants,
and drugs. They stimulate the IgE production. Bee and wasp
venoms,
tree nuts (e.g., almond, hazelnut, walnut, and cashew), eggs,
milk, latex,
antibiotics (e.g., cephalosporins), heterologous antisera,
hormones (e.g.,
insulin) and others including shellfish and anesthetics can

trigger
anaphylaxis.[21]
In type II hypersensitivity reactions, the antigens can be found
in the
membrane of erythrocytes (e.g., A, B, O, C, c, D, d, E, e, K, k,
Fy, M, and N).
In transfusion reactions, all blood groups are not equally
antigenic, e.g., A or
B evoke stronger hypersensitivity reactions in an incompatible
recipient than
other antigens such as Fy.[22]
In type III hypersensitivity reactions, the persistence of antigen
from chronic
infection or autoimmune diseases can develop complex immune
diseases,
including vasculitis and glomerulonephritis. Penicillin as an
antigen can
ble
ble
ble
ble
ble
produce any hypersensitivity reactions, e.g., anaphylactic shock,
hemolytic
anemia, and serum sickness.[23]

Epidemiology
Hypersensitivity reactions are very common. Fifteen percent of
the world
population will be affected by any type of allergic reaction
during their lives.
In the second half of this century, allergic diseases have
increased. The cause
of the increase is unknown, but it may reflect lifestyle changes,
decreased
breastfeeding, and air pollution. The hygiene hypothesis
proposes that since
IgE is no longer needed to protect against parasites in the
Western world, the
IgE-mast cell axis has evolved in type I hypersensitivity
reaction.[24][25]
European data estimate that 0.3% of the population will be
troubled by
anaphylaxis at some point in their lives. In addition, 1 out of
3000 inpatients
in the United States experiences a severe allergic reaction every
year.
However, the prevalence of bronchial asthma was 1.5% in
Korea. Fernández-
Soto et al., 2018 reported that fungal infections could be as high
as 50% in
inner cities and constitute a risk factor predisposed to the
development of
allergic bronchial asthma.[26] Worldwide epidemiological data
of
anaphylaxis are scanty and remain unavailable in many
countries.
Pathophysiology
In type I hypersensitivity reactions after a previous
sensitization, the

immunoglobulin (Ig) E is produced and binds to Fc receptors on
mast cells
and basophils. On encountering the allergen, it triggered cross -
linking of
mast-cell cytophilic IgE, causing the activation of mast cells
and their
degranulation of mediators that cause an allergic reaction. The
mediators that
participate in this type of hypersensitivity reaction include
histamine and
lipid mediators such as PAF, LTC4, and PGD2 that cause a
vascular leak,
bronchoconstriction, inflammation, and intestinal hypermotility.
Enzymes
(e.g., tryptase causes tissue damage) and TNF causes
inflammation.
Eosinophils release cationic granule proteins, e.g., major basic
protein
(causes killing of host cells and parasites) and enzymes (e.g.,
eosinophil
peroxidase, which participates in tissue remodeling).[27]
In type II hypersensitivity reaction antibodies against basement
membranes
produce nephritis in Goodpasture's syndrome. Myasthenia
gravis and
ble
ble
ble
ble

ble
Lambert-Eaton syndrome are caused by antibodies that reduce
the amount of
acetylcholine at motor endplates, and autoantibodies to an
intercellular
adhesion molecule cause pemphigus.
In type III hypersensitivity reactions immune-complex
deposition (ICD)
causes autoimmune diseases, which is often a complication. As
the disease
progresses a more accumulation of immune-complexes occurs,
and when the
body becomes overloaded the complexes are deposited in the
tissues and
cause inflammation as the mononuclear phagocytes,
erythrocytes, and
complement system fail to remove immune complexes from the
blood.
Histopathology
Human basophils present multi-lobed nuclei and distinctive
granules. They
can be found in local tissues including the nose, lungs, skin or
gut in response
to allergic and immune responses. The two populations of mast
cells are
mucosal and connective tissue. They have morphological and
pharmacological differences. The mucosal mast cells can
associate with a
parasitic infestation, and connective tissue mast cells are
smaller and live
shorter. Both contain histamine and serotonin in their granules.
Skin biopsy

of patients with allergic dermatitis shows inflammatory
infiltrate with few
eosinophils, but their degranulation in the skin demonstrated in
the biopsy
stained with antibodies against eosinophil major basic protein
(MBP). In the
nasal smear of a patient with acute bronchial asthma, an
infiltrate consistent
of eosinophils, and polymorphonuclear cells with a normal
cytoplasm stained
with hematoxylin and eosin were shown.[28][29]
In type II hypersensitivity reactions, autoantibodies bind to
desmosome
involved in cell adhesion, and autoantibodies in diabetes
mellitus bind to islet
cells. They can be demonstrated in tissues by
immunofluorescence. The
method that uses fluorescent antibodies has also been used in
type
III hypersensitivity reactions to demonstrate the presence of
immune
complexes in the intima and media of the arterial wall, as well
as IgG and C3
deposits in kidney, joints, arteries, and skin. In Goodpasture
syndrome, the
antibodies involved are IgG and have the capacity to fix
complement.
Necrosis of the glomerulus, with fibrin deposition, is a major
feature of this
syndrome.[30][31]
History and Physical
ble

ble
ble
ble
In type I hypersensitivity reactions there is a history of atopy or
a patient
suffering from an allergic condition (e.g., bronchial asthma,
allergic rhinitis,
or food allergy). It may associate with recurrent infections
caused by viruses
and bacteria. For instance, bronchial asthma may link to
recurrent bacterial
pneumonia. Clinically allergic disorders may accompany by
airways
inflammation, wheezing attack, bronchial hyper-responsiveness,
tachycardia,
tachypnea, intense itching of the eyes and nose, sneezing,
rhinorrhea,
dermatitis, and gastrointestinal symptoms. Anaphylaxis, the
most severe type
of allergy, is clinically characterized by bronchospasm,
angioedema,
hypotension, loss of consciousness, generalized skin rash,
nausea, vomiting,
and abdominal cramps among other symptoms.[32]
In type II hypersensitivity reactions, a patient may report
multiple blood
transfusions, rhesus incompatibility, and drug history.
Clinically, it may
manifest as autoimmunity, e.g., autoimmune hemolytic anemia
(characterized

by jaundice), immune thrombocytopenia (characterized by
bleeding
disorders), and other blood dyscrasia (autoimmune neutropenia).
In this type
of hypersensitivity, drugs may attach to red blood cells and
stimulate the
production of anti-red blood cell antibodies or anti-dsDNA
antibody that
causes drug-induced systemic lupus erythematosus
(SLE).[33][34]
Type III hypersensitivity reactions may manifest as immune
complex-
mediated diseases including glomerulonephritis, vasculitis,
serositis, arthritis,
and skin manifestations of autoimmunity such as malar rash,
which is due to
photosensitivity. The prevalence of serum sickness has
decreased
dramatically because animal anti-serum is rarely used to treat or
prevent
infectious diseases. General manifestations of disease including
anorexia,
loss of weight, and asthenia may report in IHR.[35]
Evaluation
The evaluation of immediate hypersensitivity includes complete
blood cell
count, assessment of immunoglobulins, skin prick test, and
detection of
autoantibodies.[4][36][37][38]
Quantitative Serum Immunoglobulins
• IgG (involved in Type II and III HR)

• IgM (involved in Type II and III HR)
ble
ble
ble
ble
ble
ble
ble
ble
• IgE (elevated in allergic diseases)
Total Leukocyte Count and Differential
• Hb (decreased in autoimmune hemolytic anemia)
• Neutrophils (decreased in autoimmune neutropenia)
• Lymphocytes (decreased in autoimmune lymphopenia)
• Platelets (decreased in immune thrombocytopenia)
Autoimmunity Studies
• Anti-nuclear antibodies (ANA, present in systemic
autoimmune

disorders, such as SLE and RA)
• Detection of specific auto-immune antibodies for systemic
disorders,
e.g., anti-ds DNA, rheumatoid factor, anti-histones, anti-Smith,
anti-
(SS-A) and anti-(SS-B)
• Detection of anti-RBC, antiplatelet, and anti-neutrophil
antibodies
• Testing for organ-specific auto-immune antibodies, e.g., the
anti-Islet
cell autoantibody that is present in diabetes mellitus
• Coombs test (positive in autoimmune hemolytic anemia)
Allergic test
• Skin prick tests using various allergens from animal, plants,
food,
pathogens and environmental pollutants
• Radioallergosorbent test (RAST): Use to determine specific
IgE
antibodies
Treatment / Management
The treatment of immediate hypersensitivity reactions includes
the
management of anaphylaxis with intramuscular adrenaline
(epinephrine),
oxygen, intravenous (IV) antihistamine, support blood pressure
with IV
fluids, avoid latex gloves and equipment in patients who are
allergic, and

surgical procedures such as tracheotomy if there is severe
laryngeal edema.
Allergic bronchial asthma can be treated with any of the
following: inhaled
short- and long-acting bronchodilators (anticholinergics) along
with inhaled
corticosteroids, leukotriene antagonists, use of disodium
cromoglycate, and
environmental control. Experimentally, a low dose of
methotrexate or
cyclosporin and omalizumab (a monoclonal anti-IgE antibody)
has been
used. Treatment of autoimmune disorders (e.g., SLE) include
one or a
combination of NSAIDs and hydroxychloroquine, azathioprine,
methotrexate, mycophenolate, cyclophosphamide, low dose IL-
2, intravenous
immunoglobulins, and belimumab. Omalizumab is a monoclonal
antibody
that interacts with the binding site of the high-affinity IgE
receptor on mast
cells. It is an engineered, humanized recombinant
immunoglobulin. Moderate
to severe allergic bronchial asthma can improve with
omalizumab.[14][32][39][40]
Differential Diagnosis
Allergic bronchial asthma must be ruled out from other classes
of asthma
based on the family history of atopy and a positive skin prick
test. Chronic
allergic bronchial asthma loses reversibility and is
indistinguishable from

chronic obstructive pulmonary disease (COPD).
Allergic rhinitis must rule out other causes of rhinitis including
vasomotor,
non-allergic rhinitis with eosinophilia, drug-induced (cocaine
abuse),
mechanical (tumors, foreign body, sarcoidosis) and infectious
including viral,
bacterial and leprosy. In allergic rhinitis, IgE is elevated, and
prick test is
positive for similar allergens as those in allergy bronchial
asthma. Also,
family predisposition to allergies may be present.
Autoimmune hemolytic anemia (AIHA) can rule out from other
anemias
based on the presence of a positive direct Coombs' test.
Sometimes the AIHA
is secondary to lymphoma or autoimmune disease, especially
SLE, where
other blood dyscrasias including immune thrombocytopenia and
autoimmune
neutropenia may be present besides with the presence of anti -
dsDNA
antibodies, and clinical signs including malar rash,
nephropathy, vasculitis,
serositis, neuropathy, and among other problems.
Prognosis
The prognosis of IHR depends on the severity of the disorders,
the extension
of the inflammation and tissue damage, and the available
treatment and their
effectiveness to control the disease. Relapsing or slow
progression

ble
ble
ble
ble
characterizes myasthenia gravis. If presents with thymoma, 68%
of the
affected have a 5-year survival. In SLE, approximately 80%
survive at 15
years if treated. Atopic eczema (dermatitis) is usual ly most
severe in infancy
and improves with age in 80% of the cases. Allergic bronchial
asthma that
does not respond to steroids has a reserved prognosis.[41]
The prognosis of other allergic disorders, including food
allergy, drug
allergy, latex allergy, allergic conjunctivitis, and allergic
rhinitis is good once
the triggers identified using skin prick test or RAST and
treatment with anti-
histamine occurs. The use of monoclonal antibodies directed to
IgE (e.g.,
omalizumab) has improved the prognosis of patients that do not
respond well
to conventional therapy, although the acquisition of these
biologicals is
expensive. The use of vaccines, some classic and recently
experimental, is
another avenue of treatment of allergic disorders that improve
the life

expectancy and quality of individuals with allergies.
Complications
Some of the complications of immediate hypersensitivity
reactions are:
Status Asthmaticus
This is a type I hypersensitivity reaction, an acute exacerbation
of bronchial
asthma that does not respond to the standard therapy with
bronchodilators. It
is a medical emergency and must require aggressive
treatment.[42]
Anaphylactic Shock
This is an allergic reaction, often life-threatening, triggered by
an allergen to
which the immune system over-reacts.[43]
Post-Transfusion Reaction
This is a hypersensitivity reaction that occurs within 24 hours
of a blood
transfusion. Hemoglobinuria that appears during or after the
procedure
becomes an alarming sign. Other manifestatio ns include back
pain, fever,
chills, dizziness, and dyspnea.[44]
Serum Sickness
This is a type III hypersensitivity reaction that commences after
the
administration of a drug (e.g., penicillin) or heterologous anti -

serum or
ble
ble
ble
ble
plasma. Clinically, it is characterized by skin rash, fever,
arthralgias, or
arthritis. Immune-complexes mediate this complication, and it
may affect
many organs.[45]
Deterrence and Patient Education
Healthcare professionals can advise allergic patients about
environmental
control at home and work. Every attempt to reduce high
humidity and to
decrease house dust-mite exposure must do. The bedroom
should be clean,
and many use mattress covers and wash bedclothes regularly.
Pets, including
cats and dogs, are often the source of allergens and should not
be in
convivence with the affected patient, nor should living plants
and flowers,
which are "a sack of antigens." Patients should be encouraged to
explore therapeutic options for acute or chronic desensitization
for "bad
allergens." This may be the only way to control their allergic
bronchial

asthma.
Enhancing Healthcare Team Outcomes
The management of an immediate hypersensitive reaction is best
done with a
multidisciplinary team that includes ICU nurses.
To improve patient outcomes, clinicians should be aware that
immediate
hypersensitivity reactions are a medical emergency. No time
should be
wasted with blood work or imaging studies. The treatment of
immediate
hypersensitivity reactions includes the management of
anaphylaxis with
intramuscular adrenaline (epinephrine), oxygen, intravenous
(IV)
antihistamine, support blood pressure with IV fluids, avoid
latex gloves and
equipment in patients who are allergic, and surgical procedures
such as
tracheotomy if there is severe laryngeal edema. These patients
are best
managed in an ICU setting.
Healthcare professionals should advise allergic patients about
environmental
control at home and work. Every attempt to reduce high
humidity and to
decrease house dust-mite exposure must do. The bedroom
should be clean,
and many use mattress covers and wash bedclothes regularly.
Pets, including
cats and dogs, are often the source of allergens and should not
be in
convivence with the affected patient, nor should living pl ants

and flowers,
which are "a sack of antigens." Patients should be encouraged to
ble
explore therapeutic options for acute or chronic desensitization
for "bad
allergens." This may be the only way to control their allergic
bronchial
asthma.
Questions
To access free multiple choice questions on this topic, click
here.
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Immunopathol (Madr). 2018 Nov - Dec;46(6):557-564.
[PubMed:
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Hypersensitivity
ReactionsAuthorsAffiliationsIntroductionEtiologyEpidemiology
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PhysicalEvaluationTreatment / ManagementDifferential
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