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Treatment

Many treatment strategies for peripheral neuropathy are symptomatic. Some current research inanimal models has shown that neurotrophin-3 can oppose the demyelination present in some

peripheral neuropathies.[10]

A range of drugs that act on the central nervous system such as drugs originally intended as

antidepressants and antiepileptic drugs have been found to be useful in managing neuropathicpain. Commonly used treatments include using a tricyclic antidepressant (such as amitriptyline)

and antiepileptic therapies such as gabapentin orsodium valproate. These have the advantagethat besides being effective in many cases they are relatively low cost.

A great deal of research has been done between 2005 and 2010 which indicates that synthetic

cannabinoids and inhaled cannabis are effective treatments for a range of neuropathic disorders.[11]

Research has demonstrated that the synthetic oral cannabinoid Nabilone is an effective

adjunct treatment option for neuropathic conditions, especially for people who are resistant,

intolerant, or allergic to common medications.[12] Orally, opiate derivatives were found to bemore effective than cannabis for most people.

[13]Smoked cannabis has been found to provide

relief from HIV-associated sensory neuropathy.[14]

Smoked cannabis was also found to relieve

neuropathy associated with CRPS type I, spinal cord injury, peripheral neuropathy, and nerveinjury.

[15]

Pregabalin (INN, pronounced /prbln/) is an anticonvulsant drug used for neuropathic

pain. It has also been found effective for generalized anxiety disorder. It was designed as a morepotent successor to gabapentin but is significantly more expensive, especially now the patent on

gabapentin has expired and gabapentin is available as a generic drug. Pregabalin is marketed byPfizer under the trade name Lyrica.

TENS (Transcutaneous Electrical Nerve Stimulation) therapy may be effective and safe in the

treatment of diabetic peripheral neuropathy. A recent review of three trials involving 78 patientsfound some improvement in pain scores after 4 and 6 but not 12 weeks of treatment, and an

overall improvement in neuropathic symptoms at 12 weeks.[16] A second review of four trialsfound significant improvement in pain and overall symptoms, with 38% of patients in one trial

becoming asymptomatic. The treatment remains effective even after prolonged use, butsymptoms return to baseline within a month of treatment cessation.

[17]

GuillainBarr syndrome (GBS) (French pronunciation: [ij bae];[1][2]

in English, pronounced

/iln bre/,[3]

/iln bre/,[4]

etc.[5]

) is an acute inflammatory demyelinating

polyneuropathy (AIDP), an autoimmune disorder affecting theperipheral nervous system,usually triggered by an acute infectious process. The syndrome was named after the French

physicians Guillain, Barr and Strohl, who were the first to describe it in 1916. It is sometimescalled Landry's paralysis, after the French physician who first described a variant of it in 1859. It

is included in the wider group ofperipheral neuropathies. There are several types of GBS, butunless otherwise stated, GBS refers to the most common form, AIDP. GBS is rare and has an

incidence of 1 or 2 people per 100,000.[6]

It is frequently severe and usually exhibits as an


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ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the facealong with complete loss of deep tendon reflexes. With prompt treatment byplasmapheresis or

intravenous immunoglobulins and supportive care, the majority of patients will regain fullfunctional capacity. However, death may occur if severe pulmonary complications and

autonomic nervous system problems are present.[7]

Guillain-Barr is one of the leading causes of

non-trauma-induced paralysis in the world.

[citation needed]

American actor Andy Griffith developed Guillain-Barr syndrome in 1983. Griffith is seen here receiving

an award at the U.S. White House in 2005

Contents

[hide]

y 1 Classification

y 2 Signs and symptoms

y 3 Cause

o 3.1 Influenza vaccine

y 4 Diagnosis

o 4.1 Diagnostic criteria

4.1.1 Required

4.1.2 Supportive

o

4.2 Differential diagnosisy 5 Management

y 6 Prognosis

y 7 Epidemiology

y 8 History

y 9 Notable sufferers

y 10 References


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y 11 External links

[edit] Classification

Six different subtypes of GuillainBarr syndrome (GBS) exist:

y Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common form of GBS,

and the term is often used synonymously with GBS. It is caused by an auto-immune response

directed against Schwann cell membranes.

y Miller Fisher syndrome (MFS) is a rare variant of GBS and manifests as a descending paralysis,

proceeding in the reverse order of the more common form of GBS. It usually affects the eye

muscles first and presents with the triad ofophthalmoplegia, ataxia, and areflexia. Anti-GQ1b

antibodies are present in 90% of cases.

y Acute motor axonal neuropathy (AMAN),[8]

aka Chinese Paralytic Syndrome, attacks motor

nodes of Ranvier and is prevalent in China and Mexico. It is probably due to an auto-immune

response directed against the axoplasm ofperipheral nerves. The disease may be seasonal andrecovery can be rapid. Anti-GD1a antibodies

[9]are present. Anti-GD3 antibodies are found more

frequently in AMAN.

y Acute motor sensory axonal neuropathy (AMSAN) is similar to AMAN but also affects sensory

nerves with severe axonal damage. Like AMAN, it is probably due to an auto-immune response

directed against the axoplasm of peripheral nerves. Recovery is slow and often incomplete.[10]

y Acute panautonomic neuropathy is the most rare variant of GBS, sometimes accompanied by

encephalopathy. It is associated with a high mortality rate, owing to cardiovascular involvement,

and associated dysrhythmias. Impaired sweating, lack of tear formation, photophobia, dryness

of nasal and oral mucosa, itching and peeling of skin, nausea, dysphagia, constipation unrelieved

by laxatives or alternating with diarrhea occur frequently in this patient group. Initial nonspecific

symptoms of lethargy, fatigue, headache, and decreased initiative are followed by autonomicsymptoms including orthostatic lightheadedness, blurring of vision, abdominal pain, diarrhea,

dryness of eyes, and disturbed micturition. The most common symptoms at onset are related to

orthostatic intolerance, as well as gastrointestinal and sudomotor dysfunction (Suarez et al.

1994). Parasympathetic impairment (abdominal pain, vomiting, obstipation, ileus, urinary

retention, dilated unreactive pupils, loss of accommodation) may also be observed.

y Bickerstaffs brainstem encephalitis (BBE), is a further variant of GuillainBarr syndrome. It is

characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness,

hyperreflexia or Babinskis sign (Bickerstaff, 1957; Al-Din et al.,1982). The course of the disease

can be monophasic or remitting-relapsing. Large, irregular hyperintense lesions located mainly

in the brainstem, especially in the pons, midbrain and medulla are described in the literature.

BBE despite severe initial presentation usually has a good prognosis. Magnetic resonance

imaging (MRI) plays a critical role in the diagnosis of BBE.

A considerable number of BBE patients have associated axonal GuillainBarr syndrome,

indicative that the two disorders are closely related and form a continuous spectrum.

[edit] Signs and symptoms


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The disorder is characterized by symmetrical weakness which usually affects the lower limbsfirst, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their

legs, manifesting as "rubbery legs" or legs that tend to buckle, with or without dysesthesias(numbness or tingling). As the weakness progresses upward, usually over periods of hours to

days, the arms and facial muscles also become affected. Frequently, the lowercranial nerves may

be affected, leading tobulbarweakness, oropharyngealdysphagia (drooling, or difficultyswallowing and/or maintaining an open airway) and respiratory difficulties. Most patients requirehospitalization and about 30% require ventilatory assistance.

[11]Facial weakness is also

commonly a feature, but eye movement abnormalities are not commonly seen in ascending GBS,but are a prominent feature in the Miller-Fisher variant (see below.) Sensory loss, if present,

usually takes the form of loss ofproprioception (position sense) and areflexia (complete loss ofdeep tendon reflexes), an important feature of GBS. Loss of pain and temperature sensation is

usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usuallyin the weakened muscles, which patients compare to the pain from overexercising. These pains

are self-limited and should be treated with standard analgesics. Bladderdysfunction may occur insevere cases but should be transient. If severe, spinal cord disorder should be suspected.

Fevershould not be present, and if it is, another cause should be suspected.

In severe cases of GBS, loss ofautonomic function is common, manifesting as wide fluctuations

inblood pressure, orthostatic hypotension, and cardiac arrhythmias.

Acute paralysis in GuillainBarr syndrome may be related to sodium channel blocking factor in

the cerebrospinal fluid (CSF). Significant issues involving intravenous salt and wateradministration may occur unpredictably in this patient group, resulting in SIADH. SIADH is one

of the causes of hyponatremia and can be accompanied with various conditions such asmalignancies, infections and nervous system diseases. Symptoms of Guillain- Barre syndrome

such as general weakness, decreased consciousness, and seizure are similar to those ofhyponatremia

The symptoms of GuillainBarr syndrome are also similar to those forprogressive

inflammatory neuropathy.[12]

[edit] Cause

Structure of a typical neuron

Neuron


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Dendrite

Soma

Axon

Nucleus

Node of

Ranvier

Axon terminal

Schwann cell

Myelin sheath

All forms of GuillainBarr syndrome are due to an immune response to foreign antigens (such

as infectious agents) that are mistargeted at host nerve tissues instead. The targets of suchimmune attack are thought to be gangliosides, compounds naturally present in large quantities in

human nerve tissues. The most common antecedent infection is the bacterium Campylobacterjejuni.

[13][14]However, 60% of cases do not have a known cause; one study suggests that some

cases are triggered by the influenza virus, or by an immune reaction to the influenza virus.[15]

The end result of such autoimmune attack on the peripheral nerves is damage to the myelin, the

fatty insulating layer of the nerve, and a nerve conduction block, leading to a muscle paralysis

that may be accompanied by sensory orautonomic disturbances.

However, in mild cases, nerve axon (the long slender conducting portion of a nerve) function

remains intact and recovery can be rapid if remyelination occurs. In severe cases, axonal damageoccurs, and recovery depends on the regeneration of this important tissue. Recent studies on the

disorder have demonstrated that approximately 80% of the patients have myelin loss, whereas, inthe remaining 20%, the pathologic hallmark of the disorder is indeed axon loss.


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Guillain-Barr, unlike disorders such as multiple sclerosis (MS) and Lou Gehrig's disease (ALS),is a peripheral nerve disorder and does not generally cause nerve damage to the brain or spinal

cord.

[edit] Influenza vaccine

GBS may be a rare side-effect ofinfluenza vaccines; a study of the Vaccine Adverse EventReporting System (VAERS) indicates that it is reported as an adverse event potentially

associated with the vaccine at a rate of an excess of 1 per million vaccines (over the normalrisk).

[16]There were reports of GBS affecting an excess of 10 per million who had received

swine flu immunizations in the 1976 U.S. outbreak of swine flu25 of which resulted in deathfrom severe pulmonary complications, leading the government to end that immunization

campaign.[17]

However, the role of the vaccine in these cases has remained unclear, partlybecause GBS had an unknown but very low incidence rate in the general population making it

difficult to assess whether the vaccine was really increasing the risk for GBS. Later research haspointed to the absence of or only a very small increase in the GBS risk due to the 1976 swine flu

vaccine.

[18]

Furthermore, the GBS may not have been directly due to the vaccine but to abacterial contamination of the vaccine.[19]

Since 1976, no other influenza vaccines have been linked to GBS, though as aprecautionary

principle, caution is advised for certain individuals, particularly those with a history ofGBS.[20][21] On the other hand, getting infected by the flu increases the risk of developing GBS to

a much higher level (approx. 10 times higher by recent estimates[22]

) and, all in all, the fluvaccination contributes protection against the risk of GBS.

[23]

From October 6 to November 24, 2009, the U.S. CDC, through the VAERS reporting system,

received ten reports of Guillain-Barre syndrome cases associated with the H1N1 vaccine and

identified two additional probable cases from VAERS reports (46.2 million doses weredistributed within the U.S. during this time). Only four cases, however, meet the BrightonCollaboration Criteria for GuillainBarr syndrome, while four do not meet the criteria and four

remain under review.[24]

A preliminary report by the CDC's Emerging Infections Programs (EIP)calculates the rate of GBS observed in patients who previously received the 2009 H1N1influenza vaccination is an excess of 0.8 per million cases, which is on par with the rate seen

with the seasonal trivalent influenze vaccine. [25]

[edit] Diagnosis

The diagnosis of GBS usually depends on findings such as rapid development of muscle

paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis(through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as

nerve conduction studies) are common tests ordered in the diagnosis of GBS.

y cerebrospinal fluid

Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes,

this is an elevated protein level (1001000 mg/dL), without an accompanying increased cell


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count pleocytosis. A sustained increased white blood cell count may indicate an alternative

diagnosis such as infection.

y Electrodiagnostics

Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distallatencies, conduction slowing, conduction block, and temporal dispersion of compound action

potential in demyelinating cases. In primary axonal damage, the findings include reduced

amplitude of the action potentials without conduction slowing.

[edit] Diagnostic criteria

[edit] Required

y Progressive, relatively symmetrical weakness of two or more limbs due to neuropathy

y Areflexia

y Disorder course < 4 weeksy Exclusion of other causes (see below)

[edit] Supportive

y relatively symmetric weakness accompanied by numbness and/or tingling

y mild sensory involvement

y facial nerve or other cranial nerve involvement

y absence of fever

y typical CSF findings obtained from lumbar puncture

y electrophysiologic evidence of demyelination from electromyogram

[edit] Differential diagnosis

y acute myelopathies with chronic back pain and sphincter dysfunction

y botulism with early loss of pupillary reactivity and descending paralysis

y diphtheria with early oropharyngeal dysfunction

y Lyme disease polyradiculitis and other tick-borne paralyses

y porphyria with abdominal pain, seizures, psychosis

y vasculitis neuropathy

y poliomyelitis with fever and meningeal signs

y CMV polyradiculitis in immunocompromised patients

y critical illness neuropathy

y myasthenia gravis

y poisonings with organophosphate, poison hemlock, thallium, or arsenic

y paresis caused by West Nile virus

y spinal astrocytoma

y Motor Neurone Disease

y West Nile virus can cause severe, potentially fatal neurological illnesses, which include

encephalitis, meningitis, Guillain-Barre syndrome, and anterior myelitis.

y Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.


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[edit] Management

Supportive care with monitoring of all vital functions is the cornerstone of successfulmanagement in the acute patient. Of greatest concern is respiratory failure due to paralysis of the

diaphragm. Early intubation should be considered in any patient with a vital capacity (VC)


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is still about 23% even in the best intensive care units. Worldwide, the death rate runs slightlyhigher (4%), mostly from a lack of availability of life support equipment during the lengthy

plateau lasting four to six weeks, and in some cases up to one year, when a ventilator is neededin the worst cases. About 510% of patients have one or more late relapses, in which case they

are then classified as having chronic inflammatory demyelinating polyneuropathy (CIDP).

Poor prognostic factors include: 1) age >40 years, 2) history of preceding diarrheal illness, 3)requiring ventilator support, 4) high anti-GM1 titre and 5) poor upper limb muscle strength.

Case reports do exist of rapid patient recovery.

[edit] Epidemiology

The incidence of GBS during pregnancy is 1.7 cases per 100,000 of the population.[28]

Themother will generally improve with treatment but death of the fetus is a risk. The risk of

GuillainBarr syndrome increases after delivery, particularly during the first two weeks

postpartum. There is evidence ofCampylobacter jejuni as an antecedent infection inapproximately 26% of disease cases, requiring special care in the preparation and handling offood. Congenital and neonatal GuillainBarr syndrome have also been reported.[29]

[edit] History

The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges

Guillain, Jean Alexandre Barr, and Andr Strohl diagnosed two soldiers with the illness anddiscovered the key diagnostic abnormality of increased spinal fluid protein production, but

normal cell count.[30]

GBS is also known as acute inflammatory demyelinating polyneuropathy, acute idiopathicpolyradiculoneuritis, acute idiopathic polyneuritis,French Polio,Landry's ascending paralysis

andLandry Guillain Barr syndrome.

[edit] Notable sufferers

y Andy Griffith, American actor onAndy Griffith Show, and Matlock. He developed GuillainBarr

in 1983.[31]

y Rachel Chagall, actress, contracted GBS in 1982. In 1987 she portrayed Gabriela Brimmer, a

notable disabilities activist.[32]

y Joseph Heller, author, contracted GBS in 1981. This episode in his life is recounted in theautobiographical No Laughing Matter, which contains alternating chapters by Heller and his

good friend Speed Vogel.[33]

y Franklin D. Roosevelt, U.S. president. In 2003, a peer-reviewed study[34] found that it was more

likely that Roosevelt's paralysislong attributed to poliomyelitiswas actually GuillainBarr

syndrome.

y Markus Babbel, former international footballer, contracted GBS in 2001, following a period

suffering from the EpsteinBarr virus. He lost almost an entire year of his footballing career


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between the two illnesses and never again demonstrated the same level of ability that won him

over 50 caps for Germany.[35]

y Serge Payer, Canadian-born professional hockey player. After battling and overcoming the

syndrome, he set up the Serge Payer Foundation, which is dedicated to raising money for

research into new treatments and cures for GuillainBarr syndrome.[36]

y Hans Vonk, Dutch conductor.[37]

y Lucky Oceans, Grammy Award winning musician with Asleep at the Wheel was diagnosed with

GBS in 2008.[38]

y William The Refrigerator Perry, former professional American football player with the Chicago

Bears was diagnosed with GBS in 2008.[39]

y Tony Benn, British politician.[40]

y Len Pasquarelli, sports writer and analyst for ESPN and resident of the Pro Football Writers of

America, diagnosed in 2008.[41]

y Hiroko Mima, Miss Universe Japan 2008, was diagnosed with GBS at the age of 13.[42]

y Norton Simon[43]

y Hugh McElhenny, former Hall-of-Fame, professional American football player with the San

Francisco 49ers.[44]

y Luci Baines Johnson, daughter of President Lyndon Johnson and Lady Bird Johnson. Diagnosedand under treatment for GuillainBarr in April 2010.

[45]

y Zeituni Onyango, paternal aunt of U.S. President Barack Obama.[46]

[edit] References

Polyarteritis nodosa (also known as "Panarteritis nodosa,"[1] and "Periarteritis nodosa"[1]) is a

vasculitis of medium-sized arteries, which become swollen and damaged from attack by rogue

immune cells. Polyarteritis nodosa is also called Kussmaul disease orKussmaul-Maierdisease.

[2]Infantile polyarteritis nodosa is a type of PAN restricted to infants.

[3]

Contents

[hide]

y 1 Causes and risk factorsy 2 Incidence

y 3 Symptomsy 4 Diagnosis

y 5 Treatment and Prognosisy 6 Complications

y 7 Preventiony 8 See also

y 9 Referencesy 10 External links

[edit] Causes and riskfactors


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Polyarteritis nodosa is a disease of unknown cause that affects arteries, the blood vessels thatcarry blood from the heart to organs and tissues. It occurs when certain immune cells attack the

affected arteries. It is caused by immune complex deposition in the walls of blood vessels, whichmakes it a type III hypersensitivity reaction.

Incidence

The condition affects adults more frequently than children and males more frequently thanfemales. It damages the tissues supplied by the affected arteries because they don't receive

enough oxygen and nourishment without a proper blood supply.

Polyarteritis nodosa is more common in people with hepatitis B infection.[4]

[edit] Symptoms

In this disease, symptoms result from ischaemic damage to affected organs, often the skin, heart,kidneys, and nervous system.

Generalised symptoms include fever, fatigue, weakness, loss of appetite, and weight loss. Muscle

and joint aches are common. The skin may show rashes, swelling, ulcers, and lumps.[citation needed]

Nerve involvement may cause sensory changes with numbness, pain, burning, and weakness.Central nervous system involvement may cause strokes or seizures. Kidney involvement can

produce varying degrees of renal failure.[citation needed]

Involvement of the arteries of the heart may cause a heart attack, heart failure, and inflammation

of the sac around the heart (pericarditis).

y Fatiguey Weakness

y Fevery Abdominal pain

y Decreased appetitey Unintentional weight loss

y Muscle achesy Joint aches

[citation needed]

[edit] Diagnosis

There are no specific lab tests for diagnosing polyarteritis nodosa. Diagnosis is generally basedupon the physical examination and a few laboratory studies that help to confirm the diagnosis:

y CBC (may demonstrate an elevated white blood count)

y ESR(elevated)


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y Perinuclear pattern of antineutrophil cytoplasmic antibodies (p-ANCA) - notassociated with "classic" polyarteritis nodosa, but is present in a form of the

disease affecting smaller blood vessels, known as microscopic polyangiitis orleukocytoclastic angiitis.

y Tissue biopsy (reveals inflammation in small arteries, called arteritis)y

Elevated C-reactive protein

A patient is said to have polyarteritis nodosa if he or she has 3 of the 10 following signs known

as the 1990 ACR (American College of Rheumatology)[5]

criteria:

y Weight loss greater than/equal to 4.5 kg.y Livedo reticularis (a mottled purplish skin discoloration over the extremities or

torso).y Testicular pain or tenderness. (occasionally, a site biopsied for diagnosis).

y Muscle pain, weakness, or leg tenderness.y Nerve disease (either single or multiple).

y

Diastolic blood pressure greater than 90mmHg (high blood pressure).y Elevated kidney blood tests (BUN greater than 40 mg/dl orcreatinine greater than

1.5 mg/dl).y Hepatitis B virus tests positive (for surface antigen or antibody).

y Arteriogram (angiogram) showing the arteries that are dilated (aneurysms) orconstricted by the blood vessel inflammation.

y Biopsy of tissue showing the arteritis (typically inflamed arteries).[6]

It should be underlined that the 1990 ACR criteria were designed for classification purposes

only. Nevertheless their good discriminatory performances, indicated by the initial ACRanalysis, suggested their potential usefulness for diagnostic purposes also. Subsequent studies

did not confirm their diagnostic utility, demonstrating a significant dependence of theirdiscriminant abilities on the prevalence of the various vasculitides in the analyzed populations.

Recently an original study, combining the analysis of more than 100 items used to describepatients characteristics in a large sample of vasculitides with a computer simulation technique

designed to test the potential diagnostic utility of the various criteria, proposed a set of eightpositively or negatively PAN discriminating items to be used a screening tool for PAN diagnosis

in patients suspected of systemic vasculitis.[7]

[edit] Treatment and Prognosis

Treatment involves medications to suppress the immune system, includingprednisone and

cyclophosphamide. Therapy results in remissions or cures in 90% of cases. Untreated, thedisease is fatal in most cases. The most serious associated conditions generally involve the

kidneys and gastrointestinal tract.A fatal course usually involves gastrointestinal hemorrhage,infection, myocardial infarction and/or renal failure.

[8]

[edit] Complications


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y Stroke[citation needed]

y Kidney failure

[citation needed]

y Heart attack[citation needed]

y Intestinal necrosis and perforation[citation needed]

[edit] Prevention

This disease cannot be currently prevented, but early treatment can prevent some damage andsymptoms.

[citation needed]

[edit] See also

y List of cutaneous conditions

ChurgStrauss syndrome (also known as "Allergic granulomatosis"[1]

) is a medium and small

vessel autoimmunevasculitis, leading to necrosis. It involves mainly the blood vessels of thelungs (it begins as a severe type ofasthma), gastrointestinal system, and peripheral nerves, butalso affects the heart, skin and kidneys. It is a rare disease that is non-inheritable, non-

transmissible. Churg-Strauss syndrome was once considered a type ofpolyarteritis nodosa due totheir similar morphologies.

The syndrome was first described by Drs. Jacob Churg and Lotte Strauss at Mount Sinai HospitalinNew York City in 1951.

[2][3]

Contents

[hide]

y 1 Diagnosis

y 2 Disease stagesy 3 Risk stratification

y 4 Treatmenty 5 Montelukast

y 6 Famous patientsy 7 Referencesy 8 External links

[edit] Diagnosis

Diagnostic markers include eosinophil granulocytes and granulomas in affected tissue and anti-neutrophil cytoplasmic antibodies (ANCA) against neutrophil granulocytes. Differentiation from

Wegener's granulomatosis can be difficult, though the increasing use of ANCA assays has made


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the leukotriene receptor antagonist, montelukast."[6]

Researchers have searched for links betweendrugs such as montelukast (Singulair)

[7]and Churg-Strauss syndrome; in another study in 2000,

researchers did not find a cause-and-effect relationship and wrote: "The occurrence of Churg-Strauss syndrome in asthmatic patients receiving leukotriene modifiers appears to be related to

unmasking of an underlying vasculitic syndrome that is initially clinically recognized as

moderate to severe asthma and treated with corticosteroids. Montelukast does not appear todirectly cause the syndrome in these patients."[8] A case study in 2006 was inconclusive butsuggested the need for further research.

[9]

[edit] Famous patients

The memoirPatient, by the musician Ben Watt, deals with Watt's mid-1990s experience withChurg-Strauss syndrome, and his recovery. Watt's case was unusual in that it mainly affected his

gastrointestinal tract, leaving his lungs largely unaffected; this unusual presentation contributedto a delay in proper diagnosis. His treatment required the removal of large sections of necrotized

intestine, leaving Watt on a permanently restricted diet.

Umaru Musa Yar'Adua, the president ofNigeria from 2007-2010, reportedly suffered fromChurg-Strauss syndrome and died in office of complications of the disease.

[10]

The DJ and authorCharlie Gillett was diagnosed with Churg-Strauss in 2006; he died four yearslater.

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