Gout

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

Gout is a common arthritis caused by deposition of monosodium urate crystals within joints after chronic hyperuricaemia. It affects 1-2% of adults in developed countries, where it is the most common inflammatory arthritis in men. Epidemiological data are consistent with a rise in prevalence of gout. Diet and genetic polymorphisms of renal transporters of urate seem to be the main causal factors of primary gout. Gout and hyperuricaemia are associated with hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular diseases. Non-steroidal anti-inflammatory drugs and colchicine remain the most widely recommended drugs to treat acute attacks. Oral corticosteroids could be an alternative to these drugs. Interleukin 1beta is a pivotal mediator of acute gout and could become a therapeutic target. When serum uric acid concentrations are lowered below monosodium urate saturation point, the crystals dissolve and gout can be cured. Patient education, appropriate lifestyle advice, and treatment of comorbidities are an important part of management of patients with gout.

Gout, otherwise called as metabolic arthritis is a congenital disorder of Uric acid metabolism. In this condition, monosodium urate or uric acid crystals are deposited on the articular cartilage of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.

• Gout was first described by Egyptians in 2640 BC.
• Hippocrates described podagra in 5th century BC as the unwalkable disease.
• Galen described the monosodium urate crystal deposition following long standing hyperuricemia as Tophi. He described gout as a discharge of the four humors of the body in unbalanced amounts into the joints.
• The word Gout was first used in 1200s AD by Dominican monk Randolphus of Bocking and was derived from the Latin word ‘Gutta’.
• Aulus Cornelius Celsus discovered many symptoms of gout.

Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Defects in the kidney may cause uric acid to build up in the blood, leading to hyperuricemia, and the subsequent formation of gout crystals.

Gout needs to be differentiated from other diseases such as cellulitis, rheumatoid arthritis, septic arthritis and sarcoidosis as they present with similar symptoms.

Gout affects men in age group 40-50 years. It is more common in people from the Pacific Islands, and New Zealand. In the United States, gout is twice as prevalent in African American males as it is in Caucasians.

Several factors may put a person at risk for developing gout. These include the presence of; hypertension, diabetes, hypercholesterolemia, obesity, and alcohol abuse. Certain medications may also put a person at a higher risk for developing gout.

The prognosis of gout is good if it is treated early, and if the person maintains a healthy lifestyle with modification of their individual risk factors.

The classic picture of an acute gouty attack, is sudden, excruciating, unexpected and burning pain. There will also be swelling, redness, warmth, and stiffness in the joint. In approximately 75% of first episodes, gout usually attacks the big toe.

A definitive diagnosis of gout is made from light microscopy of the fluid aspirated from the joint. The fluid demonstrates intracellular negatively bi-refringent monosodium urate crystals and polymorphonuclear leukocytes in the synovial fluid. Although hyperuricemia is a common feature of gout, a high uric acid level does not necessarily mean a person will develop gout.

An x-ray is done when gout is suspected to rule out other abnormalities of the bone that may be causing the pain. Most commonly in gout, the x-ray will show no abnormalities, or a small amount of soft tissue swelling.

The first goal of therapy when treating gout, is pain relief. This can be acheived with NSAIDs, and oral or intra-articular glucocorticoids. If colchicine is given, it should be taken within the first 12 hours of the attack. Other, less standard methods of treatment include the use of hemorrhoidal ointment, ice, increasing mobility, and acetazolamide.

For extreme cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.

There are several methods used to prevent a re-occurrence of gout. Dietary changes include reducing the intake of foods that increase the levels of purine in blood, such as protein and alcohol. Several foods, and vitamin C have been thought to decrease the levels of purine in the blood. Modification of the risk factors for gout has been shown to also be beneficial in reducing the reoccurrence of gout. There are medications which can increase the excretion of uric acid, and reduce uric acid levels through other mechanisms.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

• Gout was first described by Egyptians in 2640 BC.
• Hippocrates described podagra in 5th century BC as an unwalkable disease.
• Galen described the monosodium urate crystal deposition following long-standing hyperuricemia as Tophi. He described gout as a discharge of the four humors of the body is unbalanced amounts into the joints.
• The word Gout was first used in 1200s AD by Dominican monk Randolphus of Bocking and was derived from the Latin word ‘Gutta’.
• Aulus Cornelius Celsus discovered many symptoms of gout.

Gout was first identified by Egyptians around 2640 BC^[1]. This is one of the most studied diseases do far with more than millions^[2] of people still suffering from the disease until today. Out of them, the males are affected the most. The scientist has a lot to offer regarding this chronic and debilitating disease. Although it was first recognized by Egyptians the first clinical description of the disease came from Hippocrates ( 460-370)^[3]. After a century later there is another scientist named Cappadocian gave a proposal that the gout disease is caused by the toxin in the blood. Which later on given the name of Uric acid in further studies.

The first person to name the disease was “Randolph of Bocking” in the early 1200s^[1]. The term is usually derived from the Latin word gutta or drop. Till day the variation of terms is seen in different languages all over the world. In English “gout”, In French ” goutte” and in the Italian language it means ” gotta” and in German named as “gicht”

Understanding the disease

In the seventeenth century the scientist “Thomas Sydenham” was the first person to study the aspects of Gout disease in terms of Acute or chronic aspects. He also helps in explaining and differentiating gout from the other diseases related to different forms of arthritis.

The tophi that are uric acid crystal deposits those were fist identified, studied, and described these as tiny needle-like particles under the microscope by the famous scientist “Anton Von Leeuwenhoek”.

This was later identified as urate crystals by a Swedish scientist named “Carl Scheele”.

Advance Work-up

The next remarkable contribution to the study of gout was made by Alfred Baring Garrod. He conducted some great experiments and eye-opening research where he demonstrated the relation between high levels of uric acid in the bloodstream and the development of gout.

Search for to control the disease

Different treatment and management theories are studied and implemented to manage the Gout over years but the Early treatment options that came from Hippocrates included minimal water and counterirritation that is basically scorching the veins near the joint affected. Bloodletting is also one of the ancient techniques used at that time.

Introducing the colchicine

Although colchicine was used in ancient times for more than 2000 years it was first used for the treatment of Gout Alexander of Tralles in around 600 AD. Then due to any reason, this was out of use for hundreds of years before re-discovering it for use by an Australian physician Baron Anton de Stock in 1700. The most noticeable user for the colchicine was Benjamin Franklin. Till today the colchicine therapy is used to prevent gout flares and played a huge role in the management of patients with Gout.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

Hyperuricemia is considered a multifactorial metabolic disorder in the general population. The levels of uric acid are influenced by the use of drugs, medications, renal impairment, and Alcohol also. The excess of uric acid levels gets deposited in the joints, kidneys, and a lot of tissue leading to clinical manifestations such as tophi, nephrolithiasis along the presence of urate nephropathy. Decreased excretion of uric acid contributes the maximum towards the development of Hyperuricemia. Along with the minimal contribution from other factors like increased production and increased consumption of foods rich in uric acid. The deposits in the joints, skin, and other tissues compromise the function of organs and resulting in the abnormal configuration of joint with funv=ctional limitation along with the presence of clinical signs in the form of pain and swelling.

In terms of pathophysiological classification, we can categorize gout into 2 main types

1) Primary gout: Mainly hereditary or related to enzymatic abnormalities

2) Secondary Gout: Secondary to other reasons like drugs, renal insufficiency, dietary or related to malignancy

The pathophysiology^[1][2]of Gout mainly relates to hyperuricemia. Greater is the degree of hyperuricemia greater is the likelihood of developing Gout^[3].

Numerous reasons can lead to the development of an increase in the level of uric acids^[4][5]:

• Enhanced or increased purine uptake.
• Decreased excretion of uric acid
• Increased production of uric acid
• Etiology in a lot of cases with rising uric acid levels is still unknown.
  

Increased intake

The increased uptake is mainly related to

• Increases intake of purine-rich food substances by the patient such as
  • Asparagus, meat broths, mushrooms, liver, kidney, sweetbreads.
  • The increased intake of all of these substances can increase the risk of accumulation of more and more purines ultimately resulting in the excess of uric acid.

• Beer is also particularly rich in guanosine which is a purine nucleotide.

Increased production

The increased production is mainly

• Increase in turn over of cells like in various hematological conditions such as Hemolytic anemia, leukemia, and lymphoma.
• Conditions associated with an increased rate of cell proliferation and cell death.
  • Cytotoxic therapy
  • Radiation
  • Psoriasis^[6]
• Obesity – As the urate production is directly proportional to the body surface area

• Hereditary conditions

  

• Enzyme abnormalities
  • Overactivity of Phosphoribosyltransferase
  • Deficiency of HGPRT
  • Absence of HGPRT ( Lesch-Nyhan syndrome)^[7]

Decreased/Reduced renal excretion

This is the most common cause of hyperuricemia. Various factors responsible for its reduced elimination are:

• Hereditary
• Compromised renal function ( Reduced GFR)
• On Diuretics^[8]
• Alcohol intake^[9]
  • The lactic acid blocks the excretion of urate from the renal tubules. Alcohol induces the purine metabolism in the liver and increases the formation of lactic acid and
  • Alcohol also directly stimulates the synthesis of urate by the liver

• Drugs like cyclosporine that are toxic to the renal tubules leads to the decreased elimination of uric acid and ultimately resulting in the urate retention.

Copyleft images obtained courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, CA) Images courtesy of Professor Peter Anderson DVM Ph.D. and published with permission © PEIR, the University of Alabama at Birmingham, Department of Pathology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

Gout needs to be differentiated from other Crystal arthropathies and also from the diseases that present with similar symptoms. List of diseases that present with similar symptoms include cellulitis, Rheumatoid arthritis, trauma, Septic arthritis and tophaceous gout from Osteomyelitis, Dactylitis and other Autoimmune Arthritis like Reactive arthritis, sarcoidosis. Gout must also be differentiated from other causes of rash and Arthritis. Synovial fluid aspiration and analysis including Gram staining,culture and different types of microscopic examination is the Diagnostic for differentiating gout from other diseases. X-rays when combined with effective History and Physical examination also help in differentiating diseases.

Gout must be differentiated from other causes of acute and chronic inflammatory Joint Disease such as Pseudogout or Calcium pyrophosphate Dihydrate deposition disease, Calcium apatite deposition disease.

Certain diseases can present with similar symptoms like

• Cellulitis
• Rheumatoid arthritis
• Septic arthritis
• Sarcoidosis

Gout must be differentiated from other diseases that cause bone pain, edema, and erythema.

Gout must be differentiated from other causes of rash and arthritis^[11][12][13]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

Gout affects men in the age group of 40-50 years. It is more common in people from the Pacific Islands and New Zealand. In the United States, gout is twice as prevalent in African American males as it is in Caucasians^[1]. The American College of Rheumatology/European League Against Rheumatism Collaborative Initiative has noted that gout is the most common form of inflammatory arthritis, with a prevalence of 3.9% in the United States^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

Gout is a disease related to joints that usually develops in patients with high levels of uric acid. The uric acid precipitates as needle-like crystals in the tissues mainly in the joints and other articular tissues resulting in sudden severe episodic pain, redness. warmth and swelling. There are a number of factors[1] that can lead to the development of gout. Gout is seen in about 4% of people in America. It is more common in men than in women with a ratio of nearly 3:1. There are numerous risk factors like Genes, Gender, and age, Diet, Obesity, Alcohol consumption, Medical condo=itions, and medication use. All the former mentioned risk factors increase the risk of developing gout in the patients.

Gout is a disease related to joints that usually develops in patients with high levels of uric acid. The uric acid precipitates as needle-like crystals in the tissues mainly in the joints and other articular tissues resulting in sudden severe episodic pain, redness. warmth and swelling. There are a number of factors^[1][2] that can lead to the development of gout. Gout is seen in about 4% of people in America. It is more common in men than in women with a ratio of nearly 3:1. There are numerous risk factors for the development of out and can increase the chances of the patient developing the painful joint disease.

Genes

The studies conducted at MRC Human Genetic units proved that the patients who suffer from usually have a positive family history of gout. And in these patients, the most important factor noted is the presence of a gene variant that is linked to the low levels of uric acid excretion.

Gender and Age

Gout predominance is seen most commonly in men. The theory proposed by a various scientist is that the higher levels of estrogens in females play a protective role during their reproductive age group period and usually increases after the occurrence of menopause in females and matches the risk equivalent to men’s for that age group.

Diet

Diets such as Seafood consumption or consumption of a diet rich in fructose beverages have been found to be linked to the higher levels of uric acid and in turn, leading to the development of gout. The higher purine content in the seafood gets broken down to uric acid and in turn, leads to the production of gout.

Obesity

Uric acid excretion is thought to be dependent on the body surface area also. so In an obese person, the body is more likely to produce more uric acid and it can get worse if the patient also has underlying renal abnormality present along with it.

Alcohol Consumption

Alcoholic drinks especially beer are high in purine content and thus contribute the greatest to the development of gout. Even the quantity of alcohol intake also plays a huge in the development of gout. More than 2 drinks a day is also a risk factor for the development of gout. So it is always advisable to cut down the alcohol drinking to the minimal and best is to stop it completely, if possible.

Medical Conditions

The medical conditions like High Blood pressure^[3], high blood sugar, heart, and kidney diseases contribute to the greatest extent in the development of gout.

Medications

A lot of Medications are associated with the risk of developing gout. The most common amongst them are Diuretics and also the drugs that affect the immune system increase the risk of developing gout. So it is always advisable to discuss with the primary care physician before starting any other medication.

Recent Surgery or Trauma

Any surgery can increase the risk of developing gout with more correlation to joint surgery or accidents.

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The prognosis of gout is good if it is treated early, and if the person maintains a healthy lifestyle with modification of their individual risk factors.

Generally, the prognosis of gout is good. It depends on:

• Whether the patient is treated early
• Whether the patient maintains a healthy lifestyle.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Sumanth Khadke, MD[2]

In general, diagnosis (plural diagnoses) has two distinct dictionary definitions. The first definition is “the recognition of a disease or condition by its outward signs and symptoms”, while the second definition is “the analysis of the underlying physiological/biochemical cause(s) of a disease or condition”.

Diagnosis covers a broad spectrum, or spectra, of testing in some form of analysis; collective reasoning using such tests is called the method of diagnostics, leading then to the results of those tests by ideal (ethics) would then be considered a diagnosis, but not necessarily the correct one.

In medicine, diagnosis or diagnostics is the process of identifying a medical condition or disease by its signs, symptoms, and from the results of various diagnostic procedures. The conclusion reached through this process is called a diagnosis. The term “diagnostic criteria” designates the combination of symptoms which allows the doctor to ascertain the diagnosis of the respective disease.

Typically, someone with abnormal symptoms will consult a physician, who will then obtain a history of the patient‘s illness and examine him for signs of disease. The physician will formulate a hypothesis of likely diagnoses and in many cases will obtain further testing to confirm or clarify the diagnosis before providing treatment.

Medical tests commonly performed are measuring blood pressure, checking the pulse rate, listening to the heart with a stethoscope, urine tests, fecal tests, saliva tests, blood tests, medical imaging, electrocardiogram, hydrogen breath test and occasionally biopsy.

The word diagnosis is derived from the Greek words dia which means “by”, and gnosis which means “knowledge”. The verb is diagnose and a person diagnosing could be considered a diagnostician.

A physician‘s job is to know the human body and its functions in terms of normality (homeostasis). The four cornerstones of diagnostic medicine, each essential for understanding homeostasis, are: anatomy (the structure of the human body), physiology (how the body works), pathology (what can go wrong with the anatomy and physiology) and psychology (thought and behavior). Once the doctor knows what is normal and can measure the patient’s current condition against those norms, she or he can then determine the patient’s particular departure from homeostasis and the degree of departure. This is called the diagnosis. Once a diagnosis has been reached, the doctor is able to propose a management plan, which will include treatment as well as plans for follow-up. From this point on, in addition to treating the patient’s condition, the doctor educates the patient about the causes, progression, outcomes, and possible treatments of his ailments, as well as providing advice for maintaining health.

It should be noted however, that medical diagnosis in psychology or psychiatry is problematic. Apart from the fact that there are differing theoretical views toward mental conditions and that there are few “lab” tests available for various major disorders (e.g., clinical depression), a causal analysis with respect to symptomatology and disorder/disease is not always possible. As a result, most if not all mental conditions, function as both symptoms as well as disorders. There are often functional descriptions provided for psychological disorders and these are vulnerable to circular reasoning due to the etiological fuzziness inherent of these diagnostic categories. (BDG, 2006)

Diagnosis is a fluid process in which the physician responds to information garnered from the patient and others, from a physical examination of the patient, and from medical tests performed upon the patient.

The doctor should consider the patient in his ‘well’ context rather than simply as a walking medical condition. This entails assessing the socio-political context of the patient (family, work, stress, beliefs), in addition to the patient’s physical body, as this often offers vital clues to the patient’s condition and its management.

The process of diagnosis begins when the patient consults the doctor and presents a set of complaints (the symptoms). If the patient is unconscious, this condition is the de facto complaint. The doctor then obtains further information from the patient himself (and from those who know him, if present) about the patient’s symptoms, his previous state of health, living conditions, and so forth.

Rather than consider the myriad diseases that could afflict the patient, the physician narrows down the possibilities to the illnesses likely to account for the apparent symptoms, making a list of only those conditions that could account for what is wrong with the patient. These are generally ranked in order of probability.

The doctor then conducts a physical examination of the patient, studies the patient’s medical record, and asks further questions as he goes, in an effort to rule out as many of the potential conditions as possible. When the list is narrowed down to a single condition, this is called the differential diagnosis, and provides the basis for a hypothesis of what is ailing the patient.

Unless the physician is certain of the condition present, further medical tests are performed or scheduled (such as medical imaging), in part to confirm or disprove the diagnosis but also to document the patient’s status to keep the patient’s medical history up to date. Consultations with other physicians and specialists in the field may be sought. If unexpected findings are made during this process, the initial hypothesis may be ruled out and the physician must then consider other hypotheses.

Despite all of these complexities, most patient consultations are relatively brief, because many diseases are obvious, or the physician’s experience may enable him to recognize the condition quickly. Another factor is that the decision trees used for most diagnostic hypothesis testing are relatively short.

Once the physician has completed the diagnosis, he explains the prognosis to the patient and proposes a treatment plan which includes therapy and follow-up (further consultations and tests to monitor the condition and the progress of the treatment, if needed), usually according to the guideline provided by the medical field on the treatment of the particular illness.

Treatment itself may indicate a need for review of the diagnosis if there is a failure to respond to treatments that would normally work.

The history of medical diagnosis began in earnest from the enlightened days of Hippocrates in ancient Greece but is far from perfect despite the enormous bounty of information made available by medical research including the sequencing of the human genome. The practice of diagnosis continues to be dominated by theories set down in the early 1900s.

Over two thousand years ago, Hippocrates recorded the association between disease and heredity. In similar fashion, Pythagoras noted the association between metabolism and heredity (allergy to Fava beans). The medical community, however, has only recently acknowledged the importance of genetics and its relevance to mainstream medicine.

The ideals of William Osler who transformed the practice of medicine in the early 1900s were based on the principles of the diagnosis and treatment of disease. According to Osler, the functions of a physician were to be able to identify disease and its manifestations, understand its mechanisms, how it may be prevented and how it may be cured. For his medical students he believed that the best textbook was the patient himself – analysis of morbid anatomy and pathology were the keys. The Oslerian ideal continues today, as the basis of the Doctor’s strategy is, “What disease does this patient have and what is the best way for treatment?” The emphasis is on the classification of the disease in order to use the remedies available for its effects to be reversed or ameliorated. The human being in question is representative of a class of people with this type of disease whereas the biological individuality of this person is not given any great weight.

The successor to William Osler as Regius Professor at Oxford was Archibald Garrod. Garrod echoed the observations of his Greek counterparts of two millennia ago, …our chemical individualities are due to our chemical merits as well as our chemical shortcomings; and it is more nearly true to say that the factors which confer upon us our predispositions to and immunities from various mishaps which are spoken of as diseases, are inherent in our very chemical structure; and even in the molecular groupings which confer upon us our individualities, and which went into the making of the chromosomes from which we sprang. Considering that the time that he formulated these ideas were the early 1900’s, and the knowledge of DNA encoding genes that in turn encoded proteins responsible for bodily structure and functions not being discovered until some fifty years later it took some time before medicine could fully appreciate the fundamental importance of his concept of diagnosis.

Whereas Osler laid the founding principles by which medicine should be practiced, Garrod placed these principles in a greater context of a chemical individuality that is inherited and is subject to the mechanisms of evolutionary selection. The Oslerian ideal of medical practice continues to dominate medical philosophy today. The patient is a collective of symptoms to be characterized and analyzed algorithmically in order to draw a diagnosis and subsequently produce a strategy of treatment. Medicine is about problems based solutions. In keeping with this philosophy, today’s pathology reports provide a momentary snapshot of the patient’s biochemical profile, highlighting the end result of the disease process.

Garrod’s conception of biological individuality was confirmed with the advent of the sequencing of the human genome. Finally the subtle relationship between inheritance, individuality and environment became apparent via the variations detected in DNA. In each patient’s DNA lies a script for how their bodies will change and become ill as well as how they will handle the assaults of the environment from the beginning of their life to its end. It is hoped that by knowing a patient’s genes that the biological strengths and weaknesses in respect to these assaults will be revealed and disease processes can be predicted before they have the opportunity to manifest. Although knowledge in this area is far from complete, there are already medical interventions based on this. More importantly, the physician, forewarned with this knowledge can guide the patient towards appropriate lifestyle changes to anticipate and mitigate disease processes.

• GPnotebook web site GPnotebook is a British medical database for GPs that provides an immediate reference resource for clinicians worldwide. The database consists of over 30,000 pages of information.
• Free 24/7 DRG & ICD-9-CM lookup powered by Flash Code at icd9coding.com
• Differential Diagnosis
• Merck Manual of Diagnosis and Therapy

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Compliance with avoidance is important. The key to avoidance is proper evaluation and detection of causative allergen. Wear appropriate clothing to protect against irritants at home and in a work environment. ^{[1] [2]}

High-potency topical corticosteroids, e.g. clobetasol propionate 0.05% cream, may be used to reduce the inflammation. ^[3] As a general rule, high-potency corticosteroids should not be used on thin skin, e.g. face, genitals, intertriginous areas, to avoid the risk of skin atrophy. Antihistamines such as hydroxyzine and cetirizine are recommended to control pruritus. Systemic steroids are advised in severe cases but should be tapered gradually to prevent recurrences. Friction should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus ointment and pimecrolimus cream are immunomodulating drugs that inhibit calcineurin and are helpful in allergic contact dermatitis.