myselfshy

Genital warts (or condylomata acuminata, venereal warts, anal warts and anogenital warts) are symptoms of a highly contagious sexually transmitted disease caused by some types of human papillomavirus (HPV). It is spread through direct skin-to-skin contact, usually during oral, genital, or anal sex with an infected partner. Warts are the most easily recognized symptom of genital HPV infection. Although some types of HPV are known to cause cervical cancer and anal cancers, these are not the same types of HPV that cause genital warts. Although 90% of those who contract HPV will not develop genital warts, those infected can still transmit the virus. Although estimates of incidence vary between studies, HPV is so common that nearly all sexually active people will get it at some point in their lives.
HPV types 6 and 11 are most frequently the cause of genital warts. The Gardasil vaccine includes coverage for these types. While types 6 and 11 are considered low risk for progression to cancers, it is also possible to be infected with different varieties of HPV, such as a low-risk HPV that causes warts and a high-risk HPV, either at the same or different times.
A condyloma acuminatum is a single genital wart, and condylomata acuminata are multiple genital warts. The word roots mean “pointed wart” (kondylos Greek κονδυλος, “knuckle” + -oma Greek ωμα, “disease” = kondyloma, “knuckle-like growth”; acuminatum Latin=”pointed”).
CAUSES
Transmission
HPV is most commonly transmitted through penetrative sex. While HPV can also be transmitted via non-penetrative sexual activity, it is less transmissible than via penetrative sex. There is conflicting evidence about the effect of condoms on transmission of low-risk HPV. Some studies have suggested that they are effective at reducing transmission. Other studies suggest that condoms are not effective at preventing transmission of the low-risk HPV variants that cause genital warts. The effect of condoms on HPV transmission may also be gender-dependent; there is some evidence that condoms are more effective at preventing infection of males than of females.
The types of HPV that cause warts are highly transmissible. Roughly three out of four unaffected partners of patients with warts develop them within eight months. Other studies of partner concordance suggest that the presence of visible warts may be an indicator of increased infectivity; HPV concordance rates are higher in couples where one partner has visible warts.
Latency and recurrence
Although 90% of HPV infections are cleared by the body within two years of infection, it is possible for infected cells to undergo a latency (quiet) period, with the first occurrence or a recurrence of symptoms happening months or years later. Latent HPV, even with no outward symptoms, is still transmissible to a sexual partner. If an individual has unprotected sex with an infected partner, there is a 70% chance that he or she will also become infected.
In individuals with a history of previous HPV infection, the appearance of new warts may be either from a new exposure to HPV, or from a recurrence of the previous infection. As many as one-third of people with warts will experience a recurrence.
In children
Anal or genital warts may be transmitted during birth. The presence of wart-like lesions on the genitals of young children has been suggested as an indicator of sexual abuse. However, genital warts can sometimes result from autoinoculated by warts elsewhere on the body, such as from the hands. It has also been reported from sharing of swimsuits, underwear, or bath towels, and from non-sexual touching during routine care such as diapering. Genital warts in children are less likely to be caused by HPV subtypes 6 and 11 than adults, and more likely to be caused by HPV types that cause warts elsewhere on the body (“cutaneous types”). Surveys of pediatricians who are child abuse specialists suggest that in children younger than 4 years old, there is no consensus on whether the appearance of new anal or genital warts, by itself, can be considered an indicator of sexual abuse.
DIAGNOSIS
The diagnosis of genital warts is most often made visually, but may require confirmation by biopsy in some cases. Smaller warts may occasionally be confused with molluscum contagiosum. Genital warts, histopathologically, characteristically rise above the skin surface due to enlargement of the dermal papillae, have parakeratosis and the characteristic nuclear changes typical of HPV infections (nuclear enlargement with perinuclear clearing). DNA tests are available for diagnosis of high-risk HPV infections. Because genital warts are caused by low-risk HPV types, DNA tests cannot be used for diagnosis of genital warts or other low-risk HPV infections.
Some practitioners use an acetic acid solution to identify smaller warts (“subclinical lesions”), but this practice is controversial. Because a diagnosis made with acetic acid will not meaningfully affect the course of the disease, and cannot be verified by a more specific test, a 2007 UK guideline advises against its use.
EPIDEMIOLOGY
Genital HPV infections have an estimated prevalence in the US of 10-20% and clinical manifestations in 1% of the sexually active adult population. US incidence of HPV infection has increased between 1975 and 2006. About 80% of those infected are between the ages of 17-33. Although treatments can remove the warts, they do not remove the HPV, so warts can recur after treatment (about 50-73% of the time). Warts can also spontaneously regress (with or without treatment).
Traditional theories postulated that the virus remained in the body for a lifetime. However, studies using sensitive DNA techniques have shown that through immunological response the virus can either be cleared or suppressed to levels below what polymerase chain reaction (PCR) tests can measure. One study testing genital skin for subclinical HPV using PCR found a prevalence of 10%.
SIGNS AND SYMPTOMS
Genital warts may occur singly but are more often found in clusters. They may be found anywhere in the anal or genital area, and are frequently found on external surfaces of the body, including the penile shaft, scrotum, labia majora of the vagina, or around the anus. They can also occur on internal surfaces like the opening to the urethra, inside the vagina, on the cervix, or in the anus. In males they are frequently found on or around the head of the penis.
They can be as small as 1-5mm in diameter, but can also grow or spread into large masses in the genital or anal area. In some cases they look like small stalks. They may be hard (“keratinized”) or soft. Their color can be variable, and sometimes they may bleed.
In most cases, there are no symptoms of HPV infection other than the warts themselves. Sometimes warts may cause itching, redness, or discomfort, especially when they occur around the anus. Although they are usually without other physical symptoms, an outbreak of genital warts may cause psychological distress, such as anxiety, in some people.
MANAGEMENT
There is no cure for HPV. Existing treatments are focused on the removal of visible warts, but these may also regress on their own without any therapy. There is no evidence to suggest that removing visible warts reduces transmission of the underlying HPV infection. As many as 80% of people with HPV will clear the infection within 18 months.
A healthcare practitioner may offer one of several ways to treat warts, depending on their number, sizes, locations, or other factors. All treatments can potentially cause depigmentation, itching, pain, or scarring.
Treatments can be classified as either physically ablative, or topical agents. Physically ablative therapies are considered more effective at initial wart removal, but like all therapies have significant recurrence rates.
Many therapies, including folk remedies, have been suggested for treating genital warts, some of which have little evidence to suggest they are effective or safe. Those listed here are ones mentioned in national or international practice guidelines as having some evidence basis for their use.
Physical ablation
Physically ablative methods are more likely to be effective on keratinized warts. They are also most appropriate for patients with fewer numbers of relatively smaller warts.
Simple excision, such as with scissors under local anesthesia, is highly effective.

Liquid nitrogen cryosurgery is usually performed in an office visit, at weekly intervals. It is effective, inexpensive, safe for pregnancy, and does not usually cause scarring.

Electrocauterization (sometimes called “loop electrical excision procedure” or LEEP) is procedure with a longer history of use, and is considered effective.

Laser ablation has less evidence to suggest its use. It may be less effective than other ablative methods. It is extremely expensive, and often used as a last resort.

Formal surgical procedures, performed by a specialist under general anesthesia, may be necessary for larger or more extensive warts, intra-anal warts, or warts in children. It carries a greater risk of scarring than other methods.

Topical agents
A 0.15-0.5% podophyllotoxin (also called podofilox) solution in a gel or cream. Marketed as Condylox (0.5%), Wartec (0.15%) and Warticon (0.15%), it can be applied by the patient to the affected area and is not washed off. It is the purified and standardized active ingredient of the podophyllin (see below). Podofilox is safer and more effective than podophyllin. Skin erosion and pain are more commonly reported than with imiquimod and sinecatechins. Its use is cycled (2 times per day for 3 days then 4-7 days off); one review states that it should only be used for four cycles.

Imiquimod (Aldara) is a topical immune response cream, applied to the affected area. It causes less local irritation than podofilox but may cause fungal infections (11% in package insert) and flu-like symptoms (less than 5% disclosed in package insert).

Sinecatechins (marketed as Veregen and Polyphenon E) is an ointment of catechins (55% epigallocatechin gallate) extracted from green tea and other components. Mode of action is undetermined. It appears to have higher clearance rates than podophyllotoxin and imiquimod and causes less local irritation, but clearance takes longer than with imiquimod.

Trichloroacetic acid (TCA) is less effective than cryosurgery, and is not recommended for use in the vagina, cervix, or urinary meatus.

Interferon can be used; it is effective, but it is also expensive and its effect is inconsistent.

Discontinued

:

A 5% 5-fluorouracil (5-FU) cream was used, but it is no longer considered an acceptable treatment due to the side-effects.

Podophyllin, podofilox and Isotretinoin should not be used during pregnancy, as they could cause birth defects in the fetus.
PREVENTION
Gardasil (sold by Merck & Co.) is a vaccine that protects against human papillomavirus types 16, 18, 6, and 11. Types 6 and 11 cause genital warts, while 16 and 18 cause cervical cancer. The vaccine is preventive, not therapeutic, and must be given before exposure to the virus type to be effective, ideally before the beginning of sexual activity. The vaccine is approved by the US Food and Drug Administration for use in both males and females as early as 9 years of age.
In the UK, Gardasil replaced Cervarix in September 2012 for reasons unrelated to safety. Cervarix had been used routinely in young females from its introduction in 2008, but was only effective against the high-risk HPV types 16 and 18, neither of which typically causes warts.

SUMMARY

Folliculitis (also known as hot tub rash) is the infection and inflammation of one or more hair follicles. The condition may occur anywhere on the skin with the exception of the palms of the hands and soles of the feet. They may appear as red dots that come to white tips on the chest, back, arms, legs, and head.
CAUSES
Most carbuncles, furuncles, and other cases of folliculitis develop from Staphylococcus aureus and Pseudomonas aeruginosa.
Folliculitis starts when hair follicles are damaged by friction from clothing, an insect bite, blockage of the follicle, shaving, or braids too tight and too close to the scalp. In most cases of folliculitis, the damaged follicles are then infected with the bacterium Staphylococcus. Folliculitis usually affects those in their early adult life, and may persist till their early 30s. Warmer weather may worsen the condition.
Iron deficiency anemia is sometimes associated with chronic cases.
Fungal
Tinea barbae is similar to barber’s itch, but the infection is caused by the fungus T. rubrum.

Malassezia folliculitis, formerly known as Pityrosporum folliculitis, is caused by yeasts (fungi) of the genus Malassezia.

Bacterial
Hot-tub folliculitis is caused by the bacterium Pseudomonas aeruginosa. The folliculitis usually occurs after sitting in a hot tub that was not properly cleaned before use. Symptoms are found around the body parts that sit in the hot tub-typically the legs, hips, buttocks, and surrounding areas. Symptoms are typically amplified around regions that were covered by wet clothing, such as bathing suits.

Sycosis vulgaris, Sycosis barbae or Barber’s itch is a staphylococcus infection of the hair follicles in the bearded area of the face, usually the upper lip. Shaving aggravates the condition.

Gram-negative folliculitis may appear after prolonged acne treatment with antibiotics.

Viral
Herpetic folliculitis may occur when Herpes Simplex Virus infection spreads to nearby hair follicles – mostly around the mouth.

Non-infectious
Pseudofolliculitis barbae is a disorder occurring when hair curves back into the skin and causes inflammation.

Eosinophilic folliculitis may appear in persons with impaired immune systems.

Folliculitis decalvans or tufted folliculitis usually affects scalp. Several hairs arise from the same hair follicle. Scarring and permanent hair loss may follow. The cause is unknown.

Folliculitis keloidalis scarring on the nape of the neck, most common among males of curly hair.

Oil folliculitis is inflammation of hair follicles due to exposure to various oils and typically occurs on forearms or thighs. It is common in refinery workers, road workers, mechanics, and sheep shearers. Even makeup may cause it.

Malignancy may also be represented by recalcitrant cases.

TREATMENT
Topical antiseptic treatment is adequate for most cases

Topical antibiotics such as mupirocin or neomycin containing ointment

Some patients may benefit from systemic narrow-spectrum penicillinase-resistant penicillins (such as dicloxacillin in US, or flucloxacillin in UK)

Fungal folliculitis can worsen with antibiotics and may require an oral antifungal such as Fluconazole. Topical antifungals such as Econazole Nitrate may also be effective.

Folliculitis may reoccur even after symptoms have gone away.
SYMPTOMS
rash (reddened skin area)

itching skin

pimples or pustules located around a hair follicle

may crust over

typically occur on neck, armpit, or groin area

may present as genital lesions

spreading from leg to arm to body through improper treatment of antibiotics.

Hair loss or baldness (technically known as alopecia) is a loss of hair from the head or body. Baldness can refer to general hair loss or androgenic alopecia (male pattern baldness). Some types of baldness can be caused by alopecia areata, an autoimmune disorder. The extreme forms of alopecia areata are alopecia totalis, which involves the loss of all head hair, and alopecia universalis, which involves the loss of all hair from the head and the body.

Baldness and hypotrichosis can have many causes, including fungal infection (tinea capitis), traumatic damage, such as by compulsive pulling (trichotillomania), as a result of radiotherapy or chemotherapy, and as a result of nutritional deficiencies such as iron, and as a result of autoimmune phenomena, including alopecia areata and hair loss associated with systemic lupus erythematosus.

CAUSES

Although not completely understood, alopecia can have many causes:

Male pattern hair loss

More than 95% of hair thinning in men is male pattern hair loss (also known as male pattern baldness). Male pattern hair loss is characterized by hair receding from the lateral sides of the forehead (known as a “receding hairline”) and/or a thinning crown (balding to the area known as the ‘vertex’). Both become more pronounced until they eventually meet, leaving a horseshoe-shaped ring of hair around the back of the head.

The incidence of pattern baldness varies from population to population and is based on genetic background. Environmental factors do not seem to affect this type of baldness greatly. One large scale study in Maryborough, Victoria, Australia showed the prevalence of mid-frontal baldness increases with age and affects 73.5 percent of men and 57 percent of women aged 80 and over. A rough rule of thumb is that the incidence of baldness in males corresponds to chronological age. For example, according to Medem Medical Library’s website, male pattern baldness (MPB) affects roughly 40& million men in the United States. Approximately 25 percent of men begin balding by age 30; two-thirds begin balding by age 60.

There is a 4 in 7 chance of receiving the baldness gene. Onset of hair loss sometimes begins as early as the end of puberty, and is mostly genetically determined. It was previously believed that baldness was inherited from the maternal grandfather. While there is some basis for this belief, both parents contribute to their offspring’s likelihood of hair loss. Most likely, inheritance involves many genes with variable penetrance.

The trigger for this type of baldness is dihydrotestosterone, a more-potent form of testosterone often referred to by its acronym DHT. DHT is an androgenic hormone, body- and facial-hair growth promoter that can adversely affect the prostate as well as the hair located on the head. The mechanism by which DHT accomplishes this is not yet fully understood. In genetically prone scalps (i.e., those experiencing male or female pattern baldness), DHT initiates a process of follicular miniaturization, in which the hair follicle begins to deteriorate. As a consequence, the hair’s growth phase (anagen) is shortened, and young, unpigmented vellus hair is prevented from growing and maturing into the deeply rooted and pigmented terminal hair that makes up 90 percent of the hair on the head. In time, hair becomes thinner, and its overall volume is reduced so that it resembles fragile vellus hair or “peach fuzz” until, finally, the follicle goes dormant and ceases producing hair completely.

Nutrition

Studies have shown that poor nutrition, limited food intake, and deficiencies in certain nutrients can cause thinning. These include deficiencies of biotin, protein, zinc and poor human iron metabolism, although complete baldness is not usually seen. A diet high in animal fats (often found in fast food) and vitamin A is also thought to lead to hair loss.

Hypervitaminosis A
Iron deficiency or malnutrition in general
Infection

Dissecting cellulitis
Fungal infections (such as tinea capitis)
Tinea capitis
Folliculitis
Secondary syphilis
Demodex folliculorum, a microscopic mite that feeds on the sebum produced by the sebaceous glands, denies hair essential nutrients and can cause thinning. Demodex folliculorum is not present on every scalp and is more likely to live in an excessively oily scalp environment.
Drugs

Temporary or permanent hair loss can be caused by several medications, including those for blood pressure problems, diabetes, heart disease and cholesterol. Any that affect the body’s hormone balance can have a pronounced effect: these include the contraceptive pill, hormone replacement therapy, steroids and acne medications.
Medications (side effects from drugs, including chemotherapy, anabolic steroids, and birth control pills in which a large number of hairs enter the resting phase at the same time, causing shedding and subsequent thinning. The condition also presents as a side effect of chemotherapy – while targeting dividing cancer cells, this treatment also affects hair’s growth phase with the result that almost 90% of hairs fall out soon after chemotherapy starts.
Radiation to the scalp, as when radiotherapy is applied to the head for the treatment of certain cancers there, can cause baldness of the irradiated areas.
Pregnancy

Hair loss often follows childbirth without causing baldness. In this situation, the hair is actually thicker during pregnancy due to increased circulating oestrogens. After the baby is born, the oestrogen levels fall back to normal prepregnancy levels, and the additional hair foliage drops out. A similar situation occurs in women taking the fertility-stimulating drug clomiphene.

Other

Air and water pollutants as well as minerals in water and the phototoxic effects of sunlight can cause thinning by aging the scalp skin and damaging hair.
Alopecia areata is an autoimmune disorder also known as “spot baldness” that can result in hair loss ranging from just one location (Alopecia areata monolocularis) to every hair on the entire body (Alopecia areata universalis). Although thought to be caused by hair follicles becoming dormant, what triggers alopecia areata is not known. In most cases the condition corrects itself, but it can also spread to the entire scalp (alopecia totalis) or to the entire body (alopecia universalis).
Localized or diffuse hair loss may also occur in cicatricial alopecia (lupus erythematosus, lichen plano pilaris, folliculitis decalvans, central centrifugal cicatricial alopecia, postmenopausal frontal fibrosing alopecia, etc.). Tumours and skin outgrowths also induce localized baldness (sebaceous nevus, basal cell carcinoma, squamous cell carcinoma).
Hypothyroidism (an under-active thyroid) and the side effects of its related medications can cause hair loss, typically frontal, which is particularly associated with thinning of the outer third of the eyebrows (also seen with syphilis). Hyperthyroidism (an over-active thyroid) can also cause hair loss, which is parietal rather than frontal.
Temporary loss of hair can occur in areas where sebaceous cysts are present for considerable duration (normally one to several weeks).
Congenital triangular alopecia – It is a triangular, or oval in some cases, shaped patch of hair loss in the temple area of the scalp that occurs mostly in young children. The affected area mainly contains vellus hair follicles or no hair follicles at all, but it does not expand. Its causes are unknown, and although it is a permanent condition, it does not have any other effect on the affected individuals.
Gradual thinning of hair with age is a natural condition known as involutional alopecia. This is caused by an increasing number of hair follicles switching from the growth, or anagen, phase into a resting phase, or telogen phase, so that remaining hairs become shorter and fewer in number.
An unhealthy scalp environment can play a significant role in hair thinning by contributing to miniaturization or causing damage. Air and water pollutants, environmental toxins, conventional styling products and excessive amounts of sebum have the potential to build up on the scalp. This debris can block hair follicles and cause their deterioration and consequent miniaturization of hair. It can also physically restrict hair growth or damage the hair cuticle, leading to hair that is weakened and easily broken off before its natural lifecycle has ended.
Causes of alopecia include:

Alopecia mucinosa
Biotinidase deficiency
Chronic inflammation
Diabetes
Hair treatments (chemicals in relaxers, hair straighteners)
Lupus erythematosus
Pseudopelade of Brocq
Telogen effluvium
Tufted folliculitis
DIAGNOSIS

Because they are not usually associated with an increased loss rate, male-pattern and female-pattern hair loss do not generally require testing. If hair loss occurs in a young man with no family history, drug use could be the cause.

The pull test helps to evaluate diffuse scalp hair loss. Gentle traction is exerted on a group of hairs (about 40-60) on three different areas of the scalp. The number of extracted hairs is counted and examined under a microscope. Normally, fewer than three hairs per area should come out with each pull. If more than ten hairs are obtained, the pull test is considered positive.
The pluck test is conducted by pulling hair out “by the roots”. The root of the plucked hair is examined under a microscope to determine the phase of growth, and is used to diagnose a defect of telogen, anagen, or systemic disease. Telogen hairs have tiny bulbs without sheaths at their roots. Telogen effluvium shows an increased percentage of hairs upon examination. Anagen hairs have sheaths attached to their roots. Anagen effluvium shows a decrease in telogen-phase hairs and an increased number of broken hairs.
Scalp biopsy is used when the diagnosis is unsure; a biopsy allows for differing between scarring and nonscarring forms. Hair samples are taken from areas of inflammation, usually around the border of the bald patch.
Daily hair counts are normally done when the pull test is negative. It is done by counting the number of hairs lost. The hair from the first morning combing or during washing should be counted. The hair is collected in a clear plastic bag for 14 days. The strands are recorded. If the hair count is >100/day, it is considered abnormal except after shampooing, where hair counts will be up to 250 and be normal.
Trichoscopy is a noninvasive method of examining hair and scalp. The test may be performed with the use of a handheld dermoscope or a video dermoscope. It allows differential diagnosis of hair loss in most cases.
There are two types of identification tests for female pattern baldness: the Ludwig Scale and the Savin Scale. Both track the progress of diffused thinning, which typically begins on the crown of the head behind the hairline, and becomes gradually more pronounced. For male pattern baldness, the Hamilton-Norwood scale tracks the progress of a receding hairline and/or a thinning crown, through to a horseshoe-shaped ring of hair around the head and on to total baldness.

In almost all cases of thinning, and especially in cases of severe hair loss, it is recommended to seek advice from a doctor or dermatologist. Many types of thinning have an underlying genetic or health-related cause, which a qualified professional will be able to diagnose.

SIGNS AND SYMPTOMS

Symptoms of alopecia include hair loss in patches usually in circular patterns, dandruff, skin lesions, and scarring. Alopecia areata (mild – medium level) usually shows in unusual hair loss areas e.g. eyebrows, backside of the head or above the ears where usually the male pattern baldness does not effect. In male-pattern hair loss, loss and thinning begin at the temples and the crown and either thins out or falls out. Female-pattern hair loss occurs at the frontal and parietal.

Excessive daily hair loss

People have between 100,000 and 150,000 hairs on their head. The number of strands normally lost in a day varies, but on average is 100. Seborrheic dermatitis, a condition in which an excessive amount of sebum is produced and builds up on the scalp (looking like an adult cradle cap) is also a symptom of hormonal imbalances, as is an excessively oily or dry scalp. Both can cause hair thinning.

Psychological

Hair thinning and baldness cause psychological stress due to its effect on appearance. Although societal interest in appearance has a long history, this particular branch of psychology came into its own during the 1960s and has gained momentum as messages associating physical attractiveness with success and happiness grow more prevalent.

The psychology of hair thinning is a complex issue. Hair is considered an essential part of overall identity: especially for women, for whom it often represents femininity and attractiveness. Men typically associate a full head of hair with youth and vigor. Although they may be aware of pattern baldness in their family, many are uncomfortable talking about the issue. Hair thinning is therefore a sensitive issue for both sexes. For sufferers, it can represent a loss of control and feelings of isolation. People experiencing hair thinning often find themselves in a situation where their physical appearance is at odds with their own self-image and commonly worry that they appear older than they are or less attractive to others. Psychological problems due to baldness, if present, are typically most severe at the onset of symptoms.

Hair loss induced by cancer chemotherapy has been reported to cause changes in self-concept and body image. Body image does not return to the previous state after regrowth of hair for a majority of patients. In such cases, patients have difficulties expressing their feelings (alexithymia) and may be more prone to avoiding family conflicts. Family therapy can help families to cope with these psychological problems if they arise.

PATHOPHYSIOLOGY

Hair follicle growth occurs in cycles. Each cycle consists of a long growing phase (anagen), a short transitional phase (catagen) and a short resting phase (telogen). At the end of the resting phase, the hair falls out (exogen) and a new hair starts growing in the follicle beginning the cycle again.

Normally, about 40 (0-78 in men) hairs reach the end of their resting phase each day and fall out. When more than 100 hairs fall out per day, clinical hair loss (telogen effluvium) may occur. A disruption of the growing phase causes abnormal loss of anagen hairs (anagen effluvium).

MANAGEMENT

Medications

Treatments for the various forms of hair loss have limited success. Three medications have evidence to support their use in male pattern hair loss: finasteride, dutasteride and minoxidil. They typically work better to prevent further hair loss than to regrow lost hair.

Minoxidil (Rogaine) is a nonprescription medication approved for male pattern baldness and alopecia areata. In a liquid or foam, it is rubbed into the scalp twice a day. However, only 30-40% of patients experience hair growth. Minoxidil is not effective for other causes of hair loss. Hair regrowth can take eight to 12 months. Treatment is continued indefinitely because, if the treatment is stopped, hair loss resumes again. Most frequent side effects are mild scalp irritation, allergic contact dermatitis, and increased facial hair.
SUMMARY

Hair loss or baldness (technically known as alopecia) is a loss of hair from the head or body. Baldness can refer to general hair loss or androgenic alopecia (male pattern baldness). Some types of baldness can be caused by alopecia areata, an autoimmune disorder. The extreme forms of alopecia areata are alopecia totalis, which involves the loss of all head hair, and alopecia universalis, which involves the loss of all hair from the head and the body.

Baldness and hypotrichosis can have many causes, including fungal infection (tinea capitis), traumatic damage, such as by compulsive pulling (trichotillomania), as a result of radiotherapy or chemotherapy, and as a result of nutritional deficiencies such as iron, and as a result of autoimmune phenomena, including alopecia areata and hair loss associated with systemic lupus erythematosus.

CAUSES

Although not completely understood, alopecia can have many causes:

Male pattern hair loss

More than 95% of hair thinning in men is male pattern hair loss (also known as male pattern baldness). Male pattern hair loss is characterized by hair receding from the lateral sides of the forehead (known as a “receding hairline”) and/or a thinning crown (balding to the area known as the ‘vertex’). Both become more pronounced until they eventually meet, leaving a horseshoe-shaped ring of hair around the back of the head.

The incidence of pattern baldness varies from population to population and is based on genetic background. Environmental factors do not seem to affect this type of baldness greatly. One large scale study in Maryborough, Victoria, Australia showed the prevalence of mid-frontal baldness increases with age and affects 73.5 percent of men and 57 percent of women aged 80 and over. A rough rule of thumb is that the incidence of baldness in males corresponds to chronological age. For example, according to Medem Medical Library’s website, male pattern baldness (MPB) affects roughly 40& million men in the United States. Approximately 25 percent of men begin balding by age 30; two-thirds begin balding by age 60.

There is a 4 in 7 chance of receiving the baldness gene. Onset of hair loss sometimes begins as early as the end of puberty, and is mostly genetically determined. It was previously believed that baldness was inherited from the maternal grandfather. While there is some basis for this belief, both parents contribute to their offspring’s likelihood of hair loss. Most likely, inheritance involves many genes with variable penetrance.

The trigger for this type of baldness is dihydrotestosterone, a more-potent form of testosterone often referred to by its acronym DHT. DHT is an androgenic hormone, body- and facial-hair growth promoter that can adversely affect the prostate as well as the hair located on the head. The mechanism by which DHT accomplishes this is not yet fully understood. In genetically prone scalps (i.e., those experiencing male or female pattern baldness), DHT initiates a process of follicular miniaturization, in which the hair follicle begins to deteriorate. As a consequence, the hair’s growth phase (anagen) is shortened, and young, unpigmented vellus hair is prevented from growing and maturing into the deeply rooted and pigmented terminal hair that makes up 90 percent of the hair on the head. In time, hair becomes thinner, and its overall volume is reduced so that it resembles fragile vellus hair or “peach fuzz” until, finally, the follicle goes dormant and ceases producing hair completely.

Nutrition

Studies have shown that poor nutrition, limited food intake, and deficiencies in certain nutrients can cause thinning. These include deficiencies of biotin, protein, zinc and poor human iron metabolism, although complete baldness is not usually seen. A diet high in animal fats (often found in fast food) and vitamin A is also thought to lead to hair loss.

Hypervitaminosis A
Iron deficiency or malnutrition in general
Infection

Dissecting cellulitis
Fungal infections (such as tinea capitis)
Tinea capitis
Folliculitis
Secondary syphilis
Demodex folliculorum, a microscopic mite that feeds on the sebum produced by the sebaceous glands, denies hair essential nutrients and can cause thinning. Demodex folliculorum is not present on every scalp and is more likely to live in an excessively oily scalp environment.
Drugs

Temporary or permanent hair loss can be caused by several medications, including those for blood pressure problems, diabetes, heart disease and cholesterol. Any that affect the body’s hormone balance can have a pronounced effect: these include the contraceptive pill, hormone replacement therapy, steroids and acne medications.
Medications (side effects from drugs, including chemotherapy, anabolic steroids, and birth control pills in which a large number of hairs enter the resting phase at the same time, causing shedding and subsequent thinning. The condition also presents as a side effect of chemotherapy – while targeting dividing cancer cells, this treatment also affects hair’s growth phase with the result that almost 90% of hairs fall out soon after chemotherapy starts.
Radiation to the scalp, as when radiotherapy is applied to the head for the treatment of certain cancers there, can cause baldness of the irradiated areas.
Pregnancy

Hair loss often follows childbirth without causing baldness. In this situation, the hair is actually thicker during pregnancy due to increased circulating oestrogens. After the baby is born, the oestrogen levels fall back to normal prepregnancy levels, and the additional hair foliage drops out. A similar situation occurs in women taking the fertility-stimulating drug clomiphene.

Other

Air and water pollutants as well as minerals in water and the phototoxic effects of sunlight can cause thinning by aging the scalp skin and damaging hair.
Alopecia areata is an autoimmune disorder also known as “spot baldness” that can result in hair loss ranging from just one location (Alopecia areata monolocularis) to every hair on the entire body (Alopecia areata universalis). Although thought to be caused by hair follicles becoming dormant, what triggers alopecia areata is not known. In most cases the condition corrects itself, but it can also spread to the entire scalp (alopecia totalis) or to the entire body (alopecia universalis).
Localized or diffuse hair loss may also occur in cicatricial alopecia (lupus erythematosus, lichen plano pilaris, folliculitis decalvans, central centrifugal cicatricial alopecia, postmenopausal frontal fibrosing alopecia, etc.). Tumours and skin outgrowths also induce localized baldness (sebaceous nevus, basal cell carcinoma, squamous cell carcinoma).
Hypothyroidism (an under-active thyroid) and the side effects of its related medications can cause hair loss, typically frontal, which is particularly associated with thinning of the outer third of the eyebrows (also seen with syphilis). Hyperthyroidism (an over-active thyroid) can also cause hair loss, which is parietal rather than frontal.
Temporary loss of hair can occur in areas where sebaceous cysts are present for considerable duration (normally one to several weeks).
Congenital triangular alopecia – It is a triangular, or oval in some cases, shaped patch of hair loss in the temple area of the scalp that occurs mostly in young children. The affected area mainly contains vellus hair follicles or no hair follicles at all, but it does not expand. Its causes are unknown, and although it is a permanent condition, it does not have any other effect on the affected individuals.
Gradual thinning of hair with age is a natural condition known as involutional alopecia. This is caused by an increasing number of hair follicles switching from the growth, or anagen, phase into a resting phase, or telogen phase, so that remaining hairs become shorter and fewer in number.
An unhealthy scalp environment can play a significant role in hair thinning by contributing to miniaturization or causing damage. Air and water pollutants, environmental toxins, conventional styling products and excessive amounts of sebum have the potential to build up on the scalp. This debris can block hair follicles and cause their deterioration and consequent miniaturization of hair. It can also physically restrict hair growth or damage the hair cuticle, leading to hair that is weakened and easily broken off before its natural lifecycle has ended.
Causes of alopecia include:

Alopecia mucinosa
Biotinidase deficiency
Chronic inflammation
Diabetes
Hair treatments (chemicals in relaxers, hair straighteners)
Lupus erythematosus
Pseudopelade of Brocq
Telogen effluvium
Tufted folliculitis
DIAGNOSIS

Because they are not usually associated with an increased loss rate, male-pattern and female-pattern hair loss do not generally require testing. If hair loss occurs in a young man with no family history, drug use could be the cause.

The pull test helps to evaluate diffuse scalp hair loss. Gentle traction is exerted on a group of hairs (about 40-60) on three different areas of the scalp. The number of extracted hairs is counted and examined under a microscope. Normally, fewer than three hairs per area should come out with each pull. If more than ten hairs are obtained, the pull test is considered positive.
The pluck test is conducted by pulling hair out “by the roots”. The root of the plucked hair is examined under a microscope to determine the phase of growth, and is used to diagnose a defect of telogen, anagen, or systemic disease. Telogen hairs have tiny bulbs without sheaths at their roots. Telogen effluvium shows an increased percentage of hairs upon examination. Anagen hairs have sheaths attached to their roots. Anagen effluvium shows a decrease in telogen-phase hairs and an increased number of broken hairs.
Scalp biopsy is used when the diagnosis is unsure; a biopsy allows for differing between scarring and nonscarring forms. Hair samples are taken from areas of inflammation, usually around the border of the bald patch.
Daily hair counts are normally done when the pull test is negative. It is done by counting the number of hairs lost. The hair from the first morning combing or during washing should be counted. The hair is collected in a clear plastic bag for 14 days. The strands are recorded. If the hair count is >100/day, it is considered abnormal except after shampooing, where hair counts will be up to 250 and be normal.
Trichoscopy is a noninvasive method of examining hair and scalp. The test may be performed with the use of a handheld dermoscope or a video dermoscope. It allows differential diagnosis of hair loss in most cases.
There are two types of identification tests for female pattern baldness: the Ludwig Scale and the Savin Scale. Both track the progress of diffused thinning, which typically begins on the crown of the head behind the hairline, and becomes gradually more pronounced. For male pattern baldness, the Hamilton-Norwood scale tracks the progress of a receding hairline and/or a thinning crown, through to a horseshoe-shaped ring of hair around the head and on to total baldness.

In almost all cases of thinning, and especially in cases of severe hair loss, it is recommended to seek advice from a doctor or dermatologist. Many types of thinning have an underlying genetic or health-related cause, which a qualified professional will be able to diagnose.

SIGNS AND SYMPTOMS

Symptoms of alopecia include hair loss in patches usually in circular patterns, dandruff, skin lesions, and scarring. Alopecia areata (mild – medium level) usually shows in unusual hair loss areas e.g. eyebrows, backside of the head or above the ears where usually the male pattern baldness does not effect. In male-pattern hair loss, loss and thinning begin at the temples and the crown and either thins out or falls out. Female-pattern hair loss occurs at the frontal and parietal.

Excessive daily hair loss

People have between 100,000 and 150,000 hairs on their head. The number of strands normally lost in a day varies, but on average is 100. Seborrheic dermatitis, a condition in which an excessive amount of sebum is produced and builds up on the scalp (looking like an adult cradle cap) is also a symptom of hormonal imbalances, as is an excessively oily or dry scalp. Both can cause hair thinning.

Psychological

Hair thinning and baldness cause psychological stress due to its effect on appearance. Although societal interest in appearance has a long history, this particular branch of psychology came into its own during the 1960s and has gained momentum as messages associating physical attractiveness with success and happiness grow more prevalent.

The psychology of hair thinning is a complex issue. Hair is considered an essential part of overall identity: especially for women, for whom it often represents femininity and attractiveness. Men typically associate a full head of hair with youth and vigor. Although they may be aware of pattern baldness in their family, many are uncomfortable talking about the issue. Hair thinning is therefore a sensitive issue for both sexes. For sufferers, it can represent a loss of control and feelings of isolation. People experiencing hair thinning often find themselves in a situation where their physical appearance is at odds with their own self-image and commonly worry that they appear older than they are or less attractive to others. Psychological problems due to baldness, if present, are typically most severe at the onset of symptoms.

Hair loss induced by cancer chemotherapy has been reported to cause changes in self-concept and body image. Body image does not return to the previous state after regrowth of hair for a majority of patients. In such cases, patients have difficulties expressing their feelings (alexithymia) and may be more prone to avoiding family conflicts. Family therapy can help families to cope with these psychological problems if they arise.

PATHOPHYSIOLOGY

Hair follicle growth occurs in cycles. Each cycle consists of a long growing phase (anagen), a short transitional phase (catagen) and a short resting phase (telogen). At the end of the resting phase, the hair falls out (exogen) and a new hair starts growing in the follicle beginning the cycle again.

Normally, about 40 (0-78 in men) hairs reach the end of their resting phase each day and fall out. When more than 100 hairs fall out per day, clinical hair loss (telogen effluvium) may occur. A disruption of the growing phase causes abnormal loss of anagen hairs (anagen effluvium).

MANAGEMENT

Medications

Treatments for the various forms of hair loss have limited success. Three medications have evidence to support their use in male pattern hair loss: finasteride, dutasteride and minoxidil. They typically work better to prevent further hair loss than to regrow lost hair.

Minoxidil (Rogaine) is a nonprescription medication approved for male pattern baldness and alopecia areata. In a liquid or foam, it is rubbed into the scalp twice a day. However, only 30-40% of patients experience hair growth. Minoxidil is not effective for other causes of hair loss. Hair regrowth can take eight to 12 months. Treatment is continued indefinitely because, if the treatment is stopped, hair loss resumes again. Most frequent side effects are mild scalp irritation, allergic contact dermatitis, and increased facial hair.
Finasteride (Propecia) is used in male-pattern hair loss in a pill form taken on a daily basis. It is not indicated for women and is not recommended in pregnant women. Treatment is effective within six to eight months of treatment. Side effects include decreased sex drive, erectile dysfunction, ejaculatory dysfunction, gynecomastia, and myopathy. Treatment should be continued as long as positive results occur. Once treatment is stopped, hair loss resumes again.
Corticosteroids injections of into the scalp can be used to treat alopecia areata. This type of treatment is repeated on a monthly basis. Oral pills for extensive hair loss may be used for alopecia areata. Results may take up to a month to be seen.
Immunosuppressants applied to the scalp have been shown to temporarily reverse alopecia areata, though the side effects of some of these drugs make such therapy questionable.
Anthralin maybe used in alopecia areata.
Hormonal modulators (oral contraceptives or antiandrogens such as spironolactone and flutamide) can be used for female-pattern hair loss associated with hyperandrogenemia.
Surgery

Hair Transplantation is usually carried out under local anaesthetic. A surgeon will move healthy hair from the back and sides of the head to areas of thinning. The procedure can take between four and eight hours, and additional sessions can be carried out to make hair even thicker. Transplanted hair falls out within a few weeks, but regrows permanently within months. **Hair transplants, takes tiny plugs of skin, each which contains a few hairs, and implants the plugs into bald sections. The plugs are generally taken from the back or sides of the scalp. Several transplant sessions may be necessary. Egg oil, in Indian, Japanese, Unani (Roghan Baiza Murgh) and Chinese traditional medicine, was traditionally used as a treatment for hairloss.

ETYMOLOGY

The term alopecia is formed from the Greek alópex (αλώπηξ), meaning fox. The origin of this usage is because this animal sheds its coat twice a year, or because in ancient Greece foxes often lost hair because of mange.

The term bald likely derives from the English word balde, which means “white, pale”, or Celtic ball, which means “white patch or blaze”, such as on a horse’s head.

TERMINOLOGY

Baldness is the partial or complete lack of hair growth, and part of the wider topic of “hair thinning”. The degree and pattern of baldness varies, but its most common cause is androgenic alopecia, alopecia androgenetica, or alopecia seborrheica, with the last term primarily used in Europe.

Diverticulitis is a common digestive disease which involves the formation of pouches (diverticula) within the bowel wall. This process is known as diverticulosis, and typically occurs within the large intestine, or colon, although it can occasionally occur in the small intestine as well. Diverticulitis results when one of these diverticula becomes inflamed.

People often have left lower quadrant abdominal pain and tenderness, fever, and an increase white blood cell count. They may also complain of nausea or diarrhea; others may be constipated. The severity of symptoms depends on the extent of the infection and complications. Less commonly, an individual with diverticulitis may have right-sided abdominal pain. This may be due to the less common right-sided diverticula or a highly redundant sigmoid colon. Some patients report bleeding from the rectum.

CAUSES

The cause of diverticulitis is unknown. The development of colonic diverticulum is thought to be a result of raised intraluminal colonic pressures. The sigmoid colon (Section 4) has the smallest diameter of any portion of the colon, and therefore the portion which would be expected to have the highest intraluminal pressure.

Diet

The claim that a lack of dietary fiber, particularly non-soluble fiber (also known in older parlance as “roughage”) predisposes individuals to diverticular disease was long accepted within the medical literature. However, the first study to specifically test the theory has found that “A high-fiber diet and increased frequency of bowel movements are associated with greater, rather than lower, prevalence of diverticulosis.” Foods such as seeds, nuts, and corn were, in the past, thought by many health care professionals to cause or worsen diverticulitis. However, there is no evidence that suggests the avoidance of nuts and seeds prevents the progression of diverticulosis to an acute case of diverticulitis. It appears that a higher intake of nuts and corn could in fact help to avoid diverticulitis in adult males.

DIAGNOSIS

People with the above symptoms are commonly studied with computed tomography, or CT scan. The CT scan is very accurate (98%) in diagnosing diverticulitis. In order to extract the most information possible about the patient’s condition, thin section (5mm) transverse images are obtained through the entire abdomen and pelvis after the patient has been administered oral and intravascular contrast. Images reveal localized colon wall thickening, with inflammation extending into the fat surrounding the colon. The diagnosis of acute diverticulitis is made confidently when the involved segment contains diverticulae. CT may also identify patients with more complicated diverticulitis, such as those with an associated abscess. It may even allow for radiologically guided drainage of an associated abscess, sparing a patient from immediate surgical intervention.

Other studies, such as barium enema and colonoscopy are contraindicated in the acute phase of diverticulitis due to the risk of perforation.

Differential diagnosis

The differential diagnosis includes colon cancer, inflammatory bowel disease, ischemic colitis, and irritable bowel syndrome, as well as a number of urological and gynecological processes.

TREATMENT

Most cases of simple, uncomplicated diverticulitis respond to conservative therapy with bowel rest. People may be placed on a low residue diet. This low-fiber diet gives the colon adequate time to heal without needing to be overworked.

Antibiotics

If bacterial infection is suspected, antibiotics may be used. Despite being recommended by several guidelines, the use of antibiotics in mild cases of uncomplicated diverticulitis is supported with only “sparse and of low quality” evidence, with no evidence supporting their routine use.

Surgery

Surgery is often not needed. Complications, such as peritonitis, abscess, or fistula may require surgery, either immediately or on an elective basis. Whether the elective surgery should be performed is decided by external factors such as the stage of the disease, the age of the patient and his or her general medical condition, as well as the severity and frequency of attacks or if the symptoms persist after a first acute episode. In most cases, the decision to perform elective surgery is taken when the risks of the surgery are smaller than the ones resulting from complications of the condition. Elective surgery may be performed at least six weeks after recovery from acute diverticulitis.

Emergency surgery is necessary for people whose intestine has ruptured; intestinal rupture always results in infection of the abdominal cavity. During emergency diverticulitis surgery, the ruptured section is removed and a colostomy is performed. This means that the surgeon will create an opening between the large intestine and the surface of the skin. The colostomy is closed in about 10 or 12 weeks in a subsequent surgery in which the cut ends of the intestine are rejoined.

The first surgical approach consists in the resection and primary anastomosis. This first stage of surgery is performed on patients with a well vascularized, nonedematous and tension-free bowel. The proximal margin should be an area of pliable colon without hypertrophy or inflammation. The distal margin should extend to the upper third of the rectum where the taenia coalesces. Not all of the diverticula-bearing colon must be removed, since diverticula proximal to the descending or sigmoid colon are unlikely to result in further symptoms.

Diverticulitis surgery can be done in two ways: through a primary bowel resection or through a bowel resection with colostomy. Both bowel resections may be done in the traditional way or by laparoscopic surgery. The traditional bowel resection is made using an open surgical approach, called colectomy. During a colectomy, the patient is placed under general anesthesia. A surgeon performing a colectomy will make a lower midline incision in the abdomen or a lateral lower transverse incision. The diseased section of the large intestine is removed and then the two healthy ends are sewn or stapled back together. A colostomy may be performed when the bowel has to be relieved of its normal digestive work as it heals. A colostomy implies creating a temporary opening of the colon on the skin surface and the end of the colon is passed through the abdominal wall and a removable bag is attached to it. The waste will be collected in the bag.

However, most of the surgeons prefer performing the bowel resection laparoscopically mainly because the postoperative pain is reduced and the patient’s recovery is faster. The laparoscopic surgery is a minimally invasive procedure in which three to four smaller incisions are made in the abdomen or navel.

All colon surgery involves only three maneuvers that may vary in complexity depending on the region of the bowel and the nature of the disease which are the retraction of the colon, the division of the attachments to the colon and the dissection of the mesentery. After the resection of the colon, the surgeon normally divides the attachments to the liver and the small intestine. After the mesenteric vessels are dissected, the colon is divided with special surgical staplers that close off the bowel while cutting between the staple lines.

When excessive inflammation of the colon renders primary bowel resection too risky, bowel resection with colostomy remains an option. Also known as the Hartmann’s operation, this is a more complicated surgery typically reserved for life-threatening cases.

The bowel resection with colostomy implies a temporary colostomy which is followed by a second operation to reverse the colostomy. The surgeon makes an opening in the abdominal wall (a colostomy) which helps clear the infection and inflammation. The colon is brought through the opening and all waste is collected in an external bag.

The colostomy is usually temporary but it may be permanent depending on the severity of the case. Most of the time, several months later after the inflammation has healed, the patient undergoes another major surgery during which the surgeon rejoins the colon and rectum and reverses the colostomy.

EPIDEMIOLOGY

Diverticulitis most often affects middle-aged and elderly persons, though it can strike younger people as well. Central obesity may be associated with diverticulitis in younger patients, with some being as young as 20 years old.

In Western countries, diverticular disease most commonly involves the sigmoid colon – section 4 (95% of patients). The prevalence of diverticular disease has increased from an estimated 10% in the 1920s to between 35 and 50% by the late 1960s. 65% of those currently 85 years of age and older can be expected to have some form of diverticular disease of the colon. Less than 5% of those aged 40 years and younger may also be affected by diverticular disease.

Left-sided diverticular disease (involving the sigmoid colon) is most common in the West, while right-sided diverticular disease is more prevalent in Asia and Africa. Among patients with diverticulosis, 10-25% will go on to develop diverticulitis within their lifetimes.

PATHOPHYSIOLOGY

Diverticulitis is believed to develop due to changes inside the intestines including high pressures due to faulty contracting of the intestines.

Most people with diverticulosis do not have any discomfort or symptoms; however, symptoms may include mild cramps, bloating, and constipation. Other diseases such as inflammatory bowel disease (IBD) and stomach ulcers cause similar problems, so these symptoms do not always mean a person has diverticulosis.

COMPLICATIONS

In complicated diverticulitis, bacteria may subsequently infect the outside of the colon if an inflamed diverticulum bursts open. If the infection spreads to the lining of the abdominal cavity, (peritoneum), this can cause a potentially fatal peritonitis. Sometimes inflamed diverticula can cause narrowing of the bowel, leading to an obstruction. Also, the affected part of the colon could adhere to the bladder or other organ in the pelvic cavity, causing a fistula, or abnormal connection between an organ and adjacent structure or organ, in this case the colon and an adjacent organ.
Bowel obstruction
Peritonitis
Abscess
Fistula
Bleeding
Strictures.

Gastroesophageal reflux disease (GERD), gastro-oesophageal reflux disease (GORD), gastric reflux disease, or acid reflux disease is a chronic symptom of mucosal damage caused by stomach acid coming up from the stomach into the esophagus.

GERD is usually caused by changes in the barrier between the stomach and the esophagus, including abnormal relaxation of the lower esophageal sphincter, which normally holds the top of the stomach closed, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia. These changes may be permanent or temporary.

Treatment is typically via lifestyle changes and medications such as proton pump inhibitors, H receptor blockers or antacids with or without alginic acid. Surgery may be an option in those who do not improve. In the Western world between 10 and 20% of the population is affected.

CAUSES

GERD is caused by a failure of the lower esophageal sphincter. In healthy patients, the “Angle of His”—the angle at which the esophagus enters the stomach—creates a valve that prevents duodenal bile, enzymes, and stomach acid from traveling back into the esophagus where they can cause burning and inflammation of sensitive esophageal tissue.

Factors that can contribute to GERD:

Hiatal hernia, which increases the likelihood of GERD due to mechanical and motility factors.
Obesity: increasing body mass index is associated with more severe GERD. In a large series of 2000 patients with symptomatic reflux disease, it has been shown that 13% of changes in esophageal acid exposure is attributable to changes in body mass index.
Zollinger-Ellison syndrome, which can be present with increased gastric acidity due to gastrin production.
Hypercalcemia, which can increase gastrin production, leading to increased acidity.
Scleroderma and systemic sclerosis, which can feature esophageal dysmotility.
The use of medicines such as prednisolone.
Visceroptosis or Glénard syndrome, in which the stomach has sunk in the abdomen upsetting the motility and acid secretion of the stomach.
GERD has been linked to a variety of respiratory and laryngeal complaints such as laryngitis, chronic cough, pulmonary fibrosis, earache, and asthma, even when not clinically apparent. These atypical manifestations of GERD is commonly referred to as laryngopharyngeal reflux (LPR) or as extraesophageal reflux disease (EERD).

Factors that have been linked with GERD, but not conclusively:

Obstructive sleep apnea
Gallstones, which can impede the flow of bile into the Duodenum, which can affect the ability to neutralize gastric acid
In 1999, a review of existing studies found that, on average, 40% of GERD patients also had H. pylori infection. The eradication of H. pylori can lead to an increase in acid secretion, leading to the question of whether H. pylori-infected GERD patients are any different than non-infected GERD patients. A double-blind study, reported in 2004, found no clinically significant difference between these two types of patients with regard to the subjective or objective measures of disease severity.

DIAGNOSIS

The diagnosis of GERD is usually made when typical symptoms are present. Reflux can be present in people without symptoms and the diagnosis requires both symptoms or complications and reflux of stomach content.

Other investigations may include esophagogastroduodenoscopy (EGD). Barium swallow X-rays should not be used for diagnosis. Esophageal manometry is not recommended for use in diagnosis being recommended only prior to surgery. Ambulatory esophageal pH monitoring may be useful in those who do not improve after PPIs and is not needed in those in whom Barrett’s esophagus is seen. Investigations for H. pylori is not usually needed.

The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and allows monitoring GERD patients in their response to medical or surgical treatment. One practice for diagnosis of GERD is a short-term treatment with proton-pump inhibitors, with improvement in symptoms suggesting a positive diagnosis. Short-term treatment with proton-pump inhibitors may help predict abnormal 24-hr pH monitoring results among patients with symptoms suggestive of GERD.

Endoscopy

Endoscopy, the looking down into the stomach with a fiber-optic scope, is not routinely needed if the case is typical and responds to treatment. It is recommended when people either do not respond well to treatment or have alarm symptoms, including dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate either once-in-a-lifetime or 5- to 10-yearly endoscopy for people with longstanding GERD, to evaluate the possible presence of dysplasia or Barrett’s esophagus.

Biopsies performed during gastroscopy may show:

Edema and basal hyperplasia (nonspecific inflammatory changes)
Lymphocytic inflammation (nonspecific)
Neutrophilic inflammation (usually due to reflux or Helicobacter gastritis)
Eosinophilic inflammation (usually due to reflux): The presence of intraepithelial eosinophils may suggest a diagnosis of eosinophilic esophagitis (EE) if eosinophils are present in high enough numbers. Less than 20 eosinophils per high-power microscopic field in the distal esophagus, in the presence of other histologic features of GERD, is more consistent with GERD than EE.
Goblet cell intestinal metaplasia or Barrett’s esophagus
Elongation of the papillae
Thinning of the squamous cell layer
Dysplasia
Carcinoma
Reflux changes may not be erosive in nature, leading to “nonerosive reflux disease”.

Differential diagnosis

Other causes of chest pain such as heart disease should be ruled out before making the diagnosis. Another kind of acid reflux, which causes respiratory and laryngeal signs and symptoms, is called laryngopharyngeal reflux (LPR) or “extraesophageal reflux disease” (EERD). Unlike GERD, LPR rarely produces heartburn, and is sometimes called silent reflux.

TREATMENT

The treatments for GERD include lifestyle modifications, medications, and possibly surgery. Initial treatment is frequently with a proton-pump inhibitor such as omeprazole.

Lifestyle

Certain foods and lifestyle are considered to promote gastroesophageal reflux, however most dietary interventions have little supporting evidence. Weight loss and elevating the head of the bed are generally useful. Moderate exercise improves symptoms, however in those with GERD vigorous exercise may worsen them. Stopping smoking and not drinking alcohol do not appear to result in significant improvement in symptoms. Avoidance of specific foods and of eating before lying down should only be recommended to those in which they are associated with the symptoms. Foods that have been implicated include coffee, alcohol, chocolate, fatty foods, acidic foods, and spicy foods.

Medications

The primary medications used for GERD are proton-pump inhibitors, H receptor blockers and antacids with or without alginic acid.

Proton-pump inhibitors (PPIs) (such as omeprazole) are the most effective followed by H receptor blockers (such as ranitidine). If a once daily PPI is only partially effective they may be used twice a day. They should be taken one half to one hour before a meal. There is no significant difference between agents in this class. When these medications are used long term, the lowest effective dose should be taken. They may also be taken only when symptoms occur in those with frequent problems. H receptor blockers lead to roughly a 40% improvement.

The evidence for antacids is weaker with a benefit of about 10% (NNT=13) while a combination of an antacid and alginic acid (such as Gaviscon) may improve symptoms 60% (NNT=4). Metoclopramide (a prokinetic) is not recommended either alone or in combination with other treatments due to concerns around adverse effects. The benefit of the prokinetic mosapride is modest.

Sucralfate has a similar effectiveness to H receptor blockers; however, sucralfate needs to be taken multiple times a day, thus limiting its use. Baclofen, an agonist of the GABA receptor, while effective, has similar issues of needing frequent dosing in addition to greater adverse effects compared to other medications.

Surgery

The standard surgical treatment for severe GERD is the Nissen fundoplication. In this procedure, the upper part of the stomach is wrapped around the lower esophageal sphincter to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia. It is only recommended in those who improve with PPIs. Benefits are equal to medical treatment in those with chronic symptoms. In addition, in the short and medium term, laparoscopic fundoplication improves quality of life compared to medical management. When comparing different fundoplication techniques, partial posterior fundoplication surgery is more effective than partial anterior fundoplication surgery.

Pregnancy

In pregnancy, dietary modifications and lifestyle changes may be attempted, but often have little effect. Calcium-based antacids are recommended if these changes are not effective. Aluminum- and magnesium-based antacids are also safe, as is ranitidine and PPIs.

Infants

Infants may see relief with changes in feeding techniques, such as smaller, more frequent feedings, changes in position during feedings, or more frequent burping during feedings. They may also be treated with medicines such as ranitidine or proton pump inhibitors. Proton pump inhibitors however have not been found to be effective in this population and there is a lack of evidence for safety.

Overtreatment

The use of acid suppression therapy is a common response to GERD symptoms and many patients get more of this kind of treatment than their individual case merits. The overuse of this treatment is a problem because of the side effects and costs which the patient will have from undergoing unnecessary therapy, and patients should not take more treatment than they need.

In some cases, a person with GERD symptoms can manage them by taking over-the-counter drugs and making lifestyle changes. This is often safer and less expensive than taking prescription drugs. Some guidelines recommend trying to treat symptoms with an H antagonist before using a proton-pump inhibitor because of cost and safety concerns.

EPIDEMIOLOGY

In Western populations GERD affects approximately 10% to 20% of the population and 0.4% newly develop the condition. For instance, an estimated 3.4 million to 6.8 million Canadians are GERD sufferers. The prevalence rate of GERD in developed nations is also tightly linked with age, with adults aged 60 to 70 being the most commonly affected. In the United States 20% of people have symptoms in a given week and 7% every day. No data support sex predominance with regard to GERD.

SIGNS AND SYMPTOMS

Adults

The most-common symptoms of GERD are:

Heartburn
Regurgitation
Less-common symptoms include:

Pain with swallowing/sore throat (odynophagia)
Increased salivation (also known as water brash)
Nausea
Chest pain
Coughing
GERD sometimes causes injury of the esophagus. These injuries may include:

Reflux esophagitis – necrosis of esophageal epithelium causing ulcers near the junction of the stomach and esophagus
Esophageal strictures – the persistent narrowing of the esophagus caused by reflux-induced inflammation
Barrett’s esophagus – intestinal metaplasia (changes of the epithelial cells from squamous to intestinal columnar epithelium) of the distal esophagus
Esophageal adenocarcinoma – a rare form of cancer
Some people have proposed that symptoms such as sinusitis, recurrent ear infections, and idiopathic pulmonary fibrosis are due to GERD; however, a causative role has not been established.

Children

GERD may be difficult to detect in infants and children, since they cannot describe what they are feeling and indicators must be observed. Symptoms may vary from typical adult symptoms. GERD in children may cause repeated vomiting, effortless spitting up, coughing, and other respiratory problems, such as wheezing. Inconsolable crying, refusing food, crying for food and then pulling off the bottle or breast only to cry for it again, failure to gain adequate weight, bad breath, and belching or burping are also common. Children may have one symptom or many; no single symptom is universal in all children with GERD.

Of the estimated 4& million babies born in the US each year, up to 35% of them may have difficulties with reflux in the first few months of their lives, known as ‘spitting up’. One theory for this is the “fourth trimester theory” which notes most animals are born with significant mobility, but humans are relatively helpless at birth, and suggests there may have once been a fourth trimester, but children began to be born earlier, evolutionarily, to accommodate the development of larger heads and brains and allow them to pass through the birth canal and this leaves them with partially undeveloped digestive systems.

Most children will outgrow their reflux by their first birthday. However, a small but significant number of them will not outgrow the condition. This is particularly true when a family history of GERD is present.

Barrett’s esophagus

GERD may lead to Barrett’s esophagus, a type of intestinal metaplasia, which is in turn a precursor condition for carcinoma. The risk of progression from Barrett’s to dysplasia is uncertain, but is estimated at about 20% of cases. Due to the risk of chronic heartburn progressing to Barrett’s, EGD every five years is recommended for people with chronic heartburn, or who take drugs for chronic GERD.

HISTORY

An obsolete treatment is vagotomy (“highly selective vagotomy”), the surgical removal of vagus nerve branches that innervate the stomach lining. This treatment has been largely replaced by medication.

When a woman has vaginismus, her vagina’s muscles squeeze or spasm when something is entering her, like a tampon or a penis. It can be mildly uncomfortable, or it can be painful.

There are exercises a woman can do that can help, sometimes within weeks.

Symptoms
Painful sex is often a woman’s first sign that she has vaginismus. The pain happens only with penetration. It usually goes away after withdrawal, but not always.

Women have described the pain as a tearing sensation or a feeling like the man is “hitting a wall.”

Many women who have vaginismus also feel discomfort when inserting a tampon or during a doctor’s internal pelvic exam.

Causes
Doctors don’t know exactly why vaginismus happens. It’s usually linked to anxiety and fear of having sex. But it’s unclear which came first, the vaginismus or the anxiety.

Some women have vaginismus in all situations and with any object. Others have it only in certain circumstances, like with one partner but not others, or only with sexual intercourse but not with tampons or during medical exams.

Other medical problems like infections can also cause painful intercourse. So it’s important to see a doctor to determine the underlying cause of pain during sex.

Treatment
Women with vaginismus can do exercises, in the privacy of their own home, to learn to control and relax the muscles around the vagina.

The approach is called progressive desensitization, and the idea is to get comfortable with insertion.

First, do Kegel exercises by squeezing the same muscles you use to stop the flow of urine when urinating:

Squeeze the muscles.
Hold for 2 seconds.
Relax the muscles.
Do about 20 Kegels at a time. You can do them as many times a day as you want to.

After a few days, insert one finger, up to about the first knuckle joint, inside the vagina while doing the exercises. It’s a good idea to clip your fingernails first and use a lubricating jelly. Or do the exercises in a bathtub, where water is a natural lubricant.

Start with one finger and work your way up to three. You’ll feel the vagina’s muscles contracting around your finger, and you can always take your finger out if you’re not comfortable.