Alopecia Areata
Alopecia Areata (AA) manifests as focal, non-scarring hair loss and is classified as an autoimmune disease. The prevalence of this condition in the general population is 1-2%. In 50% of cases, the onset of the disease occurs during adolescence. A typical symptom is the presence of well-defined hairless areas. The pathological mechanism leading to alopecia areata is not yet fully understood. The influence of genetic factors and environmental factors (including stress) is often emphasized as triggers for the autoimmune process.
Symptoms:
In these patients, a round or oval bald patch is observed, usually appearing rapidly. The number and size of the patches may vary; sometimes, it is a patch of 1-2 cm in diameter, less frequently numerous bald patches are seen that often merge. There are several clinical forms of alopecia areata: focal alopecia, diffuse alopecia areata, ophiasis (when it affects the hairline in the occipital and temporal areas), total alopecia (loss of all hair on the scalp), and universal alopecia (total loss of body hair).
The course of the disease:
Predicting the course of the disease poses challenges. Unfavorable outcomes are more likely in individuals with an early onset of the condition, a familial history of alopecia areata, associated atopy, and concurrent autoimmune diseases or nail abnormalities. Cases displaying an “ophiasis” pattern tend to be more intricate. The extent of hair loss emerges as a pivotal prognostic factor. While some experience spontaneous remissions, approximately 5% advance to alopecia totalis, and 1% progress to alopecia universalis. Recurrent patterns may characterize the disease trajectory in some instances.
Diagnosis:
The diagnosis is established based on the clinical presentation and trichoscopy findings. Punch biopsy may be required for further confirmation.
Treatment:
Topical and systemic medications are employed in the treatment. Immunosuppressive drugs (corticosteroids, cyclosporine), photochemotherapy (PUVA), and immunomodulatory medications prove effective. Additional options include laser therapy and scalp micropigmentation.
Frontal Fibrosing Alopecia (FFA)
Frontal Fibrosing Alopecia (FFA) is a condition described by Steven Kossard in 1994. The prevalence of this condition is challenging to assess. Many authors consider AFF to be a subtype of LPP (Lichen Planopilaris). Scarring is the outcome of lymphocytic inflammation, leading to permanent damage to the hair follicles.
Symptoms:
This condition most commonly affects postmenopausal women. In patients with Frontal Fibrosing Alopecia (FFA), the percentage of premenopausal women generally does not exceed 8%, while the overall percentage of men is around 2%. The primary symptom is a slow, gradual recession of the frontal and temporal hairlines. Rarely, the same process may be observed in the parietal area. A common accompanying symptom is the thinning of eyebrows, especially the lateral parts, and hair loss in other body areas (axillae, groins, and less frequently, limbs). Occasionally, isolated hair may be seen in previously hairless skin. Within the newly formed hairline, no hair is observed, and sometimes erythema (redness) of the skin is visible. In a subset of patients with FFA, small reddish papules may form on the face, and the skin may become rough.
The course of the disease:
The onset of the condition is often challenging for the patient to notice, and only significant recession of the hairline is a reason to seek dermatological advice. The condition is slowly progressive, with the rate of hairline recession varying from 0.3 to 1.7 mm per month. Thinning of the hair within the eyebrows begins from the sides and progresses towards the center, often leading to the complete loss of eyebrows. Frontal Fibrosing Alopecia is irreversible.
Diagnosis:
The diagnosis is determined based on the clinical picture and trichoscopy.
Puncture biopsy may be necessary.
Treatment:
The treatment is challenging. Steroids, retinoids, and minoxidil are used to halt progression. Some authors emphasize the effectiveness of hydroxychloroquine, cyclosporine, and mycophenolate mofetil. Other medical options include laser hair therapy and epidermal injection of medications.
LIQUEN PLANOPILARIS (LPP)
Lichen Planopilaris (LPP), in its classic form, is the most common cause of primary alopecia in adults. LPP affects women twice as often as men. The disease progresses with the irreversible loss of hair due to damage to the hair follicles from an autoimmune process.
Symptoms:
Typically, at the onset, the presence of reddish or violaceous papules, or erythematous areas accompanied by scalp scaling, can be observed. The lesions often occur in the parietal and vertex areas. A common symptom is itching and sensitivity of the affected scalp. These conditions may worsen due to sweating, sun exposure, irritation, and stress. As inflammatory symptoms decrease, focal or diffuse alopecia can be observed, giving an image of confluent white dots or areas of milky red color.
The course of the disease:
The disease is almost always progressive, although its activity may vary from person to person. Initially, small affected areas may tend to merge and affect large areas of the scalp. In places where scarring occurs, hair growth becomes impossible.
Diagnosis:
Diagnosis is possible based on the clinical picture and trichoscopy procedure. Sometimes, a punch biopsy may be necessary to confirm the diagnosis.
Treatment:
In the initial stage of LPP, the most important treatments involve anti-inflammatory medications such as corticosteroids and retinoids. Some authors emphasize the effectiveness of hydroxychloroquine, cyclosporine, and mycophenolate mofetil. Recently, treatments with PPAR modulators are being explored.
Other medical options may be considered.
Postpartum alopecia
Postpartum alopecia is classified as telogen effluvium. This phenomenon is influenced by hormonal changes in the hair follicles, specifically the reduction of estradiol and thyroxine levels in the postpartum period.
The impact of these hormones on the hair follicles during pregnancy reduces the number of follicles in the telogen (inactive) phase by half.
The hair loss after childbirth occurs as a result of the hairs “paused” in the active growth phase due to pregnancy hormones beginning to shed, along with the hair that was supposed to fall out during this period.
Some authors suggest a correlation between postpartum alopecia and the prevalence of postpartum depression, which may be caused by similar hormonal factors.
Symptoms:
Postpartum alopecia is diffuse, with approximately 20-30% of the hair shedding suddenly, usually around the second or third month after childbirth. It’s important to note that complete hair loss does not occur.
The course of the disease:
Spontaneous hair regrowth typically occurs within 6 to 9 months after childbirth. In breastfeeding women, hair regrowth may take longer due to the influence of prolactin on the hair follicles.
Diagnosis:
It is easy to diagnose due to the history of childbirth. Trichoscopy helps to exclude other associated conditions.
Treatment:
In general, routine treatment is not used for postpartum alopecia, especially in breastfeeding women. In case of significant hormonal disorders, thyroid hormone and estradiol supplements may be given, and sometimes hormonal contraceptives are administered. During the breastfeeding period, therapeutic options are limited due to the potential adverse effects on the baby.
Telogen Effluvium
Telogen Effluvium, first described by Klingman in 1961, is a general term to explain various patterns of hair loss with different causative factors. Any hair loss or its cause can be termed Telogen Effluvium if a significantly higher percentage of hair follicles are in the resting phase. Acute and chronic Telogen Effluvium have been identified.
Telogen Effluvium is one of many non-scarring alopecias, meaning there is no irreversible damage to the hair follicle.
Normally, hair growth occurs in a cycle of hair growth (anagen phase), followed by a resting phase (telogen phase), and eventually shedding. In Telogen Effluvium, a physiological stress factor causes many follicles, more than usual, to enter the resting phase, resulting in diffuse hair shedding as a key feature.
Symptoms:
In the case of acute Telogen Effluvium, hair loss is observed throughout the scalp, although patients mainly notice deficiencies in the frontal area. Acute Telogen Effluvium starts suddenly and can be triggered by an intrinsic or extrinsic factor, causing a significant amount of hair to enter the telogen phase.
Inductive factors for TE mentioned above include: diseases with high fever, surgical treatments, psychological stress, pregnancy, thyroid function disorders, cessation of estrogen therapy, strict diets (usually low in protein), iron deficiency, medications (beta-blockers, anticoagulants, retinoids, carbamazepine, vaccines), scalp diseases (psoriasis, seborrheic dermatitis), and exposure to intense ultraviolet light.
Chronic Telogen Effluvium is less frequent and is considered a separate entity. Chronic TE can be primary or occur as a secondary condition, accompanying general disorders such as malnutrition, renal or hepatic insufficiency, systemic lupus erythematosus, or HIV infection. Clinically, chronic Telogen Effluvium manifests as diffuse hair loss affecting the entire scalp and lasting more than 6 to 8 months or even years.
Telogen Effluvium itself is a benign and self-limiting condition, although its presence may provide a clue to an underlying state of illness.
Disease Course:
In the case of acute Telogen Effluvium, the interval between exposure to the trigger and hair shedding is generally about 3 to 4 months. Sudden and sometimes massive diffuse hair loss is observed, followed by spontaneous hair growth within the next 4 to 6 months. In many cases, improvement is spontaneous. Complete hair loss is not observed.
In the case of chronic Telogen Effluvium, hair loss persists for more than 6-8 months. In the interview, patients sometimes mention many years of hair loss with periods of increased intensity and remissions. Occasionally, hair loss is accompanied by thinning affecting all areas of the head and subjective symptoms such as scalp hypersensitivity or tenderness. Complete baldness is never observed.
Diagnosis:
The diagnosis is based on a detailed medical history and an analysis of the clinical picture, in addition to a thorough trichoscopic evaluation.
Treatment:
TE therapy aims to eliminate triggering factors: endocrinopathy, metabolic disorders, nutritional deficiencies, and inducing drugs. Topical corticosteroids can be used in TE treatment. Other medical options may include laser therapy or intradermal injection of medications.
Anagen Effluvium
Anagen Effluvium (AE)” encompasses conditions related to diffuse hair loss in the active or anagen growth phase. This group of conditions includes hair loss caused by cytotoxic factors (most commonly, cytostatic drugs, radiation therapy, toxic chemical factors), loose anagen hair syndrome, and short anagen syndrome. Some authors include in this spectrum the so-called incognito alopecia areata.
Symptoms:
In the case of chemotherapy-induced alopecia, a sudden and diffuse loss of hair is usually observed 1-3 weeks after the first administration of the drug. The average incidence of hair loss is observed in approximately 65% of patients treated with cytostatic drugs, and it is often less intense with monotherapy than with therapy combining two or three drugs. Anagen Effluvium of a less intense course is observed in patients taking medications with a less drastic influence on the hair growth cycle (including retinoids, fluoxetine, carbamazepine).
Anagen Effluvium related to incorrect “anchoring” of anagen hair (the so-called loose anagen hair syndrome) results in hair that gives the impression that it “doesn’t grow.” This syndrome mainly affects young girls (1 to 6 years old).
Course:
In cases of AE related to exposure to chemotherapeutic agents, other drugs, or toxic factors, hair growth can be expected once exposure to the harmful factor ceases. When the hair grows back, it may be different from the previous hair, often differing in its tendency to curl, and it may have a slightly different color.
Diagnosis:
Anagen Effluvium related to cytostatic drugs is easy to diagnose as patients report undergoing chemotherapy/anticancer treatment. Trichoscopy is very useful in differentiating from other conditions mentioned above.
Treatment:
In the case of hair loss caused by toxic agents, harmful factors should be removed if possible. Attempts are made to prevent chemotherapy-induced anagen effluvium by applying scalp cooling systems, reducing the exposure of hair follicles to cytostatic drugs. Other medical options include Low-Level Laser Therapy (LLLT) and intradermal injection of medications.
Radiation Treatment-Induced Alopecia
Why does radiation therapy cause hair loss?
Radiation therapy (RT) not only destroys cancer cells but can also affect healthy cells in the body. Healthy cells that rapidly divide, including those in the hair follicles, are most susceptible to radiation damage. The impact of radiation can result in hair thinning, and in some cases, it may lead to complete hair loss.
Does radiation therapy cause generalized hair loss?
Radiation therapy typically causes hair loss in the specific part of the body being treated. For example, if your arm undergoes radiation, you may lose hair on that arm, but the hair on your head would not be affected. The extent of hair loss depends on factors such as the size of the treated area and the total radiation dose administered. Hair loss is more pronounced within the treatment field, but it can also occur in the area where the radiation beam exits the body.
Chemotherapy treatments can also cause hair loss. If you are undergoing chemotherapy as well, you should consider whether the medications you are receiving can cause hair loss. When chemotherapy causes hair loss, it includes all the hair on your body (head, eyebrows, body hair, etc.). Learn more about chemotherapy-induced hair loss.
Is radiation-induced hair loss permanent?
Hair loss caused by radiation therapy can be temporary or permanent. At lower doses, hair loss is often temporary, but at higher doses, it may be permanent. Your doctor can assess whether the anticipated hair loss is expected to be temporary or permanent based on the planned radiation dose and the number of sessions. However, each patient’s situation is unique, and the regeneration of hair cannot be guaranteed even with lower doses of radiation. Hair loss caused by chemotherapy is usually temporary.
When new growth occurs, there may be changes in texture and color. It’s common for regrown hair to be curlier than before; however, a change in color is less frequent.
Definitive hair loss from RT is a scarring alopecia, but it can be treated with transplantation when the microvascular network of the scalp has not been significantly damaged.
Traction Alopecia
Traction Alopecia (TA)” is a term used to describe hair loss caused by prolonged or repetitive tension on the hair. TA was first described in 1907 in Greenlanders who developed hair loss along the frontal line due to prolonged use of tight ponytails. Subsequently, most literature has focused on the prevalence of TA in individuals of African descent. However, TA affects people of different ethnic backgrounds.
It can vary significantly in its clinical presentation, and diagnosis can be challenging when there is little clinical suspicion of traction or if the history of traction is remote and not obtained in the interrogation. Because pathological features are biphasic and show variable characteristics in the early and late stages of the disease, appropriate clinical-pathological correlation is essential to ensure a TA diagnosis. In patients with no clear history of traction, the clinical differential diagnosis is broad and may include alopecia areata, androgenetic alopecia, telogen effluvium, trichotillomania, and primary lymphocytic scarring alopecias (lichen planopilaris, central centrifugal cicatricial alopecia, Brocq’s pseudopelade, and frontal fibrosing alopecia).
Clinically, TA most often affects the frontal and temporal scalp (marginal loss). However, it can be seen in other scalp areas. The location depends on hairstyling, which may or may not be related to ethnic or racial origin (braids, buns, ponytails, dreadlocks, etc.).
Treatment:
Treatment can be divided into three stages: preventive, early, and late. Prevention is key in childhood and involves educating parents about the importance of avoiding tight hairstyles or ponytails. If detected in the early stage, both in children and adults, it is important to loosen the hairstyle and avoid chemicals or heat because hair loss is reversible at this stage. Brushing the affected area “to stimulate hair growth” should be avoided. Intralesional corticosteroid injection, at the periphery of hair loss, is beneficial to suppress perifollicular inflammation. Oral or topical antibiotics may be used in the early stages of the disease for their anti-inflammatory effect. Minoxidil solution or foam at 5% can promote hair growth in some of these patients.
In the late stage, hair loss is irreversible, and hair transplantation may be considered as a solution.
Early intervention is vital to reverse hair loss in TA; the final outcome of hair loss often depends on timely diagnosis combined with appropriate patient counseling.
Trichotillomania
Trichotillomania is a self-induced and recurrent alopecia resulting from compulsive hair-pulling behavior. It is more common in women, with a ratio of 4 to 1 compared to men, and often begins before the age of 17, typically in childhood, even before the age of six.
Clinically, one observes patchy hair loss with indistinct borders, a normal scalp, and broken hairs of various lengths on the surface. Sometimes, instead of patches, it presents as a diffuse alopecia, making diagnosis challenging. The most affected areas are usually the scalp, eyebrows, eyelashes, and beard, although any hairy area of the body can be affected.
Trichotillomania can be associated with trichophagia (ingestion of pulled hair), leading to a trichobezoar or a hair mass in the shape of a cast in the stomach, which can cause various digestive symptoms, including intestinal obstruction.
After ruling out other pathologies, the treatment primarily involves medication and psychotherapy to control depression, anxiety, and habits that lead to this compulsive behavior.
