María Gabriela Garrido - Patricia Arrastía

Alopecia is defined as the total or partial loss of hair.

Physiology and Pathophysiology

Hair is a keratinized (lifeless) product of the hair follicle. Hair growth is cyclical and comprises three stages or phases:

Anagen : it is an active growth phase, it lasts from 2 to 5 years, with an average of three years.

Catagen : it is a transition phase, its duration is short, with an average of three weeks. At this stage, mitotic activity in the womb ceases and hair growth stops.

Telogenic : it is a resting phase, the average duration is three months. The hair follicle is shortened and nail hair is formed.

These stages or phases are dynamic processes and vary according to the region of the body, and in relation to genetic, hormonal, seasonal and environmental factors.

Each follicle has a cycle and is independent of neighboring follicles. The number of follicles on the scalp is approximately 100,000. Of these, 85 to 90% are in anagen and 10 to 15% in telogen. Loss of up to 100 hairs per day is normal. The length of the hair depends on the duration of the active growth phase (anagen).

The pathophysiological mechanisms that lead to alopecia, not always clear, differ according to the cause. Therefore, the pathophysiology is analyzed, in each case, taking into account the classification.

Broadly speaking, it is important to determine whether alopecia is localized, diffuse or generalized; whether it is reversible or irreversible.

Classification

1. SCAR ALOPECIAS
   1. Congenital diseases
   2. Infections
   3. Irradiation
   4. Burns
   5. Caustic
2. NON-SCAR ALOPECIAS
   1. PHYSIOLOGICAL
      1. Postpartum alopecia
      2. Neonatal alopecia
   2. SYSTEMIC DISEASES (Telogen effluvium)
      1. Fever
      2. Infectious diseases
      3. Physical stress: anemias - surgeries
      4. Endocrine diseases: hypothyroidism - hyperthyroidism
      5. Nutritional deficiencies: protein-calorie malnutrition - zinc-selenium-iron-biotin deficiency
      6. Chronic diseases: liver and kidney diseases - collagenopathies
      7. Psychological stress
   3. DRUGS AND CHEMICAL AGENTS (anagen effluvium)
      1. Irradiation
      2. Chemotherapeutic agents
      3. Metrotexate
      4. Colchicina
      5. Thallium poisoning
      6. Mercury
      7. Hypervitamosis A / Retinoids
   4. TRAUMATIC
      1. Tricotilomania
      2. Traction alopecia
   5. ALOPECIA AREATA
   6. ANDROGENETIC ALOPECIA

Scarring alopecia is caused by the destruction or lack of the hair follicle. It is final. They can be caused by defects in embryonic development, such as epidermal nevi or other congenital disorders; bacterial, fungal, or viral infections (eg herpes zoster); Neoplasms or physical or chemical agents such as burns, radiation, caustic agents.

Non-scarring alopecia can be classified into:

• Physiological: as an example, the occipital alopecia of the newborn, postpartum alopecia and senile alopecia can be named. During pregnancy 95% of the hair is in anagen, after delivery more than 50% enters the telogen stage, manifesting the fall three months after delivery. In senile alopecia the hairs increase in telogen by shortening the duration of the anagen.
• For systemic diseases: It can be produced by telogen effluvium, this means that the pathological process leads the actively growing follicles to a resting phase. It represents the precipitous passage of a percentage of anagen to telogen hairs. Telogen hair loss is the pattern of a variety of stressful physical or psychic stimuli. Hair loss occurs 3 to 4 months after the triggering process. It is always reversible and does not lead to total hair loss. Post febrile alopecia, infectious diseases, hemorrhages, anemias, stress, surgeries, low calorie diets, malabsorption syndromes, amino acid deficiencies, iron and zinc can be mentioned as an example. In the states of protein malnutrition, the hair also looks dry, brittle and with its color lightening. Secondary syphilis produces alopecia with moth-like looking hair "abrasive alopecia." In pathologies with hyperandrogenism, the hyperactivity of the androgen dependent sebaceous glands produces alterations in the scalp that can lead to a certain degree of alopecia. Thyroid hormones exert an important action on the skin and skin cells including hair.
• For drugs and chemical agents: chemotherapeutic agents (antimitotic agents) and thallium poisoning cause fall in the anagen phase (anagen effluvium), by interference in the incorporation of essential amino acids, which leads to the fracture of the stem within the follicle, and then the hair falls off when lose its root. Alopecia secondary to irradiation affects growing hairs, which is why it manifests itself on the scalp and beard, where most are in the anagen phase. Both in irradiation and chemotherapy alopecia, alopecia is complete but has full recovery. When the irradiation dose exceeds 1200R there will be follicular destruction and alopecia will be permanent. Other drugs that produce alopecia are: methotrexate, colchicine, heparin, coumarin, vitamin A (in high doses) and retinoids. In all these cases, alopecia is diffuse and transitory. Thallium poisoning results in total hair loss 2 to 3 weeks after poisoning. The patient also presents neurological symptoms such as irritability, seizures, etc.
• Traumatic: The so-called trichotillomania is produced by frequent and subconscious manipulation of the hair (curling of the hairs around the fingers). Alopecia is confined to the trauma area. When the process is chronic it can lead to scarring alopecia. Traction alopecia is related to some hairstyles such as braids, rollers, buckles, etc.
• Alopecia Areata: the pathogenesis of alopecia areata is still obscure, although most authors tend to classify it as an autoimmune disease. Emotional stress is cited as a trigger factor. Follicular damage occurs in anagen and then rapid transformation into telogen. It manifests with plaque, rounded, or confluent hair loss on both the scalp and other hairy areas of the body, or both. The scalp has a normal appearance. It can be located with one or more alopecia plates; Generalizes affecting the entire scalp or universal with total loss of hair on the body and scalp. It shows some association with autoimmune diseases, particularly those related to thyroid (hypothyroidism, chronic Hashimoto's thyroiditis) and pigmentation disorders such as vitiligo. Another association is insulin-dependent diabetes. Small depressions or pitz may be seen on the nails.
• Androgenetic Alopecia: Genetic and hormonal factors influence its etiopathogenesis. It is the result of the progressive miniaturization of the hair follicle, which leads to the transformation of the terminal hairs into hairs. Androgenic receptors exist in the hair follicle and sebaceous glands, therefore androgens are regulators of hair growth. The hormone DHEA (dehydroepiandrosterone) is metabolized into more powerful androgens such as testosterone and DHA (dehydroandrosterone) through an enzyme called 5-alpha-reductase. This enzyme would be responsible for the miniaturization of genetically marked hair follicles. It is manifested by hair loss with a characteristic distribution in vertex and temporal entrances and frontal areas.

Interrogation and study methodology

From the pathophysiology and causes of alopecia that were mentioned, it follows that on many occasions hair loss can be anticipated or its etiology easily identified as in the case of irradiation, drugs and fever.

The questioning will be aimed at ruling out systemic diseases that have repercussions at the level of the hair follicle, drugs, genetic factors. The physical examination will determine the characteristic, location and extent of the alopecia and the existence of other associated signs and symptoms.

The study methodology will depend on the clinical orientation obtained by the interrogation and the physical examination. Within laboratory studies, a blood count, blood iron, and thyroid hormones, among others, must be requested.