Abstract : The purpose of this article is to provide the information regarding the important causes of hair loss along with pathophysiology and how our repertory rubrics related with them.
Introduction : A patient who complains of too little hair should be treated with sensitivity. Particularly in women, these complaints are a source of genuine distress and the effect on a person’s self-esteem and self-image. The causes are numerous and varied but a systematic approach to the history and examination can easily be used to elicit the correct diagnosis for hair loss.
Knowledge of the normal hair cycle is fundamental to understanding hair disorders. Hair growth on the scalp is cyclical, with each follicle producing a number of different hairs during a person’s lifetime. The anagen growth phase lasts about 3 to 5 years on the scalp, during this phase hair grows at a rate of approximately 1 cm per month. The duration of anagen varies from person to person.The anagen phase is followed by an involutional stage known as catagen , which lasts 2 weeks and leads into a 3-month long dormant phase known as telogen. During telogen the hair remains anchored into the follicle but no longer grows. At the end of telogen the follicle awakens and commences production of the next anagen hair. As the new hair grows it displaces the old telogen hair from the follicle. At any one time, and depending on the age and sex of the person, up to 90% of hair follicles are in anagen, the growing phase, and only 10% in telogen, the resting phase, when hairs are normally shed. An alteration in this ratio can lead to an increased rate of hair loss and thus an impression of impending baldness.
The two major forms of alopecia are scarring and nonscarring. In scarring alopecia there are associated fibrosis, inflammation, and loss of hair follicles. A smooth scalp with a decreased number of follicular openings is usually observed clinically, but in some cases the changes are seen only in biopsy specimens from the affected areas. In nonscarring alopecia the hair shafts are gone, but the hair follicles are preserved, explaining the reversible nature of nonscarring alopecia
- Telogen effluvium:[Serious systemic illness, childbirth, weight loss, other stresses]
- Androgenic alopecia [secondary to ovarian or adrenal dysfunction]
- Alopecia areata
- Traction or other trauma (trichotillomania, heat exposure)
- Drugs[Cytotoxic agents, interferon,Oral contraceptives, Amphetamines, Anticoagulants (heparin, Coumadin), Beta-blockers, captopril, Lithium, anticonvulsants, Vitamin A, retinoids, Cholesterol-lowering agents]
- Cutaneous disease:[Seborrheic dermatitis, Eczema, Tinea capitis, Psoriasis, Cosmetics, other local irritants]
- Hypothyroidism, hyperthyroidism,Hypopituitarism
- Nutritional deficiency states (kwashiorkor, marasmus, or iron, zinc, or biotin deficiency)
- Human immunodeficiency virus (HIV) infection
- Physical and chemical agents:[Burns (hot combs or curlers), Freezing, Mechanical trauma, Acid, alkali, Radiation, Body art: tattooing, scarification]
- Infection:[Bacterial (including pyogenic infection, tertiary syphilis, leprosy, or lupus vulgaris), Fungal (e.g., ringworm), Viral (especially varicella-zoster, variola),Protozoal (leishmaniasis)]
- Systemic disease:[Lupus erythematosus, systemic or discoid, Scleroderma or morphea, Sarcoidosis, Dermatomyositis,Amyloidosis, Neoplasm]
- Cutaneous disease:[Basal cell carcinoma, Lichen planus, Cicatricial pemphigoid, Necrobiosis lipoidica diabeticorum]
The most common causes of “nonscarring alopecia” include telogen effluvium, androgenetic alopecia, alopecia areata, tinea capitis, and traumatic alopecia
1.TELOGEN EFFLUVIUM: Diffuse shedding of normal hairs follows either major stress (high fever, severe infection) or change in hormones (post partum). Stress causes the normally asynchronous growth cycles of individual hairs to become synchronous; therefore, large numbers of growing (anagen) hairs simultaneously enter the dying (telogen) phase.
The common rubrics regarding telogen effluvium found in repertories[Murphy]:
*Constitutions – HAIR, general, head and body – falling out, of hair – childbirth, after: Calc. Canth. Carb-v. hep. LYC. Nat-m. Nit-ac. Ph-ac. SEP. sil. SULPH.
*Constitutions – HAIR, general, head and body – falling out, of hair – diseases, after: lyc. manc. Ph-ac. thal.
*Constitutions – HAIR, general, head and body – falling out, of hair – grief, from:Ph-ac.
*Constitutions – HAIR, general, head and body – falling out, of hair – pregnancy, during LACH. Sep.
*Pregnancy – CONFINEMENT, general, puerperal – hair, loss: Nat-m. Sep.
*Breasts – BREAST-feeding, general – hair falls out: Nat-m. Ph-ac. sep.
*HEAD – FALLING out, hair, alopecia – toxicemia, from: crot-h.
2.ANDROGENETIC ALOPECIA: Male-pattern baldness is physiological in men over 20 years old, although rarely it may be extensive and develop at an alarming pace in the late teens. It also occurs in females, most obviously after the menopause. The well-known distribution (bitemporal recession and then crown involvement) is described as ‘male-pattern’ but this type of hair loss in females is often diffuse. Increased sensitivity of affected hairs to the effects of testosterone increased levels of circulating androgens (ovarian or adrenal source in women).
The common rubrics regarding androgenic alopecia found in repertories[Murphy]:
*Constitutions – HAIR, general, head and body – falling out, of hair – menopause: Sep.
*Constitutions – HAIR, general, head and body – loss, of hair – temples, from: calc. Kali-c. lyc. merc. Nat-m. par. sabin.
*Constitutions – HAIR, general, head and body – falling out, of hair – vertex: bar-c. graph. lyc. thuj. zinc.
*Constitutions – HAIR, general, head and body – loss, of hair – forehead, from: ars. bell. Hep. Merc. Nat-m. Phos. sil.
*FEMALE – FALLING out, hair: alum. BELL. Calc-f. Hell. Merc. NAT-C. NAT-M. NIT-AC. Ph-ac. Rhus-t. SEL. Sulph. Thal. ZINC.
*HEAD – FALLING out, hair, alopecia – climacteric period, in:LYC. SEP.
3.ALOPECIA AREATA: Well-circumscribed, circular areas of hair loss, 2–5 cm in diameter in extensive cases, coalescence of lesions and/or involvement of other hair-bearing surfaces of the body. The germinative zones of the hair follicles are surrounded by T lymphocytes. During the active stage of hair loss pathognomonic ‘exclamation mark’ hairs are seen (broken-off hairs 3-4 mm long, which taper off towards the scalp). Alopecia totalis describes complete loss of scalp hair and alopecia universalis complete loss of all hair. There is an association of alopecia areata with autoimmune disorders, atopy and Down’s syndrome.
The common rubrics regarding alopecia areata found in repertories[Murphy]:
*Constitutions – HAIR, general, head and body – baldness, head – spots, in: Apis Ars. Calc. calc-p. carb-an. FL-AC. Hep. Phos. Psor.
*HEAD – FALLING out, hair, alopecia – spots, in, alopecia areata: APIS ARS. CALC. CANTH. FL-AC. HEP. IOD. PHOS.. PSOR.
4.TINEA CAPITUS: Varies from scaling with minimal hair loss to discrete patches with “black dots” (broken hairs) to boggy plaque with pustules (kerion), Invasion of hairs by dermatophytes, most commonly Trichophyton tonsurans. Endothrix (within the hair shaft) infections, e.g. Trichophyton tonsurans, cause relatively uninflamed patchy baldness with breakage of the hairs at the skin surface (‘black dot’). There is no fluorescence under Wood’s light. Ectothrix (outside the hair shaft) species of fungi, such as Microsporum audouinii (anthropophilic), show minimal inflammation; Microsporum canis (from dogs and cats) infections are more inflamed and can be identified by green fluorescence with Wood’s light. Kerions are boggy, highly inflamed areas of tinea capitis and are usually caused by zoophilic (from animals, e.g. cattle ringworm) species of fungi (e.g. Trichophyton verrucosum).
The common rubrics regarding tinea capitus found in repertories:
*[Knerr] [Outer Head]Eruption(undefined):Tinea capitis (crusta lactea, scald head):Filthy, two-thirds of scalp one, mass of inflammation: Ustilago maydis
*Constitutions – HAIR, general, head and body – baldness, head – patches, in: Apis Ars. Calc. calc-p. carb-an. fl-ac. Graph. Hep. kali-p. lyc. morg. Phos. psor. sep.
*Constitutions – HAIR, general, head and body – brittleness: ars. bad. bell. borx. fl-ac. graph. Kali-c. plb. Psor. sec. Sep. staph. thuj.
5.TRAUMATIC ALOPECIA: Broken hairs irregular outline, Traction with curlers, rubber bands, braiding. Exposure to heat or chemicals (e.g., hair straighteners). Mechanical pulling (trichotillomania)
The common rubrics regarding traumatic alopecia found in repertories:
*HEAD – FALLING out, hair, alopecia – injury, from:hyper.
*[Complete] Mind – PULL, desires to, one’s hair: ars. BELL. Cina cupr. lach. Lil-t. med. mez. tarent. tub.
SCARRING alopecia is more frequently the result of a primary cutaneous disorder such as lichen planus, folliculitis decalvans, chronic cutaneous (discoid) lupus, or linear scleroderma (morphea) than it is a sign of systemic disease. Although the scarring lesions of discoid lupus can be seen in patients with systemic lupus, in the majority of cases the disease process is limited to the skin. Less common causes of scarring alopecia include sarcoidosis and cutaneous metastases.
In the early phases of discoid lupus, lichen planus, and folliculitis decalvans, there are circumscribed areas of alopecia. Fibrosis and subsequent loss of follicles are observed primarily in the center of the individual lesions, while the inflammatory process is most prominent at the periphery. The areas of active inflammation in discoid lupus are erythematous with scale, whereas the areas of previous inflammation are often hypopigmented with a rim of hyperpigmentation. In lichen planus the peripheral perifollicular macules are usually violet-colored. Complete examination of the skin and oral mucosa combined with a biopsy and direct immunofluorescence microscopy will aid in distinguishing these two entities. The peripheral active lesions in folliculitis decalvans are follicular pustules; these patients can develop a reactive arthritis.
The common rubrics regarding scaring alopecia found in repertories[Murphy]:
- Constitutions – HAIR, general, head and body – falling out, of hair – spots, in – and comes in white: vinc.
- HEAD – FALLING out, hair, alopecia – syphilis, from: ARS. aur. carb-v. cinnb. FL-AC. graph. HEP. kali-i. lyc. merc. merc-f. NIT-AC. PHOS. sulph.
- Skin – LICHEN, planus: agar. anac. Ant-c. apis Ars. Ars-i. chinin-ar. iod. Jug-c. Kali-bi. kali-i. led. merc. sars. staph. Sul-i.
- Skin – LUPUS erythematosum: ARS. LYC. NIT-AC.THUJ.
- Skin – LUPUS erythematosum – lupus, vulgaris: Ars. Ars-i. Aur-m Cist. Hep. Hydr. Hydrc. Sulph. Tub.
- Diseases – CANCER, general – skin, cancer, epithelioma: ARS-I.. CON. LYC. SOL
- Diseases – SCLERODERMA, skin: alum. Ant-c. arg-n. berb-a. Bry. Calc. caust. Crot-t. echi. Graph. Hydrc. lyc. petr. phos. ran-b. rhus-r. sars. sil. still. sulph. thiosin. Thyr.
- Skin – ERUPTIONS – morphea: ars. Phos. sil.
- Diseases – RADIATION, sickness, side effects: ars. CADM-S. calc-f. chin. fl-ac. Ip. nux-v. phos. rad-br. SOL x-ray
Laboratory tests, including a full blood count, erythrocyte sedimentation rate, urea and electrolytes, liver and thyroid function tests, an autoantibody profile and Treponema pallidum haemagglutination (TPHA) test, should help determine the cause of non-scarring alopecia. More specialised tests, including the hair pluck test where up to 50 hairs are removed with epilating forceps to determine the anagen:telogen ratio, are seldom necessary. Mycological assessment is advisable in cases of localised hair loss with scaling. A scalp biopsy, with direct immunofluorescence, may help to confirm a diagnosis of lichen planus of the scalp or discoid lupus erythematosus.
The scalp should be examined for evidence of disease such as scaliness, redness, injury, or scarring with its associated loss of follicles. Scarring is an important prognostic feature because hair loss is irreversible. Hair pulling gives rise to hair loss and the hair length varies because it is broken irregularly.
In modern medicine the management includes medicines and hair transplantation. Even than many patients are not improved properly. With homoeopathy it is expected that many patients will have better outcome by proper diagnosis of the case and select similimum by using correct rubrics.
- The Merc Manual Of Diagnosis And Therapy
- Davidsons Principles An Practice Of Medicine
- Harrisons Text Book Of Medicine
Dr.G.Siva Prasad, MD(Hom)