{"id":58832,"date":"2024-11-15T04:56:55","date_gmt":"2024-11-15T04:56:55","guid":{"rendered":"https:\/\/www.homeobook.com\/?p=58832"},"modified":"2024-11-15T04:56:55","modified_gmt":"2024-11-15T04:56:55","slug":"homoeopathic-management-of-eczema","status":"publish","type":"post","link":"https:\/\/www.homeobook.com\/homoeopathic-management-of-eczema\/","title":{"rendered":"Homoeopathic management of Eczema"},"content":{"rendered":"
Dr Reshma Radhakrishnan<\/strong><\/p>\n INTRODUCTION Most, but not all, dermatologists use dermatitis and eczema interchangeably. In general, dermatitis is used more commonly in the United States, and eczema is used more commonly in Europe. Dermatitis and Eczema are non-contagious inflammation of the skin, characterized by are erythema, scaling, oedema, vesiculation and oozing. It is characterized by superficial inflammatory oedema of the epidermis associated with vesicle. Itching varies from mild to severe paroxysms which may even interfere with work and sleep.<\/p>\n Dermatotic lesions pass through:<\/p>\n The acute stage<\/strong>: is characterized by itchy erythema followed by oedema, papules, vesicles, oozing and crusting. Most of the typical ecze\u0131nas of moderate intensity start with these morphological features. This stage does not last long. In about a couple of weeks the lesions start to heal.<\/p>\n Chronic<\/strong>: If the cause persists, and the eczema lasts over months or years, it becomes chronic. In such cases, the integument appears thickened and pigmented with prominent crisscross markings (Lichenification). This is the end result of all types of long-standing eczemas.<\/p>\n Sub-acute<\/strong>: In between the acute and chronic stages, is the sub-acute stage. characterized by papules and scaling with moderate oedema and erythema. Acute eczema may pass through this stage before it heals completely or becomes chronic.<\/p>\n ETIOLOGY<\/strong><\/p>\n The exact cause of eczema (atopic dermatitis) is unknown. Basically, two factors cause dermatitis and eczema.<\/p>\n Darier had correctly said that, “there is no eczema but an eczematous patient. \u201c<\/p>\n The general predisposing causes are<\/strong>:<\/p>\n Multiple precipitating, exciting and aggravating factors <\/strong><\/p>\n CLINICAL FEATURES<\/strong><\/p>\n There are several patterns of eczema but the clinical features are similar, irrespective of the cause.<\/p>\n CLASSIFICATION OF ECZEMA<\/strong><\/p>\n ENDOGENOUS ECZEMA<\/strong><\/p>\n ATOPIC DERMATITIS<\/strong> [Synonym: Besnier’s Prurigo] Besides allergens, emotional stresses and parental attitudes can also cause this condition. (The parents are usually the anxious type, and the patient is usually very sensitive and highly strung but often very intelligent. The atopic patient is also very sensitive to physical stresses like heat, cold and humidity and also infections. There is also vasomotor sensitivity.<\/p>\n Etiopathogenesis<\/strong>: The pathogenesis of atopic eczema is complex and multifactorial, involving an interplay of contributing factors:<\/p>\n Pathology<\/strong><\/p>\n Clinical features<\/strong><\/p>\n Clinically. there are four stages of atopic eczema:<\/p>\n It is marked by ill-defined, lichenoid patches, scratch marks and blood crusts with exacerbations of acute eczema from time to time. The skin is dry and injures easily. This stage is most marked till the age of 25, and may last through life. There may be associated cataract. Intolerance to high temperatures and humidity is fairly common.<\/p>\n Other features<\/strong><\/p>\n Prognosis<\/strong>: If left alone, eczema tends to continue indefinitely; but under judicious and persistent treatment can cur. Spontaneous and complete remission occurs during childhood. 30-5-% patients may develop asthma or hay fever later in life. Adult-onset AD often runs a severe course.<\/p>\n Management:<\/strong><\/p>\n SEBORRHEIC DERMATITIS It has a bimodal occurrence in infancy and adult age unlike AD it does not constitute on to adult life. It may be evident within the first few weeks of life, and within this context it typically occurs in the scalp [cradle cap], face or groin. Most common location<\/p>\n The lipophilic yeast Pityrosporum, a normal inhabitant of the skin, has been implicated recently. This conclusion is based on the finding of higher-than-normal numbers of the organisms in seborrheic areas and the response of seborrheic dermatitis to anti- fungal therapies, such as selenium sulfide and ketoconazole.<\/p>\n An increased incidence and severity of seborrheic dermatitis are seen in persons with Parkinson’s disease, facial paralysis, poliomyelitis, syringomyelia, quadriplegia, and emotional stress, suggesting that the CNS may influence seborrheic dermatitis. The mechanism is uncertain but may relate to increased rates of sebum production reported in some neurologic conditions. Severe or recalcitrant seborrheic eczema can be a marker of immune deficiency, including HIV infection.<\/p>\n Clinical features The common clinical patterns are:<\/p>\n Infantile Seborrheic Dermatitis<\/strong>: It presents in infants between 2-10 weeks of age and clears spontaneously by 8-12 months of age before reappearing at puberty. Distribution in infants includes the scalp (first site involved -cradle cap, 40% children), diaper area (napkin dermatitis), and other intertriginous folds. The primary lesions are round to oval patches of dry scales or yellowish-brown, greasy crusts with variable erythema. It presents as greasy yellowish scales without any hair loss.<\/p>\n Adult Seborrheic Dermatitis<\/strong>: Pityriasis capitis or dandruff is the adult counterpart in its mildest form or the precursor lesion. With progression, the scalp may become inflamed and covered with greasy scale. Dull or yellowish-red, sharply marginated, nonpruritic lesions covered with greasy scales are seen in areas with a rich supply of sebaceous glands. The other areas involved in adults are the central face, retro-auricular and nasolabial folds, glabella, eyebrows and external auditory canal. Lesions may also see in the axillary, pre-sternal and interscapular areas and inguinal folds. It is the one of the most common causes of chronic dermatitis of the genital area.<\/p>\n Management<\/strong><\/p>\n NUMULAR ECZEMA OR DISCOID ECZEMA Lesion sometimes clear centrally and resemble tinea corporis. Sometimes dry scaly lichenified plaque may be seen. It is considered as a variant of Atopic Dermatitis. Its etiology is unknown, but dry skin is a contributing factor. It occurs more frequently in men and is most common in middle age. Also, women aged 55-65 years. Most patients are seen in winter months. Lesions may be clustered on the extensor surface of lower parts of the legs or trunk in males and hands or fingers in females, are often bilaterally symmetrical. It may be generalized and scattered.<\/p>\n Cause<\/strong><\/p>\n It has a chronic course from weeks to months and tends to recur. Secondary bacterial infection is common. Nummular eczema should be distinguished from circular patches of infective eczema and tinea circinate. Both of these are asymmetrical, acute and non-recurring conditions. Sometimes, discoid dermatitis may be associated with dyshidrosis of palms and soles, and discoid patches of keratoderma.<\/p>\n Treatment<\/strong><\/p>\n STASIS \/ GRAVITATIONAL ECZEMA There may be concomitant irritant contact dermatitis due to secretion from stasis ulcer and allergic contact dermatitis secondary to topical medications and bacterial colonization. Typical initial site of involvement is the medial aspect of the ankle, often over a distended vein.<\/p>\n Pathogenesis<\/strong>: Incompetence of the deep perforating veins increases the hydrostatic pressure in dermal capillaries. Pericapillary fibrin deposition leads to the pathological and clinical changes.<\/p>\n POMPHOLYX \/ DYSHIDROTIC ECZEMA Pompholyx may have several causes, which include atopic eczema, irritant and contact allergic dermatitis and fungal infection. The underlying cause must be treated or removed. Being deep seated, the lesions do not rupture easily and heal instead with a dry thick scale which gradually peels off. Spontaneous remissions can occur in 2-3 weeks. Recurrence is the rule. Secondary infection may occur. Hyper hidrosis is common<\/p>\n Management<\/strong>: Emollients and topical steroids are needed. Venous insufficiency should be managed.<\/p>\n EXOGENOUS ECZEMA<\/strong><\/p>\n CONTACT DERMATITIS\/ CHEMICAL ECZEMA A minimum of 8-10 days is needed after sensitization for clinical allergy to manifest. Once sensitization to an allergen occurs, it tends to persist throughout life. However, the degree of sensitivity wanes with time unless repeated exposures occur. Depending on the degree of sensitization, even minute amounts of allergen may elicit a reaction. The eruption starts in a sensitized individual 48 hours or a few days after contact with the allergen.<\/p>\n The eruption worsens on repeated exposures (crescendo reaction). There is intense pruritus. Lesions are initially confined to the area of contact with the allergen and later spread to the surrounding areas. The distribution of eczema can be very informative with regard to possible culprits. Generalized involvement can also occur, if sensitization is strong.<\/p>\n Pathogenesis<\/strong>:<\/p>\n Many allergens are irritants, preceding irritation is common and may enhance allergen absorption. In contrast to irritant reactions, relatively small concentrations of an allergen can be enough to elicit an inflammatory reaction. ACD can be divided into acute and chronic forms.<\/p>\n Acute ACD<\/strong>: is characterized by erythema, edema, vesicle formation, and pruritus. It frequently spreads beyond the areas of contact and becomes generalized. The classic example is poison ivy dermatitis.<\/p>\n Chronic ACD<\/strong>: reactions are pruritic, erythematous, scaly, lichenified, and frequently excoriated. These may mimic chronic ICD.<\/p>\n Patch test<\/strong>: It is the only method available to diagnose ACD and differentiate it from ICD. The most widely used method involves the use of a Finn chamber. A small amount of the allergen, usually in a petrolatum vehicle, is placed into individual aluminum wells affixed to a strip of paper tape. \u00a0After 48 hours, the patches are removed and the initial readings recorded. Because these allergic reactions are delayed, a second interpretation must be per-formed at 72 hours, 96 hours, or even at 1 week after the initial test application. Additional readings beyond 48 hours increase the positive patch test yield by 34%.<\/p>\n The classic positive allergic patch test reaction shows spreading erythema, edema, and closely set vesicles that persist after removal of the patch or may appear after 2-7 days. Irritant reactions may have a glazed, scalded, follicular, or pustular appearance that usually fades after the patch is removed. Usually, patients with a suspected ACD are patch tested with a “standard” panel of 20 allergens to screen for the most common sensitivities. However, this panel only detects 75-80% of the most common allergies.<\/p>\n Additional testing with more specialized allergens is frequently warranted. Testing should only be done with known materials in accepted concentrations. The Repeated open application test [ROAT], or usage test, is used when patch testing is negative yet there remains a strong clinical suspicion for ACD. Remember, patch testing is a one-time occlusive test that does not duplicate low-level chronic daily exposure. With the ROAT, patients apply the suspected product to a quarter-sized area on the forearm twice a day for 1 week. If the patient is allergic, a localized dermatitis will occur, confirming the suspected allergy.<\/p>\n In ACD, sensitization is present on all parts of the skin as it is immunologically mediated. Therefore, application of the allergen to any area of normal skin provokes an eczematous reaction.<\/p>\n Management:<\/strong><\/p>\n Irritant contact dermatitis The potential for an individual compound to cause contact dermatitis varies greatly. Factors affecting a cutaneous response include the substance’s chemical and physical properties, concentration, vehicle, and duration of exposure; patient age, area of exposure, underlying dermatitis, and genetic makeup; and environmental factors such as humidity and temperature.<\/p>\n The most common area of involvement is the hands, where dermatitis is initiated or aggravated by chronic exposure to water and detergents. Features may include skin dryness, cracking, erythema to vesiculation, and edema. Erosion, crusting and scaling follows. Papules are not seen. ICD can be divided into acute toxic and cumulative insult subtypes.<\/p>\n Acute toxic:<\/strong> Eruptions occur from a single exposure to a strong toxic chemical, such as an acid, chloroform, methanol, phenol or propylene glycol, and cause toxic reactions after a short exposure. inducing erythema, vesicles, bullae, or skin sloughing. Reactions occur within minutes to hours after exposure, localize to the areas of maximal contact, and have sharp borders. In most cases, healing occurs soon after exposure.<\/p>\n Chronic cumulative insult<\/strong>: It is the more common type of ICD. These are due to multiple exposures of many low-level irritants, such as soaps and shampoos, over time. This dermatitis may take weeks, months, or even years to appear. It is characterized by erythema, scaling, fissuring, pruritus, lichenification, and poor demarcation from the surrounding skin.<\/p>\n Strong irritants have acute effects, whereas weaker irritants commonly cause chronic eczema, especially of the hands, after prolonged exposure. It is dependent on the concentration of the offending agent and occurs in all those who are exposed, depending on the penetrability and thickness of the stratum corneum. There is a threshold concentration for these substances above which they cause acute dermatitis and below which they do not. Individual susceptibility varies and older adults, atopic and fair skinned individuals are predisposed. Irritant eczema accounts for most occupational cases of eczema and is a significant cause of time off work. In chemical burns, necrosis of tissues leads to ulceration.<\/p>\n There is no reliable confirmatory skin test for irritants. Diagnosis is based on the exposure history and clinical picture.<\/p>\n Photosensitive\/photo dermatitis In normal persons pigmentation of the skin increases with exposure to sunlight, depending on its intensity, duration of exposure and type of skin. Ultra violet A (UVA 320-400 nm) and ultra violet B (UVB 290-320 nm) are the primary inducers of most photosensitivity reactions. The photon energy is absorbed by molecules such as skin cells (chromophores) and then either dispersed harmlessly or results in clinical disease. The chromophore can be<\/p>\n Eruption develops, or becomes aggravated on exposure to light. Seasonal variations are an Important consideration, particularly more so, in countries with extremes of climate. The common causes of photodermatitis are:<\/p>\n Photo dermatosis is broadly classified into:<\/p>\n Sunburn:<\/strong> is a transient inflammatory response of normal skin due to exposure to UVB rays. It is common in fair skinned individuals. There is uniform erythema, edema, vesicles and bullae strictly confined to the sun exposed areas. Erythema is visible 2-6 hours following exposure and reaches a maximum at 24-72 hours and fades in 3-5 days, followed by pigmentation.<\/p>\n Drug \/ chemical induced photo toxic reactions<\/strong>: In this condition interaction occurs between drugs \/chemical with ultra violet rays in the skin and manifests like an ICD (e.g. dyes, coal tar derivatives, psoralens, tetracyclines, phenothiazines, thiazides, sulfonamides and others).<\/p>\n Phytophotodermatitis: <\/strong>Photo-sensitization of the skin after contact with plants which have either phototoxic or photo allergic action. Clinically the lesions consist of a linear erythematous, bullous rash which heals in a week or two. On healing, pigmentation is left behind which takes several months to disappear. The rash develops after contact with the plant during, or followed by, exposure to sunlight.<\/p>\n Photo allergic reactions<\/strong>: A photo allergen such as fragrances like musk ambrette, PABA, phenothiazines and halogenated salicylanilides in deodorant soaps, formed in the skin initiates a type IV hypersensitivity reaction and manifests like an ACD.<\/p>\n Idiopathic- Polymorphous light eruption<\/strong>: Polymorphous light eruption (PMLE) is the most common photo dermatosis. This is common in women. UVA and UVB can evoke PMLE, UVA being more common. Lesions are papular, papulovesicular or urticarial plaques that begin within 24 hours of exposure. In the individual patient, usually one type of lesion predominates.<\/p>\n Photodermatitis must be differentiated from contact dermatitis due to pollens, particularly congress grass. Both occur on the exposed parts. While the former is seen in winter, the latter, is seen at least to begin with, in the pollinating season, in parthenium growing areas. Both get aggravated by exposure to sun, the former more than the latter. In some cases, it is difficult to distinguish the two.<\/p>\n Diagnosis of photodermatitis is based upon:<\/strong><\/p>\n Management<\/strong>:<\/p>\n UNCLASSIFIED ECZEMA<\/strong><\/p>\n This occurs in dry skin and is common in older adults. Low humidity caused by central heating, over-washing, excessive use of soap, malnutrition, diuretics and decrease in skin lipids\/cholesterol lowering drugs predispose. The most common site is the lower legs especially shin, and a \u2018crazy paving\u2019 pattern of fine fissuring on an erythematous background is seen. Dry winter climate, over washing and hypothyroidism exacerbates the condition.<\/p>\n Emollients are a mainstay, in combination with topical glucocorticoids. Patients must be advised to use caution with flammable emollients and to avoid bathroom slippages related to emollients on floor and feet, and this is particularly relevant for older individuals.<\/p>\n LSC is a localized form of lichenification due to rubbing or scratching as a habit or due to stress or anxiety. The skin becomes highly sensitive and hyperexcitable in response to minimal external stimuli. Any emotional conflicts particularly those arising from sex, financial and social problems, may initiate itching: scratching produces further irritation, and a vicious cycle is established resulting in lichenification.<\/p>\n LSC is common in elderly females [menopausal women] and neurotic people. These patients tend to tear off their skin when they cannot get at others for social reasons. It usually occurs as a single plaque of lichenification with exaggerated skin markings and hyper pigmentation associated with paroxysms of pruritus.<\/p>\n Common sites are the lower parts of the legs, back of the knee, ankles, wrists, back of the neck, scrotum and anogenital region. Sometimes a nodular lichenification known as prurigo nodularis develops on the shins and forearms. It should be explained to the patient that the rubbing and scratching must be stopped.<\/p>\n Neurodermatitis should be distinguished from lichenified eczemas, atopic dermatitis, lichen planus hypertrophicus and lichen scleroses et atrophicus. Prognosis is good if the primary emotional conflict can be resolved satisfactorily. Treatment consists of psychotherapy.<\/p>\n REPERTORIAL APPROACH<\/strong><\/p>\n SKIN AND EXTERIOR BODY, ERUPTIONS: MOIST, HUMID, ECZEMATOUS: CHRONIC ECZEMA: <\/strong>(13)\u00a0<\/strong>1 Am-c, 1 Bar-c, 1 Calc-f, 1 Cupr, 1 Cur, 1 Guai, 3 Nat-c, 3 Psor, 1 Sec, 1 Sep, 1 Sul-i, 3 Sulph, 1 Viol-t<\/p>\n SKIN AND EXTERIOR BODY,MILK-CRUST:<\/strong> (27)\u00a01 Ambr, 3 Ant-c, 2 Ars, 2 Bar-c, 2 Bell, 2 Bry, 4 CALC, 2 Carb-an, 1 Carb-v, 1 Cham, 3 Cic, 3 Dulc, 3 Graph, 2 Hep, 3 Led, 2 Lyc, 3 Merc, 2 Mez, 2 Nat-m, 1 Phos, 4 RHUS-T, 4 SARS, 3 Sep, 2 Sil, 3 Staph, 2 Sulph, 2 Viol-t,<\/p>\n SKIN AND EXTERIOR BODY, SUNBURN: <\/strong>(3)\u00a02 Camph, 3 Lyc, 3 Sulph,<\/p>\n SKIN AND EXTERIOR BODY, ULCERS: ECZEMATOUS (SALT-RHEUM): <\/strong>(16)\u00a03 Ambr, 4 ARS, 2 Calc, 1 Chin, 3 Graph, 4 LYC, 1 Merc, 1 Nat-c, 2 Petr, 2 Phos, 3 Puls, 4 SEP, 2 Sil, 2 Staph, 1 Sulph, 1 Zinc,<\/p>\n SKIN AND EXTERIOR BODY,TETTERS (INCLUDING HERPES AND ECZEMA):IN GENERAL:<\/strong> (81)\u00a01 Agar, 2 Alum, 1 Am-c, 2 Ambr, 1 Anac, 4 ARS, 1 Aur, 2 Bar-c, 2 Bell, 1 Bor, 4 BOV, 3 Bry, 1 Bufo, 1 Calad, 4 CALC, 1 Caps, 1 Carb-ac, 1 Carb-an, 2 Carb-v, 3 Caust, 1 Chel, 1 Cic, 4 CLEM, 1 Cocc, 4 CON, 2 Cupr, 1 Cycl, 4 DULC, 3 Fl-ac, 4 GRAPH, 1 Hell, 1 Hep, 1 Hyos, 1 Kali-c, 1 Kali-n, 3 Kreos, 2 Lach, 3 Led, 4 LYC, 2 Mag-c, 1 Mag-m, 1 Mang, 4 MERC, 1 Mez, 1 Mosch, 2 Mur-ac, 3 Nat-c, 2 Nat-m, 2 Nit-ac, 1 Nux-v, 2 Olnd, 1 Op, 1 Par, 3 Petr, 2 Ph-ac, 3 Phos, 1 Plb, 1 Puls, 2 Ran-b, 1 Ran-s, 4 RHUS-T, 1 Ruta, 1 Sabad, 2 Sars, 4 SEP, 4 SIL, 1 Spig, 1 Spong, 1 Squil, 1 Stann, 3 Staph, 1 Sul-ac, 1 Sulph, 1 Tarax, 3 Tell, 1 Teucr, 1 Thuj, 1 Valer, 1 Verat, 2 Viol-t, 2 Zinc,<\/p>\n AGGRAVATION SUN-BURN<\/strong>: (5)\u00a01 Acon, 4 BELL, 2 Camph, 1 Clem, 3 Hyos,<\/p>\n SKIN]ERUPTIONS:MILK CRUST<\/strong>: (28)\u00a01 Ambr, 3 Ant-c, 2 Ars, 3 Bar-c, 2 Bell, 2 Bry, 4 CALC, 2 Carb-an, 1 Carb-v, 1 Cham, 3 Cic, 3 Dulc, 3 Graph, 2 Hep, 3 Led, 2 Lyc, 3 Merc, 3 Mez, 2 Nat-m, 2 Olnd, 1 Phos, 4 RHUS-T, 4 SARS, 3 Sep, 2 Sil, 3 Staph, 2 Sulph, 3 Viol-t,<\/p>\n SKIN ULCERS: SALT RHEUM<\/strong>: (16)\u00a03 Ambr, 4 ARS, 2 Calc, 1 Chin, 3 Graph, 4 LYC, 1 Merc, 1 Nat-c, 2 Petr, 2 Phos, 3 Puls, 4 SEP, 2 Sil, 2 Staph, 1 Sulph, 1 Zinc,<\/p>\n SKIN TETTER:IN GENERAL (HERPETIC)<\/strong>: (75)\u00a01 Agar, 2 Alum, 1 Am-c, 2 Ambr, 1 Anac, 4 ARS, 1 Aur, 2 Bar-c, 1 Bell, 4 BOV, 3 Bry, 1 Calad, 4 CALC, 1 Caps, 1 Carb-an, 2 Carb-v, 3 Caust, 1 Chel, 1 Cic, 4 CLEM, 1 Cocc, 4 CON, 2 Cupr, 1 Cycl, 4 DULC, 4 GRAPH, 1 Hell, 2 Hep, 1 Hyos, 1 Kali-c, 1 Kali-n, 3 Kreos, 2 Lach, 3 Led, 4 LYC, 2 Mag-c, 1 Mag-m, 1 Mang, 4 MERC, 1 Mez, 1 Mosch, 2 Mur-ac, 3 Nat-c, 2 Nat-m, 2 Nit-ac, 1 Nux-v, 2 Olnd, 1 Par, 3 Petr, 2 Ph-ac, 3 Phos, 1 Plb, 1 Puls, 2 Ran-b, 1 Ran-s, 4 RHUS-T, 1 Ruta, 1 Sabad, 2 Sars, 4 SEP, 4 SIL, 1 Spig, 1 Spong, 1 Squil, 1 Stann, 2 Staph, 1 Sul-ac, 3 Sulph, 1 Tarax, 1 Teucr, 1 Thuj, 1 Valer, 1 Verat, 2 Viol-t, 2 Zinc,<\/p>\n SKIN, ERUPTIONS: ECZEMA<\/strong>: (68)\u00a01 Alum, 1 Am-c, 1 Am-m, 1 Anac, 1 Ant-c, 1 Arg-n, 3 Ars, 3 Ars-i, 1 Astac, 1 Aur, 2 Aur-m, 3 Bar-m, 1 Bell, 1 Bor, 1 Brom, 1 Bry, 2 Calad, 3 Calc, 3 Calc-s, 1 Canth, 1 Carb-ac, 2 Carb-v, 1 Carbn-s, 2 Caust, 3 Cic, 1 Clem, 1 Cop, 3 Croto-t, 1 Cycl, 3 Dulc, 1 Fl-ac, 3 Graph, 3 Hep, 1 Hydr, 2 Iris, 3 Jug-c, 3 Jug-r, 2 Kali-ar, 1 Kali-bi, 1 Kali-c, 2 Kali-chl, 2 Kali-s, 1 Lach, 1 Led, 2 Lith, 2 Lyc, 2 Merc, 3 Mez, 1 Nat-m, 1 Nat-p, 1 Nat-s, 1 Nit-ac, 3 Olnd, 3 Petr, 1 Phos, 2 Phyt, 3 Psor, 2 Ran-b, 3 Rhus-t, 1 Rhus-v, 2 Sars, 2 Sep, 2 Sil, 2 Staph, 3 Sul-i, 3 Sulph, 2 Thuj, 2 Viol-t.<\/p>\n SKIN, ERUPTIONS: CRUSTY: MOIST<\/strong>: (26)\u00a01 Alum, 1 Anac, 2 Anthr, 3 Ars, 2 Bar-c, 3 Calc, 3 Carbn-s, 2 Cic, 1 Clem, 3 Graph, 2 Hell, 2 Hep, 2 Kali-s, 3 Lyc, 3 Merc, 3 Mez, 2 Olnd, 1 Phos, 1 Plb, 1 Ran-b, 3 Rhus-t, 1 Ruta, 1 Sep, 2 Sil, 3 Staph, 3 Sulph,<\/p>\n SKIN, ERUPTIONS: DRY<\/strong>: (61)\u00a02 Alum, 1 Anac, 1 Anag, 3 Ars, 3 Ars-i, 3 Aur, 3 Aur-m, 3 Bar-c, 2 Bor, 2 Bry, 1 Bufo, 2 Cact, 1 Calad, 3 Calc, 3 Calc-s, 2 Carb-v, 2 Carbn-s, 1 Caust, 1 Clem, 1 Cocc, 1 Corn, 2 Cupr, 2 Dulc, 2 Fl-ac, 2 Graph, 2 Hep, 1 Hydr-ac, 1 Hyos, 2 Kali-ar, 2 Kali-c, 2 Kali-chl, 1 Kali-i, 1 Kali-s, 2 Kreos, 3 Led, 2 Lyc, 2 Mag-c, 2 Merc, 3 Mez, 1 Nat-c, 1 Nat-m, 1 Nat-p, 1 Par, 2 Petr, 2 Ph-ac, 3 Phos, 2 Psor, 1 Rhus-t, 2 Sars, 1 Sel, 3 Sep, 3 Sil, 1 Stann, 2 Staph, 2 Sulph, 1 Teucr, 1 Thuj, 1 Valer, 3 Verat, 2 Viol-t, 2 Zinc,<\/p>\n SKIN, ERUPTIONS: ECZEMA: CHRONIC: <\/strong>(39)\u00a01 Am-c, 1 Bac, 1 Bar-c, 1 Bell, 2 Berb, 1 Calc, 1 Calc-f, 1 Carb-ac, 1 Carb-v, 1 Carbn-s, 2 Chaul, 1 Clem, 1 Cupr, 1 Cur, 2 Euph-cy, 1 Graph, 1 Guai, 1 Ign, 1 Iris, 3 Kali-ar, 1 Kali-m, 1 Mang, 1 Merc, 1 Merc-pr-a, 1 Merc-pr-r, 1 Mez, 3 Nat-c, 4 PETR, 3 Psor, 2 Rib-ac, 1 Sec, 1 Sep, 3 Sin-n, 1 Skook, 2 Solid, 1 Sul-i, 3 Sulph, 2 Vero-o, 3 Viol-t,<\/p>\n SKIN, ERUPTIONS: ECZEMA: DRY: <\/strong>(28)\u00a03 Alum, 4 ALUM-SIL, 3 Am-c, 1 Ars, 1 Bar-c, 1 Berb-a, 1 Bov, 3 Bry, 1 Calc, 1 Calc-s, 1 Canth, 2 Cortico, 1 Eur-p, 1 Fl-ac, 1 Foll, 1 Kali-c, 1 Lob-e, 1 Lyc, 1 Morg, 3 Petr, 2 Platan-a, 1 Por-m, 1 Rad-br, 1 Sars, 1 Sep, 1 Sil, 1 Sulph, 3 X-ray,<\/p>\n SKIN, ECZEMA: MOIST: <\/strong>(94)\u00a01 Aethi-a, 3 Alum, 1 Am-c, 2 Ange-a, 1 Ars, 1 Ars-i, 2 Atro, 1 Bac, 3 Bar-c, 1 Bell, 4 BOV, 1 Brom, 1 Bry, 3 Calc, 1 Calc-f, 1 Calc-s, 1 Canth, 1 Carb-an, 3 Carb-v, 1 Caust, 2 Cham, 1 Chlol, 3 Cic, 3 Clem, 1 Con, 1 Cupr, 1 Cur, 1 Dulc, 1 Erig, 2 Galeg, 2 Genist, 2 Gnaph, 4 GRAPH, 1 Guai, 1 Harp, 1 Hell, 3 Hep, 2 Hoch, 1 Iod, 1 Iris, 3 Kali-br, 1 Kali-c, 1 Kali-chl, 1 Kali-sil, 1 Kreos, 1 Lach, 3 Lappa, 1 Led, 4 LYC, 1 Merc, 1 Merc-c, 1 Merc-pr-a, 1 Merc-pr-r, 3 Mez, 3 Morg, 1 Mut, 1 Nat-c, 3 Nat-m, 3 Nat-s, 1 Nit-ac, 3 Olnd, 4 PETR, 1 Ph-ac, 1 Phos, 1 Phyt, 2 Pot-t, 1 Pras, 1 Prim-o, 3 Psor, 1 Rad-br, 3 Rhus-t, 3 Ruta, 1 Sabin, 1 Sanic, 1 Sars, 2 Scab-s, 1 Sec, 3 Sel, 3 Sep, 3 Sil, 1 Squil, 3 Staph, 1 Sul-ac, 1 Sul-i, 3 Sulph, 1 Tarax, 1 Tere-ch, 1 Thuj, 1 Tub, 1 Vinc, 3 Viol-o, 1 Viol-t, 1 Wies, 1 Zinc,<\/p>\n HEAD, ERUPTIONS: MILK CRUST, CRUSTA LACTEA:<\/strong> (86)\u00a01 Acon, 1 Aethi-a, 3 Alum, 3 Ambr, 3 Ant-c, 1 Ant-t, 3 Ars, 1 Ars-i, 3 Astac, 1 Aur, 4 BAR-C, 2 Bell, 2 Betul, 1 Bor, 1 Brom, 2 Bry, 4 CALC, 1 Calc-i, 1 Calc-p, 3 Calc-s, 1 Canth, 3 Carb-an, 1 Carb-v, 1 Cham, 1 Chel, 4 CIC, 3 Clem, 3 Croto-t, 4 DULC, 3 Euph, 3 Graph, 1 Hell, 4 HEP, 1 Hydr, 1 Iod, 1 Iris, 3 Jug-r, 1 Kali-c, 1 Kali-chl, 1 Kali-m, 1 Kreos, 3 Lappa, 3 Led, 3 Lyc, 3 Mag-c, 2 Med, 2 Melit, 4 MERC, 1 Merc-i-f, 4 MEZ, 1 Mur-ac, 3 Nat-m, 1 Nat-p, 3 Nit-ac, 1 Ol-j, 4 OLND, 1 Onis, 1 Par, 3 Petr, 1 Ph-ac, 4 PHOS, 1 Phyt, 1 Plb-i, 3 Psor, 4 RHUS-T, 3 Ruta, 1 Sarr, 4 SARS, 1 Scroph-n, 1 Seneg, 3 Sep, 4 SIL, 4 STAPH, 1 Still, 1 Sul-ac, 3 Sulph, 2 Tarent, 3 Trif-p, 3 Tub, 2 Ust, 1 Vac, 1 Verat, 3 Vinc, 1 Viol-o, 3 Viol-t, 3 Zinc,<\/p>\n GENERALITIES SUN: AGG.: SUNBURN<\/strong>: (49)\u00a03 Acon, 3 Agar, 3 Ant-c, 3 Astac, 4 BELL, 3 Bov, 1 Bry, 1 Bufo, 1 Cadm-s, 3 Camph, 3 Canth, 1 Carc, 1 Chlorpr, 3 Clem, 2 Cortiso, 1 Cyt-l, 1 Epig, 1 Euphr, 1 Germ, 1 Gink, 1 Hist, 1 Hydrog, 3 Hyos, 2 Hyper, 1 Ignis, 1 Kali-c, 1 Lach, 3 Lyc, 1 Mangi, 1 Morg, 3 Mur-ac, 3 Nat-c, 2 Nelu, 1 Op, 1 Pitu-a, 4 PULS, 1 Rob, 2 Ros-d, 1 Sel, 1 Seq-g, 3 Sol, 3 Sulph, 1 Tam, 1 Tax, 1 Toxop-p, 1 Tub, 1 Uv-lux, 3 Valer, 1 Verat,<\/p>\n CLINICAL, ALLERGY: CREMES, COSMETICS<\/strong>:(2)\u00a01 Ars, 1 Puls,<\/p>\n CLINICAL, ALLERGY: CHEMICALS<\/strong>: (5)\u00a01 Antipyrin, 3 Asar, 1 Ba-tn, 1 Carc, 1 Dpt,<\/p>\n CLINICAL, ALLERGY: METAL DERMATITIS<\/strong>: (3)\u00a01 C-di-o, 1 Morg-g, 1 Pitu-a,<\/p>\n SKIN, ERUPTIONS: ALLERGIC: <\/strong>(56)\u00a04 ANT-C, 1 Apis, 3 Ars, 3 Astac, 1 Bell, 2 Bov, 1 Bry, 1 Calc, 1 Calc-ar, 1 Camph, 1 Cann-s, 1 Carb-v, 3 Chlol, 1 Chol, 1 Coloc, 3 Cop, 1 Dulc, 1 Dys-co, 1 Euph, 1 Fic, 1 Frag, 1 Galph, 4 GRAPH, 1 Hep, 1 Hom, 1 Ind, 1 Levo, 1 Lyc, 1 Mand, 1 Med, 1 Medus, 1 Morg, 1 Morg-g, 1 Nat-s, 1 Neod-c, 1 Pall, 1 Parth, 1 Petr, 1 Pot-a, 1 Prim-o, 3 Puls, 1 Rad-br, 1 Rhus-t, 1 Ruta, 1 Sep, 1 Sil, 1 Stroph, 1 Syc-co, 1 Tela, 3 Ter, 1 Terb-s, 1 Tet, 1 Thuj, 4 TUB, 1 Urea, 3 Urt-u,<\/p>\n SKIN – ERUPTIONS – chronic<\/strong>: (4) mang. sul-i. syph. vac.<\/p>\n
\n<\/strong>Dermatitis is a general term that describes an inflammation of the skin, but dermatologists use the term to refer to a specific group of inflammatory skin diseases. Eczema [atopic dermatitis] a Greek word meaning \u201ca boiling out\u201d. Atopy the strange word, coined in 1923 by Coca, means “out-of-place-ness” or “different.” Atopy refers to the predisposition to develop asthma, allergic rhinitis, and an associated skin disease appropriately called atopic dermatitis.<\/p>\n\n
\n
\n
\n
\n
\n
\nThe eczematous process is usually the result of endogenous sensitization, but exogenous allergies may also play a part. The latter can be proved by patch tests, and the former, by scratch tests, which show allergy to multiple agents. There is more than normal susceptibility to develop passive transfer antibodies in the blood serum (Prausnitz Kustner reaction).<\/p>\n\n
\n
\n
\n
\n
\n
\n<\/strong>The term seborrheic dermatitis may be a misnomer because the pathogenic role of sebum has not been established. The lipophilic yeast Pityrosporum, a normal inhabitant of the skin, has been implicated in the etiopathogenesis along with abnormalities of essential fatty acids. It is a common, chronic disorder characterized by greasy scales overlying erythematous patches or plaques. Induration and scaling are less prominent than in psoriasis, but clinical overlap exists between these diseases [sebo-psoriasis].<\/p>\n\n
\n<\/strong>It is more common in males and occurs after puberty and the incidence increases with age.<\/p>\n\n
\n
\n
\n<\/strong>It a is a chronic pruritic inflammatory dermatitis, typically affects middle aged or elderly. In Latin nummular, meaning \u201ccoinlike\u201d. Clinically characterized by circular or oval \u201ccoinlike\u201d lesions of variable sizes ranging from 1cm to 5cm, rapidly beginning as small edematous papules that become crusted and scaly. They are formed by coalescence of minute papulovesicular and are intensely pruritic, with excoriations.<\/p>\n\n
\n
\n<\/strong>It develops on the lower extremities secondary to venous incompetence. Patients may give a history of deep venous thrombosis and may have evidence of vein removal or varicose veins. Early findings consist of mild erythema and scaling associated with pruritus. Inflammatory edema, papules, scaling, loss of hair, ulceration, old hemorrhages and lipodermatosclerosis are the characteristic features.<\/p>\n
\n<\/strong>Pompholyx is an acute, chronic or recurrent dermatosis of the lateral aspects of the fingers, palms and soles characterized by sudden eruption of bilaterally symmetrical deep seated pruritic, clear vesicles. These may coalesce to form large multiloculated bullae. Later forms scaling, fissures, and lichenification. It is thought to be related to an atopic background and as a manifestation of nickel allergy.<\/p>\n
\n<\/strong>Contact dermatitis (CD) is a term applied to acute or chronic cutaneous inflammatory reaction to substances that come in contact with the skin. The eruption develops briskly, spreading far beyond original point of contact it has an ill-defined margin, fading at the periphery. Brisk oedema and uniform vesiculation are the features that dominate the eruption.\u00a0 These reactions occur through one of two mechanisms:<\/p>\n\n
\n
\n
\n
\n<\/strong>While over 2800 substances have been identified as contact allergens, almost any substance under the right circumstances can act as an irritant. It is important to note that irritating compounds can be allergenic, and allergenic compounds can be irritating. Irritants produce direct toxic injury to the skin. An irritant substance is one that causes an inflammatory reaction in most individuals when applied in sufficient concentration for an adequate length of time.<\/p>\n
\n<\/strong>Photosensitivity is an abnormal response to sunlight and affects the sun exposed parts of the body like:<\/p>\n\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n