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Erythema means redness of the skin due to dilatation of blood vessels. This will lead to hyperemia in a specific area of the skin in response to endogenous or exogenous factors. Erythema is the first and most common skin manifestation, which may be localized or generalized.

Different clinical types of erythema

  1. Localized erythema: this type involves certain areas due to different factors.

    Different clinical descriptive names are related to the localized erythema mainly:

    Erythema palmare : is localized to the palms, which may appear due to liver cirrhosis.

    Erythema intertrigo: erythema of the intertriginous areas due to excess friction and sweating.



                 Fig.220b. Erythema intertrigo

    Erythema pernio: due to exposure to cold, which affects the acral parts .

    Erythema caloricum: erythema occurring in response to any type of heat.

    Erythema solare: erythema in response of exposure to sun.


                                                             Fig. 220c. Erythema solare

    Another types of erythema may occur in response to certain types of food,chemicals, drugs, vaccines,stress, gastro-intestinal disturbances and vasomotor liability.

  2. Generalized erythema

    This type is generalized involving wide areas of the skin due to systemic factors.

    Generalized erythema presents with different clinical types.


(Erythema toxicum neonatorum)

Erythema toxicum neonatorum is a patchy benign eruption of the newborn that appears in the first three or four days of life and generally disappears by the second week.


The cause of this type of erythema of the newborn is unknown. Different factors are suspected:

An allergic origin : hypersensitivity to milk.

Drugs transmitted to the infant via the placenta .



  Fig.220d. Erythema due to drug reaction(Corticosteroids)

Due to vaginal secretions of the mother.

Allergic response to some components of sebum .

Clinical Features

Skin lesions initially appear as erythematous blotchy macules, papules or pustules mainly on the trunk , face and proximal parts of the limbs.

Rarely the palms and soles are affected.

The papules may be surmounted by small pustules, 2-4 mm in diameter.

In the mildest cases these macules fade within a day.

In more severe cases, urticarial papules arise within the erythematous areas, on the back and buttocks.

The general health of the infant is not affected and usually the lesions fade away without treatment .

Differential Diagnosis

Toxic erythema of the newborn has to be differentiated from:

Pustular miliaria, which clinically simulates toxic erythema.

Herpes simplex virus infection .

Incontinentia pigmenti .

Neonatal pustular pyoderma : The pustules show neutrophilic leukocytes.The pustules in erythema neonatorum toxicum are filled with eosinophils which are follicular and perifollicular .

The erythematous macules show slight perivascular infiltration with eosinophils.


Symptomatic and supportive measures since no specific treatment is available. Usually the skin lesion clears within few days .



Several types of exanthematous diseases manifest with erythema, which is variable and specific to such diseases. Viral and bacterial diseases are common cause of erythema in infants and children. Measles, erythema infectiosum (fifth disease), roseola and scarlet fever are some types of generalized erythema.


                                         Fig. 220d,e, Generalized exanthematous reaction


(Fifth disease)
(Margarine disease)

Epidemic types of generalized erythema were reported in Holland and Germany in 1958 in children, known as "Margarine disease" . Viral cause from certain types of diary products was suspected. The disease is slightly infectious that occurs in epidemics in spring and summer.

Clinical features

The erythema appears on the proximal parts of the extremities and sometimes on the face and spread to cover the entire skin surface.Erythema appears suddenly and usually without any prodromal symptoms. The erythematous reaction has different clinical features simulating erythema multiforme,papular and morbiliform eruption. The skin lesion on the face has the butterfly appearance and present with diffuse erythema or grouped tiny papules on an erythematous base.

Itching is severe but on the fifth day , erythema begins to regress and itching becomes less.


(Erythema exudativum)

This is a hypersensitivity syndrome due to antigen-antibody reaction, which may involve skin, mucous membranes and internal organs. Stevens and Johnson‘s syndrome is an acute and severe clinical type of erythema multiforme.

Fig. 220 Erythema multiforme

Fig. 221 Erythema multiforme

Fig.222 Erythema multiforme

Fig.223 Erythema multiforme


Clinical Features

Skin lesions present with symmetrical bright bluish to dark purple slightly infiltrated, round macules with tendency to spread peripherally.

Different clinical types of erythema multiforme may appear, which depend mainly on the shape and severity of the reaction. Skin lesions may be macular,papular,nodular, vesicular or bullous forming different shapes such as the annular, circinate, the iris lesions, purpuric and urticarial types.

The Iris lesion: The central portion of the lesion usually shows a bluish gray central depression known as the “iris lesions“ which is usually characteristic to erythema multiforme.


                                         Fig. 223a. Erythema multiforme


The most common sites involved are the dorsal aspects of the hands, fingers and feet.

The Hebra type: is characterized by symmetrical erythematous papular, urticarial, bullous or even hemorrhagic reactions appear on the sun-exposed areas of the skin. Skin lesions have the characteristic iris lesions.

The mucous membranes are usually involved. This type is usually recurrent and usually preceded by herpes labilalis before the onset of erythema.

The maculopapular type

Well-defined erythematous maculopapules, which spread peripherally forming polycyclic patches with central clearing. Erythema iris may be conspicuous.

Fig. 223b. Maculopapular erythema

The bullous type

Skin lesions may show hemorrhagic bullae on an erythematous base.

The vesiculobullous type

Discrete or grouped vesicles surrounded by an erythematous base, which may be misdiagnosed as herpes lesions.

The maculopapular type

Skin lesions present with edematous bright bluish red macules or flat-topped papules, which has the tendency to spread peripherally.



This is considered as a severe type of erythema multiforme which presents with skin , mucous membrane and internal manifestations.

General manifestations

The patient may show severe constitutional manifestations, where the severity and prognosis depend on age, cause of the disease and early management.

Constitutional symptoms : fever, headache, malaise and soreness of the mouth and throat. The syndrome may present with severe manifestations such as rapid pulse,weakness,rapid respiration, prostration and joint pains.

The syndrome may be fatal.

Mucous membrane : stomatitis is the early manifestation and may be diagnostic. Mucous membranes show ulceration with bleeding, salivation and angioedema.This may interfere with drinking or feeding causing more cachexia to the patients.Conjunctivitis, corneal ulceration,rhinitis and epistaxis are common mucous membrane manifestations.


                                          Fig. 224a. Steven’s Johnson  syndrome  


                 Fig. 224b.Steven’s Johnson  syndrome


               Fig. 224c.Steven’s Johnson  syndrome

                      (Vesiculo-bullous lesions)


         Skin manifestations: skin lesions present with multiforme, erythematous, macular with an iris,papular,vesicular reaction with large hemorrhagic bullae on an erythematous base. Rupture of the bullae lead to ulcerating abraded skin surface, which is susceptible to secondary infections.

Subungual hemorrhages are common.

Purpura is a common manifestation of the severe type.

Pruritus may be severe.


Different factors are blamed as a causative of Steven-Johnson syndrome.

Idiopathic types with unknown cause are common.

Some of the following may cause the syndrome:

  1. Bacterial infections: Diphtheria, Brucellosis, T.B.,Typhoid fever and pneumonia.

  2. Viral infections: measles, herpes, small pox vaccination, Asian flu and viral pneumonia.

  3. Mycotic infections: Coccidioidomycosis and histoplasmosis.

  4. Protozoal infections: malaria and trichomoniasis.

  5. Collagen diseases: systemic and discoid lupus erythematosus.

  6. Vaccines: BCG, small pox and poliomyelitis vaccines.

  7. Drugs: penicillin,sulfonamides, trimethoprine, salicylates, phenobarbitol, barbiturates, antipyrine and hydrazine.

  8. Loffler‘s syndrome may be accompanied with erythema multiforme.

  9. Hormonal changes.

  10. Allergic skin contactants: rhus dermatitis and fire sponges.

  11. Internal malignancy:lymphoma, carcinomas , polycythemia,myeloma and Hodjkin‘s disease.


Inflammatory infiltrate of the upper dermis.

Spongiosis and edema of the epidermis and dermis.

Perivascular inflammatory infiltrate around dilated blood vessels.

Extravasated erythrocytes.

Differential diagnosis

Toxic epidermal necrolysis.

Bullous contact dermatitis.

Pemphigus and pemphigoides.

Bullous systemic lupus erythematosus.


Treatment depends on the cause and the severity of the clinical manifestations.  



Erythema elevatum diutinum is characterized by slightly painful, red,elevated, round, polygonal nodules, usually arranged in annular shapes. The  most common sites involved are the extensor surfaces of the extremities and hands. 

Fig.224e. Erythema Elevatum diutenum


The nodules have smooth surface showing central depression. The eruption has a chronic course, which may extend for months.There is no involvement of the mucous membranes and the general health is no affected.



Erythema nodosum is characterized by symmetrical , tender, bright red nodules of different sizes, most common on the extensor surfaces of the legs. Mild constitutional symptoms such as fever,malais,myalgia and arthralgia may precede the appearance of the eruption.The disease is self-limiting.




                                                              Fig.224f. Erythema nodosum

(Erythema nodosum was discussed in the previous chapters).



This type is due to insect bites such as ticks.The erythematous reaction appears in rings spreading peripherally with raised edges and pale center.

Fig. 224. Erythema chronicum migrans


This type is common in children with rheumatic fever and rheumatic endocarditis. Skin manifestations present with pale red to livid rings of variable sizes and shapes. The commonest sites involved are thighs,abdomen, chest and the back.



The disease runs a chronic course, and may begin at any age even in newborn infants . In neonates, annular erythema may be a sign of maternal systemic lupus erythematosus. The most common sites are the buttocks, thighs and upper arms, but any area may be involved. Sometimes lesions are localized on the extremities but the face is seldom affected.

Fig. 225. Erythema annulare centrifugum

Clinical Manifestations

The lesions may be solitary or more often multiple that appear mainly on the buttocks , thighs and upper arms. Small, pink, infiltrated papule slowly enlarges and forms a ring as the central area flattens and fades. Individual lesions last for a few days, weeks, or slowly extend for months, with the appearance of purpura and pigmentation .

Extension of the lesion may be irregular to leave arciform segments. The edge may be quite flat or easily palpable, smooth or show slight scaling.

Rarely vesiculation occurs.

Itching is variable but seldom intense.



Erythroderma means erythema and skin scaling . Erythroderma may be primary or secondary that occurs in the course of different skin diseases .

Primary erythroderma

Erythroderma desquamativum (Linear‘s disease).

Erythroderma associated with lymphomas, Hodgkin‘s disease, and mycosis fungoides.

Secondary erythroderma

Extensive skin exfoliation may occur with:

Drug reactions

Chronic dermatitis


Seborrheic dermatitis


Pityriasis rubra piliaris

Fig. 226. Erythroderma (Erythema & skin exfoliation)

Fig. 226b. Erythroderma

Fig. 226c Erythroderma


Metabolic complications of erythroderma

Hyperthermia: sweat retention due to obstruction of sweat gland orifices may lead to dangerous hypothermia especially in children in the tropics .

Muscle wasting: An increase in metabolic activity provides compensatory increase in body heat production but at the expense of tissue catabolism

Cardiovascular failure: Skin blood flow, blood volume and cardiac output may all be increased. If these changes persist, they may lead to cardiovascular failure.

Malabsorption and enteropathy may occur.

Hypoalbuminaemia: Extensive scaling leads to protein and iron loss beside impaired absorption and utilization, causing edema and iron deficiency anemia . Serum B12 tend to be low, mainly due to increased utilization by the hyperplastic epidermis.

Dehydration and water loss: The barrier efficiency of the skin in psoriatic erythroderma is certainly impaired. The chief effect is the increase in water loss by diffusion since evaporation of which also contributes to heat loss.

The urine output tends to drop and if water intake is inadequate for any reason, dehydration results.


Erythroderma may be suspected in an infant with erythroderma that has persisted from birth or shortly after birth.

Failure to thrive and diarrhea.

Susceptibility to infections.

Lymphadenopathy, and/or hepatospleenomegaly will help to establish the diagnosis.

Differential Diagnosis

Non-bullous ichthyosiform erythroderma .

Omenn‘s syndrome .

Erythrodermic atopic eczema .

Psoriasis .



Urticaria is a common vascular skin reaction characterized by the appearance of wheals that are transient and recurrent. These are erythematous, elevated skin swelling surrounded by a halo and accompanied by severe itching or stinging sensation.

Urticaria may be accompanied by systemic manifestations such as asthma, abdominal cramps, joint pain and severe laryngeal edema .

Urticaria is common in children and has different clinical picture that may appear with different shapes , and varies from the simple wheal to the severe bullous type .


                                           Urticaria(Drug reaction ,Amoxycillin)




                                                                                      Fig.227 Urticaria

Neonatal hemorrhagic edema (purpura en cocarde) occurs in very young children and is on the borderline between urticaria and vasculitis.

Urticarial lesions show vascular dilatation. The reaction in urticaria is related to different factors; histamine (mediator for the common urticaria), kinins (mediator for angioedema), serotenin , prostaglandin, anaphphylatoxin and acetylcholine release .

The different factors affecting children are the same as that of adults with a tendency to be more acute in young ages .

Classification of Urticaria

Urticaria is classified according to its etiology into immunological or non-immunological type .

Fig. 227. Urticaria

Fig. 228. Urticaria

Fig. 229. Angioneurotic edema

Fig. 230. Urticaria

  1. Immunologic urticaria

    The immunologic type of urticaria may be an IgE dependent.

    Different factors that can cause immunologic urticaria are :

    Food due to a specific antigen .

    Intestinal worms .

    Physical factors due to sunlight , heat , water , and pressure urticaria.

    Hereditary angioedema 





  1. Non immunologic urticaria

    This type is due to substances that have direct effect causing degranulation of mast cells.

    Different factors that can cause non-immunologic urticaria are:

    Food stuffs containing histamine such as fish .


    Chemicals .

    Direct physical factors .


Patient presenting with chronic urticaria should be thoroughly investigated. This doesn‘t mean to do immediately every possible investigation to diagnose or exclude every possible underlying cause .

History and a careful interrogation of the patient or the child‘s mother may be very helpful to reach the diagnosis of the triggering factors.

Food: The relation to food especially food with additives, colored or preserved foods should be considered .

Drugs: taken by the child such as antibiotics or antipyretics as salicylates should be thoroughly investigated.

Systemic Diseases:

Urticaria may appear with other diseases such as systemic diseases or hormonal imbalance.

Insects: ants , mosquitoes may cause severe reaction especially in sensitive infants .

Fig. 231. Papular urticaria, Purpuric lesion
(Insect Bite)

Fig. 232. Papular urticaria (Insect Bite)

The psychological state of the child is important where some cases of urticaria are due to stress and psychological trauma .


Investigations of chronic recurrent urticaria is not always successful in detecting the offending causative factors .

Several tests may be considered such as:

  • Complete blood picture: Blood count, including eosinophils count and ESR.

  • Serum protein electrophoresis .

  • Thyroid function tests .

  • Total IgE

  • RASTs .

  • Urine for any suspected infections .

  • Liver function tests .

  • Hepatitis B surface antigen .

  • Autoantibodies .

  • Complement screen , including C1 esterase inhibitor .

  • Stool analysis for detecting any parasites .

  • Chest x-ray for the nasal sinuses to detect any septic focus .

  • Provocation tests with Tartrazine and anti candida may be of value in older children.

                                     TYPES OF URTICARIA

There are different types of urticaria :

Cholenergic urticaria

Physical urticaria .

Herido-familial urticaria

Idiopathic urticaria .

Angio neurotic edema

Urticaria pigmentosa

Papular urticaria

Bullous urticaria

Inhalant urticaria


Physical agents such as cold, heat and sun may precipitate this type of urticaria.

Cold urticaria

Cold urticaria may be transmitted as an autosomal dominant .

The skin lesions present with wheals that appear after exposure to cold . The condition begins after birth and may persist throughout life .

Another type of cold urticaria accompanies collagen diseases such as lupus erythematosus, dysproteinaemia or haemoglobinuria.

Idiopathic cold urticaria

This is a common type of urticaria, where whealing appears after exposure to cold and can be relieved after warming of the skin . Mucous membrane of the mouth , pharynx and gastrointestinal tract may be involved.

Patients having this type of urticaria should have much care and should be warned not to be exposed suddenly to cold or swimming in cold water or having a cold shower, where these may cause syncope and even sudden death.

Diagnosis of cold urticaria is by applying an ice on the skin, this will provoke an urticarial lesion .

Heat urticaria

Urticarial lesions appear due to histamine release after sweating initiated by heat or after bathing with hot water .

Solar urticaria

Urticarial lesion appears few minuets after exposure to sunlight . This condition may be associated with the delayed type of photosensitivity and polymorphous light eruption .



Demographic urticaria is a common type, characterized by linear and with sharp edged wheals, appearing after scratching of the skin by a blunt object. This is associated with increase in the circulating IgE.

Firm stroking of the skin gives rise to the triple response of Lewis with a wheal and ‘flare‘. This may appear in 25-50% of normal people.

Fig. 233. Dermographic urticaria

Clinical Features

This type of urticaria can be provoked by pressure of tight clothes or after stroking the skin, where few seconds later a wheal with a surrounding erythematous flare corresponds to the affected sites.

This may be accompanied by itching . Scratching also leads to the appearance of linear raised erythematous streaks .

Treatment of urticaria

Suspected food and drugs should be eliminated .

Hydroxyzine (Atarax) is considered specific in the treatment of such type of urticaria .

The new generation antihistamine; Cetrizine (Zyrtec) is also of value.

Topical steroids are not always recommended .

Oral and parental steroids are temporarily effective and rarely indicated in infants and children .

H2 blockers such as Cimetidine may be tried in chronic and resistant cases .

Cyproheptadine (Periactin): May be given to older children and not to young age. This drug may be effective especially if combined with hydroxazine.

Sometimes a combination of two antihistamines of the different group may be necessary in older children .  

Tricyclic antidepressants, such as doxepin, have the capability to block both H1 and H2 receptors. Leukotriene receptor antagonists and oral beta-adrenergic agents are reported to be helpful as combination therapy with antihistamines.

 Low-dose thyroid hormone for patients who have positive antithyroid antibodies .

 Cyclosporin, hydroxychloroquine, colchicine, dapsone, and COX 2 inhibitors have also been used in some cases not responding to traditional treatment.


This type of urticaria is herido-familial dominantly transmitted due to absence of C1 esterase inhibitor, which normally inhibits the activity of the first component of the complement .

Clinical Manifestations

The manifestations begin early in childhood and are characterized by recurrent attacks of swelling of the subcutaneous tissue, lips, mouth and eyes. The condition may be precipitated by injury where non-itchy, firm and painful lesions appear.

Constitutional symptoms: severe abdominal colic due to gastro-intestinal tract involvement may be a manifestation in some cases .

Respiratory tract :may be involved and in severe cases it may cause asphyxia in infants and children .


Diagnosis of herido-familial urticaria depends on :

Absence of typical urticarial lesions .

Severe angioedema .

Tender subcutaneous tissue .

Respiratory symptoms .

Abdominal colic due to gastro-intestinal involvement .

Decreased of C1 esterase inhibitor,C2 and C4 complement components.


Treatment is sometimes disappointing in such cases, where the mortality rate is considered high . Fresh plasma replacement of esterase inhibitor may have some effect .

Epsilon-aminocaproic acid and Danazol ( weak androgen which inhibits pituitary gonadotrophin ) both proved to be effective prophylactic medications.



Urticaria pigmentosa is an uncommon dermatoses that usually develops during the first year of life . The condition is characterized by urticarial lesions due to histamine release from excess mast cells in the skin and may be associated with systemic manifestations.

Types of Urticaria Pigmentosa

  1. Juvenile urticaria pigmentosa

    Begins early in infancy usually in the first year of life . The clinical picture varies from scanty urticarial lesions and pigmented flat macules with irregular edges that appear after scratching of the skin .

    The condition can be provoked mechanically by stroking normal skin.

    Fig. 234. Juvenile urticaria pigmentosa

    Fig. 235. Juvenile urticaria pigmentosa

    Fig. 236 urticaria 


    Linear urticarial lesions with beaded edges due to accumulation of mast cells under the skin may appear . Blisters may develop due to separation of the dermoepidermal junction .

    Urticaria pigmentosa may be accompanied by systemic manifestations such as abdominal colic , vomiting , tachycardia and flushing due to excess histamine release .

    Spontaneous regression of the infantile form may take place or may persist to the adult life presenting with flat-pigmented macules .

    Darier sign

     Demonstration  the presence of mast cells can appear by rubbing  the urticarial patch , where the rubbed area becomes reddened, swollen and itchy. This is known as Darier sign, and confirms the presence of mastocytosis.

Adult urticaria pigmentosa

This type may be the continuation to the infantile type or arise in the adult age . The lesions are in the form of itchy macules around 4mm in diameter, lightly pigmented appearing after rubbing or scratching of the skin surface.

Systemic manifestation of the adult type is more than in the juvenile type .

Liver and spleen may be enlarged due to diffuse mastocytosis and the bones may show osteoporosis and sclerosis .

Fig. 237. Adult urticaria pigmentosa


The patients should be warned not to rub the body vigorously especially during and after bathing with hot water, where this may activate mast cells in the skin and respiratory tract which may lead to flushing , hypotension, bronchospasm and even sudden death .


Antihistamine H1 blockers and cyproheptadine may give some relief .

H2 blockers claimed to have some effect in alleviating symptoms in urticaria pigmentosa .

Systemic manifestations can be treated accordingly .



  1. Gollhausen R, Kligman AM. Human assay for identifying substances, which induce non-allergic contact urticaria: the NICU-test. Contact Derm 1985; 13: 98-106.

  2. De Groot AK, Gerkens F. Contact urticaria from a chemical textile finish. Contact Derm 1989; 20: 63-4.

  3. Juhlin L. Recurrent urticaria: clinical investigation of 330 patients. Br J Dermatol 1981; 104: 369-81.

  4. Michaelsson G, Juhlin L. Urticaria induced by preservatives and dye additives in food and drugs. Br J Dermatol 1973; 88: 525-32.

  5. Parish WE. Possible relevance of changes in mast cells and neutrophils to perpetuation of chronic urticaria. In: Champion

  6. RH, Greaves MW, Kobza Black A et al., eds. The Urticarias. Edinburgh/ New York: Churchill Livingstone, 1985: 70-85.

  7. Kobza Black A, Greaves MW, Champion RH et al. Urticaria. Br J Dermatol 1991; 124: 100-8.

  8. Lagunoff D. The mechanism of histamine release from mast cells. Biochem Pharmacol 1972; 21: 1889-96.

  9. MacDonald SM, Lichtenstein LM, Proud LM et al. Studies of IgE-dependent histamine releasing factors: heterogeneity of IgE. J Immunol 1987; 139: 506-12.

  10. Parish RP Champion RH. Urticaria. London: W.B. Saunders, 1974.

  11. Parish WE Possible relevance of changes in mast cells and neutrophils to perpetuation of chronic urticaria. In: Champion RH, Greaves MW, Black AK, Pye RJ, eds. The Urticarias. Edinburgh: Churchill-Livingstone, 1985: 70-85.

  12. Carini C. IgE immune complexes in food allergy; significance, pathogenicity and clinical consideration. Clin Allergy 1987; 17: 485-97.

  13. Heavey DJ, Kobza-Black A, Barrow SE et al. Prostaglandin D2 and histamine release in cold urticaria. J Allergy Clin Immunol 1986; 78: 459-61.

  14. Michaelsson G, Juhlin L. Urticaria induced by preservatives and dye additives in food and drugs. Br J Dermatol 1973; 88: 525-32

  15. Thompson HL, Burbelo PD, Segui-Real B et al. Laminin promotes mast cell attachment. J Immunol 1989; 143: 2323-7.

  16. Freeman RG, Spiller R, Knox JM. Histopathology of erythema toxicum neonatorum.
    Arch Dermatol 1960; 82: 586-9.

  17. Harris R, Schick B. Erythema neonatorum. Am J Dis Child 1956; 92: 27-33.
    Keitel HG, Yadav V. Etiology of toxic erythema. Am J Dis Child 1963; 106: 306-9.

  18. Levy HL, Cothran F. Erythema toxicum neonatorum present at birth. Am J Dis Child 1962; 103: 617-19.

  19. Wakeel RA, Gavin MP, Keefe M. Severe toxic erythema caused by diltiazem. Br Med J 1988; 296: 1071.

  20. Hasan T, Jansen CT. Erythroderma: a follow-up of 50 cases. J Am Acad Dermatol 1983; 8: 836-40.

  21. Zoon JJ, Mali JWH. The influence of erythroderma on the body. Arch Dermatol 1957; 75: 573.

  22. Harris DWS, Spencer M-J, Tidman MJ. Papulo-erythroderma - clinical and ultrastructural features. Clin Exp Dermatol 1990; 15: 105-6.13.

  23. Uvnas B. Chemistry and storage function of mast cell granules. J Invest Dermatol 1978; 71: 76-80.

  24. Vella Briffa D, Eady RAJ, James MP et al. Photochemotherapy (PUVA) in the treatment of urticaria pigmentosa. Br J Dermatol 1983; 109: 67-75.

  25. Poynard T, Nataf C, Messing B et al. Secretory diarrhea and prostaglandin D2 overproduction in systemic mastocytosis. New Engl J Med 1982; 307: 186 .(Letter).

  26. Omerod AD, Herriot R, Davidson RJL et al. Adult mastocytosis, an immunophenotypic and flow cytometric investigation. Br J Dermatol 1990; 122: 737-44.

  27. Rasmussen JE. Xanthelasmoidea: an unusual case of urticaria pigmentosa. Arch Dermatol 1976; 112: 1270-1.

  28. Sutter MC, Beaulieu G, Birt AR. Histamine liberation by codeine and Polymyxin B in urticaria pigmentosa. Arch Dermatol 1962; 86: 217-21.

  29. Soter NA, Austen KF, Wasserman SI. Oral disodium cromoglycate in the treatment of systemic mastocytosis. New Engl J Med 1979; 301: 465-9.

  30. Crotty RQ. Erythroderma desquamativum (Leiner‘s disease). Arch Dermatol 1955; 71: 587-90.

  31. Den Tandt W, Eggermont E, Bourgeois N. Erythroderma desquamativum. Acta Paediatr Belg 1967; 21: 433-50.


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