Eczema is a ubiquitous, often acute, less often
chronic, recurrent skin disease that occurs at any age, characterized by
polymorphism of the morphological elements of the rash. Eczema accounts for
30-40% of all skin diseases [ Studnitsin A. A., Skripkin Yu. K., 1979]. The
name of this dermatosis is explained by the property of eczematous vesicles to
quickly open, like bubbles of boiling water ( eczeo in Greek – to boil). An
important sign of acute eczema is the presence of numerous grouped and quickly
opening with the formation of serous “wells” of small bubbles, which
have some resemblance to bubbles on the surface of boiling water.
The term “eczema” was used as early as the 2nd century BC. e., but
only to refer to various acutely occurring dermatoses. Only in the first half
of the 18th century, Willen (1808), Bateman (1813), Reye (1823) and other
scientists singled out eczema as a separate nosological form.
Etiology and pathogenesis
Eczema is formed as a result of a complex complex of etiological and
pathogenetic factors. Since the predominant value of certain endogenous and
exogenous influences remains controversial, eczema is considered to be a
polyetiological disease.
At different stages of the development of the doctrine of eczema, particular
importance in the etiology and pathogenesis of the disease was given to the
nervous system (neurogenic theory), the role of the endocrine glands, the
allergic state of the body (allergic theory), and hereditary factors. It should
be recognized that the etiology and even pathogenesis of eczema are extremely
complex, not always the same, and in many of their aspects remain unexplored.
In recent years, most authors believe that the eczematous process develops as a
result of the complex effects of neuroallergic, endocrine, metabolic and
exogenous factors [ Shakhtmeister I. Ya., 1970; Skripkin Yu. K. et al., 1975;
Antoniev A. A. et al., 1978; Kubanova A. A., 1986].
Exogenous irritants can be chemical, biological agents, bacterial allergens,
physical factors, medicines, foods, cosmetics. Allergic reactivity at the onset
of the disease is sometimes monovalent . With the further course of dermatosis,
the diseased organism qualitatively and quantitatively begins to respond to a
variety of irritants and allergens, which indicates the development of
polyvalent sensitization characteristic of eczema. An eczematous reaction is a
delayed-type allergic reaction. However, in some patients, as a result of the
use of medications (penicillin, novocaine, B vitamins, etc.), reactions of an immediately-delayed
type (anaphylactic reaction) may develop.
The reaction between antigens and antibodies occurs in a specific
humoral environment. Changes in homeostasis also have a significant impact on
the mechanisms of formation of allergic phenomena (disturbances in the activity
of the endocrine, nervous, immune systems that are in constant interaction). At
the present stage of development of the doctrine of eczema, the main importance
is attached to the pathogenetic role of various immune shifts, changes in the
state of prostaglandins and cyclic nucleotides. When studying the immune status
of patients with eczema, A. A. Kubanova (1986) established significant
violations of the cellular link of immunity and nonspecific protective factors,
manifested in severe lymphocytopenia , a decrease in the functional activity
and content of the T-lymphocyte pool, a sharp suppression of the functional
activity of T-suppressors and a decrease in the number T-helpers. The revealed
violations were directly dependent on the duration of the disease, the decrease
in the severity of clinical manifestations and changed with age. The highest
indicators, reflecting the state of the immune status, were found in the age
groups from 16 to 20 years and from 20 to 30 years, and the lowest in the age
group over 50 years. The dependence of changes in the immune status on gender
has not been established.
Violations of non-specific defense factors are manifested in a decrease in the
functional activity of neutrophils (the percentage of phagocytosis, phagocytic
number, absolute phagocytic index), the ability to spontaneous and
complementary rosette formation of neutrophilic leukocytes, in a decrease in
the number of their cytoplasmic granules (cytoplasmic granules of neutrophils
are a morphological indicator of their digestion ability, reflecting fourth
stage of phagocytosis). These disorders, perhaps, explain the often observed
complications of the eczematous process secondary streptostaphyloderma , which
aggravates the course of the disease and leads to additional sensitization of
the body. Indicators of humoral immunity (total number of B-lymphocytes,
immunoglobulins A, M, G) in patients with eczema do not change significantly.
Patients with true eczema have a positive association of histocompatibility
system antigens (HLA) B22 and CW1 [Kubanova AA, 1986]. The indicated
association of antigens was noted in persons of the Slavic race, predominantly
of Russian nationality, which allows us to consider these antigens as genetic
markers of eczema for persons of the Slavic race. The information obtained
deepens the understanding of the mechanisms of implementation of the genetic
predisposition to the development of immunopathological conditions. The
dependence of indicators of the suppressor function of T-lymphocytes and the
content of T-helpers on the HLA phenotype was revealed, as evidenced by a
decrease in suppressor function and the number of T-helpers in patients with
eczema markers HLA-B22 and CW1 [ KubanovaA . A., 1986].
A significant role in the pathogenesis of eczema is played by changes in
the state of prostaglandins and cyclic nucleotides, which occupy a central
place in intracellular regulatory mechanisms, mediate neuroendocrine
information, turn it into a specific cell response and implement normal and
pathological reactions of the body [Fedorov N. A., 1979]. Prostaglandins E1 and
F201, cyclic adenosine monophosphate and guanosine monophosphate have a
regulatory effect on the development of allergic and inflammatory reactions,
the functional activity of the body’s immune system. Antagonistic relationships
exist between prostaglandins E1 (PGE1, cyclic adenosine monophosphate ( cAMP )
and prostaglandins F2a cyclic guanosine monophosphate ( cGMP ). PGE1 stimulates
the synthesis of cAMP , which suppresses the production of histamine, serotonin
and other mediators of allergic reactions. PFG2a stimulates the synthesis of
cGMP , which activates the production of allergy mediators, thereby
contributing to the development of allergic and inflammatory reactions.In
patients with eczema, an increase in the concentration of PGE1 and PGF2a in
blood plasma was found, however, a more significant increase in PGFa , which
leads to a change in the ratio of PGE1 / PGF2 (PGF2a predominates) and the
formation of a kind of PGE1 deficiency
. disorders made it possible to develop a new concept of the pathogenesis of
eczema [Kubanova A. A., 1986].In persons with a hereditary predisposition,
confirmed by a positive association of antigens of the histocompatibility
system (B22 and Cw1), the synthesis of prostaglandin F2a increases, which in It
causes increased stimulation of the synthesis of cyclic guanosine monophosphate
, which activates the production of histamine, serotonin and other allergy
mediators, promotes the development of allergic and inflammatory reactions, and
increases vascular permeability. Simultaneously with the increase in the
formation of prostaglandin F2a, the synthesis of prostaglandin E1 increases,
but its concentration is significantly reduced in relation to the increasing
concentration of prostaglandin F201. Lack of content of prostaglandin E1,
violation of its ratio with the content of prostaglandin F2a leads to
insufficient stimulation of the synthesis of cyclic adenosine monophosphate , which
suppresses the formation of allergic and inflammatory reactions, the production
of allergy mediators. Thus, in patients with eczema, as a result of an increase
in the content of F2a and a violation of the ratio of PGE1 / PGF2a and cAMP /
cGMP , prostaglandin F2a and cyclic guanosine monophosphate predominate , which
is one of the reasons for the development of the disease. In the peripheral
blood platelets of patients with eczema, an increase in the synthesis and
excretion of serotonin into the bloodstream was found. The platelet release
reaction that releases serotonin into the blood is regulated by prostaglandins.
Prostaglandin E1 suppresses it, and prostaglandin F2a provokes it. The
predominance of prostaglandin F2a causes an increase in the content of
serotonin in the blood, which exacerbates allergic reactions. The thyroid
hormone thyrocalcitonin stimulates the activity of adenylate cyclase , an
enzyme that catalyses the synthesis of cyclic adenosine monophosphate from ATP.
An increase in the content of thyrocalcitonin in patients with eczema may be a
manifestation of the protective-compensatory reactions of the body.
Prostaglandins and cyclic nucleotides are one of the factors of the
multicomponent system of immune response regulation. An increase in their
synthesis leads to changes in immunological reactivity and causes profound
immunological disorders, manifested in the suppression of cellular immunity
(decrease in the content of T-ROK, quantitative and functional indicators of
T-helpers and T-suppressors, suppression of the suppressor activity of
T-lymphocytes) and nonspecific defense factors ( decrease in the number of
spontaneous and complementary neutrophils, the content of cytoplasmic granules
of neutrophilic leukocytes, the percentage of phagocytosis, the absolute
phagocytic index and phagocytic number). Changes in the immune status
contribute to an increase in allergic reactivity and, along with prostaglandins
and cyclic nucleotides, lead to the formation of an eczematous process. The
degree of severity of the established imbalance of prostaglandins, cyclic
nucleotides and immunological reactivity is reflected in the severity of
clinical manifestations and the course of the process.
Simultaneously with the state of immune deficiency in patients with eczema,
functional changes in the activity of the central nervous system are
ascertained, the predominance of the activity of unconditioned reflexes over
the activity of conditioned reflexes, imbalance between the activity of the
sympathetic and parasympathetic divisions of the autonomic nervous system,
changes in the functional state of skin receptors in the form of dissociation
of skin sensitivity. Thus, inhibition of immune reactivity in patients with
eczema does not develop in isolation, not only on the basis of a genetic
predisposition, but also as a result of complex neuroendocrine -humoral changes
that change tissue trophism.
The predominance of parasympathetic mediators in the skin, humoral
insufficiency of the pituitary-adrenal system [Sharapova G. Ya., 1965;
Shakhtmeister I. Ya., 1970, etc.] lead to a sharp increase in the permeability
of the walls of blood vessels and increased sensitivity of smooth muscle cells
to the action of endo- and exogenous resolving factors, including bacterial antigens.
Weakness of immunity in the presence of infectious antigenic stimuli is
manifested by the persistence of microbial and bacterial antigens, the
formation of chronic recurrent inflammation in the epidermis and dermis. In
this case, pathological immune complexes arise that damage their own
microstructures and create autoantigens that form autoaggressive antibodies.
An inflammatory chronic process in the epidermis and dermis occurs as a result
of the complex pathological functioning of various systems of the
macroorganism. Most clearly in patients with eczema, neurodermatitis and other
allergic dermatoses, violations of the functional state of the gastrointestinal
tract, nervous, endocrine systems, and metabolic processes are revealed
[Toropova NP et al., 1986].
The formation of eczema due to a genetic predisposition, which depends on the
presence of an immune response gene in lymphocytes, creates the prerequisites
for its inheritance in subsequent generations. The development of eczema in
children of the first year of life contributes to the complicated course of
pregnancy in the mother [Toropova NP et al., 1986]. When studying the anamnesis
of sick children, it was revealed that toxicosis and nutritional errors during
pregnancy, concomitant diseases in the mother (nephropathy, diabetes mellitus,
cardiovascular insufficiency, chronic hepatocholecystitis ) contribute to the
onset of the disease. According to F. A. Zverkova (1975), in 30% of mothers,
pregnancy was accompanied by toxicosis, severe vomiting. Artificial feeding
from the first days of a child’s life, early introduction of complementary
foods, especially whole cow’s milk, semolina porridge with whole or condensed
milk, concentrates, meat and fish broths, create conditions for the occurrence
of exudative diathesis and severe dermatoses, most often children’s eczema.
In the development of eczema in children, there is a polygenic multifactorial
inheritance with pronounced gene expression and penetrance. Yu. K. Skripkin
(1979) reports that with an allergic disease of one of the parents (mainly the
mother), the chance of developing eczema in a child is approximately 40%, and
if both parents are affected, the risk increases to 50-60%. The formation of
immediate-delayed hypersensitivity, manifested by eczematous rashes, is
facilitated by foci of chronic infection, gastrointestinal disorders,
dysfunction of the liver, pancreas, etc. Clinical and pathogenetic features of
eczema allow us to identify several of the most common forms.
Classification
There is currently no generally accepted unified classification of
eczema. Some scientists [L. N. Mashkilleyson , 1965; Smelov N. S. et al., 1973]
distinguish the following forms of eczema:
- sharp
- subacute
- chronic
- seborrheic
- children’s
- varicose form.
S. T. Pavlov and co-authors (1985) distinguish:
- true
- microbial
- professional eczema.
Each of them can proceed acutely, subacutely and chronically.