Ludzkie koronawirusy - autor: Krzysztof Pyrć z Zakładu Mikrobiologii, Wydział Biochemii, Biofizyki i Biotechnologii, Uniwersytet Jagielloński, Kraków

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© Borgis - New Medicine 2/2004, s. 37-40
Ewa Szpringer1, 2, Krzysztof Lutnicki1
Eccrine hyperhidrosis – new therapeutic options
1 Department of Pathophysiology, Medical University, Lublin, Poland
2 ´Laser-Medic´ Dermatology and Laser Therapy Centre, Lublin, Poland
Hyperhidrosis is a severe problem for the people affected with the disorder. Until now the treatment of local eccrine hyperhidrosis (pharmacological treatment, iontophoresis, application of antiperspirants) has not been very effective or it has carried the risk of complications (surgical excision of the skin and subcutaneous tissue, endoscopic transthoracic sympathectomy). Very good therapeutic results may be achieved by injecting botulinum toxin of type A. The procedure effectively inhibits the secretion of sweat in the face, palms, soles and axillae for a few months or even longer than a year.
Maintaining proper heat balance in homeothermic organisms depends upon the balance between heat production and heat loss. The body loses heat through radiation (45-60%), conduction and convection (20-40%), and perspiration – imperceptible and perceptible evaporation of water from the skin surface (20-25%). Sweating is one of the most important mechanisms of removing excess heat from the body. Evaporation of 1 litre of sweat from the skin surface results in the utilization of more than 2400 kJ (543 kcal) of thermal energy (1).
Hyperhidrosis is excessive perspiration not resulting from normal thermoregulatory mechanisms. In terms of its localization, hyperhidrosis may be divided into local and generalized. In terms of its causes excessive sweating may be described as idiopathic, which is usually confined to the palms, soles and axillae and secondary (symptomatic), resulting from endocrine dysfunction (diabetes mellitus, hyperthyroidism, phaeochromocytoma, menopause), neoplastic disease, neurological syndromes (spinal cord and peripheral nerves damage, diabetic neuropathy) or febrile infectious diseases. Some persons develop the so-called gustatory sweating (Luckie-Frei syndrome) which is excessive perspiration of the skin of the face and the nape of the neck following ingestion of spicy foods or tyramine (an alkaloid ergot) contained, among others, in certain types of hard cheese, the Chianti wine, certain types of beer, yeast, mushrooms and herring (2).
Sweat is a weak solution of sodium chloride, containing mineral compounds (potassium, calcium, magnesium, iron) and urea, lactic acid, carbohydrates and lipids. Specific gravity of sweat is 1.002-1.003, pH ranges from 4.2 to 7.5. The number of sweat glands in the human skin is approximately 2000/cm2 on the hands and feet and from 100 to 200/cm2 on the skin of the chest and limbs. Sweat glands are divided into eccrine and apocrine. Eccrine glands are distributed all over the body, except for the breast, vermilion border and nail bed. They are most densely located on the forehead, palms, soles and axillae and most sparsely found in the skin of the eyelids. Eccrine sweat glands play a role in thermoregulation. They are also vital in the so-called emotional perspiration. Apocrine glands are not involved in thermoregulation. They are associated with hair follicles and open onto a hair root sheath just above the opening of the sebaceous gland. The secretion of apocrine glands is thicker than that of eccrine glands and contains fragrant substances (pheromones). Apocrine glands are located (together with eccrine glands) in the anogenital area, eyelids and ears, nipples, axillae, groins. They become active at puberty (3).
Sweat glands are supplied by the autonomic nervous system. The chemical nature of transmission in the fibres of the autonomic system consists in one neuron secreting only one specific chemical transmitter. Noradrenaline is the main transmitter in postganglionic sympathetic fibres, and acetylcholine in postganglionic parasympathetic fibres and in all autonomic preganglionic fibres - both parasympathetic and sympathetic. Eccrine glands are the exception in this rule as they are innervated by postganglionic sympathetic fibres, cholinergic character, releasing acetylcholine at their endings. However, the glands are controlled by the sympathetic nervous system and respond to sympathetic and parasympathetic pharmaceutical agents; their function is stimulated by muscarine, polocarpine and acetylcholine and inhibited by atropine. Apocrine glands are innervated by noradrenergic fibres (3).
Acetylcholine is produced from choline and acetyl coenzyme A in cholinergic neurons, and is the catalyst choline acetyltransferase. The synthesized acetylcholine is stored in synaptic vesicles. It is estimated that from 1000 to 50 000 acetylcholine molecules may be found in one vesicle and there are approximately 300 synaptic vesicles at one nerve ending, which clearly manifests that the activity of the acetylcholine synthesis is very high. Some quantity of acetylcholine is continuously and spontaneously released in small amounts. The quantum release is responsible for the formation of miniature postsynaptic potentials and is the source of the parasympathetic tonus which disappears when a nerve has been severed or has degenerated. Due to irritation of parasympathetic nerves and depolarization of the nerve ending, the membranes of synaptic vesicles bind with the membrane of the nerve ending, and the contents of the vesicles are emptied into the synaptic fissure. Approximately 100 or more vesicles are simultaneously opened, and from 100 000 to 5 000 000 acetylcholine molecules are released. Each of them, having bound to a receptor, alters the postsynaptic membrane potential by 3 × 10-7 V, which results in the value of 3 to 150 mV. During the acetylcholine action the system is in the state of refraction and does not respond to further stimuli. Reactivity returns after acetylcholine is removed from the bonding sites. This function is performed by acetylcholinesterase (AChE), the enzyme hydrolyzing acetylcholine to acetic acid and choline. After passing through a depolarized presynaptic membrane into the synaptic fissure, acetylcholine binds to the muscarine receptors (M) of the postsynaptic membrane. A stimulation potential is then evoked in certain organs, which leads to muscle contraction and increased glandular secretion. Acetylcholine released by cholinergic fibres also causes dilation of the vascular bed as well as coronary and pulmonary vessels, acting on muscarine receptors. It decelerates the heart action, decreases the force of myocardial contractions and reduces conduction. It increases the tonus and amplitude of contractions and the peristalsis of the stomach and intestines. It also activates the secretion of all glands released parasympathetically, including saliva, gastric juice, digestive juices, mucus in the respiratory tract and sweat (4).
Destruction of sympathetic innervation entirely stops sweat response to an increased temperature within the range of the innervation. Sweat glands, however, still respond to acetylcholine and pilocarpine. It seems important that perspiration is induced by stimuli radiating from the centres in the cerebral cortex. The beginning of muscular work, sweating is initiated by impulsation from motor centres of the cerebral cortex, as it occurs before any change in the temperature of the internal organs. Similar impulsation from the cerebral cortex may play a role in inducting perspiration by mental and emotional stimuli. For example, cold sweat may be due to psychogenic result from psychic factors, anxiety, fear, fatigue or mental effort. Cold sweat occurs especially on the forehead, palms and soles, that is in the areas which basically do not respond with sweating to an increased temperature.
For people affected with the disorder, eccrine hyperhidrosis is a serious problem, which makes it difficult or impossible for them to function in the society, begin work and maintain normal interpersonal relationships.

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