Its pathophysiology is not well established [1, 3, 5], but nearly two-third of patients have reported a positive family history, thus a genetic predisposition is proposed [1-5]. A cholinergic sympathetic nerve overactivity, leading to an excessive production of sweat is believed to be causing the symptoms [1-5], but it is thought that a dysregulation of both sympathetic and parasympathetic nervous systems is involved. [2, 4-6]. No histopathological changes, or an increase in the number or size of sweat glands, have been observed in patients with PHH. [2, 3]. Two categories of hyperhidrosis must be distinguished. Generalized hyperhidrosis affects the entire body and is secondary to an underlying medical condition or medication, while primary focal hyperhidrosis occurs in otherwise healthy persons [1-3, …show more content…
Side effects reported include local skin irritation and burning [1, 2, 5]. It is described as the first-line treatment for mild axillary hyperhidrosis [2, 5].
Oral treatment includes anticholinergic agents such as glycopyrrolate, oxybutinin or amitriptyline which represent the main systemic medications for hyperhidrosis. They inhibit the neuroglandular signaling by blocking the binding of acetylcholine to its receptor in the nerve cells [1, 3, 5]. Their use is usually restricted to primary focal hyperhidrosis due to frequent adverse effects (dry mouth, blurred vision, constipation, and urinary retention) [1-3, 5].
Injectable therapies comprise iontophoresis and Botulinum toxin injection. As stated by Schlereth and al. and Stefaniak and al., iontophoresis, where ions are passed through an electrical current into the skin, with a medical device, occluding the eccrine duct [1, 2], is the treatment of choice for palmar and plantar hyperhidrosis [2, 3]. However, the duration and frequency of treatment required [2], and the skin irritation and dryness it produces are limiting factors [2,