: 506–8 : 213

Focal
Focal palmoplantar keratoderma, a type of palmoplantar keratoderma in which large, compact masses of keratin develop at sites of recurrent friction, principally on the feet, although also on the palms and other sites, a pattern of calluses that may be discoid (nummular) or linear. Focal palmoplantar keratoderma with oral mucosal hyperkeratosis (also known as "Focal epidermolytic palmoplantar keratoderma," "Hereditary painful callosities," "Hereditary painful callosity syndrome," "Keratosis follicularis," "Keratosis palmoplantaris nummularis", and "Nummular epidermolytic palmoplantar keratoderma") is an autosomal dominant keratoderma that represents a clinical overlap syndrome with pachyonychia congenita type I but without the classic nail involvement. : 510

Punctate
Punctate palmoplantar keratoderma is a form of palmoplantar keratoderma in which many tiny "raindrop" keratoses involve the palmoplantar surface, skin lesions which may involve the whole of the palmoplantar surface, or may be more restricted in their distribution. : 505 
Type 1: Keratosis punctata palmaris et plantaris (also known as "Autosomal-dominant hereditary punctate keratoderma associated with malignancy," "Buschke–Fischer–Brauer disease," "Davis Colley disease," "Keratoderma disseminatum palmaris et plantaris," "Keratosis papulosa," "Keratoderma punctatum," "Keratodermia punctata," "Keratoma hereditarium dissipatum palmare et plantare," "Palmar and plantar seed dermatoses," "Palmar keratoses," "Papulotranslucent acrokeratoderma," "Punctate keratoderma," "Punctate keratoses of the palms and soles," and "Maculosa disseminata") is a skin condition, an autosomal dominant palmoplantar keratoderma with variable penetrance, characterized clinically by multiple, tiny, punctate keratoses over the entire palmoplantar surfaces, beginning over the lateral edge of the digits. : 509 : 212–213  It has been linked to 15q22-q24.
Research
While many antioxidants have been researched to treat a large number of diseases by reducing the negative effect of oxidative stress, acetylcysteine is one of the few that has yielded promising results, and is currently already approved for the treatment of paracetamol overdose. In mouse mdx models of Duchennes muscular dystrophy, treatment with 1–2% acetylcysteine in drinking water significantly reduces muscle damage and improves strength. It is being studied in conditions such as autism, where cysteine and related sulfur amino acids may be depleted due to multifactorial dysfunction of methylation pathways involved in methionine catabolism. Animal studies have also demonstrated its efficacy in reducing the damage associated with moderate traumatic brain or spinal injury, and also ischaemia-induced brain injury. In particular, it has been demonstrated to reduce neuronal losses and to improve cognitive and neurological outcomes associated with these traumatic events. It has been suggested that acetylcysteine may help people with Samters triad by increasing levels of glutathione allowing faster breakdown of salicylates, although there is no evidence that it is of benefit. Small studies have shown acetylcysteine to be of benefit to people with blepharitis. It has been shown to reduce ocular soreness caused by Sjögrens syndrome. It has been shown that N-acetylcysteine may protect the human cochlea from subclinical hearing loss caused by loud noises such as impulse noise. In animal models, it reduced age-related hearing loss. It has been shown effective in the treatment of Unverricht-Lundborg disease in an open trial in four patients.