Tinea imbricata (also known in parts of Indonesia as “Kaskado”) is a superficial fungal infection of the skin limited to southwest Polynesia, Melanesia, Southeast Asia, India, and Central America. : 303  The skin lesions are often itchy, and mainly in the torso and limbs. The name is derived from the Latin for "tiled" (imbricata) since the lesions are often lamellar. It is often treated with griseofulvin or terbinafine.The risk of developing tinea imbricata is probably inherited as an autosomal recessive trait.Tinea imbricata is associated with Trichophyton concentricum. Tinea pseudoimbricata
The term "tinea pseudoimbricata" synonymous with "tinea indecisiva", was coined to describe a form of tinea mimicking the concentric rings of tinea imbricata, but is caused by local or systemic immunosuppression. Since then, 3 cases of Trichophyton tonsurans have been associated with it, as well as Trichophyton rubrum which can trigger mycosis fungoides. Mixed infections with scabies have been described to produce tinea pseudoimbricata.As of 2015 in India, corticosteroid–antifungal–antibacterial combinations sold as over-the-counter drug have led to an increase in chronic, recurrent, difficult to treat fungal infections of the skin, including tinea pseudoimbricata. See also
Skin lesion
List of cutaneous conditions

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Fortification
According to the Global Fortification Data Exchange, pantothenic acid deficiency is so rare that no countries require that foods be fortified. Absorption, metabolism and excretion
When found in foods, most pantothenic acid is in the form of CoA or bound to acyl carrier protein (ACP). For the intestinal cells to absorb this vitamin, it must be converted into free pantothenic acid. Within the lumen of the intestine, CoA and ACP are hydrolyzed into 4-phosphopantetheine. The 4-phosphopantetheine is then dephosphorylated into pantetheine. Pantetheinase, an intestinal enzyme, then hydrolyzes pantetheine into free pantothenic acid. Free pantothenic acid is absorbed into intestinal cells via a saturable, sodium-dependent active transport system. At high levels of intake, when this mechanism is saturated, some pantothenic acid may also be additionally absorbed via passive diffusion. As a whole, when intake increases 10-fold, absorption rate decreases to 10%.Pantothenic acid is excreted in urine. This occurs after its release from CoA. Urinary amounts are on the order of 2.6 mg/day, but decreased to negligible amounts when subjects in multi-week experimental situations were fed diets devoid of the vitamin. Deficiency
Pantothenic acid deficiency in humans is very rare and has not been thoroughly studied. In the few cases where deficiency has been seen (prisoners of war during World War II, victims of starvation, or limited volunteer trials), nearly all symptoms were reversed with orally administered pantothenic acid. Symptoms of deficiency are similar to other vitamin B deficiencies. There is impaired energy production, due to low CoA levels, which could cause symptoms of irritability, fatigue, and apathy.