One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male,

Signs and symptoms
There is usually an itch, with generalised dry flaky thick skin of the palm of a hand. Frequently, one hand is affected, but it can be in both. If the back of the hand is affected, it may appear as reddish circles like in ringworm. Sometimes there are no symptoms. The feet may be affected as in two feet-one hand syndrome. Cause and mechanism
The most common cause is Trichophyton rubrum. Other causes include Trichophyton verrucosum (from cattle), Microsporum canis (from a cat or dog),  Trichophyton erinacei (from a hedgehog), Trichophyton mentagrophytes, Epidermophyton floccosum, Trichophyton interdigitale, and more rarely Microsporum gypseum, Trichophyton eriotrephon, and Arhroderma benhamiae.Tinea manuum can result from touching another area of the body with a fungal infection such as athletes foot or tinea cruris, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors
Diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet are risk factors for tinea manuum. Pet owners and farmworkers are also at higher risk. Diagnosis
Diagnosis is by visualization, direct microscopy and culture. Differential diagnosis
Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment
Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole  by mouth might be options. Other options include  clotrimazole, fluconazole and ketoconazole.
These peptides are modified by tTG in two ways, deamidation or transamidation.Deamidation is the reaction by which a glutamate residue is formed by cleavage of the epsilon-amino group of a glutamine side chain. Transamidation, which occurs three times more often than deamidation, is the cross-linking of a glutamine residue from the gliadin peptide to a lysine residue of tTg in a reaction that is catalysed by the transglutaminase. Crosslinking may occur either within or outside the active site of the enzyme. The latter case yields a permanently covalently linked complex between the gliadin and the tTg. This results in the formation of new epitopes believed to trigger the primary immune response by which the autoantibodies against tTg develop.Stored biopsies from people with suspected coeliac disease have revealed that autoantibody deposits in the subclinical coeliacs are detected prior to clinical disease. These deposits are also found in people who present with other autoimmune diseases, anaemia, or malabsorption phenomena at a much increased rate over the normal population. Endomysial components of antibodies (EMA) to tTG are believed to be directed toward cell-surface transglutaminase, and these antibodies are still used in confirming a coeliac disease diagnosis. However, a 2006 study showed that EMA-negative people with coeliac tend to be older males with more severe abdominal symptoms and a lower frequency of "atypical" symptoms, including autoimmune disease. In this study, the anti-tTG antibody deposits did not correlate with the severity of villous destruction.