Onychomycosis: Rapid Evidence Review.

Onychomycosis is a chronic fungal infection of the fingernail or toenail bed leading to brittle, discolored, and thickened nails. Onychomycosis is not just a cosmetic problem. Untreated onychomycosis can cause pain, discomfort, and physical impairment, negatively impacting quality of life. Onychomycosis should be suspected in patients with discolored nails, nail plate thickening, nail separation, and foul-smelling nails. Accurate diagnosis is important before initiating treatment because therapy is lengthy and can cause adverse effects. A potassium hydroxide preparation with confirmatory fungal culture, periodic acid-Schiff stain, or polymerase chain reaction is the preferred diagnostic approach if confirmative testing is cost prohibitive or not available. Treatment decisions should be based on severity, comorbidities, and patient preference. Oral terbinafine is preferred over topical therapy because of better effectiveness and shorter treatment duration. Patients taking terbinafine in combination with tricyclic antidepressants, selective serotonin reuptake inhibitors, atypical antipsychotics, beta blockers, or tamoxifen should be monitored for drug-drug interactions. Topical therapy, including ciclopirox 8%, efinaconazole 10%, and tavaborole 5%, is less effective than oral agents but can be used to treat mild to moderate onychomycosis, with fewer adverse effects and drug-drug interactions. Nail trimming and debridement used concurrently with pharmacologic therapy improve treatment response. Although photodynamic and plasma therapies are newer treatment options that have been explored for the treatment of onychomycosis, larger randomized trials are needed. Preventive measures such as avoiding walking barefoot in public places and disinfecting shoes and socks are thought to reduce the 25% relapse rate.

Serum homocysteine and methylmalonic acid concentrations in Chinese Shar-Pei dogs with cobalamin deficiency.

Cobalamin deficiency is suspected to be hereditary in Chinese Shar-Pei dogs (Shar-Peis), and inherited causes of cobalamin deficiency may affect the cellular processing of cobalamin. In humans, a defect of the two main cobalamin-dependent intracellular enzymes (i.e., methionine synthase and methylmalonyl-CoA mutase) may lead to hyperhomocysteinemia and hypermethylmalonic acidemia. The aim of this retrospective study was to evaluate serum homocysteine (HCY) and methylmalonic acid (MMA) concentrations in cobalamin-deficient Shar-Peis and dogs of six other breeds. Serum samples (n=297) from cobalamin-deficient dogs (Shar-Peis, German Shepherd dogs, Labrador Retrievers, Yorkshire Terriers, Boxers, Cocker Spaniels, and Beagles) were analyzed for serum HCY and MMA concentrations. A Fisher's exact test was used to evaluate if cobalamin deficiency in Shar-Peis is associated with hyperhomocysteinemia. Serum HCY and MMA concentrations were higher in cobalamin-deficient Shar-Peis compared to cobalamin-deficient dogs of the six other breeds (P<0.0001). Hyperhomocysteinemia was associated with cobalamin deficiency in Shar-Peis (P=0.009). In addition, serum HCY and MMA concentrations did not differ between cobalamin-deficient German Shepherd dogs with and without exocrine pancreatic insufficiency (EPI), a potential cause of secondary cobalamin deficiency. These findings suggest that the function of the two intracellular cobalamin-dependent enzymes is impaired in Shar-Peis with cobalamin deficiency.