If the infection is continuous, the cause is often fungal and needs antifungal cream or paint to be treated.Risk factors include repeatedly washing hands and trauma to the cuticle such as may occur from repeated nail biting. or hangnails. In the context of bartending, it is known as "bar rot".Prosectors paronychia is a primary inoculation of tuberculosis of the skin and nails, named after its association with prosectors, who prepare specimens for dissection. Paronychia around the entire nail is sometimes referred to as "runaround paronychia".Painful paronychia in association with a scaly, erythematous, keratotic rash (papules and plaques) of the ears, nose, fingers, and toes may be indicative of acrokeratosis paraneoplastica, which is associated with squamous-cell carcinoma of the larynx.Paronychia can occur with diabetes, drug-induced immunosuppression, or systemic diseases such as pemphigus. Diagnosis
Types
Paronychia may be divided as occurring suddenly, acute, or gradually, chronic. Acute
Acute paronychia is an infection of the folds of tissue surrounding the nail of a finger or, less commonly, a toe, lasting less than six weeks. The infection generally starts in the paronychium at the side of the nail, with local redness, swelling, and pain. : 660  Acute paronychia is usually caused by direct or indirect trauma to the cuticle or nail fold, and may be from relatively minor events, such as dishwashing, an injury from a splinter or thorn, nail biting, biting or picking at a hangnail, finger sucking, an ingrown nail, or manicure procedures.
The absence of secondary causes of severe hypertriglyceridemia (like e.g. diabetes, alcohol, estrogen-, glucocorticoid-, antidepressant- or isotretinoin-therapy, certain antihypertensive agents, and paraproteinemic disorders) increases the possibility of LPL deficiency. In this instance besides LPL also other loss-of-function mutations in genes that regulate catabolism of triglyceride-rich lipoproteins (like e.g. ApoC2, ApoA5, LMF-1, GPIHBP-1 and GPD1) should also be consideredThe diagnosis of familial lipoprotein lipase deficiency is finally confirmed by detection of either homozygous or compound heterozygous pathogenic gene variants in LPL with either low or absent lipoprotein lipase enzyme activity.Lipid measurements
·        Milky, lipemic plasma revealing severe hyperchylomicronemia;·        Severely elevated fasting plasma triglycerides (>2000 mg/dL);LPL enzyme
·        Low or absent LPL activity in post-heparin plasma;·        LPL mass level reduced or absent in post-heparin plasma;Molecular genetic testing
The LPL gene is located on the short (p) arm of chromosome 8 at position 22. More than 220 mutations in the LPL gene have been found to cause familial lipoprotein lipase deficiency so far. Treatment
Treatment of LPLD has two different objectives: immediate prevention of pancreatitis attacks and long-term reduction of cardiovascular disease risk. Treatment is mainly based on medical nutrition therapy to maintain plasma triglyceride concentration below 11,3 mmol/L (1000 mg/dL). Maintenance of triglyceride levels below 22,6 mmol/L (2000 mg/dL) prevents in general from recurrent abdominal pain.