For example, varicose veins and prolonged bed rest both may induce SVTs due to slowing the flow of blood through superficial veins. Diagnosis
SVTs may be diagnosed based upon clinical criteria by a healthcare professional. A more specific evaluation can be made by ultrasound. An ultrasound can be useful in situations in which an SVT occurs above the knee and is not associated with a varicose vein, because ultrasounds can detect more serious clots like DVTs. The diagnostic utility of D-dimer testing in the setting of SVTs has yet to be fully established. Classification
SVTs can be classified as either varicose vein (VV) or non-varicose (NV) associated. NV-SVTs are more likely to be associated with genetic procoagulable states compared to VV-SVTs. SVTs can also be classified by pathophysiology. That is, primary SVTs are characterized by inflammation that is localized to the veins. Secondary SVTs are characterized by systemic inflammatory processes.A subclass of SVTs are septic thrombophlebitis, which are SVTs that occur in the setting of an infection. Treatment
The goal of treatment in SVT is to reduce local inflammation and prevent the SVT from extending from its point of origin. Treatment may entail the use of compression, physical activity, medications, or surgical interventions. The optimal treatment for many SVT sites (i.e. upper limbs, neck, abdominal and thoracic walls, and the penis) has not been determined. Compression
Multiple compression bandages exist. Fixed compression bandages, adhesive short stretch bandages, and graduated elastic compression stockings have all be used in the treatment of SVTs.
Adenosine deaminase deficiency (ADA deficiency)  is a  metabolic disorder that causes immunodeficiency. It is caused by  mutations in the ADA gene. It accounts for about 10–15% of all cases of autosomal recessive forms of severe combined immunodeficiency (SCID) among non-inbred populations.ADA deficiency can present in infancy, childhood, adolescence, or adulthood. Age of onset and severity is related to some 29 known genotypes associated with the disorder. It occurs in fewer than one in 100,000 live births worldwide. Signs and symptoms
The main symptoms of ADA deficiency are pneumonia, chronic diarrhea, and widespread skin rashes. Affected children also grow much more slowly than healthy children and some have developmental delay. Most individuals with ADA deficiency are diagnosed with SCID in the first 6 months of life.An association with polyarteritis nodosa has been reported. Genetics
The enzyme adenosine deaminase is encoded by the ADA gene on chromosome 20. ADA deficiency is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome (chromosome 20 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.Age of onset and severity is related to some 29 known genotypes associated with the disorder. Pathophysiology
ADA deficiency is due to a lack of the enzyme adenosine deaminase.