Management for Tietze syndrome usually consists of analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, aspirin, acetaminophen (paracetamol), and naproxen. Other methods of management include manual therapy and local heat application. These are intended to relieve pain and are not expected to treat or cure Tietze syndrome as the condition is expected to resolve on its own. Intercostal nerve block
A nerve block can be utilized in cases where symptom management is not satisfactory in relieving pain. This is usually a nerve-blocking injection that consists of a combination of steroids such as hydrocortisone, and anesthetics such as lidocaine and procaine, which is typically administered under ultrasound guidance. One study used a combination of triamcinolone hexacetonide and 2% lidocaine in 9 patients and after a week, found an average 82% decrease in size of the affected costal cartilage when assessing with ultrasound as well as a significant improvement of symptoms clinically. However, the long-term effectiveness of the injection is disputed, with multiple researchers describing recurrence of symptoms and repetitive injections. Surgical intervention
In refractory cases of Tietze syndrome, where the condition is resistant to other conservative treatment options, surgery is considered. Surgery is uncommon for cases of Tietze syndrome, as many describe Tietze syndrome as manageable under less invasive options. The use of surgery in this context refers to the resection of the affected costal cartilages and some of the surrounding areas. Some surgeons have resected cartilage matching the symptoms of Tietze syndrome under the assumption the cartilage was tubercular.
This is in contrast with mammals, some of which have mutations that show no tyrosinase or DOPA oxidase activity in albinos. The albino phenotype of the pond frog (Pelophylax nigromaculatus) has been attributed to one of three mutations that created a dysfunctional tyrosinase. Two of those mutations involve an insertion of a thymine (T), a frameshift mutation, resulting in a truncated isoform of the TYR protein that is defective. The other mutation involves the deletion of a codon, three nucleotides that code for a lysine (Lys). In the wrinkled frog (Glandirana rugosa) and in the rice frog (Fejervarya kawamurai), a substitution from a guanine (G) to an adenine (A) creates a missense mutation, in which a glycine (Gly) changes to an aspartic acid (Asp) and an arginine (Arg), respectively. These changes in the polypeptide chain causes a dysfunctional tyrosinase. In invertebrates
Albinism in molluscs has been recognized to be a hereditary phenomenon at least since 1900. Albinism in molluscs can exist to a variable degree. Sometimes an individual snail has a normally pigmented body, but the shell is completely without the normal pigmentation because of a defect in the cells of the mantle. Shells of certain mollusc species can be translucent when they lack the normal pigmentation. In insects
The neurohormone [His7]-corazonin induces darkening of the cuticle of Locusta migratoria. The Okinawa strain of this species is deficient in [His7]-corazonin and is albino. One of the typical features of Locusta migratoria is that they are gregarious locusts.