Medical imaging, consisting of x-ray, CT, MRI, or ultrasound may detect chondrocalcinosis within the affected joint, indicating a substantial amount of calcium crystal deposition within the cartilage or ligaments. Ultrasound is a reliable method to diagnose CPPD. Using ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage or fibrocartilage. By x-ray, CPPD can appear similar to other diseases such as ankylosing spondylitis and gout. Arthrocentesis, or removing synovial fluid from the affected joint, is performed to test the synovial fluid for the calcium pyrophosphate crystals that are present in CPPD. When stained with H&E stain, calcium pyrophosphate crystals appears deeply blue ("basophilic"). However, CPP crystals are much better known for their rhomboid shape and weak positive birefringence on polarized light microscopy, and this method remains the most reliable method of identifying the crystals under the microscope. However, even this method has poor sensitivity, specificity, and inter-operator agreement.These two modalities currently define CPPD disease, but lack diagnostic accuracy. Thus, the diagnosis of CPPD disease is potentially epiphenomenological. Treatment
Because any medication that could reduce the inflammation of CPPD bears a risk of causing organ damage, treatment is not advised if the condition is not causing pain. For acute pseudogout, treatments include intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or, on occasion, high-dose colchicine. In general, NSAIDs are administered in low doses to help prevent CPPD. However, if an acute attack is already occurring, higher doses are administered. If nothing else works, hydroxychloroquine or methotrexate may provide relief.
Prognosis
In most cases that begin with a small number of patches of hair loss, hair grows back after a few months to a year. In cases with a greater number of patches, hair can either grow back or progress to alopecia areata totalis or, in rare cases, alopecia areata universalis.No loss of body function occurs, and the effects of alopecia areata are psychological (loss of self-image due to hair loss), although these can be severe. Loss of hair also means the scalp burns more easily in the sun. Patients may also have aberrant nail formation because keratin forms both hair and nails.Hair may grow back and then fall out again later. This may not indicate a recurrence of the condition, but rather a natural cycle of growth-and-shedding from a relatively synchronised start; such a pattern will fade over time. Episodes of alopecia areata before puberty predispose to chronic recurrence of the condition.Alopecia can be the cause of psychological stress. Because hair loss can lead to significant changes in appearance, individuals with it may experience social phobia, anxiety, and depression. Epidemiology
The condition affects 0.1%–0.2% of the population, with a lifetime risk of 1%-2%. and is more common in females.Alopecia areata occurs in people who are otherwise healthy and have no other skin disorders. Initial presentation most commonly occurs in the early childhood, late teenage years, or young adulthood, but can happen at any ages.