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There are also a number of other conditions that affect hands, feet, and parts of the face with associated skin color changes that need to be differentiated from acrocyanosis: Raynaud phenomenon, pernio, acrorygosis, erythromelalgia, and blue finger syndrome. The diagnosis may be challenging in some cases, especially when these syndromes co-exist.
Cold agglutinin-mediated acrocyanosis differs from Raynaud phenomenon. In Raynaud phenomena, caused by vasospasm, a triphasic color change occurs, from white to blue to red, based on vasculature response. No evidence of such a response exists in cold agglutinin disease. Other symptoms
Symptoms of AIHA may be due to the underlying anemia; including shortness of breath or dyspnea, fatigue, headache, muscle weakness and pallor. [10] In cold agglutinin disease (cold antibody type), agglutination and impaired passage of red blood cells through capillaries in the extremities causes acrocyanosis and Raynaud phenomenon with a rare complication of gangrene [4]
Differential diagnosis: Circumoral cyanosis, peripheral cyanosis, central cyanosis: Prevention: Avoid exposure to freezing cold temperatures, limit smoking or caffeine, avoid touching cyanide: Medication: Antidepressants, anti-hypertension medication, or if caused by other reasons, naloxone hydrochloride
Cold agglutinin disease (CAD) is a rare autoimmune disease characterized by the presence of high concentrations of circulating cold sensitive antibodies, usually IgM and autoantibodies that are also active at temperatures below 30 °C (86 °F), [1] directed against red blood cells, causing them to agglutinate and undergo lysis. [2]
Erythrocyanosis crurum is a skin condition, a variant of acrocyanosis caused by chronic exposure to cold. See also. Chilblains; List of cutaneous conditions;
Cerebral achromatopsia is a type of color blindness caused by damage to the cerebral cortex of the brain, rather than abnormalities in the cells of the eye's retina.It is often confused with congenital achromatopsia but the underlying physiological deficits of the disorders are completely distinct.
[3] [5] After biochemical suspicion of MCADD, molecular genetic analysis of ACADM can be used to confirm the diagnosis. [6] The analysis of MCAD activity in cultured fibroblasts can also be used for diagnosis. [3] In cases of sudden death where the preceding illness would not usually have been fatal, MCADD is often suspected.