The second form of bone marrow suppression is bone marrow aplasia, which is associated with being late into toxicity and cannot be reversed in some cases. Chloramphenicol is contraindicated in persons who are breastfeeding due to the risk of toxic effects in the baby, but if maternal use of chloramphenicol cannot be avoided, close monitoring of the babys symptoms such as feeding difficulties, and blood work is recommended. Treatment
Chloramphenicol therapy should be stopped immediately if objective or subjective signs of gray baby syndrome are suspected since gray baby syndrome can be fatal for the infant if it is not diagnosed early on as it can lead to anemia, shock, and end-organ damage. After discontinuing the antibiotic, the side effects caused by the toxicity should be treated. This includes treating hypoglycemia to help prevent hemodynamic instability, as well as increasing the temperature of the infant if they have developed hypothermia. Since symptoms of gray baby syndrome are correlated with elevated serum chloramphenicol concentrations, exchange transfusion may be required to remove the drug, charcoal column hemoperfusion is a type of transfusion that has shown significant effects but is associated with numerous side effects. The associated side effects isnt the only reason why this method of treatment is not a first line therapy. According to the American Journal of Kidney Diseases, elevated cartridge prices and viable lifespan of the product are deterring factors to consider.
Treatment
Treatment largely depends upon individual disease progression and the nature of presenting symptoms. Antimalarials, corticosteroids, and other drugs may be prescribed, if deemed appropriate by the treating physician. Prognosis
Most patients will maintain a diagnosis of undifferentiated connective tissue disease. However, about one third of UCTD patients will differentiate to a specific autoimmune disease, like rheumatoid arthritis or systemic sclerosis. About 12 percent of patients will go into remission.Severe vitamin D deficiency has been associated with the progression of UCTD into defined connective tissue diseases. The presence of the autoantibodies anti-dsDNA, anti-Sm, and anti-cardiolipin has been shown to correlate with the development of systemic lupus erythematosus, specifically. References


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