Vitamin A deficiency can lead to a decrease in the number of blood lymphocytes, a decrease in natural killer cells, and a decrease in specific antibody responses. When vitamin A is insufficiently ingested, a decrease in the number of white blood cells, a decrease in the weight of lymphoid organs, a loss of T cell function, and a decrease in immunity against immunogenic tumors can be observed. In experimental animals and human experiments, vitamin A deficiency leads to abnormal humoral and cellular immune functions.
Dry eye is one of the typical clinical features of vitamin A deficiency. According to the specific eye performance, dry eye syndrome can be divided into several periods. The XN phase is the earliest stage, mainly causing night blindness caused by dark adaptation function damage. After the X1A phase, the goblet cells secrete mucus and the conjunctiva is dry. Next, in the X1B phase, the bubble-like Piedular plaque appears on the frontal surface of the conjunctiva. The X2 phase is the stage of disease progression, which is characterized by simple corneal dryness. When the cornea is softened or ulcerated, or both, the liquefaction process is X3. At this time, if the liquefaction surface is insufficient, 1/3 of the cornea area is the X3A phase, and more than 1/3 is the X3B phase. Eye damage caused by corneal softening is called dry eye disease fundus disease, also known as XF phase.
Vitamin A deficiency can damage embryo growth. Experimental animals with severe vitamin A deficiency often undergo embryo resorption, while surviving embryos also have abnormalities in the eyes, lungs, urinary tract and cardiovascular system. When the body is deficient in vitamin A, there is less morphological abnormality, but the function of the lung is abnormal.
Lack of vitamin A harm
