Deficiency, diagnosis dietary

There is a great deal of both popular and professional interest in the etiology, diagnosis, prevention, and treatment of osteoporosis. The extent of this disease in the United States is a major public health concern. No single cause can be identified. Certainly the influence of hormones, dietary intakes of Ca, fluoride and vitamin D are significant. Our results suggest that it may be prudent to consider the possibility that trace element deficiencies, particularly of Mn, may be of significance. 

The symptoms of the disease can be ameliorated by dietary zinc supplementation. The differential diagnosis of the disease includes acquired zinc deficiency condition owing to low-zinc level in mother s milk because both conditions are very similar in terms of onset and clinical features. As soon as the low-zinc breastfed infants are weaned, they no longer require supplemental zinc, but acrodermatitis enteropathica patients experience recurrence of symptoms if they discontinue oral zinc therapy. 

Breakdown of isoleucine, valine, threonine, and methionine results in the production of propionyl-CoA. Propionyl-CoA, in turn, is catabolized to succinyl-CoA via the intermediate methylmalonyl-CoA. Methylmalonyl-CoA is a compoimd of imusual interest to nutritional scientists. This compound accumulates in the cell during a vitamin B12 deficiency. Vitamin B12 deficiency is not a rare disease, as it appears in a common autoimmune disease called pernicious anemia. Vitamin B12 deficiency also occurs in strict vegetarians who avoid meat, fish, poultry, and dairy products. Methylmalonyl-CoA can also build up with rare genetic diseases that involve the production of defective, mutant forms of methylmalonyl-CoAmutase. Most of the methylmalonyl-CoAthat accumulates to abnormally high levels in the cell is hydrolyzed to methylmalonic acid (MMA), which leaves the cell for the bloodstream and eventual excretion in the urine. Some of the MMA is converted back to propionyl-CoA, resulting in the production and accumulation of propionic acid in the cell. The measurement of plasma and urinary MMA has proven to be a method of choice for the diagnosis of vitamin B12 deficiency, whether induced by pernicious anemia or by dietary deficiency. 

No definitive test will confirm a diagnosis of ACD, and the diagnosis is often overlooked The practitioner should maintain a high index of suspicion in any patient with a chronic disease. ACD may coexist with IDA and folic acid deficiency, as many of these patients will have poor dietary intake or gastrointestinal blood loss. Examination of the bone marrow reveals an abundance of iron, suggesting... 

The relative ease of treatment with vitamin B should not prevent a full investigation of the etiology of the deficiency. The initial diagnosis usually is suggested by a macrocytic anemia or an unexplained neuropsychiatric disorder. Eull understanding of the etiology of vitamin B deficiency involves studies of dietary supply, GI absorption, and transport. 

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