Vitamin manifestations

A disease resulting from a deficiency of one or more vitamins is hypovitaminosis (if vitamin is supplied in insufficient quantity) or avitaminosis (complete lack of vitamin manifested by some biochemical processes disorder). Deficiency of vitamins was formerly one of the main causes of many diseases and deaths. Pellagra (deficiency of some B-complex vitamins), scurvy (vitamin C), beriberi (thiamine), rickets (vitamin D), pernicious anaemia associated with reduced ability to absorb vitamin Bj2 (corrinoids) and xerophthalmia (vitamin A) are now well-known diseases caused by vitamin deficiency. Excessive intake of one or more vitamins (especially of lipophilic vitamins A and D) also causes an abnormal state resulting from disturbances of biochemical processes and can lead to severe diseases known as hypervitaminosis. 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

Clinical manifestation of vitamin B 2 deficiency is usually a result of absence of the gastric absorptive (intrinsic) factor. Dietary deficiency of vitamin B 2 is uncommon and may take 20 to 30 years to develop, even in healthy adults who foUow a strict vegetarian regimen. An effective enterohepatic recycling of the vitamin plus small amounts from bacterial sources and other contaminants greatly minimizes the risk of a complete dietary deficiency. Individuals who have a defect in vitamin B 2 absorption, however, may develop a deficiency within three to seven years. 

Thiamin has a very low toxicity (oral LD5o of thiaminchloride hydrochloride in mice 3-15 g/kg body weight). The vitamin is used therapeutically to cure polyneuropathy, beri-beii (clinically manifest thiamin deficiency), and Wernicke-Korsakoff Syndrome ( Wernicke encephalopathy and Korsakoff psychosis). In mild polyneuropathy, 10-20 mg/d water-soluble or 5-10 mg/d lipid-soluble thiamin are given orally. In more severe cases, 20-50 mg/d water-soluble or 10-20 mg/d lipid-soluble thiamin are administered orally. Patients suffering from beri-beri or from early stages of Wernicke-Korsakoff Syndrome receive 50-100 mg of thiamin two times a day for several days subcutaneously or intravenously until symptoms are alleviated. Afterwards, the vitamin is administered orally for several weeks. 

It is important to monitor vitamin D therapy aggressively to assure that PTH levels are not oversuppressed. Oversuppression of PTH levels can induce adynamic bone disease, which manifests as decreased osteoblast and osteoclast activity, decreased bone formation, and low bone turnover. 

The answer is c. (Hardman, p 15.33.) Enthusiastic over medication with vitamin D may lead to a toxic syndrome called hy/jervitamijmsis D. The initial symptoms can include weakness, nausea, weight loss, anemia, and mild acidosis. As the excessive doses are continued, signs of nephrotoxicity are manifested, such as polyuria, polydipsia, azotemia, and eventually nephrocalcinosis. In adults, osteoporosis can occur. Also, there is CNS impairment, which can result in mental retardation and convulsions. 

Patients typically present by 6-12 months with severe developmental retardation, convulsions, microcephaly and homocysteinemia (=50pmol/l) with hypomethioninemia (<20 pmol/1). A few individuals have had psychiatric disturbances. The blood concentration of vitamin B12 is normal, and, unlike individuals with defects of cobalamin metabolism, these patients manifest neither anemia nor methylmalonic aciduria. The blood folic acid level is usually low. 

With respect to human beings there is some question as to what level of tissue saturation should ideally be maintained. In guinea pigs defects in developing incisors appear when the tissue concentrations are about 40 per cent of the maximum. Scurvy symptoms do not appear until the tissue saturation has reached a much lower level (about 20 per cent saturation). It seems logical to suppose that in different individuals the manifestations of mild vitamin C deficiency would be different and that a high degree of saturation would be safest from the standpoint of all the vulnerable tissues. 19... 

When the patient is manifesting acute symptoms of withdrawal such as the shakes, a rapid pulse, or increased blood pressure, then detoxification with a benzodiazepine should begin immediately. When the patient s liver function is unknown, we recommend lorazepam (1-2 mg) as the treatment of choice in the emergency room setting. The lorazepam can be repeated every hour until the patient s symptoms begin to resolve. Initial treatment should also include vitamin supplements as noted earlier, especially thiamine. 

Vitamin 6 2 deficiency is known to manifest as dementia along with other neurological sequelae, as subacute combined degeneration (SCD). A study done on choline-deficient mice fed with vitamin B12 showed... 

Oxidation of nicotine with chromic acid led to the isolation of pyridine-3-carboxylic acid, which was given the trivial name nicotinic acid. We now find that nicotinic acid derivatives, especially nicotinamide, are biochemically important. Nicotinic acid (niacin) is termed vitamin B3, though nicotinamide is also included under the umbrella term vitamin B3 and is the preferred material for dietary supplements. It is common practice to enrich many foodstuffs, including bread, flour, corn, and rice products. Deficiency in nicotinamide leads to pellagra, which manifests itself in diarrhoea, dermatitis, and dementia. 

Nicotinate and nicotinamide, together referred to as niacin, are required for biosynthesis of the coenzymes nicotinamide adenine dinucleotide (NAD"") and nicotinamide adenine dinucleotide phosphate (NADP" ). These both serve in energy and nutrient metabolism as carriers of hydride ions (see pp. 32, 104). The animal organism is able to convert tryptophan into nicotinate, but only with a poor yield. Vitamin deficiency therefore only occurs when nicotinate, nicotinamide, and tryptophan are all simultaneously are lacking in the diet. It manifests in the form of skin damage (pellagra), digestive disturbances, and depression. 

Doses of folic acid greater than 0.1 mg/day may result in hematologic remission in patients with vitamin B12 deficiency. Neurologic manifestations will not be prevented... 

Deficiency of this coenzyme can lead to many manifestations. Clinical signs include retarded growth, acrodynia, alopecia, skeletal changes and anemia, while changes in neurotransmitters, such as dopamine, serotonin, norepinephrine (noradrenaline), tryptamine, tyramine, histamine, y-aminobutyric acid, and taurine, affect the brain function and can lead to seizures and convulsions. An overdose of vitamin Bg leads to neuronal damage and sensory and motor effects [417],... 

Dietary deficiency of thiamine (vitamin 6,j results In an Inability to synthesize thiamine pyrophosphate, and the pathophysiology arises from Impaired glucose utilization, especially manifested In the nervous system. 

The answer is B. This patient s greasy, foul-smelling stools indicate steatorrhea. Her vision problems may be a manifestation of vitamin A deficiency due to fat malabsorption. The most likely explanation is biliary insufficiency, ie, decreased bile salt production leading to poor emulsification of dietary fats. Active ileal disease is a possibility, but the WBC count would likely be elevated unless her condition was in remission. Infection with Giardia is less likely due to the absence of pathogenic organisms in her stool. Lactose intolerance can produce diarrhea but not steatorrhea. 

Persons with vitamin deficiency exhibit a spectrum of nonspecific neurologic manifestations, in-ciuding depression, confusion, and disorientation, which may lead to convulsions in severe cases. 

CNS toxicity occurs because isoniazid has structural similarities to pyridoxine (vitamin Be) and can inhibit its actions. This toxicity is dose-related and more common in slow acetylators. Manifestations include peripheral neuropathy, optic neuritis, ataxia, psychosis and seizures. The administration of pyridoxine to patients receiving INH does not interfere with the tuberculostatic action of INH but it prevents and can even reverse neuritis. Hematological effects include anaemia which is also responsive to pyridoxine. In some 20% of patients antinuclear antibodies can be detected but only in a minority of these patients drug-induced lupus erythematosus becomes manifest. 

Pyridoxine is indicated in vitamin B deficiency, for the treatment of some pyridoxine responsive anemia s and for isoniazid-induced neuropathy. It may relieve symptoms of pellagra when niacin fails. Long-term administration of large doses may produce neurotoxicity manifesting itself in progressive peripheral sensory neuropathy. 

Biotin (vitamin B ) is widespread in foods and is also synthesized by intestinal bacteria. It is a coenzyme for the carboxylation of pyruvate, acetyl-coenzyme-A (CoA), propionyl CoA, and /1-methyl-crotonyl CoA and is involved in fatty acid formation and in energy release from carbohydrates. In humans deficiencies only occur in patients with an abnormal gut flora and manifests itself as exfoliative dermatitis and alopecia. 

Deficiency may occur in infants if no fruits or vegetables are added to their milk formulas. In alcoholics, and in elderly subjects who consume inadequate diets vitamin C deficiencies are frequent. Severe ascorbic acid deficiency is characterized by the syndrome known as scurvy. Its manifestations are generally based on a loss of collagen. Symptoms include hemorrhages, loosening of teeth. In children cellular changes in the long bones occur. 

High daily doses of retinoids can lead to hyper-vitaminosis A manifesting itself as dermal toxicity such as erythematous dermatitis, bone pains, neurological symptoms and hepatosplenomegaly. A recent study shows a correlation between low bone mineral density and too high intake of vitamin A. 

Deficiency symptoms In vitamin E deficiency in experimental animals the manifestations are seen in several systems... 

Histamine, an important mediator of inflammation, gastric acid secretion and other allergic manifestations, contain an imidazole ring system. Thiamine, an essential vitamin, possesses a quaternized thiazole ring. 

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