Deficiency secondary deficiencies

Secondary Deficiency. Low plasma Cp levels caused by a lack of incorporation of Cu into the molecule during synthesis are much more common than primary deficiency. Secondary deficiency may be due to dietary Cu insufficiency (including malabsorption), inability to release Cu " " from the gastrointestinal epithelium into the circulation, or inability to insert Cu into the developing Cp molecule. In all cases, apoCp (noncopper containing) is stiU synthesized by the hepatic parenchymal cells. However, as mentioned previously, most apoCp is cataboHzed intracellularly before release into the plasma, and plasma apoCp has a much shorter half-life than does holoCp. Levels may also be low in blood loss or in gastrointestinal or renal protein-losing syndromes. 

Formation of strictures, abscesses, fistulae, and obstructions in patients with CD is possible. Patients with CD may develop significant weight loss or nutritional deficiencies secondary to malabsorption of nutrients in the small intestine, or as a consequence of multiple small- or large-bowel resections. Common nutritional deficiencies encountered in IBD include vitamin B12, fat-soluble vitamins, zinc, folate, and iron. Malabsorption in children with CD may contribute to significant reductions in growth and development. 

Cancer patients also may have concurrent iron deficiency secondary to erythropoietin use ( functional iron deficiency) or to cancer. Therefore, it is imperative that these patients have iron studies done to assess adequate iron stores needed to drive hematopoiesis. If the patient is determined to have sub-optimal iron stores or is iron deficient, then replacement either orally or intravenously may be necessary, in addition to the use of erythropoietin products. The use of iron in these patients is the same as discussed previously under Iron-Deficiency Anemia. ... 

Frank, A., V. Galgan, and L.R. Petersson. 1994. Secondary copper deficiency, chromium deficiency and trace element imbalance in the moose (Alces alces L.) effect of anthropogenic activity. Ambio 23 315-317. 

Cobalamin deficiency can create a secondary deficiency of active THF by preventing its release from the storage pool through the AT-methyl THF-homocysteine methyltransferase reaction, and thus also result in megaloblastic anemia. Progressive peripheral neuropathy also results from cobalamin deficiency. TTeating a cobalamin deficiency with folate corrects the megaloblastic anemia but does not halt the neuropathy. 

Addison s disease), both cortisol and aldosterone must be replaced when ACTH production is deficient (secondary AC insufficiency), cortisol alone needs to be replaced. Cortisol is effective when given orally (30 mg/d, 2/3 a.m., 1/3 p.m.). In stress situations, the dose is raised by 5- to 10-fold. Aldosterone is poorly effective via the oral route instead, the mineralocorticoid fludrocortisone (0.1 mg/d) is given. 

Zinc (Zn) deficiency is teratogenic in rats, and fetal skeletal defects are prominent. Embryofetal zinc deficiency secondary to changes induced by substances in maternal Zn metabolism is a well-established mechanism for developmental toxicity (29-31). Several substances, including urethane and alpha-hederin cause similar malformations as Zn deficiency in rodents. A number of mechanistic studies have shown that these substances act via an acute-phase reaction induction of metallothionein in the maternal liver which binds systemically available Zn in the pregnant animal. This results in a systemic redistribution of Zn. As a consequence the substances produce a transient but developmentally adverse Zn deficiency in the... 

Deficiency (vitamin deficiency secondary to reduced intake)... 

Gomes, J.A., Dos Santos, M.S., Cunha, M.C., Mascaro, V.L., Barros, J.N., De Sousa, L.B. Amniotic membrane transplantation for partial and total limbal stem cell deficiency secondary to chemical bum. Ophthalmology 110, 466-473 (2003)... 

FIGURE 10—11. Several different causes of dopamine deficiency may result in negative and cognitive symptoms. In schizophrenia itself, there may be a primary dopamine (DA) deficiency or a DA deficiency secondary to blockade of postsynaptic D2 dopamine receptor by an antipsychotic drug. If serotonin is hyperactive, this may also cause a relative DA deficiency by inhibiting DA release. Either primary or secondary DA deficiency in this pathway may cause cognitive blunting, social isolation, indifference, apathy, and anhedonia. 

Celiac disease is the result of the development of inflammatory-allergic condition due to gluten intolerance. The disease occurs both in adults and in children in a number of countries all over the world. Its occurrence is fairly frequent, it is estimated that approximately 1% of the population suffers from it. Patients manifest not only gastrointestinal symptoms, but also symptoms which are the consequence of malabsorption syndrome, such as osteoporosis, hypochromic anemia, hypoproteinaemia, hypocalcemia, short stature in children, vitamin deficiency, secondary polysensibilization, and emotional disturbances. Moreover, it has been observed that the occurrence of autoimmunological diseases and neoplasms in patients who are not treated with gluten-free diet doubles (Swinson et al., 1983 Ventura et al., 1999). 

Patients with preexisting tumors or growth hormone deficiency secondary to an intracranial lesion should be examined routinely for progression or recurrence of the underlying disease process. In pediatric patients, clinical literature has revealed no relationship between somatropin replacement therapy and central nervous system (CNS) turmor recurrence or new extrracranial tumors. However, in childhood cancer survivors, an increased risk of a second neoplasm has been reported in patients treated with somatropin after their first neoplasm. Intracranial tumors, in particular meningiomas, in patients treated with radiation to the head for their first neoplasm, were the most common of these second neoplasms. In adults, it is unknown whether there is any relationship between somatropin replacement therapy and CNS tumor recurrence... 

Although the FIGLU test depends on folate nutritional status, the metabolism of histidine wUl also be impaired and a positive result obtained, in vitamin B12 deficiency, because of the secondary deficiency of folate (Section 10.3.4.1). About 60% of vitamin Bi2-deficient subjects show increased FIGLU excretion after a histidine load. 

Again, either a primary deficiency of folic acid or functional deficiency secondary to vitamin B12 deficiencywillhave the same effect. In folate deficiency. 

The main hmiting factor in obtaining an optimal response to epoetin is the adequacy of the patient s iron stores (32,33) the response is abated in the presence of iron deficiency, occult blood loss, hemolysis, and other hematological diseases (34,35). Other causes of an inadequate response to epoetin include concurrent infection or inflammatory disease (1), aluminium toxicity, vitamin deficiencies, secondary hyperparathyroidism (36,37), and osteitis fibrosa (38,39). 

Decreased Plasma Levels. Cp levels are decreased as a result of various primary and secondary deficiencies. 

Factor H or I Rare HypercataboUsm of C3 with secondary deficiency severe and recurrent bacterial infections (as with C3, deficiency) membranoproliferative glomerulonephritis... 

The clinical importance of the complement system is demonstrated by the disease associations seen in inherited or secondary deficiencies of the various components. Several of the more important of these are listed in Table 20-9. Most of the complement components also demonstrate genetic polymorphism. The genetic aspects of C3 and C4 are discussed in the individual sections following. 

Genetic Deficiency. Inherited primary deficiency of C3 is associated with a greatly increased risk for infection, particularly with encapsulated bacteria, similar to the picture seen with the Bruton type of agammaglobulinemia. Deficiency of the inactivators of C3, including factors H and I of the alternative pathway, is associated with severe secondary deficiency of C3 and a similar clinical picture. 

Other Conditions. Other groups of individuals are considered to be at risk either from a marginal dietary deficiency or from an acquired deficiency secondary to disease. These groups would include female adolescents during pregnancy and lactation. Also affected may be patients with malabsorption syndrome, inflammatory bowel disease, alcoholic liver disease, and anorexia nervosa. A significant proportion of cases of sickle cell anemia have clinical signs and symptoms and some laboratory abnormalities of zinc deficiency. These patients respond well to zinc supplementation. ... 

Interpretation In normal subjects, plasma ACTH concentrations peak 30 minutes after CRH injection (80 7pg/mL at 0930 hr 29 2.6pg/mL at 2030 hr), and serum cortisol peaks at 60 minutes (13 Ijig/dL at 1000 17 0.7p.g/dL at 2100 hr). Patients with pituitary ACTH deficiency (secondary adrenal insufficiency) have decreased ACTH and cortisol responses. Patients with hypothalamic disease have prolonged ACTH responses and subnormal cortisol responses. Most patients with Cushing s syndrome caused by adrenal tumors or nonendocrine ACTH-producing tumors do not respond to CRH. Most patients with Cushing s syndrome respond with a normal or excessive increase in ACTH. Responses are usually normal in patients with depression. 

Secondary deficiencies are 10-100 times commoner than primary deficiencies (Section 4). Among the primary immunoglobulin deficiencies, it is also clear that DG is some 6-12 times commoner than AG (H25). In general the primary deficiencies are more severe than the secondary (see Table 3). 

Pyridoxine, a water-soluble vitamin, is used in dietary vitamin Bg deficiency, seizures related to vitamin Bg deficiency or dependency, vitamin Bg-responsive anemias or dependency syndrome (inborn errors of metabolism), prevention of vitamin Bg deficiency during isoniazid therapy, and treatment of vitamin Bg deficiency secondary to isoniazid. 

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