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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a retrovirus infection and represents the end point in a progressive sequence of immunosuppressive changes. Vitamins can enhance disease resistance in animals and humans. As such they are important co-factors in optimal functioning of the immune systems. In this article, the immunological and nutritional modifications caused by AIDS are summarized. The effects of murine and human retrovirus infection on vitamin status are analyzed as co-factors in the development of severe immune dysfunction, AIDS. The properties of immunoenhancing antioxidative vitamins, vitamin A, B6, B12, C, E, and beta-carotene, which are frequently low in AIDS patients, are evaluated relative to the development of immunodeficiency during retrovirus infection. Vitamin A, E, and B12 deficiency accelerated the development of AIDS with low T cells, whereas their normalization retarded the development of immune dysfunction. The interactions between these vitamins and the immune system in human AIDS patients and animal models of AIDS are reviewed. Our purpose is to provide data on how retrovirus infection can cause nutritional deficiencies that accentuate immune damage and to evaluate the potential therapeutic role of vitamins in the treatment of immune dysfunctions in AIDS patients.
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PMID:Vitamins and immunomodulation in AIDS. 883 29

A patient is reported on with a common variable immunodeficiency syndrome (CVID), in whom chronic gastritis with antibodies against parietal cells and a cytomegalovirus associated enteritis led to vitamin B12 deficiency with consecutive subacute combined degeneration of the spinal cord. The resulting medullary changes, most probably representing demyelination, were visualised with MRI. The effects of treatment were also monitored over three years by MRI and clinical examination. The resolution of the MRI changes correlated with clinical improvement of the patient's signs. In the medical literature only five cases of vitamin B12 related spinal cord changes have been identified by MRI; none was caused by a CVID syndrome.
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PMID:Common variable immunodeficiency leading to spinal subacute combined degeneration monitored by MRI. 959 86

Diarrhea and malabsorption are common findings in patients with the acquired immunodeficiency syndrome (AIDS). The pathogenesis and consequences of malabsorption in human immunodeficiency virus (HIV) infection are similar to those found in non-HIV-related conditions, and are related to both direct intestinal damage and alterations in the coordination of the body's response to feeding. The pathogenesis of malabsorption is multifactorial and includes primary enterocyte injury with partial villus atrophy and crypt hyperplasia, ileal dysfunction with bile salt wasting and fat malabsorption, and exudative enteropathy. Clinical studies show that intestinal cryptosporidiosis leads to excess fecal losses of about 20% for protein and fat. The consequences of malabsorption include decreased appetite; "enterogastrone" effects including dry mouth, decreased gastric acid secretion, decreased rate of gastric emptying, and slowed intestinal transit; anemia resulting from iron, folate, or vitamin B12 malabsorption; and metabolic effects including osteomalacia, gallstones, renal stones, and hypocholesterolemia. Few studies of nutritional therapy have been applied specifically to AIDS patients with malabsorption. Total parenteral nutrition promotes weight gain, although the response to this therapy depends on the underlying clinical problem, with body cell mass repletion noted in patients with malabsorption but predominantly fat gain in patients with systemic infections. Nutritional stabilization also was noted in response to oral administration of a semielemental diet.
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PMID:Human immunodeficiency virus-related wasting: malabsorption syndromes. 962 87

The relationship between asymptomatic human immunodeficiency virus (HIV) infection and blood hemoglobin (Hb) concentration was examined in anemic pregnant women from a population with high prevalence of both anemia (60%) and HIV seropositivity (30%). Sera from 155 pregnant women with Hb levels < 10.5 g/dL were tested for HIV status, C-reactive protein (CRP), vitamin B12, retinol, and folate levels. The observed prevalence of HIV seropositivity in the group of women with anemia was 47.1% (95% confidence interval=39.2-55.0%). This is significantly higher than the HIV prevalence in the whole population (30.1%; P < 0.001). Median Hb values in HIV-seropositive and -seronegative women with anemia were 8.40 g/dL and 8.95 g/dL, respectively. Serum retinol, vitamin B12, and folate levels were not significantly different in the HIV-seropositive and -seronegative groups. In women who were HIV-seropositive with normal levels of CRP, a median decrease in Hb of 0.4 g/dL was observed. For those with serum CRP levels > 25 mg/l, the median decrease in Hb was 0.7 g/dL. Results indicate that asymptomatic HIV infection is associated with increased prevalence and severity of anemia in pregnancy in this population.
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PMID:The relationship between asymptomatic human immunodeficiency virus infection and the prevalence and severity of anemia in pregnant Malawian women. 988 14

Serum vitamin B12 levels are often low in human immunodeficiency virus (HIV)-infected patients. However, only a few patients appear to have actual vitamin B12 deficiency. A low red cell folate level accompanying the low vitamin B12 level makes the presence of vitamin B12 deficiency more likely. Our experience suggests that a low red cell folate level always indicates deficiency, but does not differentiate between vitamin B12 and folate deficiency. The deoxyuridine suppression test and the assay of serum or plasma total homocysteine and/or of methylmalonic acid levels can also be useful in the identification of patients with true vitamin B12 deficiency. HIV-positive patients frequently have absorption disorders, including vitamin B12 malabsorption. However, the correlation between vitamin B12 malabsorption and serum vitamin B12 and plasma homocysteine levels is poor. Abnormalities in vitamin B12-binding proteins, which are often found in HIV-positive patients, may explain many cases of low vitamin B12 levels. Current evidence suggests that low vitamin B12 levels are more common as the HIV disease progresses. The results of vitamin B12 treatment have been disappointing thus far, including the prevention of toxicity induced by azidothymidine. The possible role of vitamin B12 treatment in the long-term survival of HIV-infected patients is at present unknown. However, it is important to identify those patients who have real vitamin B12 deficiency to treat or prevent their hematologic and/or neurological symptoms.
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PMID:Cobalamin deficiency in patients infected with the human immunodeficiency virus. 993 May 70

Micronutrient deficiencies may be common during human immunodeficiency virus (HIV) infection. Insufficient dietary intake, malabsorption, diarrhoea, and impaired storage and altered metabolism of micronutrients can contribute to the development of micronutrient deficiencies. Low plasma or serum levels of vitamins A, E, B6, B12 and C, carotenoids, Se, and Zn are common in many HIV-infected populations. Micronutrient deficiencies may contribute to the pathogenesis of HIV infection through increased oxidative stress and compromised immunity. Low levels or intakes of micronutrients such as vitamins A, E, B6 and B12, Zn and Se have been associated with adverse clinical outcomes during HIV infection, and new studies are emerging which suggest that micronutrient supplementation may help reduce morbidity and mortality during HIV infection.
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PMID:Micronutrients and the pathogenesis of human immunodeficiency virus infection. 1043 44

This case study reported a 17-year-old female of common variable immunodeficiency (CVID) associated with bronchiectasis, pernicious anemia and mosaic trisomy 8. Clinically this patient presented with recurrent sinopulmonary infections, intractable diarrhea, macrocytic anemia, and primary amenorrhea. Immunological tests showed pan-hypogammaglobulinemia and a decrease of peripheral blood B cells (4%) and CD4+ cells (25%). Lymphoproliferative responses to mitogen (PHA) and specific antigen (BCG) were profoundly impaired in the patient in comparison to those in control. Production of interleukin 4 (IL-4) and gamma interferon (IFN-gamma) in the in vitro lymphoproliferation was also profoundly depressed. Pernicious anemia demonstrated by larger MCV (112.9 fl) and hyper-segmental granulocytes on peripheral blood smear responded to parental administration of vitamin B12. Interestingly, she had a mosaic trisomy 8 in peripheral blood mononuclear cells but normal 46XX karyotype in the bone marrow cells. To our knowledge, this is the first case of CVID associated with mosaic trisomy 8 reported in the literature. As the case exemplifies, CVID should be considered when the physicians evaluate the patient presenting with recurrent sinopulmonary infections, diarrhea, malnutrition, and pernicious anemia. It requires further study to explore whether the genes in the chromosome 8 are linked to CVID.
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PMID:Common variable immunodeficiency with mosaic trisomy 8: report of one case. 1119 41

This article reviews current literature on the role of micronutrients in human immunodeficiency virus (HIV) infection. Deficiencies of micronutrients are common in HIV-infected persons. They occur due to malabsorption, altered metabolism, gut infection, and altered gut barrier function. There is a compelling association of deficiencies of micronutrients in HIV-infection with immune deficiency, rapid disease progression, and mortality. Also, there is increased risk of vertical HIV transmission from mother to child with deficiency of vitamin A, and of neurological impairment with vitamin B12. The last five years have been exciting in micronutrient research, and there is promise that some micronutrients may be key factors in maintaining health in HIV immunodeficiency, and in reducing mortality. Selenium appears important in reducing virulence of HIV and slowing disease progression. Vitamin A supplementation in pregnant women with HIV may reduce maternal mortality and improve birth outcomes. Supplementation in children with HIV may accelerate growth. Carotenoid supplementation is being evaluated. Vitamin B12 may slow HIV immune deficiency disease progression, and reverse neurological compromise. Clinical benefit of supplementation with some micronutrients may be measurable in the presence of pre-existing deficiency. Apart from improved general nutrition, the impact of micronutrient supplements on health and their optimal use in HIV infection is controversial because there are so few controlled clinical trials. Further research is needed to elucidate the role of micronutrient deficiencies on the course of HIV infection, and the preventive and therapeutic role of supplementation in its clinical management. Nevertheless, current knowledge supports the use of routine multivitamin and trace element supplementation as adjuvant to conventional antiretroviral drug treatment as a relatively low-cost intervention.
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PMID:A clinical review of micronutrients in HIV infection. 1294 78

A 54-year-old man of Persian origin presented to our department with a 1-year history of ulcers on the right leg that had been unresponsive to numerous topical treatments, accompanied by lymphedema of the right leg. Medical history included hypergonadotropic hypogonadism, which had not been further investigated. He was treated for 20 years with testosterone IM once monthly, which he stopped a year before the current hospitalization for unclear reasons. The patient reported no congenital lymphedema. Physical examination revealed two deep skin ulcers (Figure 1) on the right leg measuring 10 cm in diameter with raised irregular inflammatory borders and a boggy, necrotic base discharging a purulent hemorrhagic exudate. Bilateral leg pitting edema and right lymphangitis with lymphadenitis were noted. He had low head hair implantment, sparse hair on the body and head, hyperpigmentation on both legs, onychodystrophia of the toenails (mainly the large toe and less prominent on the other toes), which was atrophic lichen-planus-like in appearance and needed no trimming (Figure 2), normal hand nails, oral thrush, and angular cheilitis. Other physical findings were gynecomastia, pectus excavatum, small and firm testicles, long extremities, asymmetrical goiter, systolic murmur 2/6 in left sternal border, and slow and inappropriate behavior. The patient's temperature on admission was 39 degrees C. Blood cultures were negative for bacterial growth. Results of laboratory investigations included hemoglobin (11.2 g/dL), hematocrit (26.8%), normal mean corpuscular volume and mean corpuscular hemoglobin volume, and red blood cell distribution width (16%). Blood smear showed spherocytes, slight hypochromia, anisocytosis, macrocytosis, and microcytosis. Blood chemistry values were taken for iron (4 micro g/dL [normal range 40-150 micro g/dL]), transferrin (193 mg/dL [normal range 220-400 mg/dL]), ferritin (1128 ng/mL [normal range 14-160 ng/mL]), transferrin saturation (1.5% [normal range 20%-55%]), serum folate (within normal limits), and vitamin B12 (within normal limits). Direct Coombs' test equaled positive 2 + IgG. All these values indicated anemia of chronic diseases combined with hemolytic anemia. Further blood work-up tested antinuclear antibody (positive <1:80 homogeneous pattern), rheumatoid factors (143 IU/mL [positive >8.5 IU/mL]), C-reactive protein (286 mg/L [normal range 0-5 mg/L]), anticardiolipin IgM antibody (9.0 monophosphoryl lipid U/mL [normal range 0-7.00 MPL U/mL]) and antithrombin III activity (135% [normal range 74%-114%]). Results of other blood tests were within normal limits or negative, including lupus anticoagulant, beta2 glycoprotein, anticardiolipin IgG Ab, anti-ss DNA Ab, C3, C4, anti-RO, anti-LA, anti-SC-70, anti-SM Ab, P-ANCA, C-ANCA, TSH, FT4, anti-T microsomal, antithyroglobulin, protein C activity, protein S free, cryoglobulins, serum immunoelectrophoresis, VDRL, hepatitis C antibodies, hepatitis B antigen, and human immunodeficiency virus. Endocrinological work-up examined luteinizing hormone (22.9 mIU/mL [normal range for adult men 0.8-6 mIU/mL]), follicle stimulating hormone (49.7 mIU/mL [normal range for adult men 1-11 mIU/mL]), testosterone (0.24 ng/mL [normal range for adult men 2.5-8.0 ng/mL]), bioavailable testosterone (0.02 ng/mL [normal range for adult men >0.6 ng/mL]), and percent bioavailable test (8.1% [normal value >20%]). These results indicate hypergonadotropic hypogonadism. Plasminogen activator inhibitor 1 was 6 U (normal value 5-20 U/mL). Karyotyping performed by G-banding technique revealed a 47 XXY karyotype, which is diagnostic of Klinefelter's syndrome. Doppler ultrasound of the leg ulcers disclosed partial thrombus in the distal right femoral vein. X-rays and bone scan displayed osteomyelitis along the right tibia. Histological examination of a 4-mm punch biopsy from the ulcer border revealed hyperkeratosis, acanthosis, hypergranulosis, and mixed inflammatory infiltrate containing eosinophils compatible with chronic ulcer. Multiple vessels were seen, compatible with a healing process. Direct immunofluorescence of the biopsy revealed granular IgM in the dermo-epidermal junction. Indirect immunofluorescence was negative. Thyroid function tests showed normal thyroid stimulating hormone and free throxine4. Multinodular goiter was seen on thyroid scan and ultrasound. Thyroid fine needle aspiration was compatible with multinodular goiter (normal follicular cells, free colloid, macrophages with pigment). IV treatment with amoxicillin-clavulanic acid 1 g t.i.d. was administered for 2 weeks, with a decrease in temperature and normalization of the leukocyte level. Oral antibiotic treatment with amoxicillin-clavulanic acid was continued for 10 more days, followed by 25 days of ciprofloxacin for the osteomyelitis. Local treatment included saline soakings followed by application of Promogran (Johnson & Johnson, New Brunswick, NJ) and Kaltostat (ConvaTec Ltd., a Bristol-Myers Squibb Company, New York, NY) with slight improvement. At the same time, the patient was treated with warfarin sodium due to deep vein thrombosis under international normalized ratio 2-3. The patient was treated with IM testosterone once monthly for 1 year, which resulted in a reduction in the diameter and depth of the leg ulcers (Figure 3). Blood tests were not performed for follow-up of the immune state.
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PMID:Klinefelter's syndrome presenting with leg ulcers. 1536 65

The incidental discovery of neutropenia during routine blood counting represents a common problem for clinicians. However, there are no reported data of systematic evaluations of adults with incidental neutropenia. As such, this was the aim of the present study. Ninety-seven adults with incidental neutropenia were submitted to a clinical and laboratory approach including medical evaluation, complete blood count (CBC), serial CBC, direct and indirect antiglobulin test, bone marrow smear and biopsy, assessment of folate, vitamin B12 and iron status, serum liver enzymes, serum proteins, serological exams for hepatitis B and C virus, cytomegalovirus, mononucleosis, human immunodeficiency virus and toxoplasmosis, detection of lupus erythematosus cells, antinuclear and anti-DNA antibodies and rheumatoid factor, dosage of free thyroxin and thyrotropin, chest roentgenogram and abdominal echography. Chronic idiopathic neutropenia of adults was identified in 34.0% of the individuals, neutropenia due to exposure to chemical agents was seen in 16.5%, infectious diseases in 9.3%, autoimmune diseases in 9.3%, haematological diseases in 9.3%, thyroid disorders in 8.2%, ethnic neutropenia in 7.2%, drug-related neutropenia in 2.1%, cyclic neutropenia in 2.1% and iron deficiency in 2.1%. Recovery or improvement of the neutrophil count was seen upon treatment or recuperation from infectious, autoimmune, haematological and thyroid diseases and iron supplementation. We conclude that the evaluation of individuals with incidental neutropenia using a structured approach may make the identification of clinically silent diseases possible, and provide an opportunity for early treatment, avoiding complications of the diseases and consequences of neutropenia.
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PMID:Causes of incidental neutropenia in adulthood. 1680 47


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