Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied population and subpopulation composition of peripheral blood lymphocytes and HBV circulation markers in 126 patients in the acute period of the disease and prophylactic screening within 6 months. It was established that in case of complete recovery the changes of immunocompetent cells had a transitory character. Replication forms of chronic hepatitis the immune status showed marked T-lymphopenia with prevailing reduction of T-suppressors. The role of cellular immunity in the formation of chronic liver disease is discussed.
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PMID:[Cellular immunity in viral hepatitis B and its transition into chronic forms]. 182 78

The incidence of malnutrition and immunocompetence in 156 patients admitted to hospital with liver disease was investigated. Expected weight/height was within the normal range for all groups except those with carcinoma. Triceps skinfold thickness (TSF) was reduced in 49% of patients with cirrhosis and 55% with alcoholic disease. Hypoalbuminaemia was common in all groups, with 66% of those with chronic disease having concentrations below 35 g/dl. Lymphopenia was equally common, 65% of patients with fulminant hepatic failure (FHF) having counts below 1000 cells/mm3. Incidence of total anergy to standard skin tests was 54% overall: 93% in FHF and 60% in cirrhosis and alcoholic disease. There were significant links between reduced TSF and hypoalbuminaemia, lymphopenia and anergy, hypoalbuminaemia and anergy, and anergy and mortality. Reduced TSF was only associated with anergy in patients with chronic disease. The high incidence of immuno-incompetence may underlie the frequent occurrence of spontaneous infections in patients with liver disease, and the association between anergy and malnutrition in patients with chronic liver disease suggests that the anergy may be partly reversible by dietary measures.
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PMID:Malnutrition and immuno-incompetence in patients with liver disease. 610 8

Peripheral blood T lymphocytes and T-cell subsets were analyzed in 19 patients with HBV-associated chronic liver disease, in 9 "autoimmune" chronic active hepatitis patients, and in three patients with HBV acute hepatitis. The percentages of the different T-cell subpopulations were defined by indirect immunofluorescence using monoclonal antibodies against all peripheral blood T cells (OKT3), T helper cells (OKT4), T suppressor cytotoxic cells (OKT8), and Ia antigens (OKIa1). The OKT4/OKT8 ratio was significantly lower in HBsAg+ chronic liver disease patients as compared with controls (P less than 0.001), with both decreases of T helper cells and increases of T suppressor cells, while "autoimmune" chronic active hepatitis patients showed a significantly increased ratio (P less than 0.001). Acute HBV infection was associated with a reversal in the normal ratio of helper to suppressor T lymphocytes. During convalescence helper T lymphocytes increased and suppressor T lymphocytes decreased.
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PMID:Immunoregulatory T cells in HBV-induced chronic liver disease as defined by monoclonal antibodies. 622 42

Subpopulations of peripheral blood T lymphocytes (T gamma and T mu) were investigated in 36 patients with chronic liver disease. T lymphocytes decreased in percentage in all patients, except in those with chronic persistent hepatitis. In contrast, the absolute numbers did not differ from those of controls, except in patients with cirrhosis, who showed decreased values for circulating T cells. The absolute and percentage values of T gamma were increased in patients with CAH and cirrhosis but not in patients with CPH. All groups of patients with CLD showed a decrease in the absolute and percentage numbers of T mu, but patients with CPH showed absolute values similar to those of the controls. The role of this imbalance in the T cell subsets in CALD is briefly discussed.
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PMID:Subpopulations of T lymphocytes in patients with chronic active liver disease. 698

DNA repair defects are inborn errors of immunity that result in increased apoptosis and oncogenesis. DNA Ligase 4-deficient patients suffer from a wide range of clinical manifestations since early in life, including: microcephaly, dysmorphic facial features, growth failure, developmental delay, mental retardation; hip dysplasia, and other skeletal malformations; as well as a severe combined immunodeficiency, radiosensitivity, and progressive bone marrow failure; or, they may present later in life with hematological neoplasias that respond catastrophically to chemo- and radiotherapy; or, they could be asymptomatic. We describe the clinical, laboratory, and genetic features of five Mexican patients with LIG4 deficiency, together with a review of 36 other patients available in PubMed Medline. Four out of five of our patients are dead from lymphoma or bone marrow failure, with severe infection and massive bleeding; the fifth patient is asymptomatic despite a persistent CD4+ lymphopenia. Most patients reported in the literature are microcephalic females with growth failure, sinopulmonary infections, hypogammaglobulinemia, very low B-cells, and radiosensitivity; while bone marrow failure and malignancy may develop at a later age. Dysmorphic facial features, congenital hip dysplasia, chronic liver disease, gradual pancytopenia, lymphoma or leukemia, thrombocytopenia, and gastrointestinal bleeding have been reported as well. Most mutations are compound heterozygous, and all of them are hypomorphic, with two common truncating mutations accounting for the majority of patients. Stem-cell transplantation after reduced intensity conditioning regimes may be curative.
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PMID:Failing to Make Ends Meet: The Broad Clinical Spectrum of DNA Ligase IV Deficiency. Case Series and Review of the Literature. 3071 30