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)

This study surveys the extent and severity of haematological and biochemical abnormalities which occurred in 265 patients with pulmonary tuberculosis, and records the haematological changes that occur with treatment. Anaemia was present in 60 per cent of patients, more frequently in males than in females. Leucocytosis with neutrophilia occurred in 40 per cent, lymphopenia in 17 per cent and monocytopenia in 50 per cent. Platelet count and erythrocyte sedimentation rate were elevated in 52 and 80 per cent respectively. Bone marrow aspiration and trephine biopsy were of limited diagnostic value. Ferritin and vitamin B12 levels were increased in 94 and 57 per cent of subjects respectively whilst serum and red cell folic acid were within normal limits in 83 per cent. The frequency of the important biochemical changes were hyponatraemia (43 per cent) and hypoalbuminaemia (72 per cent); alkaline phosphatase, aspartic transaminase and lactic dehydrogenase levels were elevated in approximately a third of patients possibly due to unsuspected dissemination. There was a close correlation between the acid-fast bacilli in sputum and abnormal values, particularly those of body weight, haemoglobin, platelet count, white cell count and erythrocyte sedimentation rate. Failure of these indices to return to normal was invariably associated with persistent excretion of acid-fast bacilli. We have shown that haematological and biochemical abnormalities in pulmonary tuberculosis are common and may be valuable aids to diagnosis. Some haematological markers also reflect response to treatment.
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PMID:The haematological and biochemical changes in severe pulmonary tuberculosis. 261 37

A prospective study of the incidence of toxic hematologic effects of antiepileptic drugs was carried out in a series of 104 epileptic patients treated with phenytoin alone or combined with other drugs, and in 30 patients treated with other anticonvulsants. A slight decrease in hemoglobin values and a slight increase in mean corpuscular volume and mean corpuscular hemoglobin was observed in both groups. These changes are typical of the hyperchromatic megaloblastic anemias, although a statistically significant relationship between folates and hemoglobin could not be established. Moreover, we found leukopenia and lymphopenia in the group treated with hydantoins, and moderate eosinophilia in both groups. Changes in metabolism of vitamin B12 and folate were frequent, with decreased values in more than 30% of patients. A significant inverse correlation was observed between serum levels of folates and phenytoin, which suggests a direct toxic effect of the drug. No major dyscrasias were noticed.
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PMID:[Hematologic alterations and reduction in serum folate in epileptics treated with anticonvulsants]. 262 85

BB rats were found to have autoantibodies to gastric parietal cells, thyroid colloid antigens, smooth muscle, and thymocytes. No autoantibodies reactive with pancreatic islet cells (cytoplasmic), thyroid epithelial cells, adrenal cortex, testes, or anterior pituitary sections were identified. BB rats with gastric parietal autoantibodies had modest degrees of lymphocytic gastritis, but none developed iron or vitamin B12 deficiencies. These results suggest that BB rats have an underlying autoimmune diathesis. In addition, reports of peripheral T lymphopenia in such rats were confirmed, and markedly reduced helper T cell and cytotoxic-suppressor T cell subsets were demonstrated. Histological studies also revealed depletions of the T cell areas of spleen and lymph nodes. Furthermore, BB rats exhibited a profound inability to reject skin grafts across major and minor histocompatibility barriers. This was confirmed by mixed lymphocyte culture studies in vitro. BB-rat lymphocytes from either spleen or peripheral blood also showed profoundly reduced responses to T cell mitogens. Although BB-rat lymphocytes could produce normal levels of interleukin-2, they were unable to respond to this T cell growth factor. However, examination of thymuses from BB rats showed largely normal histologies, normal numbers of thymocyte subsets, and good mitogenic responses to con A. Thus, it appears that BB rats may have a thymic or post thymic defect in T lymphocyte maturation. The relevance of the immunologic lesion to the etiology of IDD in BB rats remains to be shown.
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PMID:Autoimmune diatheses and T lymphocyte immunoincompetences in BB rats. 634 99

Prognostication is one of the three cardinal clinical skills. Although it has been undervalued by modern medicine compared with diagnostics and therapeutics, poor prognostication can have dire consequences for the patient with advanced cancer, almost as serious as the wrong diagnosis or treatment. Oncologists relying on their subjective judgment for predicting survival often will be inaccurate, usually as too optimistic, which may result in overly aggressive cancer treatment. Actuarial judgment, based on assessment of statistically derived key factors, has the potential to improve prognostic accuracy. These factors in patients with advanced cancer differ from those in patients with newly diagnosed disease; they include performance status, symptoms of the cancer cachexia syndrome, and patient-rated quality of life, rather than tumor size, tumor grade, or extent of disease. Laboratory markers such as leukocytosis or lymphopenia also appear to be useful. Novel markers include acute phase reactants (C-reactive protein, vitamin B12) and cytokines that may provide more objective evidence of survival prospects. Prognostic indices, nomograms, and web-based tools are in development for the advanced cancer population. Identifying the clinical markers predicting for short-term survival in patients with advanced cancer is important to help form the basis for teaching prognostication skills to physicians.
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PMID:Clinical predictors of survival in advanced cancer. 1621 57

Vacuolar myelopathy (VM) in leukemia is rare. We report a boy with leukemia who developed isolated central nervous system (CNS) relapse during reinduction therapy. 5 months after cranial radiotherapy, he gradually developed quadriparesis. Magnetic resonance imaging revealed an intramedullary lesion which extended through the cervical spine. Serum vitamin B12, folic acid, cerebrospinal fluid methyl malonic acid were normal. Viral screening by ELISA was negative. He had lymphopenia, and reduced immunoglobulins, from a cardiac arrest. Biopsy revealed VM. He responded to weekly vitamin B12 treatment but on the 6th week of the therapy he died after developing periventricular, gliotic, hyperintense lesions in the brain.
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PMID:Progressive vacuolar myelopathy and leukoencephalopathy in childhood acute lymphoblastic leukemia and transient improvement with vitamin B12. 1639 85

The two-stage neuroinflammatory process, containment and progression, proposed to underlie neurodegeneration may predicate on systemic inflammation arising from the gastrointestinal tract. Helicobacter infection has been described as one switch in the pathogenic-circuitry of idiopathic parkinsonism (IP): eradication modifies disease progression and marked deterioration accompanies eradication-failure. Moreover, serum Helicobacter-antibody-profile predicts presence, severity and progression of IP. Slow gastrointestinal-transit precedes IP-diagnosis and becomes increasingly-apparent after, predisposing to small-intestinal bacterial-overgrowth (SIBO). Although IP is well-described as a systemic illness with a long prodrome, there has been no comprehensive overview of the blood profile. Here, it is examined in relation to Helicobacter status and lactulose-hydrogen-breath-testing for SIBO. A robust finding of reduced lymphocyte count in 126 IP-probands and 79 spouses (without clinically-definite IP), compared with that in 381 controls (p < 0.001 in each case), was not explained by Helicobacter-status or breath-hydrogen. This complements a previous report that spouses were 'down-the-pathway' to 'clinically-definite' disease. In 205 other controls without clinically-definite IP, there were strong associations between sporadic cardinal features and immunoglobulin class concentration, not explained by Helicobacter-status. Premonitory states for idiopathic parkinsonism associated with relative lymphopenia, higher serum immunoglobulin concentrations and evidence of enteric-nervous-system damage may prove viral in origin.Although only 8% of the above 79 spouses were urea-breath-test-positive for Helicobacter, all 8 spouses with clinically-definite IP were (p < 0.0001). Transmission of a 'primer' to a Helicobacter-colonised recipient might result in progression to the diagnostic threshold. Twenty-five percent of the 126 probands were seropositive for anti-nuclear autoantibody. In 20 probands, monitored before and serially after anti-Helicobacter therapy, seropositivity marked a severe hypokinetic response (p = 0.03). It may alert to continuing infection, even at low-density. Hyperhomocysteinemia is a risk factor for dementia and depression. Serum homocysteine exceeded the target in 43% of the 126 IP-probands. It was partially explained by serum B12 (12% variance, p < 0.001), but not by Helicobacter-status (gastric-atrophy uncommon in IP) or levodopa treatment. Immune-inflammatory activation increases homocysteine production. Since an estimated 60% of probands are hydrogen-breath-test positive, SIBO, with its increased bacterial utilisation of B12, is a likely cause. Thus, two prognostic indicators in established IP fit with involvement of Helicobacter and SIBO.
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PMID:Blood profile holds clues to role of infection in a premonitory state for idiopathic parkinsonism and of gastrointestinal infection in established disease. 1994 60