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 clinical and laboratory features of 18 adult pellagrins are reviewed. Only four patients (22%) had the full trial of dermatitis, diarrhea and dementia. Dermatitis alone occurred in six(33%), dementia in five(28%) and dermatitis and diarrhea in three(17%). In one patient, dermentia was the initial sign of a relapse. Steatorrhea was found in six patients and was usually associated with marked alopecia. Edema without evidence of cardiac failure was present in seven patients. A diffuse increase in slow wave activity on the electroencephalogram was characteristic in patients with dementia. Fever occurred in 14 patients, and an infection was documented in 10 of these. Common laboratory abnormalities included a normochromic, normocytic anemia, lymphopenia, eosinopenia hyperuricemia, and low serum levels of albumin, urea, cholesterol, carotene, potassium, calcium, and magnesium. Adrenal and thyroid function were normal, but a low serum T4, high serum free T4, and an elevated T3 resin uptake were frequently observed. These abnormalities were corrected with treatment of the underlying nutritional disorder. In two patients initially treated with thiamine alone, and in one who received inadequate amounts of niacin and protein, there was marked deterioration of mental function, which responded to administration of niacin and proper diet.
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PMID:Pellagra: an analysis of 18 patients and a review of the literature. 86 2

Tumor necrosis factor alpha (TNF) induces lymphopenia, neutropenia, and biphasic neutrophilia after intravenous injection of 3,000 U TNF in Lewis rats. The mechanism of TNF-induced lymphopenia was investigated by means of thoracic duct cannulation. Hourly measurements of lymphocyte recirculation via the thoracic duct failed to reveal any significant decrease in lymphocyte recirculation in TNF-treated vs. control rats, suggesting that a decrease in lymphocyte recirculation through the thoracic duct is not the mechanism for TNF-induced lymphopenia. The mechanism of TNF-induced neutropenia was investigated by administering TNF to rats in whom a neutrophilia had been induced with interleukin-1 (IL-1). In rats with neutrophilia, TNF resulted in a sharp decrease in the circulating neutrophil pool, demonstrating that TNF induces neutropenia by causing neutrophils to leave the circulating pool rather than decreasing neutrophil release from the marrow. The mechanism of neutropenia was furthermore shown to be due to the transient intravascular margination of neutrophils by administering epinephrine concomitantly with TNF. Epinephrine, which causes neutrophilia solely by demargination, abrogated the TNF-induced neutropenia and actually resulted in a neutrophilia that was greater than the neutrophilia occurring in epinephrine alone-treated rats, demonstrating both that TNF had already caused release of marrow neutrophils at the time of peripheral neutropenia, and that the paradoxical neutropenia was due to the transient intravascular margination of neutrophils. The known property of epinephrine to cause neutrophilia exclusively by demargination was proved by examination of the bone marrow of epinephrine-treated rats in whom no decrease in marrow neutrophils was observed (in contrast to TNF- and IL-1-treated rats in whom neutrophilia is accompanied by a depletion of marrow neutrophils). The mechanism of TNF-induced neutrophilia was investigated by modulating the magnitude of both the first and second peaks of neutrophilia by priming of rats with daily injections of IFN gamma for 2 days prior to administration of TNF. The first peak of neutrophilia in IFN gamma-primed TNF-treated rats was decreased in comparison to TNF alone-treated rats because of the well-known neutropenic and myelosuppressive effect of IFN gamma, which resulted in a decrease in the number of neutrophils that could be recruited to cause neutrophilia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mechanisms of tumor necrosis factor alpha-induced lymphopenia, neutropenia, and biphasic neutrophilia: a study of lymphocyte recirculation and hematologic interactions of TNF alpha with endogenous mediators of leukocyte trafficking. 249 93

Endotoxin reduces the release among other cytokines of tumor necrosis factor (TNF) and interleukin 1 (IL-1) and causes peripheral lymphopenia and a dose-response-dependent initial neutropenia followed by a monophasic neutrophilia. TNF alone induces lymphopenia and an initial neutropenia followed by a biphasic neutrophilia. IL-1 alone induces lymphopenia and a monophasic neutrophilia. TNF-plus-IL-1 caused a greater lymphopenia than either monokine alone, suggesting that both monokines contribute to LPS-induced lymphopenia. TNF-plus-IL-1 induced neutropenia similar in magnitude to that induced by TNF alone and induced a neutrophilia significantly greater than that induced by either monokine alone, suggesting that LPS-induced neutropenia is caused by TNF, while LPS-induced neutrophilia is due to the combined effects of TNF and II-1. TNF and IL-1 were administered together with LPS to simulate the in vivo condition of endogenous monokine release during gram-negative bacteremia. TNF combined with LPS increased both the duration and magnitude of LPS-induced lymphopenia, LPS-induced neutropenia, and LPS-induced neutrophilia. TNF-plus-LPS treated rats at 2 hours after injection exhibited a striking 93% decrease in bone marrow neutrophils even though no peripheral neutrophilia was yet apparent, suggesting that the subsequent neutrophilia was due to demargination and recirculation of neutrophils sequestered in the peripheral vasculature immediately after their release from the bone marrow. Epinephrine, which causes neutrophilia by demargination but not by release of marrow neutrophils, reversed the initial neutropenia in TNF-plus-LPS-treated rats and increased the neutrophilia. IL-1 combined with LPS increased LPS-induced neutrophilia, suggesting that endogenous IL-1 also contributed to LPS-induced neutrophilia. Corynebacterium parvum-primed rats with hyperplasia of the monocyte-macrophage system and treated with TNF differed from naive rats treated with TNF in that the second peak was as great as the initial peak of neutrophilia, supporting the hypothesis that the second peak of TNF-induced neutrophilia is due to the release of endogenous monokines. In conclusion, exogenous TNF, IL-1, and adrenal hormones affect circulating numbers of lymphocytes and neutrophils in a fashion consistent with their postulated endogenous role in the regulation of leukocyte trafficking during bacterial infection.
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PMID:Hematologic interactions of endotoxin, tumor necrosis factor alpha (TNF alpha), interleukin 1, and adrenal hormones and the hematologic effects of TNF alpha in Corynebacterium parvum-primed rats. 278 48

The effects of cortisol and adrenaline on natural killer (NK) cell activity and the distribution of circulating lymphocyte subpopulations were studied in twenty volunteers, using a continuous intravenous infusion pattern to simulate some of the hormonal changes induced by major surgery. The participants were allocated to receive either cortisol for 5 h, adrenaline for 1 h, cortisol for 5 h with simultaneous adrenaline during the last hour, or placebo for 5 h. Cortisol induced leucocytosis, neutrophilia, and lymphopenia with marked reduction in the number of T-lymphocyte subsets (OKT3+, OKT4+, and OKT8+ cells). No changes were induced in the activity or number of NK (Leu 11+) cells. Adrenaline produced an instantaneous increase in NK-cell activity accompanied by a selective increase in circulating NK cells. Significant leucocytosis, lymphocytosis and neutrophilia occurred. All measurements returned to preinfusion levels within 15 min after completing infusion. The effects of simultaneous infusion of cortisol and adrenaline were equal to the additive response to the hormones administered separately, except for the leucocytosis, which clearly exceeded this. In the placebo group all measurements remained unchanged. The results confirm the role of adrenaline as a potent stimulator/inducer of NK-cell activity. Adrenaline may be responsible for the increase in NK-cell activity during anaesthesia and major surgery.
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PMID:Natural killer cell activity during cortisol and adrenaline infusion in healthy volunteers. 312 49

Epinephrine (Epi) increases lymphocyte traffic to lung. We investigated whether Epi also modulates pulmonary cell-mediated immune responses in vivo. C57BL/6 mice were immunized with hen-egg lysozyme (HEL) on day 0, challenged with HEL intratracheally at day 12, and killed at day 15. Mice received Epi (0.5 mg/kg) subcutaneously during the sensitization phase, days 1-7 (Epi-SP), or the effector phase, days 12-14 (Epi-EP); controls received saline subcutaneously. Epi-SP mice showed increased airway inflammation (P < 0.03) and pulmonary angiitis (P < 0.04) characterized by endothelialitis and subendothelial fibrin deposition. Macrophages and granulocytes were increased in perivascular cuffs in situ (P < 0.001). CD3+ lymphocytes increased in the bronchoalveolar lavage fluid, whereas NK1.1+ and CD4+CD25+ lymphocytes decreased (all P < 0.05). Atenolol, a selective beta1-adrenoreceptor (AR) antagonist, inhibited the increased vascular and airway inflammation and the reduction in CD4+CD25+ lymphocytes (all P < 0.05) yielded by Epi, whereas all alpha/beta-AR blockers inhibited airway inflammation. We conclude that Epi-EP selectively promotes vascular inflammation in vivo via a beta1-receptor-mediated mechanism.
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PMID:Epinephrine promotes pulmonary angiitis: evidence for a beta1-adrenoreceptor-mediated mechanism. 1273 78