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

The Wiskott-Aldrich syndrome (WAS) is an inherited disease involving defects of platelets (small size, severe thrombocytopenia due to accelerated destruction) and T lymphocytes (progressive immunodeficiency, lymphopenia). The best-characterized molecular defect is the deficiency and, in some cases, abnormal forms of the T-lymphocyte surface mucin molecule CD43; deficiency of the platelet surface mucin GPIb was observed previously in two of four patients. Neither of these defects is primary, since CD43 and GPIb are encoded by autosomal genes and the disease is X-linked. This study uses cellular biological approaches to explore the possibility that destruction of structurally defective WAS platelets, mimicked experimentally by sonication of normal platelets, plays a role by releasing protease and generating other cellular defects. We show that a protease of normal platelets, identified as Ca(2+)-dependent neutral protease (calpain), which is known to cleave platelet GPIb, also specifically cleaves CD43 on the surface of neighboring desialylated T lymphocytes. The identification of the CD43 cleaving protease was based on its requirement for Ca2+ and inhibition by leupeptin, but not by diisopropylfluorophosphate (DFP). The approximate site of CD43 cleavage was identified by the use of a rabbit antibody. Sensitivity of GPIb to calpain is shown to be sialylation-independent and that of CD43 to be sialylation-dependent, and these findings are explained in terms of molecular structures. These and previous findings are incorporated into a putative mechanism, which explains most of the defects in the WAS. The mechanism suggests that the primary defective molecule in the WAS is unlikely to be a surface glycoprotein, but rather a cytoplasmic molecule with a function in cytoskeletal interactions and/or calcium ion regulation and calpain activation.
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PMID:Effect of platelet calpain on normal T-lymphocyte CD43: hypothesis of events in the Wiskott-Aldrich syndrome. 155 70

In case of immunization with adsorbed diphtheria-tetanus toxoid with reduced antigen content the treatment of children with calcium pantothenate in combination with chloropyramine proved to be most effective. This was confirmed by the absence of postvaccinal complications and by the most active restoration of the pool of active T cells as early as 2 months after immunization. After the preliminary treatment of children with allergic diseases with calcium pantothenate, glyceram, chloropyramine or their combinations the number of T lymphocytes decreased differently in children receiving different medicinal preparations. In 2 months after immunization the restoration of the pool of T cells was incomplete in children with allergic diseases and considerably more intensive in healthy children.
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PMID:[The clinical course of allergic diseases in children and the T-lymphocyte dynamics with adsorbed DT-m vaccination against a background of drug therapy]. 197 31

The output of lymphocytes, obtained on a ficoll-verografin gradient and intracellular free Ca2+ concentration were studied in the rat spleen 1, 3 and 6 days after X-ray irradiation in a dose of 0.5 Gy. The amount of lymphocytes decreased by 30% a day after irradiation and turned to the control level 3 days after exposure of animals. Free Ca2+ concentration remains abnormally high during all the examined period, increasing to 411 nM a day after irradiation and approaching to the control value 6 days after irradiation.
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PMID:[Increase in free Ca2+ level determined by quin-2 in spleen lymphocytes from irradiated rats]. 223 47

Withholding iron dextran treatment normally given to pigs at 1-3 days of age to prevent anemia resulted also in neutropenia. Polyinosinic acid:polycytidylic acid (poly I:C) at 0.5 mg/kg IV at 25 days of age resulted in induction of putative interferon 2 to 24 hours later, with significantly (P less than 0.05) lower concentrations in iron-deficient (Fe-) female pigs than in iron-supplemented (Fe+) female pigs. Poly I:C caused several transient toxic manifestations, including elevations in blood urea nitrogen, creatinine, aspartate aminotransferase, potassium (K), total bilirubin and phosphorus (P), marked leukopenia (both neutropenia and lymphopenia), and declines in serum albumin, calcium, cholesterol, glucose and globulin. Certain blood chemistries before poly I:C were significantly (P less than or equal to 0.05) different: albumin, globulin, cholesterol and K were higher in females than in males; albumin, globulin, glucose, P and K were higher in Fe- than in Fe+ pigs; and total carbon dioxide was higher in Fe+ than in Fe- pigs.
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PMID:Effects of poly I:C in porcine iron deficient neutropenia. 241 Jan 86

We compared the immunologic measurements from treatment of 12 healthy volunteers (six male, six female) with 800 and 1,600 mg cimetidine. In the first trial 800 mg cimetidine was administered daily to the volunteers over a period of 7 d; after an interruption of 2 months, 1,600 mg of cimetidine was applied daily for 21 d. The most striking result of our study was an increased mitogen-induced lymphocyte proliferation. This conclusion can be drawn from the fact that phytohaemagglutinin (PHA) (0.4 microgram/well) and pokeweed mitogen (PWM) (0.4 microgram/well) induced lymphocyte proliferation were found to be significantly increased in comparison to pretreatment values on day 7 in both cimetidine regimens (800 mg; PHA: mean proliferation 66,500 before treatment to 166,00 cpm, PWM: mean proliferation 8,800 before treatment to 34,000 cpm; 1,600 mg; PHA; mean proliferation 48,700 before treatment to 81,600 cpm; PWM: mean proliferation 6,300 before treatment to 16,200 cpm). Increased mitogen-induced proliferation following cimetidine intake is of special interest because the mechanisms of this activation process are incompletely known. Lymphocyte proliferation response is dependent on the availability of extracellular calcium. The function of the other bivalent cations is unknown. We found that the extent of mitogen-induced lymphocyte proliferation correlates with cellular intralymphocytic zinc and magnesium amounts (coefficients of correlation [r]) (800 mg: PHA/Mg r = 0.84; PHA/Zn r = 0.86; PWM/Mg r = 0.88; PWM/Zn r = 0.87). Though the application of both cimetidine doses causes enhanced mitogen-induced lymphocyte proliferation on day 7, T lymphocytes with different phenotypic properties appear to be influenced by cimetidine. In the first dose regimen (800 mg) the number of the CD8 lymphocytes decreased significantly from 16.1% (365 cell/microliters blood) to 12.7% (264 cells/microliters blood) after 7 d of cimetidine intake. After the period of high-dose (1,600 mg) cimetidine administration (at day 21) numbers of CD4 lymphocytes were significantly increased from 41.5% (860 cells/microliters blood) to 56.3% (1,210 cells/microliters blood). Our results show that although different cimetidine doses obviously influence different cell types of healthy volunteers, the cellular mechanisms are the same, namely, a proliferation and an increased incorporation of magnesium and zinc in lymphocytes.
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PMID:Cimetidine and the immuno-response in healthy volunteers. 257 37

We evaluated the role of gallium nitrate infusion in the treatment of metastatic breast cancer. Gallium nitrate was administered at 300 mg/m2/day for 7 days every 3 weeks by continuous infusion concomitantly with oral calcium supplement of 500 mg twice daily and oral hydration. Fifteen patients with refractory metastatic breast cancer received such treatment for a total of 30 courses. Median age was 51, and median performance status (Zubrod scale) was 1. These patients had minimal prior chemotherapy (median 1 regimen). All patients were evaluable for toxicity and 14 for response. Nine patients had one to two metastatic sites, five patients had three to four sites. No major objective response was seen, but one patient had a minor response (10 weeks), and another showed no change in disease (16 weeks). Diverse low-grade toxicities were observed, including nausea and vomiting in 11 patients, anorexia in 11, diarrhea in eight, stomatitis in five, dysgeusia in six, musculoskeletal pain in five, skin rash in seven, partially reversible tinnitus and/or mild hearing loss in four and sensory neuropathy in two. A consistent drop in hemoglobin (median of 3.2 g/dL per patient) necessitated blood transfusion in seven patients. There was no granulocytopenia or thrombocytopenia; however, significant lymphopenia was noted. Reversible, moderate nephrotoxicity occurred in two patients. The hypocalcemic effect was consistent, with a median drop in serum calcium of 1.25 mg/dL per course. There was no hepatic toxicity. While no single toxicity was severe, overall toxicity adversely influenced treatment tolerance. Gallium nitrate by continuous infusion, as given in this study, has no activity in metastatic breast cancer.
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PMID:Phase II evaluation of gallium nitrate by continuous infusion in breast cancer. 279 77

Intravenous potentiated anesthesia was made with six clinically normal boars of the White Bulgarian breed, weighing 50 kg, premedication of Atropini sulfas (50 gamma/kg M., s/c) and of a mixture of Droperidol (0.25 mg/kg M.) and Fentanyl (0.05 mg/kg M.) introduced via Sinus venosus ophthalmicus being administered 15 min. prior to 13 mg/kg M. of 5% water solution of thiopental-sodium injected in the same sinus. Prior to and following anesthesia at the 1st, 3rd, and 24th hour and on the 4th and 7th day the blood was checked with regard to hemoglobin, erythrocytes, erythrocyte sedimentation rate, hematocrit, leukocytes and leukocyte formula, total protein and protein fractions, calcium, phosphorus, magnesium, sodium, potassium, chlorides, total and direct bilirubin, and fibrinogen. Hemoglobin, erythrocytes, and hematocrit were found to drop insignificantly mathematically. The rate of increase of the sedimentation did not fully correspond to the drop of the erythrocyte count. The increase in leukocytes was accompanied by transient neutrophilia, eosinopenia, and lymphopenia in the early hours following anesthesia. The changes in the total protein and protein fractions, fibrinogen, total and direct bilirubin, and the other element indices referred to were shown to be close to the physiologic levels.
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PMID:[Hematologic and biochemical changes in the blood of boars undergoing potentiated anesthesia with droperidol, fentanyl and thiopental]. 378 57

Hematologic parameters change during the first 10 days of life. Erythrocytes increase in number but decrease in size and hemoglobin concentration. The PCV, hemoglobin, and platelet count also decrease. Total blood and plasma volume and, to lesser extent, erythrocyte volume decrease. Normal neonatal foals may have immature neutrophils (up to 5 per cent bands), and their early rapid rise in neutrophil numbers may be accompanied by a lymphopenia. Monocytes, eosinophils, and basophils are all absent or low initially. Infectious processes can cause rapid and variable changes in the leukogram. However, elevation of fibrinogen levels may lag behind the development of an inflammatory process, and this parameter should not be relied on for early evidence of infection. After 12 hours of life, there is generally a decrease in serum concentrations of Na, Cl, iron, creatinine, BUN, plasma protein, and possibly calcium. LDH, SAP, P, bilirubin, and glucose concentrations are all higher in foals than in mature horses. Creatinine may actually be elevated during the first 12 hours of life and then decreases. If azotemia, hypochloremia, hyponatremia, and hyperkalemia are found, ruptured bladder with uroperitoneum should be suspected. The creatinine concentration is preferable to BUN determination for diagnosis of this condition. Blood typing is useful for diagnosis of NI, determination of blood compatability between donor and transfusion recipient, and for verification of parentage for breed registries. Several techniques are available. Several tests are available for evaluation of the foal's immunoglobulin levels and confirmation of passive antibody transfer. Because foals suffering from FPT are more predisposed to infections, their immunoglobulin status should be determined as early as possible so that additional colostrum or plasma can be administered as needed. Neonatal isoerythrolysis is uncommon but is an important immunologic syndrome that often results in a fatal hemolytic crisis. If one suspects the condition may be likely, the optimal time for testing the mare is during the last 2 weeks of gestation. If the foal's dam is shown to have alloantibodies against a panel of known erythrocyte alloantigens, prevention is possible by feeding colostrum from another mare. If a foal develops NI, further colostrum ingestion from the dam must be prevented. Good nursing care, minimizing stress, and adequate frequent feedings are essential; prophylactic antibiotics should be used, and transfusion may be necessary.
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PMID:Hematology, blood typing, and immunology of the neonatal foal. 390 69

Zinc deficiency alters lymphocyte and monocyte function in man and animals. A patient with isolated zinc deficiency was found to have lymphopenia (420 lymphocytes/microliter), depressed T-cell mitogen response (48% of normal control), increased numbers of circulating T-suppressor cells (OKT8 reactive cells) and decreased circulating T-helper cells (OKT4 reactive cells). Activity of the patient's natural killer (NK) cells was 1 lytic unit/10(6) cells (normal 10 to 40), and monocyte cytotoxicity (MC) was four times that of normal controls. Zinc repletion in vivo improved the peripheral lymphocyte count, corrected the abnormal OKT8-to-OKT4 ratio, normalized T-cell response to mitogen, improved NK function, and lowered MC to control values. A divalent cation chelator, 1,10-orthophenanthroline (OP), was used to simulate zinc deficiency in vitro. T-cells exposed to OP are nonresponsive to mitogen unless zinc is added. NK function of lymphocytes from normal donors exposed to OP was depressed in a time- and dose-dependent manner. NK activity of peripheral blood lymphocytes (PBL) from 12 normal donors exposed to 50 microM OP for 16 hr was 10.3 +/- 7 lytic units/10(6) cells (mean +/- S.E.M.) vs. 32.6 +/- 14 for cells incubated in medium alone. When monocytes were exposed for 16 hr to 50 microM OP, however, MC significantly increased to a range two to five times that of control. OP-induced alterations of lymphocyte and monocyte function was reversed by the addition of 50 microM zinc but not calcium or magnesium. Since NK activity and MC are thought to be important in host tumor immunity, alterations in zinc metabolism may have important implications for human tumor immune surveillance mechanisms.
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PMID:Alterations in human natural killer cell activity and monocyte cytotoxicity induced by zinc deficiency. 660 71


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