Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of a low protein (6%) diet on the immunologic function of NZB mice was investigated. The low protein intake was associated with decreased weight gain in both male and female NZB mice. The mice fed the low protein diet did not develop splenomegaly, which generally occurs by 7 to 10 months of age in NZB mice fed a normal amount of protein. Further, 7- to 10-month-old NZB mice fed the low protein(6%) diet, maintained: 1) more vigorous antibody production to sheep red blood cells; 2) greater capacity to produce graft-vs-host reactions, and 3) more vigorous cell-mediated "killer" cell immunity after immunization against DBA/2 mastocytoma cells than did NZB mice on a normal (22%) protein diet. The decrease of PHA and Con A response which normally occurs with aging in NZB mice was abrogated to some degree by protein restriction. However, response to LPS, which also declines with age in NZB mice, did not appear to be influenced by diet.
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PMID:Influence of protein restriction on immune functions in NZB mice. 0 5

Corynebacterium parvum was administered to sixteen patients with malignant tumors submitted to repeated chemotherapy courses. A total of 428 injections of C. parvum at a dose of 3.5 mg/m2 in weekly, biweekly and monthly administration was given between the chemotherapy courses. Injection of C. parvum was followed by fever and local pain in 15/16 patients. Three patients presented a local ulceration during the initial period of weekly injections. Splenomegaly was observed after the second month of treatment, peripheral and bone-marrow monocytic infiltration after the second month. The decreased lymphocyte stimulation by PHA observed during the first two months was followed by an increased response. Cutaneous reactions to three antigens increased progressively in most patients and negative pre-treatment tests became positive after treatment.
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PMID:Clinical trial with Corynebacterium parvum. 34 3

Enzymaticaly homogeneous fractions of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from peripheral blood of a patient with hairy cell leukemia, or leukemic reticuloendotheliosis, LRE,(with leukopenia, neutropenia, lymphocytosis, and massive splenomegaly). To detect enzymatic deficiencies, the cells were analyzed quantitatively for six leukocytic enzymes on three occasions: 1) before splenectomy, 2) 5 days after splenectomy, and 3) 6 weeks after splenectomy. Before splenectomy, the patient's cells showed moderate deficiency of beta-glucuronidase in lymphocytes and monocytes; server to modorate deficiency of lysozyme and myeloperoxidase in monocytes and granulocytes; and complete absence of neutral protease and alkaline phosphates in neutrophils. Full restoration of neutral protease and a three-fold rise in alkaline phosphatase activities occurred in the patient's neutrophils 5 days after splenectomy. Lysozyme and myeloperoxidase returned to normal in both monocytes and neutrophils of the patient. Six weeks following splenectomy, the alkaline phosphatase activity again disappeared from patient's neutrophils, although neutral protease remained normal. The patient's lymphocytes were unresponsive to PHA and PW mitogen before splenectomy but became responsive 6 weeks postoperatively. Monocytic transfomation into macrophges was supressed before and after splenectomy. The findings indicate that developmenally, in lymphocytic leukemia, a biochemical defect involves the patient's monocytes and neutrophils much more severely than it affects the leukemic lymphocytes. Functionally, the results partly explain the susceptibility of LRE patients to microbial infections.
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PMID:Absence of neutral protease and alkaline phosphatase in neutrophils of a case of hairy cell leukemia. 43 13

Twenty-two patients with lymphocytosis and sometimes accompanied by splenomegaly selected from our difficult diagnostic cases over the past two years are presented. The clinical and laboratory features pointed to one of the following: chronic lymphatic leukaemia without lymphadenopathy, lymphosarcoma or other lymphoreticular tumour, tropical splenomegaly syndrome with a lymphatic leukaemoid reaction. The precise diagnosis was usually made by haemotological laboratory tests - viz. (a) Lymphocytes transformation test (LTT) (b) Serum/Plasma IgM estimation. It was found that: (1) There was markedly raised IgM in the responders i.e. patients with Tropical Splenomegaly Syndrome (TSS) whose spleens regressed following treatment with antimalarials, contrasting the normal levels of IgM in the non-responders to antimalarial therapy. (2) The PHA - Lymphocytes Transformation in the TSS was normal while that of Chronic Lymphatic Leukaemia (CLL) was abnormally low. These combined tests (LTT & IgM) are recommended as investigations for leukaemoid reactions involving lymphocytes.
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PMID:The use of lymphocyte transformation and IgM estimation as diagnostic aids in leukaemoid reactions. 52 52

The spleen cell population of C3H/He mice injected with a single sublethal dose of cyclophosphamide (CY) was analysed. An initial atrophy was followed by a considerable hypertrophy and a progressive return to normal. During the phase of spleen atrophy, both B and T cell compartments were depleted. During regeneration, the percentage of Ig+ cells increased rapidly, and at the peak of splenomegaly, the percentage of Ig+ cells was high while no Thy1-2+ cells were detectable. The peculiar points of histology were disappearance of normal T and B compartments, substituted by a layer of lymphoid cells. During the phase of splenectomegaly, the in vitro reactivity of spleen cells to the mitogens PHA and LPS was drastically decreased. Furthermore, the spleen cell population from CY treated mice contained suppressor cells, capable of inhibiting the in vitro reactivity of normal lymphocytes to these mitogens and the multiplication of tumour cells in culture. These cells were adherent, Ig+, Thy1-2- cells. They developed in CY treated T deprived mice. After velocity sedimentation the suppressive activity was detected in the 6 mm/h fraction.
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PMID:[Suppressive cells induced by cyclophosphamide in the spleen of C3H mice]. 84 86

The cellular and humoral immune responses of patients with S. mansoni infection were evaluated before and one month after each of two intramuscular doses of diphtheria/tetanus toxoid vaccine. Patients were divided into "responder" and "non-responder" groups based on anti-tetanus toxoid (anti-TT) IgG levels after vaccination. The specific anti-TT IgG1 response of the responder group was predominantly in the IgG, subclass. The lymphoproliferative response to PHA was also significantly higher in the responder group; this elevation was detectable before and after each vaccination. The responses to PWM and SPL were comparable in the two groups before vaccination, although the responder group had a higher response to SPL after vaccination. IgG antibodies for schistosome adult worm and egg antigens were significantly lower in the responder group prior to vaccination but not thereafter. Anti-diphtheria IgG antibodies were comparable in the two groups after vaccination at all times. Clinically, the non-responder patients had a higher incidence of splenomegaly (84.6% vs 44.8%) and were significantly older than the responder patients (mean 34.1 yrs vs 18.7 yrs). The cause for the reduced anti-tetanus IgG response in schistosomiasis patients is believed to be multifactorial. T cell or antigen presenting cell dysfunction, high levels of IgG antibodies specific for schistosome antigens, splenomegaly and age are factors that might lead to reduced anti-TT IgG response.
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PMID:Immunological response to diphtheria/tetanus vaccine in Schistosomiasis mansoni patients. 143 Dec 94

(B10.A x A/WySn)F1 mice, infected with the Friend virus (FV) complex, were used as a predictive therapeutic model for AIDS. These infected mice exhibit many of the viral and immunologic manifestations of AIDS. Bropirimine (2-amino-5-bromo-6-phenyl-4[3H]pyrimidinone, ABPP) is an immunomodulating compound which has been shown to inhibit other viral infections. Oral (per os treatment) dosages of ABPP ranging from 50 to 400 mg/kg/day for 3 days resulted in increased numbers of infectious centers in the infected mice and increased splenomegaly and percentage of Ig+ (B cells) in spleens of infected and uninfected mice. Decreased percentages of total Thy-1.2+ (total T) cells and L3T4+ (T-helper) cells were seen in both uninfected and infected mice and a slightly decreased percentage of Ly-2+ (T-suppressor/cytotoxic) cells was observed in spleens of the infected mice. No effect on Ly2+ cells in spleens of uninfected mice was found. Intraperitoneal injection, single or multiple, of 20-200 mg/kg ABPP prior to FV injection resulted in increased spleen weights but had no effect on numbers of infectious centers in the spleens or on FV antibody titers in the plasma. Intraperitoneal treatment of uninfected mice with ABPP resulted in slight or no changes in percentages of Thy-1.2+, L3T4+ and Ly-2+ cells. Mice receiving multiple exposures of ABPP had an increase in percentage of splenic B cells and a depressed response to the T cell mitogen PHA. Treatment with ABPP induced the production of interferon (IFN); however, a state of hyporesponsive IFN production was seen following multiple administrations of ABPP. These data suggest that the immunomodulator ABPP may have an enhancing effect on this retroviral disease.
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PMID:Murine retroviral disease-enhancing effects of a pyrimidinone immunomodulator. 144 28

We studied the effect of depleting NK1.1+ cells from an allograft of lymph node and spleen cells on the outcome of GVH disease in the parent----F1-hybrid combination C57BL/6----(C57BL/6xDBA/2)F1. Four treatment groups were established: group I mice were transplanted with an unmodified graft from normal donors; group II mice were transplanted with an NK1.1-depleted graft that had been harvested from normal donors; group III mice received grafts from donors that had been injected with Poly I:C (100 micrograms i.p.) 18 hr prior to harvesting (These grafts were incubated with complement, but no antibody.); group IV mice were transplanted with depleted grafts harvested from donors that had received Poly I:C. Recipients in each group were monitored for splenomegaly, mitogen responsiveness, NK and CTL activity, histopathology, weight loss, and mortality. Results showed that recipients in all four groups developed splenomegaly and unresponsiveness to LPS, PHA, and Con A by day 12. Augmented host-derived NK activity and graft-derived antihost CTL activity was also demonstrated. Group IV showed little or no weight loss, minimal histopathological changes and a marked reduction in mortality. Recipients in all other groups developed features characteristic of GVH disease and exhibited a steady decline in body weight beginning by day 12. Mortality generally began on day 18 and reached 75-90% by day 60. We postulate that anti-NK1.1 depletes cells from the graft are intimately connected with the effector mechanism in acute GVH disease.
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PMID:Prevention of acute lethal graft-versus-host disease in F1 hybrid mice by pretreatment of the graft with anti-NK-1.1 and complement. 163 23

A 1-month-old girl was admitted because of staphylococcal cellulitis of the buttock and the shoulder, and peripheral agranulocytosis. CBC on admission showed 10,100/microliters of WBC with 1% mature neutrophils, 5% monocytes, 6% eosinophils, 2% basophils and 86% lymphocytes. Bone marrow aspiration revealed maturation arrest of neutrophil precursors at the level of myelocyte. We treated the patient with subcutaneous rhG-CSF (Kirin-Amgen, Tokyo) for sequential 7-day course at the starting dose of 3 micrograms/kg, and increased weekly. The dose was escalated at the level of 18 micrograms/kg for 2 weeks subcutaneously, 8 days after effective dose of 18 micrograms/kg, the absolute neutrophil counts more than 1,000/microliters was attained, and bone marrow aspiration showed an increase of neutrophil precursors beyond the myelocyte level with maturation. Our case proved that both WBC and absolute neutrophil counts were increased parallel with the dose escalation of rhG-CSF. Shortly after the cessation of rhG-CSF, WBC and absolute neutrophil counts were decreased. No side effect was detected except for mild splenomegaly which was resolved after cessation of rhG-CSF. In methylcellulose culture with PHA-LCM, marrow cell of patient produced normal number of CFU-GM, and myeloid precursors could proliferate and differentiate to normal polymorphonuclear neutrophils, but rhG-CSF produced only small number of CFU-GM. Our case confirms that rhG-CSF is a new approach to control the life-threatening infection of congenital agranulocytosis.
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PMID:[A successful case of congenital agranulocytosis treated with recombinant human granulocyte colony-stimulating factor]. 170 2

The present paper describes the clinical and laboratory follow-up of 11 patients with the diagnosis of common variable immunodeficiency. Their age varied from 8 to 45 years. The mean disease time was 12.6 years and mean diagnosis time 4.3 years. Infectious manifestations, mainly of the respiratory and digestive tracts, occurred in all patients. Polyadenomegaly was noted in seven, hepatomegaly in six, splenomegaly in five and arthralgia in four patients. All of them presented serum IgG less than 250 mg/dl. IgA less than 33 mg/dl and IgM less than 31 mg/dl, except one with IgM = 176 mg/dl. The isohaemagglutinin titers were less than 1/20 in all but one patient. The determination of the number of B lymphocytes in the peripheral blood revealed normal counts in three, elevated in one and decreased in five patients. The CD-4/CD-8 ratio was less than 1 in 8 and greater than 1 in three of them. Five patients had positive cutaneous late reactions to at least one of the following antigens: PPD, SK-SD (Varidase), Trichophytin and Levedurin (Candidin). A decrease of the proliferative activity of peripheral blood mononuclear cells stimulated by lectins (PHA, Con-A, PWM) was also noted. Natural killer function was decreased. The association a possible role of regulatory lymphocytes in the immunopathogenesis of this disease. The data presented here emphasize the diversity of clinical and immunological manifestations of this disease, which could be noted between diverse patients and in the follow-up of a single one. In our cases the disease had an evolutive character, with a primarily humoral dysfunction followed by cellular immunity disturbances that determined poorer prognosis and progressive difficulties in the therapeutics. We suggest a conceptual reevaluation of this condition and a new denomination, for instance "Late-Onset Combined Immunodeficiency". The long delay between the initial clinical manifestations of the disease and its diagnosis was a handicap for an adequate treatment. Early intervention could certainly decrease the morbidity and mortality of the disease.
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PMID:[Common variable immunodeficiency (hypogammaglobulinemia of late onset or acquired hypogammaglobulinemia): initial follow-up of 11 cases]. 172 73


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