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)

Generalized but well-circumscribed lymphadenopathy and rash-like skin changes were observed in three men, aged 58 to 75 years. There was a reticular appearance in the chest X-ray. Dyspnoea, weakness, marked weight loss, changing but marked lymphopenia, markedly increased blood-sedimentation rate, and an always negative Tine test were present in all three. Despite antibiotics, cytostatic drugs and prednisolone the disease quickly ended fatally with high fever, general debilitation and pneumonia. Post-mortem examination revealed diffuse lymphatic hyperplasia with plasma-cell infiltration in the lymph nodes, tonsils and lymphatic tissue of the intestines, and diffuse hyperplasia of the endothelial venules, together with basophilic blast cells, eosimophilic granulocytes and reticulum cells with broad nucleoli. The spleen was normal or enlarged. Spleen, lung tissue and lymphatics, the skin in the area of the small vessels, hair follicles and sweat glands contained lymphocytes, plasma cells and eosinophilic leucocytes. The spleen, if enlarged, also had focal necroses in its periarteriolar septa. In two cases electrophoresis revealed beta-globulin poorly demarkated from gamma-globulin, doubling and increase. In the third case, IgA was markedly increased with one each monoclonal IgG1 und IgA, and corresponding shift in the chi/lambda relationship in serum. Immunohistologically, lymphocytes were made up of about 20 percent IgG-containing and about 25 percent IgA-containing cells. Lymphopenia, if present, was associated with markedly reduced blast transformation of peripheral lymphocytes to phytohaemagglutinin. The granulocytes were defective (intracellular killing of Candida albicans and Staphylococcus aureus), while the nitrobluetetrazolium test was normal. There was RBC phagocytosis in the macrophages of bone marrow and in Kupffer cells of all three cases.
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PMID:[Rapidly debilitating disease with generalized lymphadenopathy, skin involvement and interstitial pulmonary infiltration (report of three cases)]. 23 37

The effects of the intravenous administration of triazinate by single and multiple injections were studied in beagle dogs and rhesus monkeys. In dogs, dose levels ranging from 0.3125 to 40 mg/kg were given either as single doses daily for 5 days, or once weekly for 6 weeks. The 5-day regimen was also studied in monkeys with dose levels from 2.5 to 40 mg/kg/day. Prominent drug-related and drug-dependent effects which appeared in both species were piloerection, muscular weakness, and respiratory difficulty which occurred during and immediately after the administration of dose levels of 10 mg/kg or greater. Gastrointestinal toxicity was severe in dogs but mild in monkeys. Lymphoid tissue toxicity was manifested by a circulating lymphopenia and localized cellular depletion in the germinal centers of lymphoid tissues. In dogs, signs of bone marrow toxicity consisted of a circulating neutropenia and, at necropsy, a reduction in the number of erythroid and myeloid elements plus megaloblastosis. Only the latter change was observed in monkeys. This difference in the hematopoietic toxicity between the beagle dog and the rhesus monkey was corroborated by the findings from in vitro studies with bone marrow. DNA synthesis in beagle bone marrow cells was depressed significantly by triazinate as compared with cells from rhesus marrow. A direct renal toxic effect was observed in monkeys given high doses of triazinate (20 and 40 mg/kg/day or 240-280 mg/m/day) for 5 days.
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PMID:Preclinical studies with triazinate (NSC-139105), an antifolate drug, in beagle dogs and rhesus monkeys. 81 4

The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.
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PMID:Skeletal muscle toxoplasmosis in patients with acquired immunodeficiency syndrome: a clinical and pathological study. 145 37

A porcine strain of Pasteurella multocida (serotype D:3) produced a toxin causing turbinate atrophy (TA) in pigs. The toxin (TAT), processed on a high performance liquid chromatography size exclusion column, eluted as a single peak (molecular weight of about 160,000) containing trace amounts of endotoxin (lipopolysaccharide, LPS; protein:LPS, 85:1). The eluted fraction migrated on sodium dodecyl sulfate polyacrylamide gels as a single band. It could be prevented from dissociating into two prominent polypeptides by addition of a protease inhibitor. A single dose (2.0 to 79.0 micrograms/kg) of TAT given to pigs intravenously was lethal. Doses from 0.02 to 1.0 microgram/kg caused transient clinical signs of porcine systemic toxicosis with reduced appetite, generalized weakness, depression, lethargy, weight loss, and in some instances, death. Intradermal doses of TAT (greater than or equal to 0.1 microgram/site) produced hemorrhagic areas within four hours. Systemically, TAT causes bilateral TA, lymphopenia, liver dysfunctions, and possible renal impairment. Affinity of TAT for cells of epithelial origin was demonstrated in mice given 125I-TAT. In vitro, TAT stimulated DNA and protein syntheses of peripheral blood lymphocytes and suppressed syntheses in turbinate and kidney cell cultures without being cytolytic. Biological effects of TAT were eliminated by exposure to either heat, trypsin or anti-TAT antibody.
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PMID:Host response to Pasteurella multocida turbinate atrophy toxin in swine. 230 67

Despite the recognition of Mycobacterium avium complex (MAC) infection as a common complication of AIDS, the specific clinical features, significance, and need for treatment have been difficult to assess. We reviewed the clinical records and autopsy material of 68 patients dying with AIDS, 32 (47 percent) of whom had MAC isolated from autopsy tissue. All had postmortem evidence of systemic infection. Eleven (34 percent) had MAC isolated from lung tissue. Little, if any, local tissue inflammation and destruction were associated with MAC infection. Patients with autopsy evidence of MAC infection had a longer time interval from diagnosis of AIDS to death. The infection was detected antemortem in 14 (44 percent), blood culture being the most sensitive means (86 percent yield). Although recurrent fever was noted among both MAC infected and uninfected patients, weight loss greater than 20 lb, weakness, anorexia, abdominal pain, and diarrhea were more frequent among infected patients. Severe anemia, thrombocytopenia, lymphopenia, and reduced mean CD-4 percentages and CD-4/CD-8 ratios were associated with MAC infection. Of eight patients who had MAC cultured antemortem and received multidrug antituberculosis therapy, none responded clinically, and all but one had MAC isolated at autopsy. Because MAC is associated with significant discomfort and disability, development of more effective treatment regimens could be beneficial for some affected AIDS patients.
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PMID:Mycobacterium avium complex infection in patients with the acquired immunodeficiency syndrome. A clinicopathologic study. 335 47

Of cases of hyperadrenocorticism in small animals 80-85% are the result of adrenocortical hyperplasia. Middle-aged or older Poodles, Dachshunds, Boston Terriers and Boxers are most commonly affected, and cats rarely. Clinical signs include polydipsia, polyuria, alopecia, abdominal distension, lethargy, weakness, hepatomegaly, calcinosis cutis, testicular atrophy and anestrus. Hematologic and biochemical changes may include neutrophilia, lymphopenia, monocytosis, eosinopenia, increased blood levels of alkaline phosphatase, SGPT, cholesterol, Na and glucose, and decreased K and T4 levels. The high-dosage dexamethasone suppression test helps differentiate pituitary-dependent hyperadrenocorticism from that caused by adrenal tumors. The low-dosage dexamethasone suppression test, determination of plasma ACTH levels, and ACTH response test are additional diagnostic aids in the diagnosis of Cushing's disease. Medical treatment involves oral use of mitotane (o,p'-DDD) at 50 mg/kg/day for 7 days and prednisone or prednisolone at 0.05 mg/kg/day. Hypophysectomy has been used with only 5% mortality in cases of pituitary-dependent hyperadrenocorticism. Adrenalectomy is indicated in cases of adrenal neoplasia.
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PMID:Diseases of the adrenal cortex of dogs and cats. 633 May 21

Nemaline-rod myopathy was recently reported in eight young males infected with human immune deficiency virus type 1 (HIV-1). A 41-year-old woman had a 2-year history of progressive proximal-muscle weakness. Muscle biopsy demonstrated the presence of nemaline rods, predominantly in type 1 fibers. She was coinfected with HIV-1 and HTLV-2, as evidenced by positive polymerase chain reaction and serology. There was no lymphopenia or CD4 lymphopenia, despite an abnormal T-cell subset ratio, high CD8 count, skin anergy, and depressed in vitro response to mitogens. This case raises the possibility that dual infection may play a role in the pathogenesis of the rare nemaline-rod myopathies of HIV-infected patients.
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PMID:Progressive nemaline rod myopathy in a woman coinfected with HIV-1 and HTLV-2. 834 53

A 22-year-old male with juvenile dermatomyositis presented with fever up to 40 degrees C and acute pain in his right thigh accompanied by muscle weakness, a skin rash and a tender swelling. Serum aspartate aminotransferase (AST) and aldolase were mildly elevated. C-reactive protein (CRP) and fibrinogen were markedly increased. The differential white blood cell count revealed relative lymphopenia. Radiography showed diffuse calcifications particularly around the thighs and knees of both legs. Magnetic resonance imaging (MRI) demonstrated inflammatory infiltrates in the right thigh. The lesions were identified as phlegmone by immunoszintigraphy with 99mTc-labelled antigranulocyte antibodies. On the 10th day of treatment Staphylococcus aureus was cultured from blood. Patients with juvenile dermatomyositis and calcinosis may develop bacterial infections of soft tissue which sometimes mimic a disease flare. For differential diagnosis plain radiographs, CT scans and MRI are of limited value. Immunoszintigraphy is able to differentiate between infiltrates caused by granulocytes and lymphocytes.
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PMID:[Juvenile dermatomyositis--acute recidivism or sepsis?]. 1041

Preparturient hypocalcemia was identified in 4 cats in a specific pathogen-free colony between 1995 and 1996. All cats had an acute onset of clinical signs, 3 to 17 days prior to parturition. Signs of depression, weakness, tachypnea, and mild muscle tremors were the most common clinical signs, following by vomiting and anorexia. Additional abnormalities included hypothermia, third eyelid prolapse, dehydration, pallor, lethargy, flaccid paralysis, and hyperexcitability. Hematologic abnormalities included leukocytosis with neutrophilia and lymphopenia. Hypocalcemia was documented in each queen. Common serum biochemical abnormalities included high aspartate aminotransferase and creatine kinase activities. All cats responded to IV or SC administration of 10% calcium gluconate. Queens were then given calcium orally prior to and following parturition. The queens did not have additional complications for the duration of the gestational or lactational periods.
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PMID:Preparturient hypocalcemia in four cats. 1053 Mar 27

The aim of this study was to characterize the metabolic disturbance associated with the skeletal myopathy resulting from extreme weight loss in anorexia nervosa. Muscle function was examined in eight female patients with severe (40%) weight loss due to anorexia nervosa and histologically confirmed myopathy. A wide range of biochemical and hematologic investigations were carried out, including serum enzymes and the response of plasma lactate to ischemic exercise of forearm muscles. All patients showed proximal muscular weakness. A diminished lactate response to ischemic exercise was a consistent finding, and a reduction of serum carnosinase activity was also found. There were no other consistent biochemical or hematologic abnormalities apart from lymphopenia of no clinical consequence. These findings contribute to our understanding of severe protein-energy malnutrition on the musculoskeletal system. The resulting disorder is a metabolic myopathy from which the patients recover rapidly as their nutrition improves. Although the patients admitted to a variety of abnormal eating behaviors, no correlation was found between a specific type of abnormal eating behavior and subsequent biochemical abnormalities. Reinstating appropriate eating behavior will treat the myopathy.
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PMID:Metabolic abnormalities associated with skeletal myopathy in severe anorexia nervosa. 1070 74


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