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Biomedical subjects

J I Allen

Publications and source records attributed to J I Allen.

30 records · Page 2Linked to original sources
PubMed1985

Association between urinary zinc excretion and lymphocyte dysfunction in patients with lung cancer.

Patients with bronchogenic carcinoma often have low serum zinc concentrations and sometimes have markedly elevated renal zinc losses. Since normal zinc metabolism is critical for the proper function of T lymphocytes and natural killer cells, the effect of zinc status on T cell phytohemagglutinin response and peripheral blood lymphocyte natural killer cell activity was studied in patients with lung cancer. Mean (+/- SEM) serum zinc concentration in 75 patients with cancer was 67.4 +/- 2.2 micrograms/dl versus 96.0 +/- 8.0 micrograms/dl for normal subjects. Patients with low serum zinc levels (less than 70 micrograms/dl) had significantly higher urine zinc excretion than patients with normal serum zinc levels (1,385 +/- 240 micrograms per 24 hours versus 392 +/- 107 micrograms per 24 hours) (p less than 0.001). This pattern of zinc concentrations (i.e., low serum zinc in combination with high urine zinc) is typical of patients with mild zinc deficiency, and suggests that a mild chronic zinc deficiency state was present in some of these patients. When lymphocyte data were analyzed according to serum zinc concentrations and urinary zinc excretion, low serum zinc concentration and high urine zinc excretion both correlated with depressed T cell phytohemagglutinin response (p less than 0.005 and p less than 0.001, respectively). For instance, mean maximal phytohemagglutinin response in patients with urinary zinc excretion of more than 700 micrograms per 24 hours was 22,132 +/- 3,201 cpm (n = 14) compared with 68,130 +/- 6,850 cpm for patients with normal zinc excretion (n = 7). Peripheral blood lymphocyte natural killer cell activity did not correlate with either serum or urine zinc values. Oral zinc sulfate (220 mg, three times daily for six weeks) was then administered to patients with hyperzincuria (mean = 992 micrograms per 24 hours). Zinc-supplemented patients had normalization of T cell phytohemagglutinin response after zinc therapy, whereas control patients demonstrated continued T cell dysfunction. Natural killer cell activity did not change in either group during the study period. These data suggest that a mild subclinical zinc deficiency state may exist in some patients with lung cancer and may be an important cause of abnormal T cell function. Furthermore, zinc supplementation may be useful to improve lymphocyte function in selected patients. Whether zinc supplementation would alter the course of the disease or the patient's prognosis is presently unknown.

Adenocarcinoma↗
PubMed1984

Peritoneovenous shunt therapy for leaking ascites in the cirrhotic patient.

Review of clinical and operative records of 86 patients at the Minneapolis VA Medical Center and Mount Sinai Hospital undergoing peritoneovenous (PV) shunt for intractable ascites revealed a subgroup of patients (n = 9) who developed leaking ascites prior to shunting. The etiology of leaking ascites was as follows: 1) ruptured umbilical hernia ( UH ) (four patients), 2) repeated paracentesis (three patients), and 3) postoperative incisional ascitic fluid leak (two patients). Initial therapy included local sterile compression dressing, intravenous antibiotics, and management of fluid and electrolytes. All nine patients underwent subsequent closure of the fascial defect and PV shunt to prevent reaccumulation of ascites (simultaneous procedures were performed in five patients). No patient developed postoperative septic complications, organ failure, gastrointestinal bleeding, or encephalopathy. There were no early deaths; however, three late deaths (18 months, 2, and 4 years) were due to variceal bleeding and/or liver failure. Ascites was well controlled in seven patients with PV shunt alone, the other two ultimately responding to medical therapy. We conclude that peritoneal fluid leaks can be treated successfully by repairing the fascial defect and placing a PV shunt. In the absence of infected ascites and clinical peritonitis, PV shunt may be performed simultaneously with closure of UH , thus preventing the reaccumulation of ascites during the immediate postoperative period.

Aged↗
PubMed1983

Alterations in human natural killer cell activity and monocyte cytotoxicity induced by zinc deficiency.

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.

Chlorides↗
PubMed1982

Scurvy: bilateral lower extremity ecchymoses and paraparesis.

A 46-year-old man presented with two weeks of progressive paraparesis and large confluent ecchymoses of both thighs. There was a history of poor dietary intake and daily alcohol use. He had had similar problems each of the past two winters. In 1979 he required hospitalization for "sciatica." In 1980 he was bedridden for two months because of lower extremity weakness. Examination revealed poorly fitting dentures, large confluent ecchymoses of both thighs, perifollicular hemorrhages, and a low serum ascorbic acid concentration. Oral ascorbic acid was begun in the hospital and all clinical symptomatic consequences of scurvy rapidly resolved. We present this case to reiterate the clinical presentation of scurvy and to emphasize the importance of recognizing early signs of nutritional deficiencies that may be confused with more common, but often less treatable, diseases.

Ascorbic Acid↗
PubMed1982

Zinc and T-lymphocyte function in hemodialysis patients.

Thirteen patients maintained on long-term hemodialysis were studied with respect to their serum zinc concentration and T-lymphocyte response to phytohemagglutinin. Six patients demonstrated depression of T-cell mitogen response, while seven patients demonstrated a normal response. The mean serum zinc concentration of the patients with abnormal response was lower than those patients with a normal response (63 +/- 11 versus 75 +/- 14 microgram/di, respectively). There was no significant correlation between an individual's serum zinc concentration and T-cell response (r = 0.16). Five patients whose T-cell responses were depressed were given intravenous zinc chloride during each dialysis run for 6 wk (10 mg intravenous zinc, three times weekly) and were evaluated before and after therapy. All five patients remained anergic to four skin tests antigens. Only one patient (who had the lowest pretreatment serum zinc concentration at 48 micrograms/dl) demonstrated significant improvement in mitogen response after zinc therapy. Although dialysis patients commonly have low serum zinc concentrations and depressed mitogen response, in our patients these two findings were generally unrelated. Additionally, supplemental zinc did not change base-line measurements of T-lymphocyte mitogen response in four of five patients studied.

Chlorides↗
PubMed1981

Cytomegalic inclusion disease diagnosed endoscopically.

Two patients who received renal transplants developed erosions or ulcers in the upper gastrointestinal tract. In both cases endoscopic evaluation enabled a diagnosis of cytomegalovirus (CMV) infection to be made quickly and safely. We emphasize the importance of early diagnosis of CMV infection and how endoscopy may be helpful.

Adult↗
PubMed1981

Severe zinc deficiency in humans: association with a reversible T-lymphocyte dysfunction.

Two patients developed severe zinc deficiency with acrodermatitis during parenteral hyperalimentation. The response of circulating T-lymphocytes to phytohemagglutinin was assessed both during the episode of clinical zinc deficiency and after intravenous zinc supplementation as the sole means of nutritional intervention. Maximum T-cell response to phytohemagglutinin, expressed as percent of simultaneous normal control response, was 2.1% and 27.9% in Patients 1 and 2 respectively. After 20 days of intravenous zinc supplementation (12 mg/d), repeat studies showed the T-cell response of Patient 1 to be 221% of the control, and that of Patient 2 to be 139% of control. In addition, Patient 1 was anergic during the period of zinc deficiency and normally reactive after zinc supplementation. These findings agree with extensive animal studies showing the detrimental effect of zinc deficiency on cellular immunity.

Acrodermatitis↗
PubMedDate not supplied

Molecular biology of colon polyps and colon cancer.

From a histologic and endoscopic standpoint, colon and rectal cancer (CRC) begins as a small neoplastic polyp which progressively enlarges and transforms through a dysplasia stage into invasive cancer. Recently, molecular abnormalities underlying the adenomacarcinoma progression have been defined. The adenomatous polyposis coli (APC) gene and mismatch repair genes are found to be dysfunctional early in the neoplastic process; either as inherited or somatic mutations. Subsequently, polyps progress to cancer along one of two paths depending on which gene is abnormal. When the APC gene is the initial mutation tumor development follows the "loss of heterozygocity" (LOH) pathway. If mismatch repair genes are altered, the "replication error" (RER) pathway is followed. Somatic mutations of the K-ras oncogene and the MCC, DCC, and p53 tumor suppressor genes accumulate in the LOH pathway and mark the progression through polyp stages. Microsatellite instability is a characteristic of the RER pathway but the precise genes involved in this pathway currently are not known. Defining these pathways has led to a new classification scheme for CRC with resultant changes in our clinical approach to screening, surveillance, and treatment.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

A carbon and nitrogen flux model of mussel digestive gland epithelial cells and their simulated response to pollutants.

The mussel digestive gland epithelial cells provide a key interface between the organism and pollutants such as aromatic hydrocarbons. The simulation of their uptake and export mechanisms as well as an internal protein degradation pathway, and any subsequent disruption to any of them, has been undertaken. A computational model is described, which simulates the flow of carbon and nitrogen through a mussel's digestive cell. The model uses a compartmentalised view of the cell with inviolate 'pipelines' connecting each of the volume-variable partitions. Only the major physiological pathways relevant to the flow of either carbon or nitrogen or volume are modelled. Simulated response to hydrocarbon exposure is examined.

Animals↗
PubMedDate not supplied

Protein energy malnutrition in severe alcoholic hepatitis: diagnosis and response to treatment. The VA Cooperative Study Group #275.

BACKGROUND: Active nutrition therapy and the anabolic steroid oxandrolone (OX), in selected patients with severe alcoholic hepatitis, significantly improved liver status and survival. We report here on the changes in their nutritional parameters. METHODS: Protein energy malnutrition (PEM) was evaluated and expressed as percent of low normal in 271 patients initially, at 1 month and at 3 months. Active therapy consisted of OX plus a high caloric food supplement vs a matching placebo and a low calorie supplement. RESULTS: PEM was present in every patient; mean PEM score 60% of low normal. Most of the parameters improved significantly from baseline on standard care; the largest improvement seen in visceral proteins, the smallest in fat stores (skinfold thickness). Total PEM score significantly correlated with 6 month mortality (p = .0012). Using logistic regression analysis, creatinine height index, hand grip strength and total peripheral blood lymphocytes were the best risk factors for survival. When CD lymphocyte subsets replaced total lymphocyte counts in the equation, CD8 levels became a significant risk factor (p = .004). Active treatment produced significant risk factor (p = .004). Active treatment produced significant improvements in those parameters related to total body and muscle mass (ie, mid arm muscle area, p = .02; creatinine height index, p = .03; percent ideal body weight, p = .04). CONCLUSION: Deterioration in nutritional parameters is a significant risk factor for survival in severe patients with alcoholic hepatitis. This deterioration is reversible with standard hospital care. Active therapy further improves creatinine height index, mid arm muscle area and total lymphocyte counts. Hence, these later parameters appear to be the best indicators for follow-up assessments.

Adult↗