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Biomedical subjects

R M Russell

Publications and source records attributed to R M Russell.

At least 217 records · Page 12Linked to original sources

Night driving (mesopic) visual acuity in sober male alcoholics with and without liver disease.

Night driving (mesopic) visual acuity and recovery after dazzle has been reported to be reduced in patients with liver disease. Mesopic visual acuity and dazzle recovery were evaluated in 32 patients with alcoholic cirrhosis, 29 alcoholics without liver disease, and 27 age-matched normal controls. All subjects were sober for at least 7 days prior to visual testing, a mean sobriety period of 22 and 39 weeks in alcoholics and cirrhotics, respectively. Serum vitamin A levels and/or dark adaptation were normal in all. Mean best decimal acuities were not significantly different among the groups: alcoholic cirrhotics, 0.32 +/- 0.02; alcoholics, 0.32 +/- 0.02; and normals 0.33 +/- 0.03 at 2 min. Although cirrhotics had significantly higher SGOT and lower albumin levels than alcoholics, mesopic acuity did not relate to liver blood tests. Decimal acuity following a dazzle stimulus was not significantly worse in cirrhotics and alcoholics compared to normals. Sober patients with alcoholic cirrhosis or a history of alcoholism have no evidence of a static mesopic visual defect and therefore may not have impaired night driving vision.

Alcoholism↗

Impairment of folic acid absorption by oral pancreatic extracts.

Higher serum folate levels were found among newly diagnosed, untreated patients with pancreatic insufficiency than among treated patients despite greater fat malabsorption in the former group. In vivo folate absorption tests using Tritium-labeled pteroylmonoglutamatic acid showed folate absorption to be enhanced in pancreatic insufficiency patients as compared to control subjects (P less than 0.01). Moreover, pancreatic extract significantly inhibited folate absorption in both normal subjects (P less than 0.05) and pancreatic insufficient patients (P less than 0.001). In vitro testing showed pancreatic extract to form insoluble complexes with folate. Such complex formation may diminish absorption of dietary folate and lead to folate deficiency. Since both pancreatic extract and bicarbonate are used in the treatment of pancreatic insufficiency and both are known to impair folate absorption, folate status should be monitored in patients being treated for pancreatic insufficiency; supplementation may be indicated.

Administration, Oral↗

Vitamin A and zinc metabolism in alcoholism.

Vitamin A and zinc metabolism are affected both by ethanol and by hepatic cirrhosis. Ethanol causes abnormal dark adaptation by acting as a competitive inhibitor with retinol for alcohol dehydrogenase in the eye. In animals oral ethanol intake results in increased losses of zinc by the urinary and fecal routes. Vitamin A malnutrition in cirrhotics may be caused by poor diet, malabsorption, decreased hepatic vitamin A uptake, and decreased hepatic storage capacity for vitamin A. In some cirrhotic patients zinc deficiency and or protein deficiency may limit the ability to respond to vitamin A. Combined vitamin A and zinc deficiencies are common in cirrhotics and either may result in abnormal dark adaptation or impaired taste and smell. The interaction of these two micro-nutrients must be kept in mind by the clinician caring for alcoholic or alcoholic cirrhotic patients.

Alcoholism↗

Deficiency of fat soluble vitamins after jejunoileal bypass surgery for morbid obesity.

Significant vitamin A, E, or 25-hydroxy D deficiency occurred in 76% of 40 patients studied up to 6 years after jejunoileal bypass surgery for morbid obesity. Vitamin A was significantly lower in those who had lost 30% of their initial weight than in those who had lost less weight; however, there was no correlation of vitamin A, E, or D levels, time elapsed since surgery, or with daily intake of vitamins as subnormal values were found despite multivitamin supplementation and consumption of twice the recommended daily allowance of vitamin A. Functional derangement of retinal adaptation to darkness secondary to vitamin A deficiency was found in four of nine stable, healthy patients studied at least 18 months after surgery. There was no linear relationship between vitamin A levels and dark adapted final thresholds or with serum albumin, prothrombin time, or degree of steatorrhea. Three patients with abnormal adapted final thresholds were treated with vitamin A. Total daily intake of up to 65,000 IU of vitamin A daily for several months resulted in normalization of function in all.

Calcifediol↗

Correlation of dark adaptation test results with serum vitamin A levels in diseased adults.

Dark adaptation, is a reliable and highly reproducible indicator of vitamin A nutritional status in terms of function. Abnormal dark adaptation occurs over a fairly wide range of serum vitamin A values; however, the lower limit of serum vitamin A which is related to normal ocular function has not been determined. We studied dark adaptation in 67 patients with a variety of hepatic and gastrointestinal diseases or with chronic alcoholism. We found that a serum vitamin A level greater than or equal to 40 micrograms % predicted normal dark adaptation 95% of the time, a serum vitamin A level greater than or equal to 30 micrograms predicted normal retinal function 68% of the time and a level greater than or equal to 20 micrograms % predicted normal function 27% of the time. Thus, in individual patients with serum vitamin A levels less than 40 micrograms % one can be sure of vitamin A sufficiency only if a normal dark adaptation response is elicited.

Adult↗

Acute ethanol administration causes transient impairment of blue-yellow color vision.

The higher incidence of blue-yellow color blindness (tritanopia) found among alcoholics could be due to genetic or acquired factors. The acute administration of ethanol to alcoholics and normal subjects transiently resulted in poorer color discrimination in all spectra but with significantly more errors in the blue-yellow versus the red-green color range (p < 0.005, p < 0.01). Thus, ethanol appears to act as a toxin to inner retinal layers, which could account for the higher incidence of tritanopia found among alcoholics.

Adult↗

Celiac disease.

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Celiac Disease↗

Impaired acid neutralization in the duodenum in pancreatic insufficiency.

The influence of severe exocrine pancreatic disease on the acid-neutralizing capacity of the duodenum was studied in five patients with pancreatic insufficiency (PI) and six control subjects using duodenal perfusion-marker technique. Hydrochloric acid (0.1 N containing 1% PEG) was infused at constant rates (1.2, 4.5 and 7.0 ml/min) into the duodenum just distal to the duodenal bulb. Samples were aspirated from the tip of the duodenal perfusion tube located at the ligament of Treitz. All samples were analyzed for volume, pH, titrable acidity, PEG and [14C]PEG (gastric marker) determination. Patients with PI demonstrated significantly diminished ability to neutralize various acid loads as compared to controls who virtually completely neutralized acid loads in the range of maximal gastric acid secretion. Exogenous secretin did not significantly improve percent acid neutralized in PI. These data clearly indicate that patients with PI have significantly impaired ability to neutralize even small loads of acid in the duodenum.

Bicarbonates↗

Vitamin and mineral supplements in the management of liver disease.

While pharmacologic doses of specific vitamins or minerals are probably not warranted as a therapy for acute or chronic liver disease, deficiencies of micronutrients among patients with liver disease are extremely common, act to the detriment of the patient, and should be corrected so that normal metabolic processes can allow both regeneration of tissue and resistance to infection.

Humans↗

N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders.

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.

Adult↗

Zinc deficiency: a cause of abnormal dark adaptation in cirrhotics.

Six stable alcoholic cirrhotics with serum zinc less than 70 microgram/100 ml had abnormal dark adaptation responses (mean dark adapted final threshold 3.2 +/- 0.6 versus 2.1 +/- 0.2 log lux in 21 age matched controls, P less than 0.01). Serum vitamin A ranged from 15 to 37 microgram/100 ml. Zinc sulfate (220 mg/day) was fed to three patients for 1 to 2 weeks and dark adapted final thresholds fell 0.9, 0.4, and 1.2 log lux without concurrent rises in serum vitamin A. Two patients were treated initially with oral vitamin A (10,000 IU/day) for 2 to 4 weeks, but their final thresholds fell to normal (2.1, 2.2 log lux) only after the addition of zinc for 1 to 2 weeks. The sixth patient, treated with vitamin A and zinc together, attained a normal final threshold in 2 weeks. The improvement in dark adaptation by zinc may be due to enhanced activity of previously depressed retinol dehydrogenase.

Aged↗

Vitamin-A reversal of abnormal dark adaptation in cirrhosis. Study of effects on the plasma retinol transport system.

Of 26 patients hospitalized with mild to moderate alcohol-associated cirrhosis, 14 had dark-adaptation abnormalities consistent with marginal vitamin-A status. The response of dark adaptation and the plasma retinol transport proteins, retinol-binding protein and prealbumin, was studied in 12 of these patients after daily oral vitamin-A supplements of 3300 microgram. Vitamin-A supplementation was associated with significant (p less than 0.05-0.005) improvement in dark adaptation and increased plasma concentrations of retinyl esters, retinol, and retinol-binding protein. Thus in patients with cirrhosis and marginal vitamin-A status, supplemental vitamin-A therapy appears to stimulate retinol-binding protein release from the liver. This enhancement of plasma retinol transport and delivery of retinol to peripheral tissues such as the retina is one of several factors that may serve to optimize vitamin-A nutritional status in patients with cirrhosis.

Dark Adaptation↗

Role of bacterial overgrowth in the malabsorption syndrome of primary small intestinal lymphoma in Iran.

Malabsorption studies were performed on five Iranian patients with primary small intestinal lymphoma. The effect of oral tetracycline (1.0 g daily) was also studied in three of the above subjects. The results of breath tests (utilizing glycine-1-14C-cholic acid) were abnormal in all five subjects before the antibiotic treatment. Oral tetracycline had a striking effect towards normalizing the results of breath tests. Schilling tests (with intrinsic factor) improve in two patients and steatorrhea improved in all and there was significant weight gain. The antibiotic had no apparent effect on D-xylose or folate absorption tests. It is concluded that bacterial overgrowth in the small intestinal lumen is an important contributory factor to the malabsorption syndrome of this disease.

Adult↗