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PubMed1998

Mechanisms of diarrhoea in myotonic dystrophy.

BACKGROUND: Gastrointestinal (GI) symptoms are common in myotonic dystrophy (MD). Diarrhoea is one of the more disabling of these GI complaints. The mechanisms behind diarrhoea in MD have not previously been investigated systematically. OBJECTIVE: To elucidate the mechanisms behind diarrhoea in MD. METHODS: Twenty patients with MD and suffering from diarrhoea were investigated in order to detect malabsorption (blood tests and faecal fat excretion) and bile acid malabsorption ([75Se]selenahomocholic acid-taurine (SeHCAT) retention) and to study intestinal morphology (duodenal and rectal biopsies). RESULTS: Two patients had deficiency of folic acid and four showed reduced levels of pancreatic isoamylase, but none of them had steatorrhoea. Two out of eight patients had abnormal bile acid breath tests with normal SeHCAT, indicating small bowel bacterial overgrowth and 12 displayed reduced SeHCAT retention. Duodenal biopsies were normal in eight patients and five out of nine rectal biopsies displayed slight inflammation. CONCLUSIONS: A possible mechanism of diarrhoea in MD could be identified in most of the patients. Bile acid malabsorption seems to be a frequent cause and can be treated successfully.

Adult↗
PubMed1969

Separation of folic acid reductase from Streptococcus faecium (ATCC 8043).

A strain of Streptococcus faecium (ATCC 8043) which is highly resistant to the antifolic acid compound, amethopterin, was gently ruptured by exposing protoplasts of the organism to a hypotonic solution. The crude lysate resulting there-from was treated by various chemical and physical techniques designed to separate folic acid reductase from dihydrofolic acid reductase. In the process, the enzyme was purified approximately 160-fold; however, throughout the process, the enzyme preparation maintained the ability to reduce folic acid to tetrahydrofolic acid. Attempts to isolate mutants showing a deficiency in either folic acid reductase or dihydrofolic acid reductase were unsuccessful. Based on these results, it is concluded that folic acid is reduced to tetrahydrofolic acid by one enzyme in S. faecium (ATCC 8043). The crude lysate was also subjected to ultracentrifugation. An analysis of the supernatant fluid and the sediment indicated that the reductive activity is located in the soluble fraction of the cell.

Bacterial Proteins↗
PubMed2006

Predicting iron and folate deficiency anaemias from standard blood testing: the mechanism and implications for clinical medicine and public health in developing countries.

BACKGROUND: Developing countries have high prevalence of diseases, but facilities to diagnose and treat them are limited. We must use available resources in ways not needed where there are sophisticated equipment and trained staff. Anaemia is common; iron deficiency affects health and productivity; folate deficiency in pregnant women causes foetal abnormalities. Few developing countries can measure serum folate or ferritin, but standard automated blood analyses are widely available and can help predict folate and iron deficiency. The RDW-CV% (coefficient of variation of the red cell width) measures the variability in the size of red blood cells (RBC) in routine automated analysis of blood cells, but is seldom reported. Levels of RDW-CV% and haemoglobin (Hb) can predict iron deficiency anaemia. METHOD AND RESULTS: I have written a computer model based on the standard mechanism for blood formation and destruction. This shows that before anaemia develops and during recovery, there are both normal and abnormal RBC (small in iron deficiency and large in folate deficiency) in the circulation. The model calculates the abnormality in the RDW-CV% in standard automated blood analyses. In early iron deficiency and during recovery the full blood count shows the Hb near the lower limit of normal, a low MCV and a high RDW-CV%. A similar pattern, but with a higher MCV, develops in folate deficiency. Folate deficiency is often brief and may not cause anaemia. The high RDW-CV% may persist for three months. CONCLUSION: This long footprint could be medically useful for detecting folate deficiency and so limiting foetal damage in individuals and communities. Few clinicians or public health workers know about RDW-CV%. Standard blood reports for clinical use should include the RDW-CV% and note the possible significance of abnormal values.

Adult↗
PubMed1998

A new concept in the control of iron deficiency: community-based preventive supplementation of at-risk groups by the weekly intake of iron supplements.

Iron deficiency (ID), defined as an insufficient supply of iron to the cells of the body after iron reserves have been exhausted, is the most prevalent single nutritional deficiency, affecting over 2,000 million people, mostly in the developing world. Infants, small children, adolescents and pregnant and fertile-age women are most vulnerable. Only about 50% of people with ID develop iron deficiency anemia (IDA), since this is a late manifestation of chronic ID. Based on the average daily iron requirement and on the rate of iron reutilization from red cell hemoglobin destruction, it can be estimated that after iron stores have been depleted, it takes about 4 months of ID erythropoiesis for adult women to have a drop in hemoglobin concentration [Hb] of 10 g/l, if the iron intake is only 70% of requirement. IDA can be defined by a [Hb] below an appropriate cut-off point for age, sex, physiological condition and altitude above sea level, or by a [Hb] increment of more than 10 g/l to the administration of adequate doses of iron. More than 85% of the nutritional anemias are IDA alone, or of iron combined with folate or other nutrient deficiencies.

Adult↗
PubMedDate not supplied

Folate and cobalamin in psychiatric illness.

The linkage of cobalamin and folate deficiency to psychiatric illness has been studied and debated since these vitamins were first discovered in the 1940s. The clinical relevance of these deficiencies remains the subject of investigation and scholarly discussion. This article reviews case reports and studies derived from a MEDLINE search for English-language articles related to folate, cobalamin, and psychiatric illness. Emphasis is given to clinical research and recent developments. Preclinical evidence for direct effects of folate and cobalamin on brain functioning is compelling, and numerous associations of their deficiencies to psychiatric illness are evident. These vitamin deficiencies may typically present initially with psychiatric symptoms, but any direct causal relationship to specific neuropsychiatric illnesses are not well defined. The relationship of these vitamins in dementia is significant, but they may only rarely be a cause of truly reversible dementia. Folate deficiency appears most tightly connected with depressive disorders, and cobalamin deficiency with psychosis. Contrary to intuition, vitamin deficiencies appear to occur infrequently with eating disorders. Other diagnoses have been investigated much less extensively. The diagnosis and management of these deficiencies in the context of neuropsychiatric illness is still a matter of discussion. The quality of clinical research in this area is improving, but there are many unanswered questions that affect clinical practice. Clinicians should remain vigilant to the possibility of deficiencies of folate and cobalamin in diverse psychiatric populations. Normal hematological indices do not rule out the deficiencies. Further study is needed to refine the detection and clinical management of these vitamin deficiencies in psychiatric populations.

Brain↗
PubMed1995

Metabolite assays in cobalamin and folate deficiency.

Cbl and folate are both necessary for the metabolism of HCYS, whereas only Cbl is required for MMA metabolism. During the past decade, analytical methods have been developed that are sensitive enough to detect low levels of MMA and HCYS normally present in the plasma. These methods are sufficiently precise to be used in the clinical laboratory and measurements of the serum levels of the metabolites provide sensitive and specific techniques for the identification of Cbl and folate deficiencies. These techniques constitute an important addition to the battery of diagnostic tests that are available for detecting the vitamin deficiencies and for distinguishing each from the other. By virtue of the role of Cbl and folate in the metabolic pathways that involve MMA and HCYS, levels of both metabolites rise in Cbl deficiency, but only HCYS rises in folate deficiency. During the development of Cbl or folate deficiencies, accumulation of these metabolites in the plasma signals the existence of a condition of biochemical vitamin deficiency of sufficient degree to cause impairment in the metabolic pathways which are dependent on these vitamins. Circulating metabolite levels appear to accurately reflect the nutritional status of the vitamins and a rise in serum metabolite levels is therefore one of the earliest and most reliable indicators of developing Cbl and folate deficiencies. Elevations of serum metabolites above the reference range not only precede a fall in the serum vitamin levels but also show a more consistent correlation with objective evidence of vitamin deficiency than do low blood vitamin levels. The advent of serum metabolite measurements has also made it possible to identify subtle or atypical forms of vitamin deficiency that may be associated with unusual or previously undiscovered disease manifestations. Thus, in patients who display only neurological manifestations of disease, underlying Cbl deficiency may be revealed by the finding of raised serum or urine levels of MMA. Similarly, unsuspected folate deficiency may be disclosed by the finding of a raised serum HCYS. This may have important implications with respect to disease risk, since there is mounting evidence that sub-optimal folate nutritional status may be associated with increased risks of vascular disease, neoplasia and birth defects. Finally, the measurement of serum levels of MMA, HCYS and other metabolites that accumulate in Cbl and folate deficiencies may provide important new insights into the mechanism whereby these vitamin deficiencies lead to different patterns and manifestations of disease.

Folic Acid Deficiency↗
PubMed1985

Plasma cobalamin-binding and serum cobalamin in patients with folate deficiency.

Plasma unsaturated R-binder and transcobalamin 2 (TC 2) levels were measured in 62 patients with folate deficiency and compared with 80 control subjects and 52 patients with pernicious anaemia. An increase in unsaturated R-binder concentration was found in the majority of patients with folate deficiency and with PA. In folate deficiency, however, the unsaturated R-binder was often elevated whether the serum cobalamin (Cbl) was low or normal, more frequently when the serum Cbl was normal. Results of a separate in vivo study of plasma retention of injected 57Co cyanocobalamin were consistent with these findings. An elevated TC2 was found in a small number of patients with folate deficiency and with PA. The serum Cbl appears to the maintained at a normal level in some patients with folate deficiency by an increase in R-binder, which is caused by folate deficiency itself.

Adult↗
PubMed1994

Possible folate deficiency with postsurgical infection.

A 51-year-old obese woman was transferred to our hospital for management of a complicated laparoscopic cholecystectomy accompanied by fever and malaise. A liver abscess was discovered. On postoperative day 52 it was noted that the patient's tongue was magenta and sore and that she had altered taste, pallor, severe weight loss, diarrhea, and poor appetite and mood. A dermatology consult suggested that her tongue abnormalities were most likely nutrition-related, and a hematologic blood smear was suggestive of folate deficiency. Premorbidly, the patient had consumed a diet chronically low in folate and had received estrogen therapy for 15 years. Throughout the patient's hospitalization, she had bouts of fever and received numerous antibiotics. Within a month of initiating nutrition support and vitamin/mineral supplements, her nutritional status improved dramatically. This patient's poor diet, long-term estrogen use, surgical stress, infection, and lack of early nutrition support may have contributed to her possible folate deficiency and her prolonged hospital stay.

Cholecystectomy, Laparoscopic↗
PubMed1988

Haematological and tissue abnormalities in chicks caused by acute and subclinical folate deficiency.

1. Haematological, histological and ultrastructural findings in young chicks fed on a purified diet severely deficient in folate are reported. 2. Growth of the birds was greatly depressed and they had a macrocytic anaemia. Other haematological changes included abnormal nuclear formations in erythrocytes, numerous mitoses and hypersegmented granulocytes. 3. Megaloblasts were observed in bone marrow and their fine structure is described for the first time in an avian species. 4. Morphological changes occurred also in the liver. The parenchyma had damaged sinusoidal endothelium, inflammatory cells and no glycogen. Mitochondria were damaged and many were associated with unusual crystalline structures. 5. Chickens fed on a semi-purified diet of low folate content showed no growth depression or clinical signs of deficiency but had abnormal haematological values and morphological changes that resembled those seen in birds fed on the purified diet. 6. These abnormalities responded to dietary supplements of pteroylmonoglutamic acid in a dose-related manner and may be useful in diagnosing subclinical folate deficiency.

Animals↗
PubMed1993

Elevation of 2-methylcitric acid I and II levels in serum, urine, and cerebrospinal fluid of patients with cobalamin deficiency.

Citrate synthase catalyzes the condensation of acetyl-coenzyme A (CoA) and oxaloacetic acid to form citric acid. The enzyme also catalyzes the condensation of propionyl-CoA and oxaloacetic acid with a maximal reaction velocity (Vmax) approximately 10(-4) times that of acetyl-CoA to form 2-methylcitric acid, which contains two asymmetric carbon atoms and exists as two pairs of related enantiomers designated as 2-methylcitric acid I and II. Cobalamin (Cbl) deficiency can lead to increases in intracellular levels of propionyl-CoA. To assess the magnitude of increased synthesis of 2-methylcitric acid in Cbl deficiency, we developed a new capillary gas chromatographic-mass spectrometric assay and measured 2-methylcitric acid levels in serum and cerebrospinal fluid (CSF) of normal subjects and patients with clinically confirmed Cbl deficiency. The normal range for 2-methylcitric acid level was 60 to 228 nmol/L for serum in 50 normal blood donors and 323 to 1,070 nmol/L for CSF in 19 normal subjects. In 50 patients with clinically confirmed Cbl deficiency, values for 2-methylcitric acid in serum ranged from 93 to 13,500 nmol/L; 44 (88%) had values above the normal range. In five patients with clinically confirmed Cbl deficiency, levels of the sum of 2-methylcitric acid I and II ranged from 1,370 to 16,300 nmol/L in CSF, and all five (100%) patients had levels above the normal range. We conclude that levels of 2-methylcitric acid are elevated in serum and CSF of most patients with Cbl deficiency.

Adolescent↗
PubMed1986

A patient with bulimia nervosa and profound folate deficiency.

A case is reported of a young woman with bulimia nervosa who presented with profound folate deficiency. This association has not been reported before despite the increased theoretical possibility. Initially she has responded well to folic acid therapy and social support.

Adolescent↗
PubMed1988

[Folate deficiency in medical intensive care: incidence, predictive factors and consequences. Results of a prospective study with 105 patients].

Among 105 patients admitted to a medical intensive care unit over a five-month period, 53 per cent had a fall in serum folate concentration (less than 5 ng/ml), and 19 per cent had a concomitant fall in erythrocyte folate concentration (less than 170 ng/ml). Acute folate deficiency with severe haematological changes was observed in 2 patients. Apart from these 2 cases, the usual haematological parameters were not significantly different in patients with or without folate deficiency. On admission, there was a significant correlation between folate status, severity index and serum albumin and transferrin, all variables which reflect the patient's nutritional status. Patients with infection and fever, and those who have recently been operated upon are at a higher risk of folate deficiency. These findings suggest that patients admitted to a medical intensive care unit should receive an early supplement of folic acid.

Adolescent↗