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Biomedical subjects

R Carmel

Publications and source records attributed to R Carmel.

At least 73 records · Page 4Linked to original sources
PubMed1988

Food cobalamin malabsorption occurs frequently in patients with unexplained low serum cobalamin levels.

Malabsorption of food-bound or protein-bound cobalamin with normal absorption of free cobalamin has been described in studies of patients with gastric dysfunction. We used the egg-yolk cobalamin absorption test to study 47 patients selected not because of known gastric disorders but because they had low serum cobalamin levels with normal Schilling test results. Their egg test results were significantly lower than in normal controls, while Schilling test results were normal. Twenty of the subjects had egg test excretion below 1.5%. No features distinguished them from the 27 who excreted more than 1.5% other than the presence of lower pepsinogen I:II ratios. Eight of 19 tested patients with food cobalamin malabsorption had no evidence of abnormal gastric status by blood tests and/or gastric analysis. Also noteworthy was the finding of food cobalamin malabsorption in 60% of tested patients who had neurologic, cerebral, or psychiatric abnormalities. Food cobalamin malabsorption appears to be associated frequently with otherwise unexplained low cobalamin levels. Low cobalamin levels in patients with normal Schilling test results cannot be dismissed as insignificant without also testing for food cobalamin malabsorption, whether or not the patients have known gastric dysfunction.

Adult↗
PubMed1987

Iron deficiency occurs frequently in patients with pernicious anemia.

We assessed iron status in patients with pernicious anemia. Iron deficiency coexisted as a presenting finding in 25 (20.7%) of 121 patients for whom data could be evaluated. Another 27 patients (22.3%) developed iron deficiency one month to 14 years later (median, two years). It was impossible to predict such a development in these 27 patients from any of their initial findings. The cause of the iron deficiency was identified in 17 of the 52 iron-deficient patients and suspected in another four. These findings show that patients with pernicious anemia are at high risk for iron deficiency, both at initial presentation and subsequently. Although the cause of the iron deficiency is often not identifiable, clinically important entities are detected often enough to warrant routine investigation for iron deficiency in such patients.

Adult↗
PubMed1987

Lymphocyte surface phenotypes in pernicious anemia.

Because an immunological defect of an unknown nature is thought to be a factor in the pathogenesis of pernicious anemia, we studied lymphocyte surface phenotypes in 40 patients and compared them with 113 healthy controls. The only significant difference that emerged was in their slightly decreased number and proportion of surface immunoglobulin (lambda chain) -bearing cells. Of specific interest, the numbers of OKT4+ and OKT8+ lymphocytes and the T4+/T8+ ratios were not significantly different from control values. A sizable minority of patients had increased ratios, while a smaller number had decreased values. No explanation or identifying feature was apparent for those patients with either increased or decreased T4+/T8+ ratios. (One patient with a very low ratio, who was excluded from our analysis, developed acquired immune deficiency syndrome.) No differences were apparent in T4+/T8+ ratios or any other lymphocyte surface phenotypic characteristics when patients were segregated by presence of anti-intrinsic factor antibody or anti-parietal cell antibody, or by race, sex, or age. Our results in a racially heterogeneous group of patients do not support the suggestion that T4+/T8+ ratios are usually abnormal in prenicious anemia or that the presence of anti-intrinsic factor antibody is associated with such abnormality.

Anemia, Pernicious↗
PubMed1987

Platelet counts in three racial groups.

Documented differences exist in red blood cell (RBC) and granulocyte counts between black and white people. However, little comparative information is available on differences in platelet counts in the two racial groups. Therefore, this study was performed to compare platelet counts in healthy white (94), black (92), and Latin-American (63) persons. Black women had significantly higher platelet counts than did white women (P less than 0.025). Latin-American women were between the other two groups. No differences were noted among men. Black women also had a significantly higher prevalence of iron deficiency and microcytosis of RBCs than did white women. After exclusion of women with either microcytosis or iron deficiency, racial differences in platelet counts were no longer evident. The authors conclude that the differences in the platelet counts between black and white women were secondary to common RBC differences (such as iron deficiency and other causes of microcytic anemia) and were not intrinsic to the platelets. These and other factors that can affect platelet counts should be excluded before determining the reference ranges for proper interpretation of the platelet counts.

Black or African American↗
PubMed1987

Racial differences in vitamin B12 levels in the United States.

Studies from Africa have demonstrated that black people have higher vitamin B12 (cobalamin) levels than do white people. The authors compared healthy white people, black people, and Latin-Americans in the United States. Their study is also the largest in which the effect of race and sex on the cobalamin levels has been examined. Analysis of 233 healthy subjects showed that black people had significantly higher (P less than 0.0001) vitamin B12 levels than did white people. Latin-Americans had levels intermediate between those of white and black people, although their levels were significantly different only in comparison with white people (P = 0.0029). Based on the study of 305 healthy subjects, no sex difference in vitamin B12 levels was noted. Conflicting claims have been made on sex difference in the past. The authors conclude that there is a racial but not a sex difference in vitamin B12 levels in the United States. Like African black people, black people and Latin-Americans in this country have significantly higher vitamin B12 levels than do white people. This finding supports the thesis that genetic factors contribute to the racial differences in vitamin B12 levels.

Black or African American↗
PubMed1987

Increased sensitivity of detection of the blocking (type I) anti-intrinsic factor antibody.

Increasing the ratio of test serum to the intrinsic factor (IF) antigen should increase the sensitivity of anti-IF antibody assay, a useful, specific tool for diagnosing pernicious anemia. We therefore designed an assay in which this ratio was increased 25-fold over that of our current standard assay and 1,000-fold over that of most described methods. This assay was then compared with our standard assay, with one of the original assays, and with a commercial kit. Both of our assays, especially the newer sensitive method, detected antibody in much greater dilutions of positive serum than the other assays. The sensitive assay also detected antibody in 17% of pernicious anemia sera negative by our standard technique. We calculated that anti-IF antibody can be detected with the sensitive assay in 78% of our patients with pernicious anemia, compared with 73% by our standard assay, 65% by the commercial kit, and 61% by the original method of Gottlieb and colleagues. No antibody was detected in 35 control sera with the new assay, which suggests that the increased sensitivity did not come at the expense of diminished specificity. The increased sensitivity enhances the value of the anti-IF antibody as a major screening and diagnostic tool in pernicious anemia.

Anemia, Pernicious↗
PubMed1987

Low serum cobalamin levels occur frequently in the acquired immune deficiency syndrome and related disorders.

Low serum cobalamin levels in 10 patients with AIDS or AIDS-related complex led us to also prospectively survey 40 homosexual men in our AIDS clinic. 8 of the latter (20%) had low cobalamin values. We found no evidence of megaloblastic changes in the blood or bone marrow. Assessment disclosed malabsorption of cobalamin in only 1 of 6 cases tested for it. 6 of the patients were treated with cobalamin and had no hematologic response. It appears that low serum cobalamin levels in AIDS and related disorders do not usually represent overt cobalamin deficiency. While malabsorption is occasionally responsible for the low cobalamin level, in most cases the cause is unknown and may reflect a serum abnormality similar to that in multiple myeloma. AIDS and related disorders should be considered in the differential diagnosis of unexplained low cobalamin levels.

AIDS-Related Complex↗
PubMed1987

Unsuspected pernicious anemia in a patient with sickle cell disease receiving routine folate supplementation.

Although the issue of folate supplementation in sickle cell anemia remains controversial, routine supplementation has become common. The major drawback to indiscriminate folate therapy is the potential of masking findings of vitamin B12 (cobalamin) deficiency. This has been dismissed as a problem in sickle cell anemia because of the generally young age of the patients. However, because young blacks, especially women, are at higher risk for developing pernicious anemia than whites, sickle cell anemia and pernicious anemia can be expected to coexist occasionally. In this article we describe such a patient and recommend that routine folate supplementation should not be given in sickle cell anemia before determining the vitamin B12 status.

Adult↗
PubMed1987

Pernicious anemia in Latin Americans is not a disease of the elderly.

Pernicious anemia is widely regarded as a disease of the elderly. However, it is expressed differently in black women, among the most striking differences being their younger age at presentation of the disease compared with whites. We now compared 92 Latin-American patients with 115 white and 100 black patients to see if similar age differences occur in other racial groups. Latin-American men and women were both significantly younger than white men and women, and were similar in age to blacks. Only 21% of Latin-American patients were 70 years of age or older, compared with 49% of whites. It is apparent that pernicious anemia is indeed predominantly a disease of the elderly in whites but that this is not the case in other racial groups.

Adolescent↗
PubMed1987

Atypical cobalamin deficiency. Subtle biochemical evidence of deficiency is commonly demonstrable in patients without megaloblastic anemia and is often associated with protein-bound cobalamin malabsorption.

We performed studies in 25 patients with low serum cobalamin levels who had few if any clinical or hematologic findings of cobalamin deficiency. All but three had morphologically normoblastic hematopoiesis, and 15 were not even anemic. None of those tested excreted methylmalonic acid or homocystine. Nevertheless, the dUST identified metabolic abnormalities in 18 of the 25 cases. In vitro additives were essential in the dUST. Especially noteworthy was MTHF, whose addition unmasked an otherwise undetectable dUST abnormality in four cases. Why MTHF appears to act as a "stress test" in this setting is unknown but deserves further attention. Seven patients had early forms of classical malabsorptive states such as pernicious anemia, defined by abnormal Schilling test results. Among the rest, seven of 13 patients displayed malabsorption of protein-bound cobalamin despite normal absorption of free cobalamin by the Schilling test. In two patients, initially normal Schilling test results became abnormal the following year. These findings demonstrate that seemingly falsely low serum cobalamin levels often indicate subtle biochemical cobalamin deficiency. Early stages of pernicious anemia or other classical malabsorptive states are sometimes responsible for such subtle deficiency. However, malabsorption confined to protein-bound cobalamin is an equally common cause. Current concepts of cobalamin deficiency and the absorptive defects that can cause it should be expanded to include atypical defects requiring newer methods of identification.

Adult↗
PubMed1987

Low serum cobalamin levels in primary degenerative dementia. Do some patients harbor atypical cobalamin deficiency states?

Serum cobalamin (vitamin B12) levels were analyzed retrospectively in 17 patients with primary degenerative dementia and 11 with specific demonstrable causes of dementia (secondary dementia). The prevalence of low cobalamin levels was significantly increased in primary dementia (29% vs 0% in secondary dementia). Because typical findings of deficiency often seemed absent, we prospectively studied two other patients with primary dementia and low cobalamin levels. Neither of these two had megaloblastic anemia; one had a normal Schilling test while the other's was borderline. Despite this absence of the expected findings, the deoxyuridine suppression test gave biochemical evidence of cobalamin deficiency in both cases. Our survey of 28 patients thus established that low serum cobalamin levels are frequent in primary dementia. Our findings in the two prospectively studied cases (as well as in some of the patients in the survey) indicate that these levels are associated in at least some cases with an atypical deficiency state rather than with disorders such as pernicious anemia. Such atypical deficiency states cannot be identified by classic hematological criteria or by the Schilling test.

Aged↗
PubMed1986

Physician response to low serum cobalamin levels.

Physician response to a low serum cobalamin result was evaluated in 250 patients. In 42% of cases, no response whatsoever to the low level was found. In 24%, response was suboptimal. In only 34% of cases was management adequate from a diagnostic and therapeutic aspect. Moreover, 13% of all patients were treated with folic acid alone. In addition to the lack of attention to the bulk of cases that had subtle abnormalities or that were not truly cobalamin-deficient, many cases with typical findings of deficiency were ignored. It should also be noted that many truly deficient patients had quite atypical clinical and hematologic features, and the classic picture emphasized in textbooks probably applies mainly to late cases with florid manifestations. These findings raise disturbing questions about the medical management of cobalamin deficiency. They also touch on the more general issue of how physicians view and respond to laboratory abnormalities.

Adult↗
PubMed1985

Racial differences in serum total bilirubin levels in health and in disease (pernicious anemia).

Common usage prescribes a single normal range for serum bilirubin levels. However, we have not only confirmed that men have higher levels than women but have discovered significant racial differences as well. Among 1,538 healthy Americans, blacks had lower mean bilirubin levels than whites of European origin, Latin Americans, and Asians. These racial differences, which were more pronounced among women than men, were maintained in pernicious anemia. Even though bilirubin levels rose in our 174 patients with this disease, they continued to be lower among blacks than among whites and Latin Americans. Moreover, the actual bilirubin level changes caused by pernicious anemia were themselves smaller among blacks. The racial differences, thus, persisted in pernicious anemia despite similar degrees of anemia, whereas the sex differences disappeared. We suggest that the lower serum bilirubin levels in blacks in health and disease do not stem primarily from lower bilirubin production than in whites.

Anemia, Pernicious↗
PubMed1985

The deoxyuridine suppression test identifies subtle cobalamin deficiency in patients without typical megaloblastic anemia.

Four patients had serum cobalamin levels that were initially thought to be falsely low. None of the patients had the typical hematologic and clinical features of cobalamin deficiency and the three so tested had normal cobalamin absorption and/or gastric function. However, the deoxyuridine suppression test result was abnormal in all four cases. The abnormality was improved by adding cobalamin in vitro but, in three of the four cases, was not corrected and, indeed, was made worse by the addition of methyl tetrahydrofolate. These results established metabolically the presence of cobalamin deficiency. The recently improved cobalamin radioassays may be unmasking some atypical and, heretofore, unappreciated cobalamin-deficiency states (only one of our four patients would have come to attention with the older radioassays). These can be identified with the deoxyuridine suppression test, particularly when specific in vitro additives are included.

Aged↗
PubMed1985

The distribution of endogenous cobalamin among cobalamin-binding proteins in the blood in normal and abnormal states.

Our information about cobalamin transport in the blood is largely based on studies of unsaturated cobalamin-binding proteins. Therefore, the distribution of endogenous cobalamin among these proteins was examined. Normally, R binder (transcobalamin I) carries most of the cobalamin circulating at any given moment, but the proportion varies greatly. Transcobalamin II carries a larger fraction of the cobalamin present in portal vein blood than in hepatic and axillary vein blood. In disease, transcobalamin II occasionally holds the bulk of the vitamin present in peripheral blood. Such was observed in three patients showing quantitative changes of unsaturated binder (either diminished R binder or increased transcobalamin II), but in two cases of chronic liver disease this was independent of unsaturated transcobalamin levels. Four patients with low serum cobalamin levels maintained normal distribution, indicating proportional cobalamin depletion from both binder pools. Small amounts of vitamin were attached in many sera to minor binders, and occasionally seemed to circulate free. These results demonstrate that assumptions that cobalamin is always attached largely to transcobalamin I are not warranted. Cobalamin distribution appears to be governed by many factors, of which the amounts of the binding proteins is only one.

Axillary Vein↗
PubMed1985

Pure human pancreatic juice directly enhances uptake of cobalamin by guinea pig ileum in vivo.

Although pancreatic enzymes clearly degrade R binder, a nonintrinsic factor binder, the full scope of the pancreatic role in cobalamin absorption remains the subject of debate. Therefore the direct effect of pure human pancreatic juice (PPJ) on ileal cobalamin absorption in the absence of intrinsic factor was studied. PPJ significantly enhanced cobalamin uptake in guinea pig ileal loop perfused in vivo. It did not do so in the jejunum. This PPJ activity in the ileum was further stimulated by enteropeptidase and inhibited by aprotinin. The intestinal mucosa remained intact during our study by morphologic and inulin clearance criteria and behaved normally with respect to intrinsic factor and nonintrinsic factor binders. Since no intrinsic factor was present in the perfusate, PPJ must directly enhance cobalamin uptake by the ileum, perhaps promoting cobalamin attachment to receptor sites for subsequent transport by intrinsic factor. PPJ thus seems to affect cobalamin absorption at several levels. Previous studies have established its interaction with luminal R binders and with bile. The findings now indicate that pancreatic juice may have an additional, more direct role in promoting cobalamin absorption in the ileum.

Animals↗
PubMed1985

Hair and fingernail changes in acquired and congenital pernicious anemia.

Pigmentation changes limited to skin appendages accompanied pernicious anemia in four patients. Two Latin-American patients, one with congenital and one with acquired pernicious anemia, had reddish hair while they were cobalamin deficient. With treatment, the new hair growth assumed its normal premorbid dark brown color. Two black patients with pernicious anemia had blue fingernails. The new nail growth after treatment was of normal color. Pigmentation changes seem to be more frequent in nonwhite than in white patients with cobalamin deficiency and may have various expressions.

Adolescent↗