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Biomedical subjects

R Carmel

Publications and source records attributed to R Carmel.

At least 127 records · Page 7Linked to original sources
PubMed1977

Serum vitamin B12 and transcobalamin abnormalities in patients with cancer.

One hundred and thirty-nine patients with non-hematologic malignancy were studied to define the incidence of vitamin B12-related abnormalities and correlate them with clinical findings. Based on vitamin B12-binding patterns, the following relatively distinct groups were defined: (A) 50% had normal results; (B) 6% had very high transcobalamin (TC) I and vitamin B12 levels as reported in isolated instances previously: most had hepatic metastases and early death, and all had definite metastatic disease; (C) 11% had high vitamin B12 levels with little or no unsaturated TC I elevation: most also had hepatic and other metastases and early death; (D) 23% had high vitamin B12-binding capacity with normal TC I and vitamin B12 levels: there were no distinguishing features for this group other than an increased proportion of black patients; and (E) 10% had low vitamin B12 levels, in many cases not associated with vitamin B12 deficiency or other known causes of low serum levels. Thus, high serum vitamin B12 level, with or without unsaturated TC I elevation, usually implies a poor prognosis in a patient with cancer. However, while most such patients have hepatic and other metastases, hepatic involvement was not universal nor did most patients with hepatic disease have high vitamin B12 levels. High serum TC I thus is not always due to increased granulocytic proliferation or to hepatic tumor, and alternative mechanisms for TC I accumulation should be sought.

Black People↗
PubMed1977

Circulating antibody to transcobalamin II causing retention of vitamin B12 in the blood.

A patient with recurrent pulmonary abscess, weight loss, and alcoholism was found to have extremely high serum vitamin B12 and unsaturated vitamin B12-binding capacity (UBBC) levels. While transcobalamin (TC) II was also increased, most of his UBBC was due to an abnormal binding protein which carried greater than 80% of the endogenous vitamin B12 and was not found in his saliva, granulocytes, or urine. This protein was shown to be a complex of TC II and a circulating immunoglobulin (IgGkappa and IgGlambda). Each IgG molecule appeared to bind two TC II molecules. The reacting site did not interfere with the ability of TC II to bind vitamin B12, but did interfere with its ability to transfer the vitamin to cells in vitro. The site was not identical to that reacting with anti-human TC II antibody produced in rabbits. Because of this abnormal complex, 57Co-vitamin B12 injected intravenously was cleared slowly by the patient. However, no metabolic evidence for vitamin B12 deficiency was demonstrable, although the patient initially had megaloblastic anemia apparently due to folate deficiency. The course of the vitamin B12-binding abnormalities was followed over 4 yr and appeared to fluctuate with the status of the patient's illness. The IgG-TC II complex resembled one induced in some patients with pernicious anemia by intensive treatment with long-acting vitamin B12 preparations. The mechanism of induction of the antibody formation in our patient is unknown.

Adult↗
PubMed1975

Extreme elevation of serum transcobalamin I in patients with metastatic cancer.

Elevation of transcobalamin I and serum vitamin B12 levels has usually been associated with increased granulocytic proliferation, such as occurs in chronic myelogenous leukemia. Two patients with metastatic cancer had extremely high serum vitamin B12 and transcobalamin I levels--greater than those seen in even the most intense granulocytic proliferation--that were not explainable by leukocytosis. The subjects' serum vitamin B12 levels were 18,750 and 21,221 pg per milliliter (normal, 471 plus or minus 174 pg per milliliter, mean plus or minus S.D.) and unsaturated vitamin B12 binding capacity 158,750 and 5,400 pg per milliliter (normal, 1153 plus or minus 313 pg per milliliter) respectively. The abnormally elevated serum binder was shown to be identical with transcobalamin balamin I in every respect. Levels of transcobalamin II and serum third binder were normal. The cause of the binder abnormality is unknown, but factors other than granulocyte proliferation may control or contribute to the production or accumulation of transcobalamin I.

Adenocarcinoma↗
PubMed1975

Serum vitamin B12-binding proteins in a case of eosinophilic leukemia.

A patient with subacute eosinophilic leukemia is presented, with full recognition of the controversy surrounding that entity. Serum vitamin B12 and B12-binding protein studies and simultaneous complete blood counts were done before and during 6 months of high-dose, intermittent combination chemotherapy. The patient presented with extremely high levels of serum vitamin B12, unsaturated B12-binding capacity, and transcobalamin I, all of which resembled the highest values seen in chronic myelogenous leukemia. Serial studies, during and after remission induction, showed a precipitous fall of serum vitamin B12 and unsaturated B12-binding capacity to normal levels. The data show that transcobalamin I levels, which eventually reached low-normal range, correlate best with the level of circulating and bone marrow eosinophils. Transcobalamin II and serum third binder appeared to be normal throughout the patient's course. The B12-binding protein abnormalities are not considered diagnostic of eosinophilic leukemia.

Adult↗
PubMed1975

Serum vitamin B12- binding proteins in neutropenia.

Serum unsaturated vitamin B12-binding capacity (UBBC) has been shown to fluctuate with neutrophil levels and has been reported to correlate with TBGP in normal and hyperleukocytic states. However, the present report demonstrates that the above relationship is not present in neutropenia, suggesting that some of our concepts regarding UBBC may have to be reexamined, since factors other than TBGP appear to be operative. There was a wide scatter of UBBC values among the 39 neutropenic subjects studied, the mean being significantly above normal. There were few low values. High UBBC was primarily confined to subjects with transient neutropenia. Normal values were generally seen in steady neutropenia. The difference in UBBC was primarily due to Transcobalamin I, the other serum binders being similar in both groups. No other significant diagnostic pattern of UBBC was found. Recovery from neutropenia was accompanied by a rise in UBBC in all cases except in four patients whose UBBC was initially very high and fell with recovery. No discernible pattern of serum B12 levels existed, although subnormal levels without evidence of B12 deficiency were found in three of the seven patients with aplastic anemia. Serum B12 levels did not change with recovery in approximately half of the neutropenic subjects, change being variable in the others. Neither serum B12, UBBC, total B12-binding capacity, or any of the three serum B12 binders correlated with neutrophil count, bone marrow findings, TBGP, or granulocyte turnover rate.

Agranulocytosis↗