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PubMed1964

FOLIC ACID AND VITAMIN B12 LEVELS IN PREGNANCY AND THEIR RELATION TO MEGALOBLASTIC ANAEMIA.

There is a significant fall in the serum folic acid level during pregnancy, reaching its lowest level at term. This is most pronounced in twin pregnancies. A similar but less spectacular fall occurs in the vitamin B(12) concentration. In megaloblastic anaemia both folic acid and vitamin B(12) levels are lower than in other pregnant women. The degree of megaloblastic change in the bone marrow, as measured by the type and number of megaloblasts, is reflected in the vitamin levels, cases with florid megaloblastosis showing the most marked depression of vitamin B(12) and folic acid activity. Although there is a significant difference in the mean folic acid levels between megaloblastic and normoblastic pregnant women, a considerable overlap exists between individual values in the two groups. When the labile folic-acid factor is determined separately the test becomes much more specific. In the present series, all cases of megaloblastic anaemia yielded labile-factor levels below 1.0 mmug. per ml., while a similar value was encountered in only one of 35 normal pregnancies. In five women with megaloblastic anaemia the vitamin B(12) concentration was less than 100 mumug. per ml. but rose to normal levels on folic acid therapy alone.

Anemia↗
PubMed1980

Reduced rate of DNA replication fork movement in megaloblastic anemia.

Chromatography on benzoylated naphthoylated DEAE-cellulose has been used to fractionate fully double-stranded from partially single-stranded DNA molecules. DNA was extracted from phytohemagglutinin-stimulated lymphocytes from patients with megaloblastic anemia resulting from vitamin B12 or folate deficiency after pulse-labeling the cells with [3H]thymidine for 5 min and chasing in unlabeled medium for 24 h. No gross accumulation of partially single-stranded material was observed in the DNA of these cells when compared with DNA from similarly labeled control cells obtained by the addition of 5-formyl tetrahydrofolic acid to the culture medium. When DNA from lymphocytes labeled with a 5-min pulse of [3H]thymidine and sheared to fragments of an average length of 18 micrometer was chromatographed on benzoylated naphthoylated DEAE-cellulose, approximately 80% of the label was recovered in the partially single-stranded fraction. After chasing in unlabeled medium the label was progressively transferred to the double-stranded fraction over a period of 2--3 h. The rate of transfer was slower in megaloblastic lymphocytes than in controls. The difference in rate suggested a slower rate of replication fork movement in megaloblastic lymphocytes and so the density shift technique of Painter and schaeffer (J. Mol. Biol. 45: 467--479, 1969) was used to measure the fork rate directly. [3H]Deoxycytidine was used as the labeled nucleoside to avoid possible complications arising from [3H]thymidine labeling of megaloblastic cells. Investigations on the lymphocytes from four patients showed that the replication fork rate in vitamin-treated control lyphocytes was about 1 micrometer/min. The fork rates in the corresponding untreated cells were invariably lower and rates ranging from 40 to 92% of those of controls were observed. Normal lymphocytes treated with the deoxynucleotide pool-depleting drugs methotrexate or hydroxyurea displayed defects in DNA synthesis similar to those of untreated megaloblastic lymphocytes. We propose that the delayed DNA replication fork movement in cells of patients with megaloblastic anemia results from impaired biosynthesis of DNA precursors.

Anemia, Macrocytic↗
PubMed2003

Red cell indices for distinguishing macrocytosis of aplastic anaemia and megaloblastic anaemia.

Megaloblastic anaemia and aplastic anaemia are important causes of pancytopenia in India. Since both may have presence of macrocytes, peripheral smear examination alone may pose a difficulty in distinction between the two in the absence of macro-ovalocytes and hypersegmented neutrophils. The present study was conducted to evaluate the role of red cell indices in differentiation between macrocytosis of aplastic anaemia and megaloblastic anaemia. Haemogram from 25 cases each of biopsy proven megaloblastic anaemia and aplastic anaemia were reviewed. It was observed that MCV was greater than 97 fl in 15 cases of aplastic anemia (mean MCV 109.7 fl), and 25 cases of megaloblastic anaemia (mean MCV 113.2 fl). Hb, MCV & MCHC were comparable in the two groups. However, mean RDW in megaloblastic anaemia (mean 87.7 fl) was significantly higher than those in aplastic anaemia (mean 71.4 fl). The difference in RDW of patients with megaloblastic anaemia and aplastic anaemia was statistically significant. We conclude that RDW can be of help to differentiate between the two conditions.

Adolescent↗
PubMed1966

An account of 335 cases of megaloblastic anaemia of pregnancy and the puerperium.

The incidence of megaloblastic anaemia in pregnancy and the puerperium in north Staffordshire has steadily declined as a result of prophylaxis with folic acid. In the presence of advanced folic acid deficiency and with a florid megaloblastic marrow, the anaemia is usually severe, but in many patients the disease is relatively mild and the degree of anaemia is determined more by blood loss or associated iron deficiency than by the megaloblastosis. Microscopic examination of marrow films is still the most reliable method of diagnosis, although estimation of the labile serum folate has produced a 95% correlation with the marrow findings. There are three main factors which operate in the pathogenesis of megaloblastic anaemia in pregnancy and the puerperium. First, the maternal stores of folic acid are used up by the growing foetus, and this process is accelerated in multiple pregnancies, after haemorrhage, or in women with haemolytic anaemia. Secondly, an insufficient intake of folic acid, due to poor diet in pregnancy, plays a part in many cases. The third, and possibly the most important, factor is an absorption defect. Folic acid absorption is usually impaired in established cases, and this can still be demonstrated years later in a majority of patients, when they are neither pregnant nor anaemic. More than 20% of all cases also show abnormal fat absorption. An inherited defect in folic acid absorption may also explain why certain women appear to be constitutionally predisposed to megaloblastic anaemia of pregnancy and the puerperium, as shown by the abnormal blood group distribution in these patients and by the tendency of megaloblastic anaemia to recur not only in subsequent pregnancies, but, as in six of our cases, following other kinds of stress. The significance of commonly associated conditions like pre-eclampsia and infection is still incompletely understood. Although the treatment of megaloblastic anaemia is simple and effective, the main emphasis should be placed on prophylaxis by administering folic acid to all pregnant women.

Adult↗
PubMed1970

Megaloblastic anaemia of pregnancy: a clinical and laboratory study with particular reference to the total and labile serum folate levels.

It has been shown that the incidence of megaloblastic anaemia in a group of 463 randomly selected pregnant women receiving iron was 12 times as high as in a control group of 235 pregnant women receiving iron and folic acid. The incidence of all types of anaemia in the women receiving iron alone was more than three times the incidence in those having iron and folic acid. Some women who were not anaemic or who had normoblastic anaemia had serum folate levels in the same range as the women with megaloblastic anaemia, but none of the women with megaloblastic anaemia had high serum folate levels. The labile fraction of the serum folate was no more reliable than the total serum folate as a diagnostic criterion of megaloblastic erythropoiesis in the individual case. The blood group distribution in the women with megaloblastic anaemia was the same as in the general population. Babies born to mothers with megaloblastic anaemia tended to be smaller than the rest, although there was no difference in the placental weights. The significance of these findings is discussed.

Anemia, Macrocytic↗
PubMed1996

Elevated deoxyuridine triphosphate nucleotidohydrolase (dUTPase) activity in the cobalamin-deficient megaloblastic bone marrow cells.

The biochemical basis underlying the pathogenesis of megaloblastic anemia due to vitamin B12 deficiency was examined. Megaloblastic bone marrow cells show a marked imbalance in the deoxynucleoside triphosphate pools. If cellular dUTP concentration is elevated due to metabolic block in a similar way to dCTP, ensuing uracil misincorporation into DNA would result in deranged DNA composition and impaired cell function. Therefore, dUTP-degrading activity was measured in blood cells from various diseases. dUTPase (dUTP nucleotidohydrolase) activity of bone marrow cells was, on average, 4.4 times higher in 8 patients with untreated megaloblastic anemia than that of other normoblastic conditions. Such elevated dUTPase may help lower cellular dUTP levels in megaloblastic anemia. However, it is not clear whether the observed increase of dUTPase in megaloblastic cells is sufficient to suppress uracil misincorporation below the harmful level.

Anemia, Megaloblastic↗
PubMed1986

Methionine partially corrects the impaired deoxyribonucleic acid synthesis of B12-deficient megaloblastic bone marrow cells at low concentration.

The effects of methionine on deoxyribonucleic acid (DNA) synthesis of B12-deficient megaloblastic bone marrow cells were investigated over a wide concentration range. Deoxyuridine (UdR) incorporation and the UdR suppression test were employed as an indicator for DNA synthesis. Only a low and limited concentration range of methionine improved significantly the impaired DNA synthesis of megaloblastic cells, although the extent of improvement was less than those by either B12 or folate. Higher concentrations of methionine (greater than or equal to 150 micrograms/ml), however, were suppressive for both megaloblastic and normoblastic cells. In contrast, homocysteine did not affect DNA synthesis of megaloblastic cells at low concentration. Improving effect of methionine at low concentration appeared to be characteristic to megaloblastic cells, since such effect disappeared on hematologic recovery following B12 administration.

Anemia, Macrocytic↗
PubMed2000

Apoptosis in megaloblastic anemia occurs during DNA synthesis by a p53-independent, nucleoside-reversible mechanism.

Deficiency of folate or vitamin B(12) (cobalamin) causes megaloblastic anemia, a disease characterized by pancytopenia due to the excessive apoptosis of hematopoietic progenitor cells. Clinical and experimental studies of megaloblastic anemia have demonstrated an impairment of DNA synthesis and repair in hematopoietic cells that is manifested by an increased percentage of cells in the DNA synthesis phase (S phase) of the cell cycle, compared with normal hematopoietic cells. Both folate and cobalamin are required for normal de novo synthesis of thymidylate and purines. However, previous studies of impaired DNA synthesis and repair in megaloblastic anemia have concerned mainly the decreased intracellular levels of thymidylate and its effects on nucleotide pools and misincorporation of uracil into DNA. An in vitro model of folate-deficient erythropoiesis was used to study the relationship between the S-phase accumulation and apoptosis in megaloblastic anemia. The results indicate that folate-deficient erythroblasts accumulate in and undergo apoptosis in the S phase when compared with control erythroblasts. Both the S-phase accumulation and the apoptosis were induced by folate deficiency in erythroblasts from p53 null mice. The complete reversal of the S-phase accumulation and apoptosis in folate-deficient erythroblasts required the exogenous provision of specific purines or purine nucleosides as well as thymidine. These results indicate that decreased de novo synthesis of purines plays as important a role as decreased de novo synthesis of thymidylate in the pathogenesis of megaloblastic anemia.

Anemia, Megaloblastic↗
PubMed1975

Arsenic intoxication as a cause of megaloblastic anemia.

We have described a case of chronic arsenic intoxication associated with pancytopenia and megaloblastic erythropoiesis. The patient had the typical laboratory manifestations of effective erythorpoiesis due to a megaloblastic process, including macroovalocytes, mild pancytopenia, low reticulocyte index, increased marrow cellularity with erythroid hyperplasia, and morphologic evidence of megaloblastic maturation in the marrow. The patient's serum folate and vitamin B12 were normal, and the anemia regressed without therapy. Our case suggests that the combination of megaloblastosis with normoblastic or megaloblastic karyorrhexis,should raise the suspicion of arsenic intoxication in the mind of the observer. In addition, arsenic should be added to the list of agents causing a reversible megaloblastic anemia.

Anemia, Macrocytic↗
PubMed2000

Serum lactate dehydrogenase in diagnosis of megaloblastic anaemia.

The present study was carried out in 75 patients of macrocytic anaemia categorised on bone marrow examination (into megaloblastic and non-megaloblastic anaemia) to evaluate the efficacy of total serum LDH levels and LDH isoenzyme pattern in the diagnosis of megaloblastic anaemia. 25 healthy adults were taken as controls. From this study it can be concluded that total serum LDH levels more than 3000 IU/L are diagnostic of megaloblastic anaemia. Reversed LDH isoenzyme pattern (LDH1 > LDH2) by chloroform inhibition test is an adjuvant in the diagnosis where total serum LDH levels are between 451-3000 IU/L and it will also differentiate megaloblastic anaemia from haemolytic anaemia.

Adolescent↗
PubMed1990

Neutrophil myeloperoxidase measurement uncovers masked megaloblastic anemia.

We report the observation of a high neutrophil myeloperoxidase activity (MPXI) in patients with megaloblastic anemia. MPXI is rapidly measured as part of an automated complete blood count (Technicon H*1, Technicon Instruments Corp, Tarrytown NY). We describe the range of MPXI levels in healthy and patient populations and in 10 cases of megaloblastic anemia, including five having elevated mean cell volume (MCV) and five without macrocytosis. Regardless of the MCV, our megaloblastic patients had hypersegmented neutrophils and elevated MPXI levels without visible alteration of granule content. MPXI measurement may be particularly useful in identifying cases of "masked megaloblastic anemia" where the MCV is below 100 fL. The advantage of the MPXI over other methods of uncovering masked megaloblastic anemia is its simplicity when performed as part of a routine complete blood count on an automated hematology instrument.

Adolescent↗
PubMed1982

Further characterization of the erythrocyte membrane protein abnormality in megaloblastic anemia.

Erythrocyte membranes obtained from patients with severe megaloblastic anemia contain spectrin as indicated by double immunodiffusion against anti-spectrin raised in rabbits. These membranes have normal protein patterns determined by polyacrylamide gel electrophoresis in sodium dodecyl sulfate after solubilization at 100 degrees C for 3 min in SDS. When incubation is carried out at 37 degrees C for 3 hours, however, the membrane protein patterns become grossly abnormal, lacking spectrin, band 3 and having several diffuse smaller bands. Cross-linking of these membranes with SH oxidizing agents, such as diamide prevented this dissociation phenomenon. The SH group content of megaloblastic membranes, both from severe and mild megaloblastic anemia, was significantly higher than that of control membranes. This was also confirmed by the greater incorporation of 3H-N-ethylmalemide into red cell membranes from mild and severe megaloblastic anemia than controls. Incorporation of this probe was greatest into the band 3 region. These findings indicate that the erythrocyte membrane proteins in megaloblastic anemia have an intrinsic abnormality which renders them more susceptible to degradation by their endogenous proteases.

Anemia, Macrocytic↗
PubMed1982

Characteristic abnormality of deoxyribonucleoside triphosphate metabolism in megaloblastic anemia.

To elucidate the biochemical basis of megaloblastic hematopoiesis, the cellular content and metabolism of deoxyribonucleoside triphosphates (dNTPs) were investigated using the bone marrow cells from nine patients with untreated vitamin B12 deficiency and one with folic acid deficiency. The marked imbalance among four dNTPs was noted in all patients. dTTP was invariably elevated rather than depressed. The most striking abnormality, however, was the excessive accumulation of dCTP, which represented the consistent feature exclusive for megaloblastic anemia. Purine nucleotides were also involved to a lesser extent. The apparent turnover pattern of the dTTP pool of megaloblastic anemia marrow cells, in the presence or absence of hydroxyurea, did not differ significantly from that of normoblastic hematopoiesis. The megaloblastic cells assimilated exogenous thymidine into dTTP pool in vitro with enhanced efficiency. It was suggested that the excessive accumulation of dCTP may be related more closely to the pathogenesis of megaloblastic hematopoiesis than to the presumed but not proved deficiency of dTTP.

Anemia, Macrocytic↗
PubMed1995

[Megaloblastic changes in cervical epithelium associated with oral contraceptives and changes after treatment with folic acid].

OBJECTIVE: To study the influence of oral contraceptives on cervical epithelium, serum and red blood cell folate levels of users and to observe the changes after treatment with folic acid. METHODS: Morphology of cervical epithelium, serum folate and red blood cell folate levels were studied in 101 women who had used oral contraceptives for over 6 months and 33 intrauterine devices users served as controls, 29 women using oral contraceptives with cervical megaloblastic changes were treated with folic acid (5mg daily) for 3-4 weeks and followed up for observation on morphological changes of cervical epithelium. RESULTS: The mean nuclear diameter of cervical epithelial cells was larger in the oral contraceptive group than that in the control group (P < 0.001). Megaloblastic changes in cervical epithelium occurred in 29 women in the oral contraceptive group (28.7%). There was significant difference in the occurrence of cervical megaloblastic changes between the two groups (P < 0.01). The level of red blood cell folate was lower in the oral contraceptive group than that in the control group (P < 0.05). There was no difference in serum folate, hemoglobin and neutrophil nuclear index between the two groups (P > 0.05). The mean nuclear diameter of cervical epithelial cells decreased significantly (P < 0.001) and multinuclear and vacuolar changes disappeared after folic acid therapy in 26 women with megaloblastic changes. CONCLUSIONS: Oral contraceptives reduced folate storage in the body and resulted in megaloblastic changes in cervical epithelium. This condition was improved with folic acid therapy.

Adult↗
PubMed1979

Defective DNA synthesis in megaloblastic anaemia. Studies employing velocity sedimentation in alkaline sucrose gradients.

1. Autoradiographic experiments revealed that the average size of the replicating unit (replicon) in human phytohaemagglutunin-stimulated lymphocytes is 45 (+/- 1.3) micron. 2. A 5 min pulse of [3H]thymidine labelled DNA chains of approximately 40 S (15 micron) in control lymphocytes as revealed by velocity sedimentation in alkaline sucrose density gradients. Upon chasing in the absence of [3H]-thymidine the labelled DNA increased in size. By 6 h the bulk of the label co-sedimented with full-sized chromosomal DNA. 3. In untreated lymphocytes from patients with megaloblastic anaemia due to vitamin B-12 or folate deficiency or lymphocytes treated with methotrexate (10(-5) M) or hydroxyurea (5 . 10(-4) M) the increase in size of pulse-labelled DNA was slower than in control cells. 4. The block in maturation of pulse-labelled DNA to bulk DNA was not permanent. At 24 h of chase 75-80% of the pulse-label in both control and megaloblastic lymphocytes co-sedimented with bulk DNA. 5. We conclude that the lesions seen in DNA synthesis in megaloblastic anaemia due to folate or vitamin B-12 deficiencies occur through impaired biosynthesis of nucleotide precursors of DNA. Possible explanations of why the defects in DNA synthesis cause altered morphology of proliferating cells in megaloblastic anaemia are suggested.

Anemia, Macrocytic↗
PubMed2003

Oral versus intramuscular cobalamin treatment in megaloblastic anemia: a single-center, prospective, randomized, open-label study.

BACKGROUND: Cobalamin (vitamin B12) deficiency, the most common cause of megaloblastic anemia, is treated with intramuscular (IM) cobalamin. It has been suggested by some investigators that oral (p.o.) cobalamin treatment may be as effective in the treatment of this condition, with the advantages of ease of administration and lower cost. OBJECTIVE: This study assessed the effects and cost of p.o. versus i.m. cobalamin treatment in patients with megaloblastic anemia due to cobalamin deficiency. METHODS: This was a 90-day, prospective, randomized, open-label study conducted at the Division of Hematology, Department of Internal Medicine, Adnan Menderes University Research and Practice Hospital (Aydin, Turkey). Patients aged > or =16 years with megaloblastic anemia due to cobalamin deficiency were randomized to receive 1000-microg cobalamin p.o. once daily for 10 days (p.o. group) or 1000-microg cobalamin i.m. once daily for 10 days (i.m. group). After 10 days, both treatments were administered once a week for 4 weeks, and after that, once a month for life. Patients were assessed for the presence of reticulocytosis between treatment days 5 and 10 until it was detected. Therapeutic effectiveness was assessed by measuring hematologic parameters on days 0, 10, 30, and 90 and serum vitamin B12 concentration on days 0 and 90. The Mini-Mental State Examination was used before and after the B12 therapy for cognitive function assessment and 125-Hz diapozone was used for vibration threshold testing. Neurologic sensory assessment, including soft-touch and pinprick examinations, was used to identify neuropathy at baseline and study end. Tolerability was assessed using laboratory tests and patient interview. Cost was assessed using the cost of the study drug and of the injection. RESULTS: Sixty patients completed the study 26 in the p.o. group (16 men, 10 women; mean [SD] age, 60 [15] years) and 34 in the i.m. group (17 men, 17 women; mean [SD] age, 64 [10] years). Reticulocytosis was observed in all patients. In the p.o. group, at days 30 and 90, all hematologic parameters changed significantly versus day 0 (mean hemoglobin levels increased [both P<0.001]; mean corpuscular volume decreased [both P<0.001]; mean white blood cell count increased [day 30, P<0.01; day 90, P<0.001]; and mean platelet count increased [both P<0.001]). The mean serum vitamin B12 concentration increased significantly from day 0 to 90 (P<0.001). These hematologic parameters and the recovery patterns were similar between the 2 groups. Neurologic findings included sensitive peripheral neuropathy in 9 patients (15.0%), alteration of cognitive function (loss of memory, impaired concentration) in 7 patients (11.7%), and loss of sense of vibration in 5 patients (8.3%). Neurologic improvement was detected in 7 of 9 patients (77.8%) in the p.o. group and 9 of 12 patients (75.0%) in the i.m. group at day 30. CONCLUSIONS: In this study of patients with megaloblastic anemia due to cobalamin deficiency, p.o. cobalamin treatment was as effective as i.m. cobalamin treatment. P.o. treatment also was better tolerated and less expensive compared with IM treatment. However, because of the small sample size and the short term of this study, further long-term studies are needed to determine the efficacy of p.o. cobalamin treatment.

Administration, Oral↗
PubMed1976

Thymidine kinase in megaloblastic anaemia.

Thymidine kinase has been measured in phytohaemagglutinin (PHA)-stimulated lymphocytes from 13 normal subjects and eight patients with megaloblastic anaemia. The levels in normal subjects ranged from 0.20 to 2.10 units/mg protein (mean 0.903 units/mg protein) and in megaloblastic anaemia from 2.99 to 9.97 units/mg protein). All the patients showed raised levels of the enzyme which were partly but not completely reduced to normal by addition of folic acid in vitro. Vitamin B12 in vitro had a lowering effect in the five vitamin-B12-deficient patients and two patients with combined deficiencies but not in one 'pure' folate-deficient patient. Thymidine kinase activity was highest in the cells of the least anaemic patients, suggesting that the degree of anaemia in megaloblastic anaemia may be determined in part by the ability of the cells to utilize thymidine by the 'salvage' pathway when the de novo pathway of thymidylate synthesis is failing. The rise in thymidine kinase activity in megaloblastic anaemia is presumably due to induction of the enzyme. Addition of methotrexate or 5-fluorouracil, drugs known to inhibit de novo thymidylate synthesis, caused an increase in thymidine kinase activity in normal PHA-stimulated lymphocytes after 24 h (but not after 1 h) which could be completely blocked by addition of puromycin. Thymidine mono- and di-phosphate kinases were also measured in normal PHA-stimulated lymphocytes. The activities were substantially higher than that of thymidine kinase and their activities were unaffected by methotrexate addition.

Anemia, Macrocytic↗
PubMed1978

The effect of deoxyuridine, vitamin B12, folate and alcohol on the uptake of thymidine and on the deoxynucleoside triphosphate concentrations in normal and megaloblastic cells.

Deoxyuridine suppression of labelled thymidine uptake tests were performed in the bone marrows of 58 patients with megaloblastic anaemia (haemoglobin less than 10.0 g/dl) and invariably gave values (range 10.3-58.8%) above the range in 16 control marrows (range 1.0-9.0%). Folinic acid corrected the test equally well in either folate or vitamin B12 deficiency, even at concentrations as low as 60 ng/ml. Folic acid also corrected the test equally well in either deficiency but was only effective at concentrations down to 5 microgram/ml. Vitamin B12 (100 microgram/ml) only corrected the test in vitamin B12 deficiency and 5-methyltetrahydrofolate only corrected the test in folate deficiency at the concentrations tested between 60 and 1.2 microgram/ml. Among 16 patients with subnormal serum levels of both vitamin B12 and folate, vitamin B12 partially corrected the test in eight, including all five with pernicious anaemia, but had no effect in the other eight. Despite the clear-cut results of the dU suppression test, measurement of the deoxythymidine triphosphate (dTTP) concentration in normal and megaloblastic phytohaemagglutinin stimulated lymphocyte cultures or short-term bone marrow cultures gave no clear-cut differences between normal and megaloblastic cells after addition of deoxyuridine nor did the addition of vitamin B12, folic acid or folinic acid either alone or with deoxyuridine produce consistent changes in the dTTP concentration in lymphocytes or bone marrow cells in megaloblastic anaemia. Alcohol caused a rise in deoxyadenosine triphosphate concentration in normal PHA-stimulated lymphocytes which was concentration dependent but caused no consistent change in any of the other three deoxynucleoside triphosphate (dNTP) concentrations. Diphenylhydantoin (10(-3)M, 10(-4)M) had no consistent effect on any of the four dNTP concentrations.

Anemia, Macrocytic↗