scholarly journals Hipotiroidismo primario, déficit de vitamina B12 y tiroiditis subaguda sobreagregada: informe de caso

2017 ◽  
Vol 2 (4) ◽  
pp. 51-54
Author(s):  
Carlos Alfonso Builes Barrera ◽  
María Gabriela García Orjuela

El hipotiroidismo primario es la patología tiroidea más frecuente. El manejo estándar de esta enfermedad es con levotiroxina, cuya absorción puede verse afectada por distintas condiciones médicas, medicamentos e incluso la dieta del paciente. Los requerimientos de levotiroxina podrían variar debido a factores sobre agregados como la tiroiditis subaguda, la deficiencia de vitamina B12 y el uso de medicamentos, elementos que afectan el control del hipotiroidismo. Se presenta el caso de una paciente con hipotiroidismo primario con necesidad de ajuste en la dosis de levotiroxina a través del tiempo debido a comorbilidades agregadas. Se presentan claves para la evaluación del paciente con dificultad para lograr una TSH dentro del rango normal.Abstract Hypothyroidism is the most common thyroid disease. This disease is managed with hormonal replacement therapy using levothyroxine, whose absorption can be affected by various medical conditions, drugs and even patient´s diet. Levothyroxine requirements could vary according to co-morbidities such as subacute thyroiditis, vitamin B12 deficiency and the use of drugs, factors that can affect the control of hypothyroidism. The case of a patient with primary hypothyroidism who required dose adjustments of levothyroxine over time due to added co-morbidities is presented. Clues are given for evaluation of the patient with difficulty in achieving maintenance of TSH within the normal range. 

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4278-4278
Author(s):  
Muhammad K Siddique ◽  
Hafiz M. Y. Sarwar

Abstract High vitamin B12 (cobalamin) levels have been documented in patients with untreated chronic myeloid leukemia. However, the literature about vitamin B12 deficiency in patients with chronic myeloid leukemia who are receiving imatinib is scarce. The objective of this study was to investigate the prevalence of vitamin B12 deficiency in patients with chronic myeloid leukemia. We retrospectively reviewed the medical records of 195 patients with chronic myeloid leukemia seen in the outpatient clinic of our institution between 2006 and 2007. The median age of patients was 35 (range 9 – 77); 118 (60%) patients were males and 77 (40%) were females. All patients included in the study were receiving imatinib. Macrocytic anemia at any given time during the course of treatment was documented in 61 (31%) out of 195 patients. Serum vitamin B12 and folate levels were measured in all patients with macrocytic anemia using chemiluminescent enzyme immunoassay. Among these 61 patients, 33 (54%) had low vitamin B12 levels (< 200 pg/ml), 12 (20%) had indeterminate levels (200 – 300 pg/ml) and 16 (26%) patients had levels > 300 pg/ml. Folate levels were within normal range (3 – 17 ng/ml) in all but two patients and both of these patients had folate levels < 3 ng/ml and vitamin B12 levels > 300 pg/ml. Among 195 study patients, 33 (17%) had macrocytic anemia with low vitamin B12 levels and 12 (6%) had macrocytic anemia with indeterminate vitamin B12 levels. We conclude that vitamin B12 deficiency is prevalent in our patients with chronic myeloid leukemia who are taking imatinib. This is of significance because our patient population is non-vegetarian. Serum vitamin B12 should be measured as a part of work up for anemia in patients with chronic myeloid leukemia. Correction of vitamin B12 deficiency in these patients could improve their tolerance to imatinib, which potentially is a myelosuppressive drug. In our study, measurements of serum methylmalonic acid (MMA) and homocysteine levels in patients with indeterminate vitamin B12 levels were not performed; although these measurements could have confirmed the diagnosis of vitamin B12 deficiency in this subgroup. We suggest that a similar study be conducted in a different patient population elsewhere.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5038-5038
Author(s):  
Stefani Parmentier ◽  
Jörg Meinel ◽  
Christiane Jakob ◽  
Anke Frömmel ◽  
Brigitte Mohr ◽  
...  

Abstract Abstract 5038 Case Report We report of a 53 year old woman who presented repeatedly with syncopes over a period of 3 months. Laboratory results revealed severe pancytopenia (Hb 4.6 mmol/l (7.4 g/dl), WBC 1.22 Gpt/L, platelet count 13 Gpt/L) and severe hemolysis (haptoglobin < 0.20 g/l, normal range 0.3–2.0 g/l; LDH 33.1 μmol/s*l, normal range 2.25–3.55 μmol/s*l). Routine examination of the bone marrow aspirate showed typical features of megaloblastic erythropoiesis, which could be confirmed by a low serum cobalamin level (53 pg/ml, normal 211–911 pg/ml) and the presence of anti-intrinsic factor antibody (16.84 U/ml). Additionally, atrophic gastritis was seen in biopsies taken of gastric mucosa. The diagnosis of pernicious anemia was suspected and the patient treated with cobalamin. Except for hemoglobin, the peripheral blood counts recovered within one week. Meanwhile, cytogenetics from the bone marrow revealed metaphases with del(3p) and histopathological results were suspicious of an increased number of blast cells with highly expression of CD163 possibly mimicking MDS or (acute) monocytic leukemia. Therefore, bone marrow examination was repeated two weeks after recovery, which still showed dysplastic changes paralleling hematopoietic recovery but no increased number of blast cells. Additionally, the cytogenetic aberration had disappeared. Discussion Diagnostic work-up for megaloblastic anemia rarely includes cytogenetic analysis of bone marrow cells. Therefore, the finding of a transient cytogenetic aberration has possibly not reported frequently before in the literature. In our case, the initial finding of del(3p) appears to be due to ineffective hematopoiesis caused by vitamin B12 deficiency which leads to impaired DNA synthesis and genomic instability. This might be an explanation for this cytogenetic abnormality which disappeared after substitution of cobalamin. CD163 is exclusively expressed on monocytes and macrophages and with signs of (slightly) increased blast counts might mimic (acute) monocytic leukemia. However, in pernicious anemia with severe hemolysis as seen in this case it might reflect an acute phase reaction, as CD163 represents a signal-inducing macrophage receptor that scavenges haemoglobin by mediating endocytosis of haptoglobin-hemoglobin complexes. In conclusion, vitamin B12 deficiency might be associated with cytogenetic abnormalities and thus in addition to the bone marrow morphology feign certain haematological diseases. Disclosures: No relevant conflicts of interest to declare.


2020 ◽  
Vol 9 (8) ◽  
pp. 2335 ◽  
Author(s):  
Sopak Supakul ◽  
Floris Chabrun ◽  
Steve Genebrier ◽  
Maximilien N’Guyen ◽  
Guillaume Valarche ◽  
...  

Sole measurement of plasma vitamin B12 is no longer enough to identify vitamin B12 (B12) deficiency. When plasma vitamin B12 is in the low-normal range, especially between 201 and 350 ng/L, B12 deficiency should be assessed by measurements of plasma homocysteine and/or plasma methylmalonic acid (MMA). However, these biomarkers also accumulate during renal impairment, leading to a decreased specificity for B12 deficiency. In such cases, urinary methylmalonic acid/creatinine ratio (uMMA/C) could be of interest, due to the stable urinary excretion of MMA. The objectives were to evaluate the influence of renal impairment on uMMA/C compared to plasma homocysteine and plasma methylmalonic acid, and to determine the diagnostic performances of uMMA/C in the diagnosis of B12 deficiency. We prospectively studied 127 patients with a plasma B12 between 201 and 350 ng/L. We noticed that uMMA/C was not dependent on renal function (p = 0.34), contrary to plasma homocysteine and plasma methylmalonic acid. uMMA/C showed a perspective diagnostic performance (AUC 0.71 [95% CI: 0.62–0.80]) and the threshold of 1.45 umol/mmol presented a high degree of specificity (87.9% [95% CI: 72.0–98.9]). In conclusion, uMMA/C is a promising biomarker to assess vitamin B12 status in doubtful cases, notably during renal impairment.


2021 ◽  
Vol 8 (8) ◽  
pp. 415-419
Author(s):  
Priyadarshini Raju ◽  
Shreyas Kumar V

BACKGROUND Hypothyroidism is a common endocrine disorder which affects 11 % of the adult population in western countries. Hypothyroidism can cause a wide variety of anaemic disorders. Patients with both hypothyroidism and Vitamin B12 deficiency also have similar symptoms. Thus, this study was conducted to evaluate the relationship between the two and also hypothyroidism due to autoimmune cause. METHODS This was a descriptive study of 50 newly detected hypothyroid patients from Rajarajeswari Medical College evaluated for vitamin B12 deficiency. The study was conducted between January 10th 2019 to July 21st 2019. Lab parameters analysed included haemoglobin, thyroid function test (TFT), vitamin B12 levels and antithyroid peroxidase (anti-TPO) antibody levels. RESULTS Of the 50 hypothyroid patients evaluated, 23 were males and 27 were females between the age of 18 to 70 years. Anti TPO antibodies were present in 24 patients (48 %) out of 50, out of which 17 (70 %) patients had vitamin B12 deficiency. Out of 50 hypothyroid patients, 26 patients (52 %) had vitamin B12 deficiency. Thus hypothyroidism and autoimmune thyroid disease was associated with Vitamin B12 deficiency which was statistically significant. CONCLUSIONS Patients with hypothyroidism were studied for the incidence of deficiency of vitamin B12. It was found that 26 of 50 (52 %) patients had low B 12 levels. Incidence in females (54 %) was more than in males (46 %). Our study showed association between hypothyroidism and vitamin B12 deficiency and also autoimmune thyroid disease. KEYWORDS Hypothyroidism, Autoimmune Thyroid Disease, Vitamin B12 Deficiency


2020 ◽  
Vol 38 (4_suppl) ◽  
pp. 338-338
Author(s):  
Yasushi Rino ◽  
Toru Aoyama ◽  
Norio Yukawa ◽  
Haruhiko Cho ◽  
Takashi Oshima ◽  
...  

338 Background: Postgastrectomy vitamin B12 deficiency is common metabolic sequel and worsens the quality of life of gastric cancer survivors. Recently, oral vitamin B12 replacement is reported. Therefore, we investigated retrospectively the efficacy of oral vitamin B12 replacement for gastric cancer patients with vitamin B12 deficiency after total gastrectomy. Methods: We reviewed 73 patients with gastric cancer who underwent total gastrectomy and were treated vitamin B12 replacement. Patients were consisted of 56 males and 17 females and median age was 70 y/o. We investigated initial treatment of vitamin B12 replacement and improvement of vitamin B12 deficiency. Results: Initial treatment of vitamin B12 replacements were intramuscular injection for 42 patients, per oral replacement for 28 patients and intravenous injection for 3 patients. Finally, all patients were treated with per oral replacement and the serum vitamin B12 levels became within normal range. Final vitamin B12 doses of replacement therapy were 500 µg of 20 out of 73 pts, respectively. Conclusions: Vitamin B12 replacement therapy should be necessary and continued. According to our results, one vitamin B12 tablet a day is enough. The vitamin B12 deficiency symptoms could be prevented. 500 micrograms vitamin B12 replacement orally is maybe effective and necessary. Our prospective clinical protocol (UMIN000030727): In this study, an oral vitamin B12 preparation (1500 μg/day, administered daily) was set as the control treatment, and a specific clinical trial was started to determine whether 500 μg/day daily administration would be sufficient for replacement therapy. Clinical trial information: UMIN000030727.


2004 ◽  
Vol 171 (4S) ◽  
pp. 15-15
Author(s):  
Urs E. Studer ◽  
Richard Aebischer ◽  
Katharina Ochsner ◽  
Werner W. Hochreiter

2010 ◽  
Vol 80 (45) ◽  
pp. 330-335 ◽  
Author(s):  
Lindsay Helen Allen

Vitamin B12 deficiency is common in people of all ages who consume a low intake of animal-source foods, including populations in developing countries. It is also prevalent among the elderly, even in wealthier countries, due to their malabsorption of B12 from food. Several methods have been applied to diagnose vitamin B12 malabsorption, including Schilling’s test, which is now used rarely, but these do not quantify percent bioavailability. Most of the information on B12 bioavailability from foods was collected 40 to 50 years ago, using radioactive isotopes of cobalt to label the corrinoid ring. The data are sparse, and the level of radioactivity required for in vivo labeling of animal tissues can be prohibitive. A newer method under development uses a low dose of radioactivity as 14C-labeled B12, with measurement of the isotope excreted in urine and feces by accelerator mass spectrometry. This test has revealed that the unabsorbed vitamin is degraded in the intestine. The percent bioavailability is inversely proportional to the dose consumed due to saturation of the active absorption process, even within the range of usual intake from foods. This has important implications for the assessment and interpretation of bioavailability values, setting dietary requirements, and interpreting relationships between intake and status of the vitamin.


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