So is there a translation out there? I haven’t see anything but what has been posted on this thread. Which suggests that RK’s defense is, my parameters were completely normal, but just in case they weren’t, I have this thyroid problem that explains everything. Let’s recall that if JTL hadn’t had an off-score of 155, he would have skated on his other test, which was estimated to be significant at the level of < 0.001.
Anemia is often present in patients with hypothyroidism, and treatment with thyroxine or related hormones can stimulate reticulocyte synthesis and raise red blood cell levels. But assuming his suspicious values were a high Hb/retic ratio, I’m not sure how his defense is going to argue that thyroxine is the cause of the abnormalities.
Here are some useful studies:
Q J Med. 1976 Jan;45(177):101-23.
The haematology of hypothyroidism.
Horton L, Coburn RJ, England JM, Himsworth RL.
Abstract
In an unselected series of 202 patients with hypothyroidism anaemia was present on diagnosis in 39 of 172 women and 14 of 30 men. Microcytic anaemia was present in only nine patients in the entire series. The average of the mean corpuscular volume (MCV) of all the patients was 90 fl. Fifty-three of 118 patients who were studied in detail had normal serum concentrations of vitamin B12, folic acid and iron.
The haemoglobin was low in 13 of these 53 patients and rose on treatment with thyroxine alone. The MCV exceeded 90 fl in 29 of these 53 patients and in three it was greater than 100 fl. The MCV invariably fell on treatment with thyroxine even if the initial value was within the normal range. Nine of this group of 53 patients had both anaemia and an increased MCV--the macrocytic anaemia of hypothyroidism. A minor degree of anisocytosis of the red blood cells, which was reduced by treatment with thyroxine, was also demonstrated. Acanthocytes were present in the blood films of 32 out of 172 patients but in only five did the abnormal cells comprise more than 0-5 per cent of the red cell population. The incidence of new cases of pernicious anaemia diagnosed concurrently with the hypothyroidism in the carefully studied group of 118 patients was 8-5 per cent. The MCV of hypothyroid patients with low levels of vitamin B12 was often no greater than in patients with uncomplicated hypothyroidism. The MCV is not therefore a useful discriminant in the diagnosis of pernicious anaemia in hypothyroidism. The serum iron concentration was less than 12 mumol/1 in 60 out of 118 patients. The total iron binding capacity of the serum was increased in only 21 of these 60 patients. In 42 hypothyroid patients the low serum iron concentration was not associated with low levels of either vitamin B12 or folate and of these patients 22 were anaemic. Despite the very low percentage saturation of the iron binding capacity in all of these patients with a low serum iron, a lack of iron did not seem to be the usual determinant of anaemia when it occurred.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Horton+AND+England+JM
J Clin Endocrinol Metab. 1975 Feb;40(2):211-20.
Erythropoiesis and erythropoietin in hypo- and hyperthyroidism.
Das KC, Mukherjee M, Sarkar TK, Dash RJ, Rastogi GK.
Abstract
Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin.
A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow.
Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H-thymidine labeling index [i.e, reduced reticulocyte synthesis]. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique.
These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate.
The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism [increased reticulocyte synthesis]; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow.
It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients.
Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.
http://www.ncbi.nlm.nih.gov/pubmed/1117976
Med Clin North Am. 1975 Sep;59(5):1133-45.
Anemia in thyroid diseases.
Fein HG, Rivlin RS.
Abstract
Thyroid hormones generally stimulate erythropoiesis. These agents also increase erythrocyte 2,3-DPG concentrations, which serve to enhance the delivery of oxygen to tissues. In the absence of thyroid hormones, anemia frequently develops and may be normocytic, hypochromic-microcytic, or macrocytic. Anemia is an uncommon finding in hyperthyroidism but when present may be morphologically similar to that observed in hypothyroidism. Pernicious anemia has been strongly associated with hypothyroidism, hyperthyroidism, and thyroiditis. Complete correction of anemia often requires restoration of thyroid function as well as specific hematinic therapy. Continued attention to hematologic status is essential in the management of patients with thyroid diseases.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Fein+HG+AND+Rivlin+RS
Effect of Restoration of Euthyroidism on Peripheral Blood Cells and Erythropoietin in Women with Subclinical Hypothyroidism
Mirjam Christ-Crain1, Christian Meier1, Peter Huber2, Henryk Zulewski1, Jean-Jacques Staub1, Beat Müller1
Abstract
Background: In overt hypothyroidism (OH) anemia is common, while less frequently basophilia has been described. In subclinical hypothyroidism (SCH), however, data on the distribution of peripheral blood cells are lacking. Therefore, we evaluated the effects of L-T4 replacement therapy on peripheral blood elements in female patients with SCH before and after restoration of euthyroidism in a randomized, double-blind and placebo-controlled study. Patients and Methods: Sixty-six women with SCH (TSH 12.9 ± 8.2 mU/L) were randomly assigned to receive L-thyroxine or placebo for 48 weeks. 63 of the 66 women completed the study. Peripheral blood cells were measured at baseline and 48 weeks after L-thyroxine or placebo treatment, respectively. Results: The percentage of lymphocytes decreased (p<0.05), whereas percent of monocytes (p<0.05) and eosinophiles (p<0.05) increased significantly upon restoration of euthyroidism after 48 weeks. Hemoglobin and hematocrit remained unchanged throughout the study period. However, erythropoietin levels increased significantly (p<0.01) during L-T4 treatment. In the placebo group all parameters remained unchanged throughout the study. Conclusions: Overall, we observed subtle alterations of the leuco-lympho-monocytic distribution of the peripheral blood cells upon restoration of euthyroidism in patients with SCH.
Hemoglobin and Hematocrit remained unchanged; however, the increasing level of erythropoietin during L-T4 treatment suggests an already stimulated, yet compensated erythropoietic system in mild thyroid failure.
http://www.hormones.gr/120/article/article.html
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