Effect of Severe, Chronic Illness on Thyroid Function

Carter, J.N.; Corcoran, J. M.; Eastman, Creswell J; Lazarus, L.

doi:10.1016/s0140-6736(74)92070-4

Cited by 202 publications

(76 citation statements)

References 19 publications

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“…4,[8][9][10]14 When the thyroid function of 100 CKD cases (Group-A+B) were compared with the control (Group-C), it was found that TT4, TT3, FT4 and FT3 values were lower and only TT3 was significantly low (P=0.0011). This result is concordant with the studies of Victoria et al, Silverberg et al, Carter et al, Grantham et al 4,5,6,10,15 The mean TSH of all CKD patients (Group A+B) was higher than that of controls (Group C) but was not statistically significant (P=0.0994).…”

Section: Discussionsupporting

confidence: 91%

“…With the introduction of radioimmunoassay and chemiluminescense assay methods for estimation of thyroid hormones, the thyroid status in CKD has been studied extensively by a host of workers. Most of the authorities have demonstrated biochemical evidence of hypothyroidism and a few have detected hyperthyroidism, even goiter and exophthalmos like Silverberg et al and carter et al 4,5 Although uremia shares some of the clinical features of myxedema, overt clinical disturbances of thyroid function ordinarily does not occur Grantham et al and Spector et al 6,7 In CKD Ramirez et al and Lim et al observed biochemical evidence of hypothyroidism but in contrast Spector et al reported clinical euthyroidism in CKD patients on HD. [7][8][9] Various workers have attributed different causes for thyroid dysfunction however Victoria et al in their study of CKD patients before HD, during HD and after renal transplant comprehended the abnormalities at three different levels.…”

Section: Introductionmentioning

confidence: 99%

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Study of thyroid dysfunction and dyslipidemia in chronic kidney diseases

Tripathy

Dhal

Kanungo³

et al. 2017

Int J Res Med Sci

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Background: Though there are many studies on thyroid dysfunction and dyslipidemia in Chronic Kidney Disease (CKD), no study is conclusive. Aim of this study was to correlate abnormalities in thyroid function and lipid profile with the severity of renal failure and also to observe the difference of these abnormalities between patients on conservative management verses hemodialysis. Methods: Hundred consecutive CKD cases admitted to Medicine Department were taken up for the study. They were divided into two groups as Group-A [on conservative management] and Group-B [on regular Hemodialysis (HD)]. Hundred healthy persons were taken as control in Group-C. After evaluation of thyroid function and lipid profile statistical analysis was done by students t-test, chi-square and regression analysis. Results: Hundred CKD cases with 74% male (n=74) and 26% female (n=26) in a M: F ratio of 2.9:1 were found to be in different stages CKD (0, 2, 20, 28 and 50 in stage-1 to stage-5 respectively). In 50 cases of stage-5 CKD, 30 were on HD and 20 on conservative management. Diabetes Mellitus (DM) (40%) was the commonest etiology of CKD followed by Hypertension (HTN), obstructive uropathy, chronic glomerulonephritis (CGN) and polycystic kidney disease (PKD). Thyromegaly was not found in a single case. In all CKD cases (Group-A+B) TT3 (TT3) was significantly low (P =0.0011) when compared with control (Group-C) and no difference was found between Group-A and Group-B. Fall in TT3 worsened with increasing severity of CKD. Lipid profile study revealed Decreased HighDensity Lipoprotein Cholesterol (HDLc) and increased Triglyceride (TG), Total Cholesterol (TC), Low Density Lipoprotein Cholesterol (LDLc), TC/HDLc and LDLc/HDLc in Group-A than Group-B but only TG and TC increase was statistically significant. The levels of TG and TC and TC/HDLc increased as the stage of CKD progressed and was statistically significant (P= 0.035). Conclusions: There occurs a state of biochemical hypothyroidism without overt clinical hypothyroid state in CKD, the extent of which correlates with the severity of CKD. Increased cardiovascular complications occur due to accelerated atherosclerosis in CKD. This study confirmed that atherogenic lipid profile and thyroid dysfunction worsen with the progression of disease. Difference between patients on conservative management and HD was not found.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Study of thyroid dysfunction and dyslipidemia in chronic kidney diseases

Tripathy

Dhal

Kanungo³

et al. 2017

Int J Res Med Sci

View full text Add to dashboard Cite

show abstract

“…Compared to normal controls, plasma ACTH and serum cortisol concentrations were not fully suppressible by dexamethasone [mean ± SEM: plasma ACTH, 21 ± 4 VS. 3 ± 0.5 pg/mL (4.7 ± 0.9 VS. 0.7 ± 0.1 pmol/ L); serum cortisol, 13.9 ± 1.9 VS. 1.5 ± 0.3 J.l.g/dL (390 ± 50 VS. 40 ± 10 nmol/L); P = 0.0001), demonstrating an altered glucocorticoid feedback in the ICU patients. Patients undergoing hCRH stimulation had clearly P REVIOUS studies demonstrated that critical illness, such as in patients in intensive care units (lCU), is associated with changes in the hypothalamic-pituitary-adrenal (HP A) (1-10), hypothalamic-pituitary-thyroid (11)(12)(13), and gonadal (14)(15)(16)(17)(18) axes; the renin-angiotensin system (19)(20)(21)(22); and the sympathoadreno-medullary system (6,23). The response of the HPA axis has been shown to be essential for adaptation and maintenance of homeostasis during critical illness (24).…”

Section: Introductionmentioning

confidence: 99%

The hypothalamic-pituitary-adrenal axis in critical illness: response to dexamethasone and corticotropin-releasing hormone.

Reincke

Allolio

Würth

et al. 1993

The Journal of Clinical Endocrinology & Metabolism

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“…These include fasting or partial caloric deprivation (8)(9)(10)(11)(12); diabetes (13)(14)(15); surgical stress (16,17); moderate or severe chronic illness (18)(19)(20); cirrhosis (21,22); and a number of drugs, including Abbreviationis used in this paper: I-, iodide; T3, 3,5,3'-triiodothyronine; T4, thyroxine; T3-neogenesis, generation of T3 from T4.…”

mentioning

confidence: 99%

Observations on the factors that control the generation of triiodothyronine from thyroxine in rat liver and the nature of the defect induced by fasting.

Balsam¹,

Ingbar²

1979

J. Clin. Invest.

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A B S T R A C T Studies were performed to explore the mechanism underlying the impaired generation of 125-I-3,5,3'-triiodothyronine (T3) from 1251-thyroxine (T4) (T3-neogenesis) in preparations of liver from rats fasted for 48 h and the prevention of this effect by the feeding of glucose. T3-neogenesis in livers from fasted animals and those fed chow or glucose was assessed in various mixtures of crude microsomal fractions with either buffer or cytosols. T3-neogenesis was mediated by an enzyme present in the microsomal fraction whose activity was enhanced by cytosolic cofactor(s). In livers from animals fasted for 48 h, the supporting activity of cytosol was decreased, whereas the activity of the enzyme was unaffected. Administration of glucose as the sole nutritional source prevented the decrease in the supporting activity of hepatic cytosol that was regularly observed in the case of animals totally deprived of food.The diminished supporting activity for T3-neogenesis provided by liver cytosol from fasted animals was restored to normal by enrichment with either NADPH or GSH, but the two cofactors appeared to act at different loci. GSH stimulated T3-neogenesis in microsomes incubated in the absence of cytosol, i.e., in buffer, whereas NADPH did not. The stimulatory effect of both agents was blocked by the sulfhydryl oxidant, diamide, which also inhibited T3-neogenesis in mixtures of microsomes with cytosols. Taken together, these observations suggest that GSH acts directly on the enzyme in the crude microsomal fraction, whereas NADPH acts within the cytosol, possibly by increasing the concentration of GSH through the action of the enzyme glutathione reductase, for which NADPH is a cofactor. In this light, the decreased supporting activity of hepatic cytosol

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Effect of Severe, Chronic Illness on Thyroid Function

Cited by 202 publications

References 19 publications

Study of thyroid dysfunction and dyslipidemia in chronic kidney diseases

Study of thyroid dysfunction and dyslipidemia in chronic kidney diseases

The hypothalamic-pituitary-adrenal axis in critical illness: response to dexamethasone and corticotropin-releasing hormone.

Observations on the factors that control the generation of triiodothyronine from thyroxine in rat liver and the nature of the defect induced by fasting.

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