Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic acidosis is noted in the majority of patients with chronic kidney disease (CKD) when glomerular filtration rate (GFR) decreases to less than 20% to 25% of normal, although as many as 20% of individuals can have acid-base parameters close to or within the normal range. Acidosis generally is mild to moderate in degree, with plasma bicarbonate concentrations ranging from 12 to 22 mEq/L (mmol/L), and it is rare to see values less than 12 mEq/L (mmol/L) in the absence of an increased acid load. Degree of acidosis approximately correlates with severity of renal failure and usually is more severe at a lower GFR. The metabolic acidosis can be of the high-anion-gap variety, although anion gap can be normal or only moderately increased even with stage 4 to 5 CKD. Several adverse consequences have been associated with metabolic acidosis, including muscle wasting, bone disease, impaired growth, abnormalities in growth hormone and thyroid hormone secretion, impaired insulin sensitivity, progression of renal failure, and exacerbation of beta 2 -microglobulin accumulation. Administration of base aimed at normalization of plasma bicarbonate concentration might be associated with certain complications, such as volume overload, exacerbation of hypertension, and facilitation of vascular calcifications. Whether normalization of plasma bicarbonate concentrations in all patients is desirable therefore requires additional study. In the present review, we describe clinical and laboratory characteristics of metabolic acidosis, discuss potential adverse effects, and address benefits and complications of therapy.
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PMID:Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. 1595 26

Acromegaly is associated with a two to three-fold increase in mortality related predominantly to cardiovascular disease. The excess mortality is associated most closely with higher levels of growth hormone (GH). Survival in acromegaly may be normalized to a control age-matched rate by controlling GH levels; in particular, GH levels less than 2.5 ng/mL are associated with survival rates equal to those of the general population. Hyperhomocysteinemia has also been recognized as a risk factor for cardiovascular disease, yet there are limited data on the prevalence of hyperhomocysteinemia in patients with acromegaly. Eighteen acromegaly patients (7 male, 11 female, mean age 42.8 +/- 11.0 years) in our endocrine clinic consented to having the following tests performed: complete blood count (CBC), thyroid hormones, folic acid, vitamin B12, plasma homocysteine levels, uric acid, fibrinogen, CRP, fasting glucose, insulin, C-peptide, total serum cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, GH, insulin-like growth factor-1 (IGF-1) and GH levels after an oral glucose tolerance test (OGTT). By history, fourteen had macroadenomas and four had microadenomas; eight had hypertension; two had glucose intolerance, and four had diabetes. Fifteen had had transsphenoidal or transfrontal surgery: two had been cured, but 13 others were taking long-acting octreotide. Five patients had undergone radiotherapy and the acromegaly in two was treated primarily with long-acting octreotide. CBC, thyroid hormone, folic acid, and vit B12 levels were normal in all patients. We divided the patients into two groups according to mean GH levels after an OGTT: Group 1 (GH<2.5 ng/mL, n=10), and Group 2 (GH<2.5 ng/mL, n=8). Comparison of the two groups using Mann-Whitney U testing revealed statistically significant lower levels in Group 1 of the following parameters: GH (1.91 +/- 0.90 vs. 8.58 +/- 5.55 ng/mL, p=0.002), IGF-1 (338.30 +/- 217.90 vs. 509.60 +/- 293.58 ng/dL, p=0.06), GH after an OGTT (1.42 +/- 0.81 vs. 9.01 +/- 4.53 ng/mL, p=0.001), plasma homocysteine (12.85 +/- 4.47 vs. 18.20 +/- 4.99 micromol/L, p=0.05), total cholesterol (164.0 +/- 20.81 vs. 188.0 +/- 22.26 mg/dL, p=0.05) and LDL cholesterol (81.0 +/- 9.64 vs. 116.70 +/- 13.03 mg/dl, p=0.01). Differences between the other parameters were not significantly different. Acromegaly patients with high GH levels after an OGTT have much higher levels of homocysteine than patients with lower GH levels. The role of elevated homocysteine levels as an independent cardiovascular risk factor in the mortality of acromegaly patients should be determined in future studies.
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PMID:Homocysteine levels in acromegaly patients. 1638 Jul

This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper- and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the renin-angiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.
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PMID:Vascular and renal function in experimental thyroid disorders. 1645 32

Radioiodine is considered the treatment of choice for hyperthyroidism, but in some situations, methimazole therapy is preferred, such as in cats with pre-existing renal insufficiency. Methimazole blocks thyroid hormone synthesis, and controls hyperthyroidism in more than 90% of cats that tolerate the drug. Unfavorable outcomes are usually due to side effects such as gastrointestinal (GI) upset, facial excoriation, thrombocytopenia, neutropenia, or liver enzyme elevations; warfarin-like coagulopathy or myasthenia gravis have been reported but are rare. Because restoration of euthyroidism can lead to a drop in glomerular filtration rate, all cats treated with methimazole should be monitored with BUN and creatinine, in addition to serum T4, complete blood count, and liver enzymes. Transdermal methimazole is associated with fewer GI side effects, and can be used in cats with simple vomiting or inappetance from oral methimazole. Hypertension may not resolve immediately when serum T4 is normalized, and moderate to severe hypertension should be treated concurrently with-atenolol, amlodipine, or an ACE inhibitor. Alternatives to methimazole include carbimazole, propylthiouracil, or iodinated contrast agents.
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PMID:Medical management of hyperthyroidism. 1658 27

Hyponatremia, albeit common in chronic renal insufficiency, necessitates a detailed search of the underlying hidden causes. We report on a 67-year-old woman with chronic kidney disease (creatinine 230 micromol/L) and hypertension who suffered from general fatigue, dizziness, nausea, vomiting and abdominal fullness off and on for 6 months. Hyponatremia (plasma Na(+) 106-125 mmol/L) on 4 occasions during the past 6 months was noticed. Her extracellular volume status was apparently normal. Plasma Na(+) concentration 110 mmol/L was the most striking laboratory abnormality with mild metabolic acidosis (HCO(3)- 19.8 mmol/L). Her urine Na(+) concentration and osmolality were inappropriately high. Her hyponatremia was refractory to normal saline, hypertonic NaHCO(3) and 0.1-microg 9 alfa-fludrocortisone. Despite normal plasma cortisol and thyroid hormone concentrations, a provocation test with cosyntropin (250 microg) showed a blunted cortisol (<579 nmol/L) but intact aldosterone response. Magnetic resonance imaging of her brain displayed a normal pituitary gland and hypothalamus. A history of intermittent intravenous steroid therapy to treat her allergic rhinitis for 3 years was uncovered. Steroid supplements induced water diuresis and corrected hyponatremia to 135 mmol/L in 5 days. With nonspecific clinical symptoms, glucocorticoid insufficiency must be kept in mind as a cause of hyponatremia even in patients with impaired renal function and normal plasma cortisol concentration.
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PMID:Recurrent hyponatremia in a patient with chronic kidney disease. 1687 5

Thyroid hormone has been studied in cardiovascular disease but rarely in cerebrovascular disease (CVD). Recently, hypothyroidism has been suggested to be related to risk factors such as atherosclerosis but not directly to CVD. We reported a 52-year-old woman with acute ischemic stroke, and greatly improved general conditions after thyroid hormone replacement. Hypothyroidism is reported to be one of the causes of hypertension or elevated cholesterol levels, the established risk factors of CVD. Further studies of the possible association of thyroid hormone and CVD are warranted. Thyroid hormone might need to be surveyed in CVD patients especially if there are symptoms and signs of thyroid disorders.
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PMID:Hypothyroidism and cerebral infarction: a case report and literature review. 1699

The syndrome of apparent mineralocorticoid excess (AME) is characterized by persistent hypertension and hypokalemia, which is caused by impaired inactivation of cortisol (F) to cortisone (E). The thyroid hormone has been known to influence the F to E conversion leading to efficacious inactivation of F into E. However, there have been no reports regarding the clinical manifestation of secondary AME due to hypothyroidism. Here we report an elderly patient who manifested AME, showing persistent hypertension with hypokalemia induced by primary hypothyroidism. Maintenance of euthyroid conditions ameliorated the concurrent AME and restored adrenal secretion of aldosterone after the recovery of the F to E shuttle. This case report would broaden our clinical recognition regarding acquired AME in relation to thyroid dysfunction.
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PMID:Apparent mineralocorticoid excess manifested in an elderly patient with hypothyroidism. 1719 20

Symptomatic ascites as a presenting symptom of hypothyroidism is quite rare. In most of the case reports, patients with ascites requiring therapeutic abdominal paracentesis have long-standing hypothyroidism. We present a case of symptomatic ascites in a subject with hypothyroidism following radioiodine therapy for Graves disease. A 70-year-old African-American man presented with increasing weakness, shortness of breath, weight gain, constipation, and abdominal distention. Past history was significant for coronary artery disease, diabetes, hypertension and history of radioiodine therapy for Graves disease 9 months prior to the presentation. He was taking levothyroxine at 50 microg per day for 3 months prior to the presentation. Physical examination findings were significant for puffiness around the eyes, decreased breath sounds at the lung bases, and distended abdomen with free fluid, hung-up reflexes, and cold extremities. The thyroid-stimulating hormone level at the time was 64 with a free T4 less than 0.4 ng/dL. Analysis of the ascitic fluid revealed an exudative effusion with a serum to ascitic fluid albumin gradient of 1.2. The patient required therapeutic abdominal paracentesis twice, with 4 L each time, to relieve the symptoms. Work-up to rule out other causes did not reveal any other relevant abnormality. After initiation of thyroid hormone replacement, the patient responded very well and the ascites resolved within 2 months. We conclude that ascites associated with hypothyroidism is rare but must be recognized early, since thyroid replacement is the definitive therapy.
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PMID:Symptomatic ascites in a patient with hypothyroidism of short duration. 1722 Jun 93

Obesity is associated with increased cardiovascular morbidity and mortality, in part through development of hypertension. Leptin promotes weight loss by reducing food intake and increasing energy expenditure through sympathetic stimulation. It also counteracts the starvation-induced suppression of thyroid hormone by up-regulating the expression of TRH. On the other hand, it is known that the extrahypothalamic TRH system participates in cardiovascular function modulating sympathetic system activity. In order to challenge the testable hypothesis that obesity may raise arterial blood pressure (ABP) through TRH system activation, we herein analyze the participation of the TRH system in the elevation of ABP in the obese agouti yellow mice. These mice are characterized by resistance to the weight reducing effect of leptin although they show a preserved sympathetic response to leptin along with a mild hypertension compared with the control strain (121+/-2 vs 102+/-2 mmHg, p less than 0.001, n=10). We report here that hyperleptinemic agouti mice showed a 1.8-fold elevation of diencephalic TRH content compared with controls, and we demonstrate that a long lasting specific inhibition of TRH system by icv treatment with siRNA against preproTRH normalizes systolic ABP independently of the thyroid status. These results suggest that the interaction leptin-diencephalic TRH may be one of the mechanisms involved in the mild hypertension of the obese agouti mice.
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PMID:SiRNA-mediated silencing of the diencephalic thyrotropin-releasing hormone precursor gene decreases the arterial blood pressure in the obese agouti mice. 1748 11

A 72-year-old white woman with an abnormal serum thyroid-stimulating hormone (TSH) concentration was referred to our facility for a comprehensive evaluation. Circulating thyroxine (T4) and free thyroxine (FT4) concentrations were all in the normal range. Tri-iodothyronine (T3) concentrations were in the low end or slightly below the normal range. TSH was detectable but was below the limits of the normal range. The patient was clinically euthyroid and was receiving medication only for treatment of hypertension. The clinical and laboratory thyroid function status was consistent with a diagnosis of subclinical hyperthyroidism. The physical examination did not reveal thyroid enlargement, nor was there any evidence for the presence of thyroid nodules or ocular changes suggestive of Graves disease. Among thyroid autoantibodies of particular interest was the presence of a moderate thyroid-stimulating immunoglobulin (TSI) level that was stable and consistently present during a 7-month observational period. At 13 months after the initial visit, TSI antibodies were absent and TSH concentration had returned to the normal range. Based on the TSH agonist activity of TSI and the observed reciprocal relation of TSI and TSH, there was no need to suggest pituitary hypersensitivity to thyroid hormone.
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PMID:Reciprocal relation of thyroid-stimulating hormone and thyroid-stimulating immunoglobulin in a patient with endogenous subclinical hyperthyroidism. 1750 73


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