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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid hormones have been shown to be absolutely necessary for early brain development. During pregnancy, both maternal and foetal thyroid hormones contribute to foetal brain development and maternal supply explains why most of the athyreotic newborns usually do not show any signs of hypothyroidism at birth. Foetal and/or neonatal hypothyroidism is a rare disorder. Its incidence, as indicated by neonatal screening, is about 1:4000. Abnormal thyroid development (i.e. agenesia, ectopic gland, hypoplasia) or inborn errors in thyroid hormone biosynthesis are the most common causes of permanent congenital hypothyroidism. Recent studies reported that mutations involving Thyroid Transcriptor Factors (TTF) such as TTF-1, TTF-2, PAX-8 play an important role in altered foetal thyroid development. Deficiency of transcriptor factor (Pit-1, Prop-1, LHX-3) both in mother and in the foetus represents another rare cause of foetal hypothyroidism. At birth clinical picture may be not always so obvious and typical signs appear only after several weeks but a delayed diagnosis could have severe consequences consisting of delayed physical and mental development. Even if substitutive therapy is promptly started some learning difficulties might still arise suggesting that intrauterine adequate levels of thyroid hormones are absolutely necessary for a normal neurological development. Placental transfer of maternal antithyroid antibodies inhibiting fetal thyroid function can cause transient hypothyroidism at birth. If the mother with thyroid autoimmune disease is also hypothyroid during pregnancy and she doesn't receive substitutive therapy, a worse neurological outcome may be expected for her foetus. Foetal and/or neonatal hyperthyroidism is a rare condition and its incidence has been estimated around 1:4000-40000, according to various authors. The most common causes are maternal thyroid autoimmune disorders, such as Graves' disease and Hashimoto's thyroiditis. Rarer non autoimmune causes recently identified are represented by TSH receptor mutations leading to constitutively activated TSH receptor. Infants born to mothers with Graves' history may develop neonatal thyrotoxicosis. Foetal/neonatal disease is due to transplacental thyrotrophin receptor stimulating antibodies (TRAb) passage. It's extremely important recognizing and treating Graves' disease in mothers as soon as possible, because a thyrotoxic state may have adverse effects on the outcome of pregnancy and both on the foetus and newborn. Thyrotoxic foetuses may develop goitre, tachycardia, hydrops associated with heart failure, growth retardation, craniosynostosis, increased foetal motility and accelerated bone maturation. Neonatal Graves' disease tends to resolve spontaneously within 3-12 weeks as maternal thyroid stimulating immunoglobulins are cleared from the circulation but subsequent development may be impaired by perceptual motor difficulties. Hashimoto's thyroiditis is a very common autoimmune thyroid disease. In presence of maternal Hashimoto's thyroiditis, there are usually no consequences on foetal thyroid, even if antiTPO and antiTg antibodies can be found in the newborn due to transplacental passage. However there are some literature reports describing foetal and neonatal hyperthyroidism in the affected mothers' offspring.
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PMID:Foetal and neonatal thyroid disorders. 1224 77

We report a case of a fifty year old woman with Graves' disease with positive AntiTPO antibodies and positive AntiTSH receptor antibodies, who was hospitalized with a right cardiac failure. A pulmonary hypertension was discovered on echocardiography. After adequate antithyroid therapy, the right cardiac failure regressed rapidly and pulmonary pressure normalised. An autoimmune process has often been proposed to explain the association between pulmonary hypertension and hyperthyroidism. We report the arguments supporting this autoimmune etiopathogenesis. We also discuss an other hypothesis based on a direct effect of thyroid hormones on the pulmonary circulation and the effects of high cardiac output associated with hyperthyroidism.
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PMID:[Primary pulmonary hypertension arterial and Basedow disease]. 1252 39

We report the case of a 48-year-old woman with a diagnosis of pulmonary hypertension and hyperthyroidism (Graves' disease) in whom pulmonary artery pressures became normal after treatment of thyroid disease. The possible pathogenic mechanisms involved in this association include the presence of hyperdynamic heart failure and/or the presence of immune alterations underlying both conditions.
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PMID:[Reference figures for pulmonary artery pressures after effective treatment of Graves' disease]. 1255 20

The authors report on 30 cases of cardiothyrotoxicosis in the young adult with Basedow's disease. Cardiac arrhythmia represented the most frequent clinical form of dysfunction, mainly atrial fibrillation. Conductive disorders came second, with seven cases of first-degree atrioventricular block [AVB], one case of second-degree AVB, and two cases of sinusoidal bradycardia. Three cases of ballooning of the mitral valve were detected by echocardiography. Myocardial hypertrophy was found in one case. The authors discuss the various physiopathological hypotheses regarding conduction and myocardial hypertrophy anomalies. No cases of severe cardiac insufficiency or coronaropathy were noted, which is explained by the absence of cardiopathic antecedents and the young age of the patient population. Treatment is more complicated in the case of a preexisting cardiac event.
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PMID:[Cardiothyrotoxicosis in the young adult in Basedow disease: report of 30 cases]. 1255 75

First cause of hyperthyroidism among women of childbearing age, Graves' disease raises the risk of maternal and fetal complications, including eclampsia, cardiac failure, abortion, prematurity, fetal death, all of which can be avoided if maternal hyperthyroidism is closely controlled. The risk of transplacental hyperthyroidism has been shown to correlate to the titre of anti-TSH receptor antibodies and has to be evaluated not only in women treated for Graves' disease during pregnancy, but also in women who have previously received radio iodine treatment or undergone surgery for Graves' disease: TSH-receptor antibodies may indeed remain at a high level several years after initial treatment. Both methimazole and propylthiouracil are equally effective to restore maternal euthyroidism. Accumulation of case-reports relating congenital malformations (mostly aplasia cutis, but in some cases, severe malformations) among the offspring of methimazole-treated women suggests the possibility of a teratogenic effect of methimazole. Despite the fact that the link between severe congenital defects and methimazole exposure during pregnancy is not formally established, propylthiouracil should be preferred to methimazole for the treatment of young hyperthyroid women.
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PMID:[Antithyroid agents and embryopathies]. 1506 47

Today, dilated cardiomyopathy (DCM) represents the main cause of severe heart failure and disability in younger adults and thus is a challenge for public health. About 30% of DCM cases are genetic in origin; however, the large majority of cases are sporadic, and a viral or immune pathogenesis is suspected. Following the established postulates for pathogenesis of autoimmune diseases, here we provide direct evidence that an autoimmune attack directed against the cardiac beta(1)-adrenergic receptor may play a causal role in DCM. First, we immunized inbred rats against the second extracellular beta(1)-receptor loop (beta(1)-EC(II); 100% sequence identity between human and rat) every month. All these rats developed first, receptor-stimulating anti-beta(1)-EC(II) Ab's and then, after 9 months, progressive severe left ventricular dilatation and dysfunction. Second, we transferred sera from anti-beta(1)-EC(II)-positive and Ab-negative animals every month to healthy rats of the same strain. Strikingly, all anti-beta(1)-EC(II)-transferred rats also developed a similar cardiomyopathic phenotype within a similar time frame, underlining the pathogenic potential of these receptor Ab's. As a consequence, beta(1)-adrenergic receptor-targeted autoimmune DCM should now be categorized with other known receptor Ab-mediated autoimmune diseases, such as Graves disease or myasthenia gravis. Although carried out in an experimental animal model, our findings should further encourage the development of therapeutic strategies that combat harmful anti-beta(1)-EC(II) in receptor Ab-positive DCM patients.
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PMID:Direct evidence for a beta 1-adrenergic receptor-directed autoimmune attack as a cause of idiopathic dilated cardiomyopathy. 1514 32

The abundance of published data on the neonatal effects of maternal Graves' disease (GD) contrasts with the paucity of information on fetal effects. In our yet unpublished study, we prospectively studied 72 pregnant women with a history of Graves' disease. Fetal ultrasonography was done at 22 and 32 weeks of gestational age. Fetal goiter was found at 32 weeks in 11 of the fetuses of the 41 mothers with positive TSH-receptor antibodies and/or antithyroid treatment and in none of the fetuses of the 31 other mothers. In the 11 fetuses with goiter, ultrasound findings (thyroid Doppler and bone maturation), fetal heart rate, and maternal antibody and antithyroid drug status effectively discriminated between hypothyroidism (n=7) and hyperthyroidism (n=4). One fetus with hyperthyroidism died in utero at 35 weeks from heart failure. Treatment was successful in the ten other fetuses. One fetus without goiter had moderate hypothyroidism at birth. This study showed that it is of the utmost importance to have the fetal thyroid scrutinized by an expert ultrasonographist and to have team work with obstetricians and paediatric endocrinologists in pregnant mothers with GD. This allowed us to accurately determine fetal thyroid status and to adapt the treatment in mothers successfully. Fetal hyperthyroidism does exist and needs an appropriate aggressive treatment.
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PMID:Fetal and neonatal thyroid function in relation to maternal Graves' disease. 1515 41

Edema develops as one of symptoms and signs in several endocrine disorders, and sometimes can be important clue in detecting the basal endocrine disorder. In patients with long-standing hypothyroidism, characteristic edematous skin changes develop and be called myxedema. In hyperthyroid patients with Graves' disease, peripheral edema sometimes develop with or without heart failure. Severe eyelid puffiness composing Graves' ophthalmopathy and 'circumscribing myxedema', mostly in the pretibial regions, are also highly disease-specific disorders. In Cushing's syndrome, both adrenal and ACTH-dependent, peripheral edema is sometimes important sign leading suspicion of this syndrome. In diabetic patients, attention should be paid to edema constantly especially with nephropathy and hypertension. In diabetic nephropathy stage 3B, aggravation of renal function is often progressive. Recently the range of therapeutic options of glycemic controls has been extended with introduction of thiazolidinediones (TZDs). Weight gain and peripheral edema are recognized side effects of these drugs, particularly when used in combination with insulin. The potential risk of worsened heart failure should be taken into consideration when TZDs are used in patients with diabetes and heart diseases.
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PMID:[Edema in endocrine and metabolic diseases]. 1567 23

A 60-year-old woman was admitted to a hospital complaining of dizziness and general fatigue in October, 2004. Because of heart failure and severe anemia, she was referred to our hospital. Based on a positive direct Coombs test and an elevated level of platelet-associated IgG (PAIgG), the patient was diagnosed as having autoimmune hemolytic anemia (AIHA) associated with idiopathic thrombocytopenic purpura (ITP), i.e., Evans syndrome. Basedow disease was also diagnosed due to hyperthyroidism with an elevation of anti-thyroid stimulating hormone (TSH) receptor antibodies. Both the Evans syndrome and Basedow disease were considerably ameliorated with plasma exchange, corticosteroid and thiamazole therapy. Although Basedow disease is known to be associated with hematological disorders such as AIHA or ITP, the combination of Basedow disease and Evans syndrome is rare. We report here a case of Basedow disease associated with Evans syndrome.
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PMID:[Basedow disease associated with Evans syndrome]. 1644 Jul 74

A 53-yr-old previously healthy man was admitted to our hospital for thyrotoxicosis without ophthalmopathy. Initial therapy with propylthiouracil caused an acute elevation of liver enzymes. Then, he received a first course of 131I therapy (20 mCi). At the end of 6-mo follow-up after 131I, he was still thyrotoxic and developed moderately severe ophthalmopathy. The patient refused thyroid surgery and decided to undergo second course of 131I therapy (30 mCi). Concomitantly with the 131I, we opted to give high-dose pulse glucocorticoid therapy (PGT) to prevent further deterioration of GO. The patient was started on intravenous methylprednisolone pulse therapy 1 g daily in a cycle (one cycle every 2 wk, each cycle comprising two infusions on alternate days). After the end of the second day of PGT administration, he suddenly developed onset of acute pulmonary edema and hypertension. There was no previous history of cardiac disorder or conditions predisposing to cardiac failure other than thyrotoxicosis. A presumptive diagnosis of fluid overload and/or hypertension- induced acute heart failure was made. After prompt investigations excluding cardiogenic causes, we thought that this condition was triggered by PGT that was superimposed on thyrotoxicosis-related hemodynamic instability. Graves' patients with uncontrolled thyrotoxicosis should be under careful surveillance when PGT is planned. To our knowledge, this is the first reported case of life-threatening acute pulmonary edema caused by PGT in GO.
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PMID:New-onset acute heart failure after intravenous glucocorticoid pulse therapy in a patient with Graves' ophthalmopathy. 1694 91


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