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)

The coexistence of organ-specific and nonorgan-specific autoimmune diseases is an interesting phenomenon. A 52-year-old woman was admitted with fever, general discomfort, polyarthritis, and Raynaud's phenomenon. Physical examination revealed a goiter of stony consistency, hardening, paleness, and atrophy of the skin on the face and upper limbs, and blood hypertension (180/110 mmHg). The biological data included leukopenia, moderate anemia, and a very high sedimentation rate. The latex test was positive (+++); LE cells positive (+); hypergammaglobulinemia (3.5 g); antinuclear antibodies, 1/1280 with an immunofluorescence granular pattern; antithyroid antibodies, 1/160. There was pulmonary, renal, and gastrointestinal involvement compatible with scleroderma, which was confirmed by skin biopsy. A thyroidectomy revealed the existence of a papillary carcinoma with thyroiditis. Responde to treatment with immunosuppressive agents, hypotensive drugs, and thyroid substitution therapy was initially good. The patient was readmitted 8 months later with general discomfort and a severe hyperproteinemia (10 g/100 ml), including 65 percent gammaglobulin and requiring various sessions of plasmapheresis. The patient was discharged, but died suddenly 4 months later. The association of lupus and scleroderma in this patient is discussed and the possibility of its being a mixed connective tissue disease is discarded. The association of this condition with Hashimoto's thyroiditis, and the latter with papillary carcinoma of the thyroid are analyzed. The peculiar features of this case are pointed out. The authors postulate that the cause of the sudden death was a vascular cerebral complication induced by the extreme hyperproteinemia.
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PMID:[Scleroderma with traces of disseminated lupus erythematosus associated with Hashimoto's thyroiditis and papillary carcinoma of the thyroid gland (author's transl)]. 58 90

A 65-year-old female patient suffering from hypertension and myxedema due to chronic thyroiditis developed anginal attacks under trichlormethiazide therapy. The ECG revealed a SA block with reciprocal beats and aberrant ventricular conduction in a form of bigeminy. Upon substitution of desiccated thyroid for the antihypertensive drug, the anginal attacks subsided, the conduction disturbances disappeared and the blood pressure returned to normal without hypotensive treatment. This observation suggests that replacement therapy should precede diuretics in hypertensive patients with myxedema.
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PMID:Sinus arrest following diuretic therapy in a patient with myxedema and hypertension. 124 Jul 90

We experienced 41 cases of Cushing's syndrome (12 males and 29 females, 15 years old - 65 years old) during the last 20 years. These included 20 patients with unilateral adrenal adenoma (Cushing's syndrome), 19 patients with bilateral adrenal hyperplasia (Cushing's disease), one patient with adrenal carcinoma and one patient with primary adrenocortical nodular dysplasia (PAND). Moreover, these cases included some special ones, i.e. 5 cases with destructive thyroiditis after treatment, 2 cases with aggravation of arthritis after treatment, a case of Carney's complex with PAND, one case with paradoxical response to dexamethasone, and one case combined with empty sella syndrome. The most specific clinical signs were moon face (95% occurrence), hypertension (95%) and subcutaneous bruising (80%). Other significant signs were eye edema (66%), buffalo hump (68%), subcutaneous purpura (63%) and osteoporosis (49%). Skin striae was not a common sign in our cases (41%). Renal stone was observed in only 20% of our patients but was a significant sign in this syndrome. There was no difference in the occurrence of each clinical sign between Cushing's syndrome and Cushing's disease. The elevation of white blood cell count (WBC) and serum sodium, a decrease of serum potassium, and a decrease of reabsorption of phosphate (%TRP) were observed. Thyroid-stimulating hormone (TSH) and human growth hormone (HGH) were suppressed in patients with Cushing's syndrome and patients with Cushing's disease. These results were consistent with those of previous reports. However, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were high in those patients with Cushing's syndrome and those with Cushing's disease. Oral glucose tolerance test was carried out in 34 patients before and after treatment. Thirty-one percent of those had diabetes mellitus and 26% had impaired glucose tolerance (IGT). The response of IRI in this test was high in patients with Cushing's syndrome and patients with Cushing's disease, and decreased 4 weeks after treatment in those with Cushing's syndrome but remained high in those with Cushing's disease. Plasma ACTH level and urinary 17-OHCS excretion were significantly higher in Cushing's disease than in Cushing's syndrome. During an 8mg-high-dose dexamethasone suppression test, urinary 17-OHCS excretion in 13 of 14 patients with Cushing's disease (93%) was suppressed by more than 50% of baseline on the second day of testing. However, all of 18 patients with Cushing's syndrome, who had an 8mg-dexamethasone suppression test, failed to suppress urinary 17-OHCS by 50% of baseline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Forty-one cases of Cushing's syndrome: a comparison between Cushing's syndrome (adrenal adenoma) and Cushing's disease (adrenal hyperplasia)]. 163 31

In order to assess the Japanese dietary iodine intake, we examined the urinary iodine excretion of those on an ordinary Japanese diet chosen at random and observed whether the thyroid function might affect the amounts of urinary iodine excretion. The subjects consisted of cases of untreated hypothyroidism and chronic thyroiditis (CT) and euthyroid controls who were healthy people or had non-thyroidal disorders such as diabetes mellitus or hypertension. Eight cases of hypothyroidism were composed of 3 cases of secondary hypothyroidism with empty sella syndrome and 5 cases of primary hypothyroidism and 32 patients with CT have been maintained in euthyroid states with T4 medication. We selected 32 cases of sex and age-matched healthy people as controls. The mean levels of excreted urinary iodine were 465.6 micrograms/day in the healthy controls and 471.8 micrograms/day in patients with CT, respectively. Urinary iodine excretion was significantly correlated to serum inorganic iodide in both controls and CT patients, of which correlation coefficients were +0.35 and +0.5, respectively. Urinary iodine and serum inorganic iodide ratios (U/S) in hypothyroidism were significantly (p less than 0.05) depressed compared with those in CT. The present study indicated that recent Japanese dietary iodine intake was estimated to be approximately 470 micrograms/day and that the urinary iodine excretion would be influenced not only by iodine intake but also by thyroid function.
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PMID:[Urinary iodide excretion in Japanese people and thyroid dysfunction]. 164 7

To study whether there is an association between hypertension and hypothyroidism, measurements of blood pressure and thyroid function were determined in 477 female patients with chronic thyroiditis. Based on the blood levels of thyroxine (T4) and thyroid stimulating hormone (TSH), 308 patients were considered euthyroid and 169 were hypothyroid [T4 = 2.9 +/- 0.1 micrograms/dl and TSH = 105.8 +/- 6.8 microU/ml (mean +/- SEM)]. Diastolic, but not systolic, blood pressure in hypothyroid patients over 50 years was higher than in euthyroid patients of corresponding age groups. The prevalence of hypertension was higher in hypothyroid patients when hypertension was defined as the systolic and/or diastolic blood pressure above 160/95 mm Hg (14.8% vs 5.5%; p less than 0.01). Correlations between diastolic, but not systolic, blood pressure and either the blood level of triiodothyronine (T3) or T4 was significant (r = - 0.174, p less than 0.01, and r = 0.208, p less than 0.01, respectively) when data from both euthyroid and hypothyroid patients were combined. Adequate thyroid hormone replacement therapy for an average 14.8 months in 14 patients resulted in a normalization of thyroid function and a reduction of blood pressure (p less than 0.01). In four who showed no change in thyroid function due to inadequate replacement therapy, blood pressure remained elevated. These results suggest a close association between hypertension and hypothyroidism.
Hypertension
PMID:Hypothyroidism as a cause of hypertension. 684 58

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

Various forms of cellular injury, whether induced by immune effector cells, aberrant metabolic processes, chemotherapeutic drugs or temperature shifts, result in common morphological changes consisting of the formation and shedding of membrane vesicles from the injured cell surfaces, i.e., apoptosis. This dynamic cell surface membrane behavior appears to be dependent on the disruption of cytoplasmic microtubules. Concomitant with the altered cell surface morphology, certain physiological and biochemical events have been found to be associated with cell injury. These include changes in membrane permeability, elevated oxygen consumption rates and nuclear DNA fragmentation. However, it remains to be experimentally established which of these biological changes defines a state of irreparable cell injury and/or programmed cell death (PCD). Selective cell injury and death is the goal of many therapeutic modalities aimed at the destruction of malignant cells. On the other hand, prevention of cell injury is desirable in autoimmune diseases such as systemic lupus erythematosus, thyroiditis, insulin dependent diabetes and many others. Injury to the vascular endothelium may play a role not only in thrombosis, atherosclerosis and hypertension, but may also provide the avenues for the metastasis of malignant cells. The objective of the present review is to compare and evaluate the cell injury process induced by effector lymphocytes with that caused by low temperature. The latter mimics most, if not all, the currently known criteria of immune effector cell mediated PCD of target tumor cells.
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PMID:Cell injury and apoptosis. 774 62

The author describes briefly some little known paraneoplastic syndromes: hypertension, circulatory failure, arterial ischaemia, Stauffer's syndrome, visceral neuropathy, thyroiditis and others. He comments on them, based on his own experience.
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PMID:[Little known paraneoplastic syndromes]. 851 47

Physiologic changes in metabolism may make thyroid diseases difficult to diagnose during pregnancy. Such diagnoses depend principally on clinical acumen and an understanding of the alterations of laboratory values, particularly thyroid-stimulating hormone (TSH), induced by pregnancy. Untreated thyrotoxicosis may lead to abortion, stillbirth, neonatal death and low birth weight. The principal cause of thyrotoxicosis in pregnancy is Graves' disease, which may be treated with antithyroid drugs or surgery. The use of radioactive iodine is absolutely contraindicated during pregnancy. Hypothyroidism during pregnancy is associated with hypertension and premature labor. The goal of thyroxine replacement therapy is to maintain serum TSH levels in the normal range. Many thyroid conditions and treatments directly affect the fetus and the principal antithyroid drugs are secreted in breast milk. Both the mother and neonate require monitoring. In addition, autoimmune postpartum thyroiditis may recur following each pregnancy in susceptible patients.
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PMID:Thyroid disease during pregnancy. 854 48

Hypothyroidism during pregnancy occurs in 1/1600-2000 deliveries, according to the most recent publications. The most common causes are chronic autoimmune thyroid disease, radiodine-131 treatment, or surgical removal. The diagnosis is difficult to make on clinical grounds alone, even in advanced cases, and a high index of suspicion is needed. Some women are at high risk of developing hypothyroidism, and they should be screened. These women may have had previous treatment for hyperthyroidism; high-dose neck irradiation, evidence of thyroid autoimmunity, amiodarone therapy, suspected hypopituitarism, and type I diabetics. The best laboratory test is the serum TSH, followed, if elevated, by a free T4 index and a TPO-ab titer. Thyroid antibodies have been associated with an increased (double) risk of miscarriage and postpartum thyroiditis. Frequent (22-44%) pregnancy-induced hypertension leading to preterm delivery, and prematurity is the main complication observed in those still hypothyroid near term. Proper therapy eliminates or reduces the risk. No congenital anomalies have been reported in the most recent studies, and the data available shows that both physical and mental development have been normal until children are 10 years old. However, one study reported lower IQs in children of euthyroid women with positive TPO-ab than in children of TPO-ab negative mothers. Levothyroxine is the treatment of choice. Euthyroidism must be reached and maintained in a timely fashion. Many women need more thyroxine during pregnancy, and surveillance of thyroid function is needed throughout gestation to make dose adjustments when needed. During the postpartum periods the thyroxine requirements decrease to preconception levels.
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PMID:Management of hypothyroidism during pregnancy. 910 50


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