Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothyroidism affects 4% to 10% of women, increasing with age. Symptoms, which are often nonspecific and subtle, can include: lethargy, mild weight gain, edema, cold intolerance, constipation, mental impairment, dry skin, depression, irregular menses, hoarseness, myalgias, hyperlipidemia, and bradycardia. TSH determination is usually warranted when some of these are present. Confirmation of diagnosis is based on laboratory tests, not symptoms. With Hashimoto's thyroiditis, the most common cause, the thyroid is usually firm and irregular to palpation. Screening is recommended by the American Thyroid Association, American Association of Clinical Endocrinologists and ACOG. Studies indicate that even slight hypothyroidism is associated with increased miscarriage, late fetal demise and lower IQ of offspring. Many believe all women intending conception or pregnancy should be screened. Most patients with even slightly elevated TSH should be treated, though controversy remains. Hypothyroidism is usually permanent, and treatment is life-long; postpartum thyroiditis may be transient. Levothyroxine is the standard treatment. Because of variable bioavailability of some levothyroxine preparations, designation of a specific high-quality brand is appropriate; TSH should be monitored to titrate the dose. The third-generation super-sensitive TSH is the most accurate test for both hypo- and hyperthyroidism. Because estrogen increases levels of thyroid binding globulin, women who are on HRT or OCs, or are pregnant, usually have total T4 levels above the reference range.
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PMID:Hypothyroidism and women's health. 1208 Dec 57

We present a 5 years 8 months old girl with severe hyperlipidemia (high total cholesterol, and low density lipoprotein values, and also, ectopic fat pericardial deposit). She was treated with diet and cholestyramine, without diagnosis of her disease etiology. Growth detention, weight loss, retarded bone age and clinical signs of hypometabolism were recorded. Thyroid profile confirms hypothyroidism diagnosis. Based on positive anti-thyroid antibodies and clearly reduced thyroid volume, a diagnosis of autoimmune atrophic thyroiditis was made, a very unusual pathology in early infancy. Linear growth was affected by late diagnosis.
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PMID:[Severe hyperlipidemia, secondary to hypothyroidism due to atrophic thyroiditis in a girl]. 1935 Jan 45

Mitochondrial disorders (MIDs) require biochemical or genetic investigations for being diagnosed. In some cases, however, the diagnosis can be suspected upon the syndromic phenotype or upon clinical presentation and family history, as in the following case. The patient was a 74-year-old male admitted for worsening of pre-existing left-sided ptosis and ophthalmoparesis after a birthday party. The history was positive for arterial hypertension, hypertrophic cardiomyopathy with systolic dysfunction, diabetes-type 2, mild renal insufficiency, thyroiditis, and polyneuropathy. Instrumental investigations additionally revealed hepatopathy, hyperlipidemia, hyperuricemia, bifascicular block, white matter lesions, and subacute stroke. Systolic dysfunction resolved upon adequate cardiac treatment. On hospital day 11 the patient suddenly developed asystole. He was successfully resuscitated but died a few hours later from acute myocardial infarction. Surprisingly, a more extensive family history was positive for myopathy (patient, brother, daughter), neuropathy (patient), hypoacusis (patient), Parkinson syndrome (mother), spasticity (son), diabetes (patient, son), renal failure (patient), and generalized atherosclerosis (patient). The individual and family history was strongly suggestive of an MID. In conclusion, individual and family history may strongly suggest MID. Phenotypic variability may be high between family members affected by an MID. MID may be associated with an increasing atherosclerotic risk lastly resulting in coronary heart disease and death.
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PMID:Diagnosing Mitochondrial Disorder without Sophisticated Means. 2661 82

Gallbladder mucocele formation is an emerging disease in dogs characterized by increased secretion of condensed granules of gel-forming mucin by the gallbladder epithelium and formation of an abnormally thick mucus that can culminate in obstruction of the bile duct or rupture of the gallbladder. The disease is associated with a high morbidity and mortality and its pathogenesis is unknown. Affected dogs have a significantly increased likelihood of concurrent diagnosis of hyperadrenocorticism, hypothyroidism, and hyperlipidemia. Whether these endocrinopathies represent coincidental primary disease processes that exacerbate gallbladder mucocele formation in predisposed dogs or reflect a concurrent disruption of endocrine and lipid metabolism is unclear. In this study, we investigated a hypothesis that dogs with gallbladder mucocele formation would have a high prevalence of occult and atypical abnormalities in adrenal cortical and thyroid gland function that would suggest the presence of endocrine disruption and provide deeper insight into disease pathogenesis. We performed a case-control study of dogs with and without ultrasonographic diagnosis of gallbladder mucocele formation and profiled adrenal cortical function using a quantitative mass spectrometry-based assay of serum adrenal-origin steroids before and after administration of synthetic cosyntropin. We simultaneously profiled serum thyroid hormone concentrations and evaluated iodine sufficiency by measurement of urine iodine:creatinine ratios (UICR). The studies were complemented by histological examination of archival thyroid tissue and measurements of thyroid gland organic iodine from dogs with gallbladder mucocele formation and control dogs. Dogs with gallbladder mucocele formation demonstrated an exaggerated cortisol response to adrenal stimulation with cosyntropin. A prevalence of 10% of dogs with gallbladder mucocele formation met laboratory-based criteria for suspect or definitive diagnosis of hyperadrenocorticism. A significantly greater number of dogs with gallbladder mucocele formation had basal serum dehydroepiandrosterone (DHEAS) increases compared to control dogs. A high percentage of dogs with gallbladder mucocele formation (26%) met laboratory-based criteria for diagnosis of hypothyroidism, but lacked detection of anti-thyroglobulin antibodies. Dogs with gallbladder mucocele formation had significantly higher UICRs than control dogs. Examination of thyroid tissue from an unrelated group of dogs with gallbladder mucocele formation did not demonstrate histological evidence of thyroiditis or significant differences in content of organic iodine. These findings suggest that dogs with gallbladder mucocele formation have a greater capacity for cortisol synthesis and pinpoint DHEAS elevations as a potential clue to the underlying pathogenesis of the disease. A high prevalence of thyroid dysfunction with absent evidence for autoimmune thyroiditis suggest a disrupted thyroid hormone metabolism in dogs with gallbladder mucocele formation although an influence of non-thyroidal illness cannot be excluded. High UICR in dogs with gallbladder mucocele formation is of undetermined significance, but of interest for further study.
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PMID:Investigation of adrenal and thyroid gland dysfunction in dogs with ultrasonographic diagnosis of gallbladder mucocele formation. 3081 73