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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of four successive siblings, age 9, 12, 14 and 16 years with cretinism associated with congenitial central hypothyroidism (central cretinism), born to a mother in the endemic goitre region of the Jos Plateau, Nigeria, is presented. Biochemically, the defects were characterized by abnormally low basal thyroxine, triiodothyronine and thyroid stimulating hormone, as well as refractory TSH response to thyrotrophin releasing hormone and gross hyperlipidaemia. Clinically, the intellectual, physical and neurological impairment varied from moderate in the youngest to very severe in the oldest. Contrasting clinical pictures of cretinism, which appeared related to age and previous treatment were found with a spectrum ranging from predominantly myxoedematous in the youngest to predominantly neurological in the 16 year old male. Response to adequate treatment was dramatic, with restoration of severe gait disturbance occurring almost completely, but the imprints of thyroid hormone deficiency on mental defects and intellectual performance remained almost unaltered. The parents and two older sisters were normal with normal thyroid function.
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PMID:Central cretinism in four successive siblings. 212 28

A study of the blood plasma content of total cholesterol in 575 healthy persons and 675 patients with diffuse toxic goiter (DTG), and the content of total lipids and triglycerides in 52 healthy persons and 132 DTG patients showed the development of adaptation hyperlipidemia in persons living long in the North. It was preserved in DTG patients irrespective of the gravity of thyrotoxicosis, stages of its therapy and the patients' age. Basing on the analysis of the level of lipid indices of erythrocytic membrane malonic dialdehyde and their refractoriness to peroxide hemolysis in 52 healthy persons and 53 DTG patients, a conclusion was made of excessive stable activation of lipid peroxidation biomembranes which can underlie the development of visceral complications.
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PMID:[Lipids of blood and erythrocyte membranes in healthy persons and in patients with diffuse toxic goiter, residing in the European North of the USSR]. 321 80

Benign symmetrical lipomatosis of the neck is a rare disease that has to be differentiated from goiter, sialadenitis, obesity or a lymphatic tumor. Most patients are severe alcoholics, but they may have other endocrine disorders, such as diabetes mellitus, hyperuricemia, or hyperlipidemia. Aside from the cosmetic disfigurement and consequent psychological stress, respiratory distress may be the indication for surgical treatment. Excision of the lipomatosis requires technical skill because the extensive and sometimes infiltrative growth makes dissection of muscle and nerves difficult. The computer tomogram provides good information on the extent of the disease. Three of our 5 patients died 2 1/2 to 6 years after the first operation because of their primary disease.
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PMID:Lipomatosis of the neck (Madelung's neck). 327 65

In patients treated with cyclosporine, an increase in the incidence of goiter has been demonstrated. This agent produces changes in the lipidic metabolisms, among which the increase in VLDL stands put. Given that the hyperlipemia more frequently associated to hyperuricemia is the increase of such lipoprotein, we decided to study the behaviour of plasmatic uric acid in patients receiving treatment with cyclosporine. The study was conducted in patients with bone marrow transplant undergoing immunosuppressive therapy, considering the effect of cyclosporine as the only drug or following a scheme of mixed immunosuppression associated to prednisone. We observed a reversible increase in the plasmatic levels of uric acid in patients treated with cyclosporine, which was positively correlated to an increase in VLDL triglycerides. Hence, the cyclosporine produced an increase of uric acid which was neither observed when associated to prednisone nor in the group of self-transplanted patients.
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PMID:[Effect of cyclosporine on plasma levels of uric acid in patients treated with bone marrow transplantation]. 765

The aim of the study was to specify postprandial hyperlipidemia (PHL) and the level of hormones which regulate metabolism, lipids in particular, in patients with ischemic heart disease (IHD) vs those in healthy persons and patients with thyrotoxicosis as well as to clarify whether IHD pathogenesis correlates with fat metabolism disturbance. Lipid and apoprotein parameters of dyslipoproteinemia, concentrations of insulin, hydrocortisone, T3, T4 and thyrotropic hormone were tested before and 3, 6 hours after fat loading in IHD patients with angiographically documented coronary atherosclerosis, in healthy persons and patients with diffuse toxic goiter. In IHD patients postprandial PHL differed from that in healthy persons and thyrotoxicosis patients by higher and growing up to hour 6 after fat loading hypertriglyceridemia associated with lowering of antiatherogenic cholesterol of HDLP. In thyrotoxicosis both fasting and afterload lipid and apoprotein indices of the lipoprotein spectrum continued at low level except triglycerides the level of which returned to normal level. The hormonal spectrum in IHD patients was characterized by higher fasting insulin and its noticeable rise after fat loading. As healthy persons and patients with thyrotoxicosis had no significant changes in hormones levels after fat loading, it is suggested that development of atherogenic postprandial PHL caused primarily by hormone dysregulation of fat metabolism with a leading role of hyperinsulinemia contributes much to pathogenesis of IHD.
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PMID:[Hormonal dysregulation of lipid metabolism in pathogenesis of ischemic heart disease]. 1502 92

Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of insulin-producing beta cells and is characterised by the presence of insulitis and &and beta-cell autoantibodies. Up to one third of patients develop an autoimmune polyglandular syndrome. Fifteen to 30% of T1DM subjects have autoimmune thyroid disease (Hashimoto's or Graves' disease), 5 to 10% are diagnosed with autoimmune gastritis and/or pernicious anaemia (AIG /PA), 4 to 9% present with coeliac disease (CD), 0.5% have Addison's disease (AD), and 2 to 10% show vitiligo. These diseases are characterised by the presence of autoantibodies against thyroid peroxidase (for Hashimoto's thyroiditis), TSH receptor (for Graves' disease), parietal cell or intrinsic factor (for AIG /PA), tissue transglutaminase (for CD), and 21-hydroxylase (for AD). Early detection of antibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown disease. Hashimoto's hypothyroidism may cause weight gain, hyperlipidaemia, goitre, and may affect diabetes control, menses, and pregnancy outcome. In contrast, Graves' hyperthyroidism may induce weight loss, atrial fibrillation, heat intolerance, and ophthalmopathy. Autoimmune gastritis may manifest via iron deficiency or vitamin B12 deficiency anaemia with fatigue and painful neuropathy. Clinical features of coeliac disease include abdominal discomfort, growth abnormalities, infertility, low bone mineralisation, and iron deficiency anaemia. Adrenal insufficiency may cause vomiting, anorexia, hypoglycaemia, malaise, fatigue, muscular weakness, hyperkalaemia, hypotension, and generalised hyperpigmentation. Here we will review prevalence, pathogenetic factors, clinical features, and suggestions for screening, follow-up and treatment of patients with T1DM and/or autoimmune polyglandular syndrome.
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PMID:Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. 2000 14

A 56-year-old white man presented with a lesion on the right shoulder. The lesion developed during a short period and recently became irritated with occasional bleeding and mild pruritus. The patient denied pain. Medical history included melanoma, nonmelanoma skin cancer, diabetes mellitus type II, hyperlipidemia, multinodular thyroid goiter, and obesity. Medications and family and social history were noncontributory. Review of systems was negative. Examination revealed a slightly raised, friable yellow-pink waxy plaque located on the right shoulder (Figure 1). There was no evidence of excoriation, secondary infection, drainage, scale, crust, atrophy, lichenification, or telangiectasia. The patient had no mucosal or nail changes and the remainder of his skin examination was normal. A shave biopsy on the right shoulder revealed a nodular deposit of homogenous eosinophilic material associated with extravasated erythrocytes within the dermis. An infiltrate of lymphocytes and plasma cells was associated with the deposits. Immunohistochemical stains revealed positive plasma cells with kappa light chain and negative with lambda light chain. Congo red stain was positive and supported the diagnosis. The findings were consistent with nodular cutaneous amyloidosis (NCA) of the amyloid light-type. Initial work-up included referrals to hematology/oncology and to general surgery. The patient had a complete blood cell count (CBC), complete metabolic profile (CMP), serum protein electrophoresis (S-PEP), urine protein electrophoresis (U-PEP), 24-hour urine creatinine clearance, and protein, serum immunoglobulins and 132 microglobulin. These were all within normal limits. Abdominal/pelvic computed tomography and positron emission tomography scan also were within normal limits. Bone marrow biopsy showed no abnormalities. The patient underwent both an abdominal fat pad biopsy as well as a colonoscopy with rectal biopsy. Both were negative for amyloidosis. Initially, the patient's cutaneous amyloidosis remained localized and mild pruritus was controlled with low potency topical steroids. The patient was closely monitored by hematology/oncology and general surgery on a biannual basis to assess the possibility of progression to systemic amyloidosis. Over the course of the subsequent two years, the patient developed multiple similar lesions across the back, shoulders, and chest, which were biopsied and found to be consistent with NCA. Progression of the cutaneous nodules led to disfiguring, painful, and friable pink to yellow waxy papules coalescing into plaques with obvious hemorrhage diffusely over the trunk (Figure 2). In lieu of the painful and disfiguring progression of disease, the patient desired a more aggressive treatment plan. At present, the treatment option recommended to the patient is carbon dioxide laser ablation. Hematology/oncology recommendation consists of a general systemic amyloid reevaluation annually, including CBC, CMP, S-PEP, U-PEP, 24-hour urine collection with creatinine clearance, and history and physical examination.
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PMID:Nodular cutaneous amyloidosis. 2216 48

Aborted sudden cardiac death (SCD) has not been reported as initial manifestation of cardiac involvement in metabolic myopathy (MM). A 20-year-old female with a previous history of three syncopes, hyperhidrosis, and recurrent tick bites experienced aborted SCD. Her mother presented with MM, and a history of pituitary adenoma, nephroptosis, arterial hypertension, depression, migraine, goiter, pancreatitis, osteoporosis, hyperhidrosis, multiple muscle ruptures, and hyperlipidemia. After a few days of disorientation and amnesia, the young female recovered completely. Clinical neurological examination was noticeable for partial ophthalmoparesis and mild hyperprolactinemia. She received an implantable cardioverter defibrillator, which did not discharge so far. Recurrent syncopes and aborted SCD may be the initial manifestation of MM with multiple organ involvement. The family history is important in cases with aborted SCD to guide the diagnostic work-up. Phenotypic heterogeneity between the family members may be an indicator of MM.
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PMID:Aborted sudden cardiac death and a mother with suspected metabolic myopathy. 2518 45

One of the many challenges for any physician is determining the correct course of treatment for patients with more than 1 area of complaint. Should the physician treat the symptoms or the underlying cause of a condition? If treating the cause, what and who determines the cause? Further complicating the issue, doctors must succeed in getting patients to follow the prescribed treatment, which has always been and will continue to be an issue in reaching therapeutic goals. In late 2009, a 49-year-old Caucasian woman visited the Natural Health Center of Medical Lake (NHCML) in Medical Lake, WA, complaining of multiple symptoms. One symptom was a goiter that had not been relieved with a prescription for 0.375 mg of Synthroid daily. Her comorbidities included mixed hyperlipidemia; multiple joint pains; alopecia; fatigue; bilateral, lower-extremity edema; and severe gastric disruption with bloating and acid reflux. After initial success from treatment, with a complete reduction of her presenting goiter and most of her other symptoms, the patient withdrew herself from her prescription medication and her nutritional supplementation. After 4 wk, the patient visited NHCML with indications of severe hypothyroidism, including a severely enlarged goiter of the right wing. After 6 wk of treatment with iodine and a glandular nutritional supplement (GTA Forte), her symptoms of severe hypothyroidism abated. Subsequent treatment for adrenal insufficiency, which was diagnosed at NHCML using salivary adrenal stress-index testing for cortisol rhythm and load, allowed complete resolution of her presenting complaints. This result persisted even at the 3-y follow-up to a greater degree than did the results from the use of thyroid nutritional supplementation and Synthroid, both alone and combined. The hypothalamus-pituitary-adrenal (HPA) axis may contribute to the existence of thyroid-type symptoms, particularly for those individuals with subclinical thyroid conditions. The treatment of the feedback mechanisms for the HPA axis may provide a valuable framework for treatment of mixed hyperlipidemia because normalizing or improving thyroid stimulating hormone (TSH) levels can reduce serum cholesterol levels.
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PMID:Adrenal and Thyroid Supplementation Outperforms Nutritional Supplementation and Medications for Autoimmune Thyroiditis. 2677 99

BACKGROUND Basal ganglia calcification (BGC) is a rare sporadic or hereditary central nervous system (CNS) abnormality, characterized by symmetric or asymmetric calcification of the basal ganglia. CASE REPORT We report the case of a 65-year-old Gypsy female who was admitted for a tetanic seizure, and who had a history of polyneuropathy, restless-leg syndrome, retinopathy, diabetes, hyperlipidemia, osteoporosis with consecutive hyperkyphosis, cervicalgia, lumbalgia, struma nodosa requiring thyroidectomy and consecutive hypothyroidism, adipositas, resection of a vocal chord polyp, arterial hypertension, coronary heart disease, atheromatosis of the aorta, peripheral artery disease, chronic obstructive pulmonary disease, steatosis hepatis, mild renal insufficiency, long-term hypocalcemia, hyperphosphatemia, impingement syndrome, spondylarthrosis of the lumbar spine, and hysterectomy. History and clinical presentation suggested a mitochondrial defect which also manifested as hypoparathyroidism or Fanconi syndrome resulting in BGC. After substitution of calcium, no further tetanic seizures occurred. CONCLUSIONS Patients with BGC should be investigated for a mitochondrial disorder. A mitochondrial disorder may also manifest as tetanic seizure.
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PMID:Basal Ganglia Calcification with Tetanic Seizure Suggest Mitochondrial Disorder. 2839 Dec 86


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