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

A 76-year-old female patient is presented who suffered from muscular weakness in arms and legs. She was obese and had a symmetric accumulation of fatty tissue with a bumpy structure at both arms which gave the patient a pseudoathletic appearance. Fatty tissue accumulations were present at both shoulders, arms, at both thighs, at the back and the abdomen. She suffered from benign symmetric lipomatosis (BSL), also called Launois-Bensaude syndrome (LBS), which is a rare disorder of unknown origin and poorly understood pathophysiology. It is believed to be a disease of disturbed lipogenesis induced by catecholamines. The syndrome is often associated with features of metabolic syndrome such as diabetes mellitus, hyperuricemia, hyperlipidemia and hypertension and is associated with polyneuropathy which is an integral part of the disease. Therapeutic options are pharmacological treatment with salbutamol and surgical procedures such as lipectomy or liposuction.
 ...
PMID:Benign symmetric lipomatosis (Launois-Bensaude syndrome). A rare cause of muscular weakness. 1718 68

Hypothyroidism is one of the common causes of the secondary hypercholesterolemia. The prevalence of hypothyroidism in the general population is estimated to be as high as about 1.5%. Frequency of the hypothyroidism in patients with hyperlipidemia is high, and can be observed in 4.2-10% in different populations. Most commonly, there is no need to treat the hypothyroid patients with the hypolipidemic drugs. Substitution treatment with the thyroid hormones usually results in either normalization or significant decreasing of the lipid levels. Hypothyroidism with symptoms of involvement of skeletal muscles is referred as to hypothyroid myopathy in English literature, and can be present in 30-80% patients with deficiency of the thyroid hormones. Hypothyroidism is a risk factor of developing of toxic injury of muscles, what is thought to be related to hypolipidemic drug intake. We report a case of a patient with undiagnosed hypothyroidism with muscle involvement manifestation, who was treated with fenofibrate due to accidentally diagnosed hypercholesterolemia. Hypolipidemic management resulted in rapid exacerbation of previously moderate myopathy. High concentrations of muscle enzymes and moderate increasing of creatinine concentration were detected. Improvement was observed after discontinuation of fenofibrate administration, but muscle symptoms and elevation of muscle enzymes and creatinine persisted. After administration of levothyroxin, muscle weakness and laboratory abnormalities were observed no longer. After several months of follow-up we believe that treatment with fenofibrate in our patient was complicated with muscle tissue damage and exacerbated symptoms of myopathy originally related to decompensated hypothyroidism.
 ...
PMID:[Fenofibrate--induced myopathy in a patient with undiagnosed hypothyroidism--case report and a review of the literature]. 1727 84

A retrospective cohort study was carried out of new referrals to transient ischaemic attack (TIA) clinics in Glasgow. The aims of the study were to describe the profile of referrals and to assess the odds ratios for TIA, minor stroke or amaurosis fugax of both cardiovascular risk factors and clinical features. In total, data were collected for 813 new referrals in a period of six months. Thirteen point eight percent of referrals were from other Health Boards. The overall referral rate among residents of Greater Glasgow NHS Board was 165.6 per 100,000 per year. About 20% of referrals were made by clinicians in secondary care. The specialties from which referrals were most commonly made were accident and emergency, general medicine, ophthalmology and geriatric assessment. The most common risk factors in patients referred were hypertension (52.9%), smoking (31.7%), ischaemic heart disease (22.7%) and former smokers (22.4%). The most common clinical features were hemiparesis (13.3%), weakness of an upper limb (8.7%), vertigo (7.9%) and dysphasia (7.3%). In 48.7% of cases, a non-cerebrovascular diagnosis was made. Separate multivariate models were established for risk factors and clinical features. In the model for risk factors, five factors were significant for risk of TIA, stroke or amaurosis fugax. These were hyperlipidaemia, age over 64 years, hypertension, smoking and ex-smoking. In the model for clinical features, five factors were also significant. These were visual field defect, speech defact, facial weakness and hemiparesis.
 ...
PMID:Epidemiological aspects of referral to TIA clinics in Glasgow. 1737 16

We describe a patient with hypothyroidism displaying "dropped head" syndrome. A 50-year-old man visited our clinic because he was unable to hold his head in the natural position. He had weakness and hypertrophy of the neck extensor muscles. Tendon reflexes were diminished or absent in all limbs. Mounding phenomena were observed in the bilateral upper extremities. Blood biochemical analysis revealed hypothyroidism, hyperlipidemia, and elevated levels of muscle-derived enzymes. Magnetic resonance imaging (MRI) of the neck demonstrated swelling and hyperintensity of the neck extensor muscles on T2-weighted images. The result of biopsy of the right biceps brachii muscle suggested mild atrophy of type 2 fibers. The diameters of the muscle fibers exhibited mild variation. No inflammatory changes were observed. We diagnosed hin as having "dropped head" syndrome due to hypothyroidism. Administration of thyroid hormone agent gradually improved his condition, and he became able to hold his head in the natural position. Levels of muscle-derived enzymes normalized and his hyperlipidemia remitted. Neck MRI also revealed improvement. Our findings suggest that hypothyroidism should be considered in the differential diagnosis of "dropped head" syndrome, although only a few cases like ours have been reported.
 ...
PMID:[A case of hypothyroidism displaying "dropped head" syndrome]. 1749 34

The many similarities between the metabolic syndrome and Cushing's syndrome led to the hypothesis that excess glucocorticoids (GC) are part of the pathogenesis linking their features. We review recent work that confirms the initial similarities (obesity, glucose intolerance, hypertension, and hyperlipidemia) and extends them to associated features of both syndromes (osteopenia, hypogonadism, leukocytosis, depression, and muscle weakness). Recent studies report that these features also occur in subclinical Cushing's syndrome, hypercortisolemic depression, and the transgenic overexpression of 11beta-hydoxysteroid dehydrogenase type 1 (11beta-HSD1) in mouse models of excess GC in adipose tissue. Reducing excess GC--in the clinical syndromes and in the mouse model-reverses many of these features. Because local tissue excess GC may have a central role in the pathogenesis of the metabolic syndrome, selective 11beta-HSD1 inhibitors are under active development by several pharmaceutical companies.
 ...
PMID:Adrenal steroids and the metabolic syndrome. 1836 16

Glycogen storage disease type III (GSD III) is a very rare disorder caused by a deficiency in the activities of glycogen debranching enzymes (amylo-1-6-glucosidase and 4-alpha-glucanotransferase). GSD III is characterized by the accumulation of abnormal glycogen in the liver and skeletal muscle. The primary clinical manifestations are hepatomegaly, fasting hypoglycemia, and hyperlipidemia in infants. We report a rare case of GSD III in an adult. A 52-year-old woman presented to our clinic due to dyspnea on exertion, severe general weakness, and hepatomegaly. Hypertrophic cardiomyopathy was diagnosed based on echocardiogram findings. The microscopic findings of liver and skeletal muscle biopsies were consistent with the diagnosis of GSD. DNA analysis prompted by clinical and pathologic findings led to a definitive diagnosis of GSD IIIa. Diet therapy with cornstarch was started, and the patient was followed closely. This represents the first reported case of GSD IIIa diagnosed in an adult in Korea.
 ...
PMID:An adult case of glycogen storage disease type IIIa. 1861 70

Recently, there have been many reports on the efficacy and safety of tacrolimus (FK506) treatment for adult patients with intractable generalized myasthenia gravis (MG). There have also been a few reports of successful FK506 therapy in patients with severe childhood-onset generalized MG involving a myasthenic crisis. Herein, we report the efficacy of FK 506 for refractory ocular symptoms in a 3-year-old girl with ocular type MG. Ptosis and alternating strabismus had appeared at 10 months of age. No bulbar signs, respiratory failure or generalized muscle weakness had been seen during her course. Her ocular symptoms had persisted despite repeated steroid pulse therapy, high dose oral prednisolone and thymectomy. Adverse effects of steroids, including obesity, growth retardation, osteoporosis, cataracts and hyperlipidemia, gradually worsened. After obtaining written informed consent from her parents, we started oral tacrolimus at a dose of 0.5mg/day and her symptoms resolved completely within 3 weeks at a maximum dose of 2.5mg/day. No adverse effects, such as renal failure or glucose intolerance, were seen. FK506 treatment allowed the steroid dose to be reduced, eliminating its adverse effects. In patients with intractable childhood-onset MG with ocular manifestations, FK506 is an alternative to steroid therapy or thymectomy.
 ...
PMID:Benefits of FK 506 for refractory eye symptoms in a young child with ocular myasthenia gravis. 1884 8

A 75-year-old woman with diabetes mellitus, hypertension, and hyperlipidemia came to the emergency department with generalized and upper-extremity weakness; she had experienced a fall 2 months earlier. On admission, her drug therapy included lovastatin 40 mg/day, controlled-release diltiazem 240 mg/day, and glimepiride 1 mg/day. Nineteen days earlier, sitagliptin 100 mg/day had been started; it was discontinued 2 weeks later, and glimepiride was begun. A cardiology consultation performed on the day of admission determined that a markedly elevated creatine kinase-myocardial band isoenzyme level and borderline-high troponin I level were diagnostic of rhabdomyolysis secondary to statin use. Because the patient had been taking lovastatin for the past 12 years, the possibility that the rhabdomyolysis may have been caused by a drug interaction between lovastatin and a concomitant drug was evaluated. As it had been 10 months since her last dosage adjustment of diltiazem, it was unlikely that the statin-induced rhabdomyolysis was precipitated by diltiazem. Use of the Drug Interaction Probability Scale to determine the strength of a lovastatin-sitagliptin interaction indicated a possible association (score of 4). Multiple drug interactions have been reported with lovastatin. To our knowledge, however, this is the first case report of a possible sitagliptin-lovastatin interaction that may have caused rhabdomyolysis. Studies must be performed to further evaluate the in vivo effect of sitagliptin on the cytochrome P450 3A4 enzyme system and to elucidate other mechanisms that may potentiate such a drug-drug interaction. In the meantime, however, clinicians should be aware of this possible drug interaction.
 ...
PMID:Rhabdomyolysis caused by a potential sitagliptin-lovastatin interaction. 1924 53

A 66 year-old woman with no history of renal or liver disease presented with progressive asthenia and diffuse myalgia. She cited 5 months history of mild hyperlipidemia under treatment with rosuvastatin (10 mg/day). Clinical examination documented both an increase in liver size and proximal muscle weakness, with difficulty in raising arms above the head. Blood tests showed the presence of renal, liver and muscle failure, with no evidence of virological, immunological or haematological diseases. Rosuvastatin treatment was stopped and blood values normalised within five days; but because of an increase in cholesterol plasma levels, rosuvastatin (10 mg/day) was restarted. Two days later, the patient returned to our observation due to the development of asthenia and muscle weakness, with an increase in creatine phosphokinase, 12,165 U/l. Rosuvastatin was discontinued and replaced with pravastatin (40 mg/day) with a complete resolution of clinical and laboratory findings in about six days. Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.
 ...
PMID:Rosuvastatin-induced rhabdomyolysis probably via CYP2C9 saturation. 1935 2

A 45-year-old man with a past history of hypertension and hyperlipidemia presented with right dorsal pontine hemorrhage manifesting as transient burning pain in the right orbital region, followed by numbness and mild weakness of the left side of the body. Magnetic resonance imaging showed a hyperintense lesion in the right dorsal pons on T(1)-weighted and T(2)-weighted images, but no other abnormalities suggesting vascular lesions in the midbrain, medulla, cerebellum, or cerebrum. These findings were consistent with the subacute stage of small pontine hemorrhage. He was treated to decrease his blood pressure. The symptoms gradually improved and he has suffered neither recurrence of the orbital pain nor migraine for several months after the first episode of headache. The trigeminal nociceptive system in the dorsal lateral pons may be linked to this characteristic pain, as suggested by reports of secondary migraine caused by cavernous hemangioma and arteriovenous malformation, and activation of the dorsal lateral pons during migraine attacks on positron emission tomography.
 ...
PMID:Transient burning pain in the ipsilateral orbit as an initial manifestation of dorsal pontine hemorrhage: case report. 1946 91


<< Previous 1 2 3 4 5 6 7 Next >>