Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the last years the occurrence of type 2 diabetes mellitus has rapidly increased. The presence of cardiovascular complications, retinopathy, nephropathy and neuropathy are the results of delayed diagnosis. In the year 2004, in the Internal Diseases Depertment in Dabrowa Tarnowska, type 2 diabetes mellitus was diagnosed for the first time in 62 patients. In this group the majority of patient suffered from I-III degree hypertension, 27% had ishaemic heart disease, and 11% were hospitalized because of heart infarction. Heart failure was present in 20% and paroxysmal atrial fibrillation in 21% of them. The other diabetic complications diagnosed in this group were: microalbuminuria (43%), proteinuria (27%), simple retinopathy (64%), proliferative retinopathy (21%), and peripheral neuropathy in 40 of patients.
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PMID:[Organ complications in patients with diabetes mellitus type 2 diagnosed during hospitalization due to other diseases in the year 2004]. 1778 45

Amiodarone chlorhydrate is a diiodated benzofuran derivative, and it is used to treat cardiac rhythm abnormalities. Hepatotoxicity is a relatively uncommon side effect of amiodarone, and symptomatic hepatic dysfunction occurs in fewer than 1% of the patients taking amiodarone. Cirrhosis is a rare complication that's been confirmed in 12 cases. Peripheral neuropathy occurs in 10% of patients taking aminodarone. We report here on an unusual case of amiodarone-induced hepatotoxicity and peripheral neurotoxicity. A 75 year old man with normal liver function was given amiodarone for treating his atrial fibrillation and heart failure. He developed nausea, vomiting, muscle weakness and wasting after 17.8 months therapy with amiodarone (400 mg orally once per day). Liver biopsy showed the presence of foam cells in the hepatic sinusoids and Mallory bodies in the periportal hepatocytes on light microscopy. Sural nerve biopsy showed demyelination, and nerve conduction studies showed mixed sensorimotor polyneuropathy. These observations show the necessity of monitoring the hepatic function and conducting neurologic examination of the patients treated with amiodarone.
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PMID:Amiodarone-induced hepatitis and polyneuropathy. 1793 44

Pregabalin is an analog of the neurotransmitter gamma-aminobutyric acid that exhibits analgesic, anticonvulsant, and anxiolytic properties. Owing to its pharmacologic properties, the drug has been used worldwide in the management of diabetic peripheral neuropathy, postherpetic neuralgia, generalized anxiety disorder, and social anxiety disorder. Although central nervous system disturbances account for the majority of pregabalin's side effects, dose-dependent peripheral edema and weight gain have also been reported. Recently, three case reports have been published documenting a possible association between pregabalin administration and chronic heart failure decompensation. We present three additional cases of possible heart failure exacerbation in patients with clinically stable heart failure who received pregabalin for neuropathic pain. Additionally, we review the literature addressing the nature and possible etiology for this adverse effect.
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PMID:Possible heart failure exacerbation associated with pregabalin: case discussion and literature review. 1869 30

A 52-year-old woman was admitted to the hospital because of appetite loss, unsteadiness, psychogenic symptoms, ataxia, and consciousness disturbance as a result of the ingestion of a diet restricted to only carbohydrates for a long term. Laboratory examination indicated the presence of pancytopenia with macrocytic anemia; further, decreased vitamin B1 and B12 levels were detected in her serum. Magnetic resonance imaging fluid attenuated inversion recovery (FLAIR), revealed high-signal intensity in the bilateral corpus striatum, third ventricle circumference, and cerebellar cortex. Thereafter, she received drip infusion that did not include vitamin B1 or B12 and subsequently suffered a cardiac arrest due to the aggravation of cardiac insufficiency; consequently, she was transferred to our hospital. Upon admission the patient was diagnosed to have obvious cardiomegaly with pleural effusion; further, a negative T-wave was obtained on the electrocardiogram. A diagnosis of beriberi heart disease was made because of thiamine deficiency. She was treated by thiamine administration, following which the cardiac symptoms improved immediately. Various neurological symptoms caused by encephalopathy, peripheral neuropathy and subacute combined spinal cord degeneration improved by treatment with thiamine and cyanocobalamine administration; however, some of these symptoms still remained. General awareness of the fact that neurological symptoms can be caused by vitamin deficiency is essential.
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PMID:[Case of Wernicke's encephalopathy and subacute combined degeneration of the spinal cord due to vitamin deficiency showing changes in the bilateral corpus striatum and cardiac arrest due to beriberi heart disease]. 1980 6

Churg-Strauss syndrome (CSS) is a rare type of necrotizing vasculitis affecting small to medium-sized vessels typically characterized by asthma, lung infiltrates, necrotizing granulomas and hypereosinophilia. Herein, we describe a case of CSS presenting severe and aggressive course. A 35-year-old male patient with weight loss, dyspepsia, dyspnea and hemoptysis was admitted. The laboratory analyses indicated a remarkable eosinophilia, elevated levels of serum total IgE and positive cANCA. Thorax CT findings were suggestive of alveolar hemorrhage. Bronchoalveolar lavage revealed alveolar hemorrhage with eosinophilia and transbronchial lung biopsy showed eosinophilic vasculitis. Cardiac enzymes were increased and murmurs were audible revealing cardiomyopathy proven by echocardiography. Pulse cyclophosphamide and methyl prednisolone was immediately started. On the 21st day, intestinal perforation developed and urgent surgery was performed. During a follow-up, although a radiological improvement was observed in the chest X-ray, cardiac failure, peripheral neuropathy and skin lesions developed and high-dose intravenous immunoglobulin and anti-TNF therapy (adalimumab) were applied. Despite the therapy, he died from heart failure and septicemia at 68th day of therapy.
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PMID:An aggressive and lethal course of Churg-Strauss syndrome with alveolar hemorrhage, intestinal perforation, cardiac failure and peripheral neuropathy. 2002 52

MoM hip bearings are being scrutinized due to high early failure rates and concerns that the results of the revision surgeries will be poor. However, orthopedic surgeons and the general medical community are unaware that patients with MoM bearings are also at risk for cobaltism. Medical providers need to know that hip arthroplasty implantees that present with symptom complexes that include tinnitus, deafness, vertigo, visual changes, rashes, hypothyroidism, tremor, dyspnea on exertion, mood disorders, dementia, heart failure, and peripheral neuropathy may be presenting arthroprosthetic cobaltism. These patients need to be asked if they have had a hip replacement and if so what type. For those patients implanted with a MoM bearing or those with a history of hip revision for a failed ceramic bearing obtaining a [Co] is indicated. MoM implantees with renal failure are a particularly high risk for cobaltism. A [Co] can be measured by many reference laboratories from royal blue top trace elements tube of venous blood. Venipuncture with a standard needle is adequate as long as a red stoppered tube is drawn first. The radiographic appearance of a MoM bearing is readily apparent to an orthopedic surgeon. The patient's operative report will usually specify the bearing type. Given that the publicity of the recent ASR bearing recall medical providers will be contacted by worried patients concerned about their hip implants. Most patients with hip replacements will not know the brand or material of their bearings. Providing patients with copies of their hip implant inventory might avoid worry by the majority of patients with hip arthroplasties that are not at risk. Patients with a cobalt levels of greater than 7 mcg/l bear observation of neurologic and cardiac function. Those patients with levels greater than 20 should be advised to have revision of their hip arthroplasty to a bearing that eliminates cobalt. Most patients implanted with MoM bearing have cobalt levels greater than those allowed in industry and cobalt exposed workers may have an increased incidence of subclinical cognitive and cardiac impairments. This association merits further study. Table 1 is a summation of the previously referenced data of this paper that might assist the clinician in interpreting a [Co].
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PMID:Arthroprosthetic cobaltism: identification of the at-risk patient. 2106 26

We report a case of Churg-Strauss syndrome (CSS) complicated by severe cardiac failure and peripheral neuropathy. Two courses of methylprednisolone pulse therapy were unable to control the disease activity. Repeated intravenous administration of high-dose human immunoglobulin (IVIg) was added together with intravenous cyclophosphamide pulse therapy (IVCY), and the patient's cardiac function and neurological symptoms were gradually ameliorated without any adverse event. Although glucocorticoid and cyclophosphamide comprise the standard therapy for patients with CSS, a number of patients with severe complications appear to be resistant to such conventional treatment. IVIg is thought to be an effective therapeutic option for such patients.
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PMID:A severe form of Churg-Strauss syndrome complicated with acute cardiac failure and rapidly progressive peripheral neuropathy--a possible effect of intravenous immunoglobulin therapy. 2149 44

The clinical presentation of beriberi can be quite varied. In the extreme form, profound cardiovascular involvement leads to circulatory collapse and death. This case report is of a 72 year-old male who was admitted to the Neurology inpatient ward with progressive bilateral lower extremity weakness and parasthesia. He subsequently developed pulmonary edema and high output cardiac failure requiring intubation and blood pressure support. With the constellation of peripheral neuropathy, encephalopathy, ophthalmoplegia, unexplained heart failure, and lactic acidosis, thiamine deficiency was suspected. He was empirically initiated on thiamine replacement therapy and his thiamine level pre-therapy was found to be 23 nmol/L (Normal: 80-150 nmol/L), consistent with the diagnosis of beriberi. Cardiovascular magnetic resonance (CMR) showed severe left ventricular systolic dysfunction, markedly increased myocardial T2, and minimal late gadolinium enhancement (LGE). After 5 days of daily 100 mg IV thiamine and supportive care, the hypotension resolved and the patient was extubated and was released from the hospital 3 weeks later. Our case shows via CMR profound myocardial edema associated with wet beriberi.
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PMID:Cardiovascular magnetic resonance in wet beriberi. 2183 1

The treatment of familial amyloid polyneuropathies (FAP) is complex and requires a neurological and cardiological multidisciplinary coverage. It includes specific treatments to control the progression of the systemic amyloidogenesis, the symptomatic treatment of the peripheral and autonomic neuropathy (digestive, urinary, sexual, postural hypotension) and the treatment of organs severely involved by amyloidosis (heart, eyes, kidneys). First line specific treatment of met30 TTR-FAP is liver transplantation (LT) which allows to suppress the main source of mutant TTR, to stop the progression of the neuropathy in 70 % of cases at long-term (with an experience of 18 years) and to double the median survival. In case of severe renal or cardiac insufficiency, a double transplant kidney-liver or heart-liver can be discussed. The tafamidis (in temporary authorization of use in France) is a stabilizing medicine of the tetrameric TTR which showed in very early stages of met30 TTR-FAP short-term capacities to stop the progress of the peripheral neuropathy in 60 % of the cases versus 38 % with placebo. It should be proposed in case of contraindication of TH (age>70 years [20 % of the cases]), of very early stages (very low NIS-LL score), or for the period of wait of LT. Other innovative medicines issued from biopharmaceutical companies have been developed to block the hepatic production of both mutant and wild TTR which are noxious in the late forms NAH (>50 years old) (RNAi [RNA interference] therapeutics, AntiSens oligonucleotids), for removing the amyloid deposits (monoclonal antibody anti-SAP), or to slow down the formation of deposits of TTR and amyloidosis (combination of doxycycline-TUDCA). Clinical trials should be first addressed to the patients with a late onset of FAP or non-met30 TTR-FAP who are less responding to LT and patients with contraindications in the LT. Initial cardiac assessment and periodic cardiac investigations are important for the FAP according to the frequency of cardiac impairment which is responsible of high rate of mortality. Conduction disorders (atrio-ventricular blocks) require the implantation of a pacemaker in about one third of the cases during the evolution of the disease. A myocardial infiltration is detected in two third of the cases and is for a long time latent; it remains often limited to a diastolic dysfunction which can be responsible for hemodynamical difficulties during the LT; it evolves sometimes, late, towards a systolic dysfunction of bad prognosis. A combined liver-heart transplantation is proposed in cases of severe cardiac involvement which are contraindication to the LT only, essentially in forms "not met30". In every case of FAP, a regular cardiological follow-up is required for life, because of the progress of the cardiac involvement, which is not always stopped by the liver transplantation. The symptomatic treatments are indispensable to improve the quality of life of the patients: neurogenic pains, urinary disorders, liqueurs, sexual impotence, postural hypotension. The familial screening of the carriers of the TTR gene mutation and their regular follow-up by appropriate clinical examination and complementary investigations are major to detect early the onset of the disease to start as soon as possible specific therapy.
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PMID:[Treatment of familial amyloid polyneuropathy]. 2234 49

The treatment of familial amyloid polyneuropathy (FAP) requires a multidisciplinary approach, mainly neurological and cardiological. It includes specific treatments to stop the progression of systemic amyloidogenesis, the symptomatic treatment of the peripheral and autonomic neuropathy and the treatment of organs severely involved by amyloidosis (heart, eyes, kidneys). First-line specific treatment of met30 transthyretin (TTR) FAP is liver transplantation, which allows suppression of the main source of mutant TTR, to stop the progression of the neuropathy in 70% of cases in the long term and to double the median survival. In cases of severe renal or cardiac insufficiency, a combined kidney-liver or heart-liver transplantation can be discussed. Tafamidis (Vyndaqel) is a novel specific stabilizer of TTR which, in the very early stages of met30 TTR FAP, slows the progress of peripheral neuropathy. This drug should be proposed in cases of stage 1 symptomatic polyneuropathy. Other innovative medicines have been developed by biopharmaceutical companies to block the hepatic production of mutant and wild type TTR which are harmful in late-onset FAP (> 50 years old), including RNA interference therapeutics and antisense oligonucleotides, and to remove the amyloid deposits (monoclonal antibody antiserum amyloid P). Clinical trials should first assess patients with late onset FAP or non-met30 TTR FAP who are less responsive to liver transplantation or in case of significant progression of the neuropathy with Vyndaqel. Initial cardiac assessment and periodic cardiac investigations are important for patients with FAP because of the frequency of cardiac impairment, which is responsible for the high rate of mortality. Prophylactic pacemaker treatment should be discussed. Symptomatic treatments are required to improve patients' quality of life. Familial screening of people with TTR mutation and regular follow up are essential. Appropriate clinical examination and complementary investigations are vital for the early detection of disease onset and to start specific therapy as soon as possible.
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PMID:Recent advances in the treatment of familial amyloid polyneuropathy. 2348 84


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