Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with peripheral cranial nerve paresis and bilateral myokymia is described during the course of acute co-infection with hepatitis B and delta viruses. Specific circulating hepatitis B immune complexes were found by electron microscopy concomitantly with the neurological symptoms.
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PMID:Seventh cranial nerve paralysis with myokymia during acute co-infection with hepatitis B and delta viruses. 339 24

Yeast-derived recombinant DNA hepatitis B vaccine usage has been widely accepted since the early 1990s, especially for high-risk patients. Severe adverse effects have been reported infrequently. Certain neurological complications raise concern for hepatitis B vaccine: central nervous system demyelination, acute myelitis, acute cerebellar ataxia, and various peripheral mononeuropathies. Case reports on tinnitus, hearing loss, and vestibular damage are extremely scarce. The case presented here concerns a professionally active nurse, born in 1953, with a medical history of progressive renal failure and hemodialysis. Eleven hours after a second injection of the hepatitis B vaccine Engerix B, an acute left-sided tinnitus occurred and, a few hours later, severe left hearing loss and intense vertigo. Tinnitus and the sensation of vertigo regressed fairly quickly, but the hearing loss and the vestibular paresis were permanent. Increased interpeak intervals on auditory brain responses and lack of recruitment suggested that the lesion probably is located at the level of cranial nerve VIII. From a medicolegal point of view, this audiovestibular damage had to be considered an accident at work and not as an occupational disease.
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PMID:Acute tinnitus and permanent audiovestibular damage after hepatitis B vaccination. 1497 38

Portosystemic encephalopathy (PSE) is a well-known, common complication of portal hypertension. It is thought to be caused by nitrogenous substances such as ammonia, which are normally cleared from the blood stream by the liver. In cirrhosis and other hepatic disorders with portosystemic shunting (PSS)-- either surgical portosystemic anastomoses (PSA) or spontaneous PSS-- the collateral vessels bypass the liver allowing the accumulation of toxic, ammoniacal substances in the blood and tissues. PSE is characterized by encephalopathy; portosystemic myelopathy (PSM) is characterized by paresis of the extremities, Babinski signs and muscle spasticity in patients with cirrhosis and/or PSS. Usually only the lower extremities are involved. This report presents the first case of this syndrome observed 5 years after a transjugular intrahepatic portosystemic shunt. The 31 year old man with chronic Hepatitis B developed complete spastic paraparesis within 4 weeks after onset of clinical/neurological symptoms, accompanied by an episode of severe hepatic encephalopathy. The transcortical magnetic stimulation showed normal motoric stimulation times to the abductor digiti minimi muscles but no stimulation to the tibialis muscles was seen. Lumbar stimulation to the tibialis muscles, however, was normal. This indicates loss of motor neurons in the spinal cord, a characteristic finding in patients with portosystemic myelopathy. We performed a search of the literature for all reported cases of cirrhosis and/or PSS that developed PSM. However, the intervals between the construction of a shunt and the diagnosis of portosystemic myelopathy were shorter in total portacaval shunts (median 16 months) than in partial, non-portacaval shunts (median 60 months, p < 0.01). This suggests that not only the shunt itself but also the shunted volume contributes to the development of the syndrome Sixty-one patients with PSM have been reported in the literature since 1944. PSE had developed before PSM in almost all cases. PSM occurred from 1 month to 10 years after the creation of portacaval anastomoses (PCA) or splenorenal shunts (SRS) or in cirrhotic patients without shunts. No one type of liver disease or type of shunt appears to predispose to PSM. The mechanisms of PSE and PSM are thought to be similar and of nitrogenous origin, but their pathogenesis remains unknown. Lathyrism, a toxic syndrome with similar symptoms and signs, is caused by the ingestion of a legume, Lathyrus sativa, which contains beta-N-oxalo-L amino-L-alanine (BOAA). This animal model with or without BOAA appears to offer a reliable way of studying PSM experimentally.
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PMID:Portosystemic myelopathy: spastic paraparesis after portosystemic shunting. 1663 7

We describe a rare and interesting progressive case of lymphocytic hypophysitis accompanied later by paresis of the left abducens nerve. A 42-year-old woman was diagnosed as having lymphocytic hypophysitis accompanied by diabetes insipidus and hypopituitarism. She had no symptoms of visual disturbance at that time. She was not treated with steroids because she is a carrier of the hepatitis B virus. Later, in 2006, she complained of progression of symptoms and double vision for a few months. Her pituitary gland showed further enlargement. The patient was diagnosed as having progressive lymphocytic hypophysitis accompanied by paresis of the left abducens nerve, which was subsequently confirmed by biopsy. The progression of lymphocytic hypophysitis in patients not receiving steroid therapy should be carefully monitored.
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PMID:A progressive case of lymphocytic hypophysitis accompanied by paresis of the left abducens nerve. 1859 49

A wild-born, 34-yr-old female western lowland gorilla (Gorilla gorilla gorilla) was transferred between zoologic collections in the United Kingdom. Adjustment to its new environment was difficult and a series of health problems ensued. Progressive severe illness of multiple etiologies, and a failure to respond to multiple therapies, led to its euthanasia 5 mo later. Disease processes included severe thoracic and axillary cutaneous ulceration of T2-3 dermatome distribution, gastroenteritis, ulcerative stomatitis, emaciation, hind limb weakness or paresis, and decubitus ulcers of the ankles and elbows. Ante- and postmortem infectious disease screening revealed that this animal was not infected with Mycobacterium tuberculosis, simian varicella virus (SVV), simian immunodeficiency virus (SIV), or hepatitis B virus; but was infected with varicella-zoster virus (VZV) and simian T-lymphotropic virus (STLV). It is hypothesized that recrudescence of VZV and other disease processes described were associated with chronic STLV infection and the end of a characteristically long incubation period.
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PMID:Debilitating clinical disease in a wild-born captive western lowland gorilla (Gorilla gorilla gorilla) co-infected with varicella zoster virus (VZV) and simian T-lymphotropic virus (STLV). 2137 Jun 55

Acute-on-chronic liver failure (ACLF) is a distinct clinical entity and differs from acute liver failure and decompensated cirrhosis in timing, presence of acute precipitant, course of disease and potential for unaided recovery. The definition involves outlining the acute and chronic insults to include a homogenous patient group with liver failure and an expected outcome in a specific timeframe. The pathophysiology of ACLF relates to persistent inflammation, immune dysregulation with initial wide-spread immune activation, a state of systematic inflammatory response syndrome and subsequent sepsis due to immune paresis. The disease severity and outcome can be predicted by both hepatic and extrahepatic organ failure(s). Clinical recovery is expected with the use of nucleoside analogues for hepatitis B, and steroids for severe alcoholic hepatitis and, possibly, severe autoimmune hepatitis. Artificial liver support systems help remove toxins and metabolites and serve as a bridge therapy before liver transplantation. Hepatic regeneration during ongoing liver failure, although challenging, is possible through the use of growth factors. Liver transplantation remains the definitive treatment with a good outcome. Pre-emptive antiviral agents for hepatitis B before chemotherapy to prevent viral reactivation and caution in using potentially hepatotoxic drugs can prevent the development of ACLF.
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PMID:Acute-on-chronic liver failure: terminology, mechanisms and management. 2683 12