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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe accidental hypothermia in an urban environment is usually associated with drug or alcohol abuse or serious illness in elderly or debilitated patients. In the presence of cardiovascular instability, extracorporeal rewarming by cardiopulmonary bypass is the gold standard of treatment of such patients. Three cases of profound hypothermia with circulatory collapse are presented. Each was successfully resuscitated to a full neurological recovery using this method in an accident and emergency (A&E) department, although one died later of respiratory complications. All three cases had a serum potassium in the normal range at the start of treatment. Where facilities exist, extracorporeal rewarming can be performed in A&E for patients with profound hypothermia and circulatory collapse. Cardiopulmonary resuscitation must be continued throughout the rewarming process.
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PMID:Back from the dead: extracorporeal rewarming of severe accidental hypothermia victims in accident and emergency. 947 31

Adult rats intubated with a single dose of ethanol (alcohol; approximately 5 g/kg) for 5 to 10 successive days incur neurodegeneration in the entorhinal cortex, dentate gyrus, and olfactory bulbs accompanied by cerebrocortical edema and electrolyte (Na+, K+) accumulation. The brain damage is not lessened by cotreatment with the NMDA receptor antagonist MK-801; also, as reported elsewhere, MK-801 as well as non-NMDA receptor and Ca2+ channel antagonists are not neuroprotective in a similar, but more compressed, intoxication protocol. However, cotreatment with the electrolyte transport inhibitor/diuretic furosemide reduces alcohol-dependent cerebrocortical damage by 75-85% while preventing brain hydration and electrolyte elevations; olfactory bulb neurodegeneration is not attenuated. In parallel in vitro studies, rat organotypic entorhinal/hippocampal slice cultures exposed to alcohol (50-200 mM) 15 h/day for 6 days, mirroring episodic intoxication in vivo, demonstrate concentration-related release of the cytotoxic indicator, lactate dehydrogenase. Analogous to the in vivo findings, furosemide blocks this alcohol-induced in vitro cytotoxicity. Our results showing neuroprotection by furosemide indicate that brain edema and swelling are essential events in the brain damage induced by episodic alcohol exposure. Furosemide and related agents might be useful as neuroprotective agents in alcohol abuse. We suggest that the neurodegeneration is elicited in part by edema-dependent oxidative stress, but the regional selectivity of the damage may be best explained by physical (mechanical) compression of the limbic cortex against the adjacent tympanic bulla and subsequent neuronal cytoskeletal collapse. A scheme for these apparently nonexcitotoxic metabolic and mechanical pathways initiated by repeated alcohol exposure is proposed.
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PMID:Brain damage due to episodic alcohol exposure in vivo and in vitro: furosemide neuroprotection implicates edema-based mechanism. 947 87

A 31-year-old pregnant woman suddenly complained of bilateral hip pain 2 weeks before delivery. She was delivered of triplets by Caesarean section. She had been treated with human menopausal gonadotropin and human chorionic gonadotropin (hMG-hCG) before pregnancy. Radiograms of the hip joint showed collapse of the femoral heads bilaterally. Magnetic resonance imaging revealed a band pattern of low signal intensity for both hips on T1- and T2-weighted images. She had no history of steroid therapy or alcohol abuse. Osteonecrosis of the femoral heads bilaterally associated with pregnancy was confirmed. Pathology of the femoral head showed typical empty lacunae and necrosis of the trabecula.
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PMID:Osteonecrosis of the femoral head associated with pregnancy. 1007 61

An increase in osteoblast and osteocyte apoptosis has been demonstrated in mice and humans receiving glucocorticoids and may be involved in the pathogenesis of the associated osteonecrosis. To examine the spatial relationship between osteocyte apoptosis and glucocorticoid-induced osteonecrosis, we determined the prevalence of osteocyte apoptosis in whole femoral heads obtained from patients who underwent prosthetic hip replacement because of osteonecrosis due to chronic glucocorticoid treatment (n = 5), alcoholism (n = 3), and trauma (n = 1) as well as in femoral neck cores from patients with sickle cell disease (n = 5). Abundant apoptotic osteocytes and cells lining cancellous bone were found juxtaposed to the subchondral fracture crescent in femurs from the patients with glucocorticoid excess. In contrast, apoptotic bone cells were absent from the specimens taken from patients with trauma or sickle cell disease and were rare with alcohol abuse. These results indicate that glucocorticoid-induced osteonecrosis is a misnomer. The bone is not necrotic; instead, it shows prominent apoptosis of cancellous lining cells and osteocytes. Glucocorticoid-induced osteocyte apoptosis, a cumulative and irreparable defect, could uniquely disrupt the mechanosensory function of the osteocyte network and thus start the inexorable sequence of events leading to collapse of the femoral head.
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PMID:Apoptosis of osteocytes in glucocorticoid-induced osteonecrosis of the hip. 1094 2

Published cases of non-traumatic avascular necrosis of the femoral head associated with pregnancy are rare. We report a case of a 41-year-old woman who suddenly complained of bilateral hip pain 3 weeks after delivery by Caesarean section. For a problem of sterility, she had been treated with human menopausal gonadotropin and human chorionic gonadotropin (hMG-hCG). Initial radiographs of both hip joints were considered regular. After 4 years' evolution, radiographs of the hip joint showed collapse of both femoral heads. Bilaterally, osteonecrosis of the femoral heads was confirmed by MRI. MRI revealed a band pattern of low signal intensity for both hips on T1- and T2-weighted images. She had no history of steroid therapy or alcohol abuse. Osteonecrosis was related to pretentaine. A bilateral total hip arthroplasty was performed. The literature about avascular necrosis of the femoral head associated with pregnancy in previous cases is reviewed.
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PMID:Bilateral osteonecrosis of the femoral head after pregnancy. 1572 94

A 53-year-old man with a known history of alcohol abuse was admitted to hospital after a minor collapse. He had a laceration to the forehead and three rib fractures. Laboratory blood-analysis showed raised non-cholestatic liver-enzyme levels suggesting alcohol-abuse. On history taking the patient was shown to have been suffering from personality changes and multiple hallucinogenic episodes for the previous two years. He had been seen and evaluated by a neurologist to that effect. The patient's family had accepted the situation and thought of it as dementia, probably caused by alcohol abuse. He had been treated for atrial flutter and was taking acenocoumerol, atorvastatin, quinapril and metoprolol 50 mg twice daily as medication. During admission the patient appeared to be suffering from a delirium with complex visual and auditory hallucinations, for which he was given haloperidol. Revision of medication use led to the stopping of metoprolol, which had been started two years earlier. Within 24 hours the delirium had disappeared completely. There was spontaneous fall in the liver enzymes. At his last follow-up, the patient had had no psychiatric symptoms for 6 months. The relationship between stopping metoprolol and the disappearance of the psychosis appeared to be a causal one and this is supported by the limited literature available on this subject.
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PMID:[Delirium attributed to the use of metoprolol]. 1622 79

Infliximab, a chimeric monoclonal antibody that binds the tumor necrosis factor alpha (TNFalpha), is used in the treatment of rheumatoid arthritis (RA) and Crohn's disease (CD). Previous cases of significant secondary liver disease associated with infliximab treatment have been reported in patients with RA, CD, and psoriatic arthritis. Two additional patients with RA who developed a serious liver disease associated with infliximab treatment are reported here. A 39-year old RA patient was admitted with cholestatic liver disease after 8 months of treatment with infliximab. She had no history of hepatic diseases, exposure to hepatotoxic or illicit drugs, or alcohol abuse. A liver biopsy showed severe ductal proliferation with collapse and enucleation of the hepatocytes. Despite aggressive treatment with oral prednisolone, she developed hepatic failure. On the 45th day, a liver transplant was performed. The second patient, a 54-year old RA patient, was diagnosed with autoimmune hepatitis after 12 infliximab infusions. She fulfilled autoimmune hepatitis type 1 criteria. A liver biopsy disclosed an altered lobulillar structure with chronic inflammation and the formation of collagen bands. She was treated with prednisolone and azatioprine and a complete recovery was noted 1 month later. These cases should alert rheumatologists to the possibility of new adverse reactions (liver injury) associated with the use of TNFalpha blockers in an autoimmune setting.
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PMID:Serious liver disease induced by infliximab. 1654 95

Osteonecrosis of the femoral head in the setting of alcohol abuse is a potential important cause of symptomatic hip disease in young patients. All cases of uncemented primary total hip arthroplasty (THA) with a primary operative diagnosis of osteonecrosis of the femoral head secondary to alcohol abuse treated at our institution from January 1990 to February 2002 were identified. Twenty-three patients with 28 hips were identified; all patients had advanced disease (subchondral collapse) that was unresponsive to conservative treatment modalities. Within 5 years of index THA, 2 patients were lost to follow-up, and 2 patients died from causes unrelated to their surgery. The remaining 19 patients underwent 24 THAs. Unilateral THA was performed in 14 patients, and bilateral THA was performed in 5 patients. Seventeen men and 2 women with an average age of 41.8 years (range, 30-59 years) at the time of THA were included in the study. The average duration to clinical follow-up was 7.6 years. There was significant improvement in hip pain and hip function scores. Seven THAs were revised at a mean 6.7 years following index THA. Five- and 10-year implant survivorship free of revision was 96% and 64%, respectively (Kaplan-Meier Survivorship Analysis). The continued use of alcohol was associated with a slightly increased risk of failure (61% implant survivorship at 10 years in those with continued alcohol intake vs 75% 10-year survivorship in those without).
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PMID:Total hip arthroplasty for alcoholic osteonecrosis of the femoral head. 1963 30

Ketoacidosis is a metabolic condition that occurs as a result of an insufficient amount of insulin. The lack of insulin results in an increased release of glucose from the liver and an excess of ketone bodies as a result of the breakdown of adipose tissue. This occurs when carbohydrates are unable to be properly processed for needed energy requirements during cellular metabolism. Ketoacidosis is commonly linked to diabetes mellitus. Diabetes mellitus is a condition where the body is unable to produce the proper amount of insulin or is unable to effectively respond to insulin stimulation. Excessive alcohol use can damage the pancreas, reducing insulin secretion. Other conditions such as pneumonia or urinary tract infections can trigger the release of counter-regulatory hormones that may contribute to the decrease in insulin's activity and secretion. Symptoms of diabetic ketoacidosis often include nausea and vomiting, increased thirst and urine production, hyperglycemia, abdominal pain, shortness of breath, confusion, headache, general weakness, fatigue and increased heart rate. If left untreated, diabetic ketoacidosis can lead to more serious complications including circulatory collapse, decreased blood potassium levels, infection and cerebral edema. The following case study presents a complex condition of ketoacidosis associated with a bacterial infection compounded by the patient's history of alcohol abuse.
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PMID:Alcohol induced diabetic ketoacidosis exacerbated by an acute respiratory infection with Klebsiella pneumoniae. 2377 71

Endocannabinoid (eCB) signaling has been identified as a modulator of adaptation to stress, and is integral to basal and stress-induced glucocorticoid regulation. Furthermore, interactions between eCBs and glucocorticoids have been shown to be necessary for the regulation of emotional memories, suggesting that eCB function may relate to the development of post-traumatic stress disorder (PTSD). To examine this, plasma eCBs were measured in a sample (n=46) drawn from a population-based cohort selected for physical proximity to the World Trade Center (WTC) at the time of the 9/11 attacks. Participants received a structured diagnostic interview and were grouped according to whether they met diagnostic criteria for PTSD (no PTSD, n=22; lifetime diagnosis of PTSD=24). eCB content (2-arachidonoylglycerol (2-AG) and anandamide (AEA)) and cortisol were measured from 8 a.m. plasma samples. Circulating 2-AG content was significantly reduced among individuals meeting diagnostic criteria for PTSD. The effect of reduced 2-AG content in PTSD remained significant after controlling for the stress of exposure to the WTC collapse, gender, depression and alcohol abuse. There were no significant group differences for AEA or cortisol levels; however, across the whole sample AEA levels positively correlated with circulating cortisol, and AEA levels exhibited a negative relationship with the degree of intrusive symptoms within the PTSD sample. This report shows that PTSD is associated with a reduction in circulating levels of the eCB 2-AG. Given the role of 2-AG in the regulation of the stress response, these data support the hypothesis that deficient eCB signaling may be a component of the glucocorticoid dysregulation associated with PTSD. The negative association between AEA levels and intrusive symptoms is consistent with animal data indicating that reductions in AEA promote retention of aversive emotional memories. Future work will aim to replicate these findings and extend their relevance to clinical pathophysiology, as well as to neuroendocrine and molecular markers of PTSD.
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PMID:Reductions in circulating endocannabinoid levels in individuals with post-traumatic stress disorder following exposure to the World Trade Center attacks. 2403 86


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