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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A longitudinal study with follow up to the end of 1989 was carried out on 23 patients with AIDS who had attended St. James's Hospital, Dublin, by the end of 1987. Until then only 33 cases of AIDS had been reported in Ireland. The patients, all of whom had antibodies to human immunodeficiency virus (HIV), were predominantly male, young (mean age 31.3 years) and belonged about equally to three major risk groups: homosexuals, intravenous drug abusers (IVDA) and haemophiliacs. AIDS was diagnosed because of oesophageal candidiasis (8 cases), Kaposi's sarcoma (4), mycobacterial infection (4), pneumocystis carinii pneumonia (3), toxoplasmosis (2) or encephalopathy (2). Malignant lymphoma and a variety of infections occurred in the course of illness, and neurological involvement developed in 11 patients (48%). Mortality following diagnosis of AIDS was 39% at one year and 64% after two years. Autopsy in 10 of the 16 deaths contributed much to defining the extent and nature of the disease. The demographic pattern, risk group status, survival and range of complications were broadly similar to the pattern of AIDS as seen elsewhere in developed countries. However, compared to the profile of disease reported from the United States, oesophageal candidiasis (52%) and Mycobacterium tuberculosis (22%) were more prominent, pneumocystis carinii pneumonia (39%), Kaposi's sarcoma (22%) and Mycobacterium avium intracellulare (13%) were less frequent and cryptococcal infection was not identified. These regional variations in the frequency of the various complications and particularly the prominence of tuberculosis, probably reflect the interaction of the immunocompromised patient with the local environment and may have important diagnostic and therapeutic implications.
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PMID:The emerging AIDS epidemic in Ireland--clinicopathological findings in 23 early cases. 239 Dec 9

It is currently controversial whether all the brain damage in alcohol abusers in the result of thiamine deficiency (Wernicke-Korsakoff's disease) or whether, in addition, alcohol abuse may affect the brain by other mechanisms as well. The purpose of this study was to determine if alcohol abuse affects muscarinic cholinergic and benzodiazepine receptors in histologically normal brains obtained at autopsy in a general hospital population. Patients were excluded from this study if they had clinical brain diseases (including Wernicke's disease), died in coma, or had liver disease, significant brain atrophy, or dementia severe enough to require institutionalization. We found that muscarinic cholinergic synaptic receptor density determined with [3H] quinuclidinly benzilate was decreased by 40% in homogenates of the tempeoral cortex of 26 alcohol abusers compared with 26 matched nonalcoholic controls. The affinities of the muscarinic receptors were not significantly different between the two groups. In contrast, receptor densities and affinities of benzodiazepine receptors determined with [3H]flunitrazepam were not significantly different in the two groups. Age and death-autopsy time interval had no significant effects on either wet tissue protein concentrations, yields of protein after centrifugation, or receptor binding. The contributions of age and time interval were each less than 2% of the total variance of protein concentrations and receptor binding. When patients were excluded or included who had received cholinergic, anticholinergic, or benzodiazepine medications before death, no significant effects on the final results were observed. Pneumonia, known to be associated with acute hypoxia, and chronic obstructive pulmonary disease, known to be associated with chronic hypoxia, where approximately equally distributed between the two groups and had no significant effects on the results reported here. The loss of muscarinic and the sparing of benzodiazepine receptors occurs in the temporal cortex of histologically normal brains in the absence of significant atrophy and of gross dementia. This means that these changes are early in the development of an alcohol encephalopathy. We have previously reported a decrease in both muscarinic and benzodiazepine receptor binding in the frontal cortex and a decreasing muscarinic but not benzodiazepine receptors in the temporal cortex of alcohol abusers. Taken together, these findings suggest that alcohol neurotoxicity does not simply result in a random loss of neurons and or their associated synapses with their receptors. Instead, different types of receptors, depending upon their location in different brain regions, are specifically affected or spared. This suggests the involvement of region- and receptor-specific mechanisms in chronic alcohol toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Loss of muscarinic cholinergic receptors from the temporal cortex of alcohol abusers. 254 45

In a group of 1,025 cases of alcoholic liver the authors detected 28 cases (2.73%) of acute alcoholic hepatitis on the basis of the morphologic examination, 75% were males, mean age 45 +/- 18 years. The mean amount of alcohol consumed daily was 106.7 g for a mean duration of 19.78 years. The hepatic lesional substrate was hepatic steatosis and cirrhosis in 7 cases (25%) and steatofibrosis in the other 14 cases (50%). The triggering factors were the abuse of alcohol in 27 cases and a pneumonia in the last case. The disease was characterized by fever, encephalopathy, hepatomegaly, hepatocytolytic-cholestatic syndrome. The evolution was dictated by the gravity of the background hepatic lesional substrate.
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PMID:[Acute alcoholic hepatitis]. 257 74

During a 2-year period after the introduction of an intensive chemotherapeutic protocol, alpha-hemolytic streptococci accounted for 75% of all episodes of sepsis among children with acute nonlymphocytic leukemia at our institution. Only one case had occurred in the previous 8 years. Fourteen of 15 episodes of streptococcal sepsis occurred after therapy with either continuous or large dosage intermittent cytosine arabinoside. Eleven episodes occurred at two specific treatment points. Septic episodes were complicated by shock (2 of 15), encephalopathy (2 of 15), pneumonia (3 of 15) and death (1 of 15). Oral mucosal lesions may provide a portal of entry for alpha-hemolytic streptococci. These data suggest that children receiving continuous or large dosage intermittent cytosine arabinoside for treatment of acute nonlymphocytic leukemia may be at increased risk for alpha-hemolytic streptococcal sepsis. Empiric antimicrobial therapy in these children when febrile and neutropenic should include antibiotics effective against alpha-hemolytic streptococci.
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PMID:Alpha-streptococcal septicemia in leukemic children treated with continuous or large dosage intermittent cytosine arabinoside. 223 81

Recent improvements in the results of orthotopic liver transplantation (OLT) have made this a well-accepted treatment for patients with severe hepatic failure. Current problems encountered following OLT are discussed. Immediate complications comprise surgical bleeding, primary graft non-function, and graft failure due to hepatic artery occlusion. Secondary complications are frequent. Surgical ones include biliary and vascular (hepatic artery thrombosis most often) problems, as well as intra-abdominal abscesses associated with gastrointestinal perforation, biliary leak, graft ischaemia or an infected haematoma. 40% of patients having undergone OLT will be reoperated on, 2/3 of them within 3 months. Non-surgical complications are mostly pulmonary. The risk of pneumonitis is increased by prolonged mechanical ventilation; it is always potentially disastrous in the immunosuppressed, transplanted patient. Hypertension is also often seen in the early postoperative period; it requires prompt treatment. Early renal impairment after OLT is common, and of better prognosis than late onset renal failure, which is generally associated with shock, graft failure, sepsis or use of nephrotoxic agents. Seizures, usually only one, occur in about 10% of patients; recovery is complete. Encephalopathy with intracranial oedema related to fulminant hepatitis has a worse prognosis, but survival figures are quite encouraging. Three type of rejection are described after OLT: 1) severe accelerated rejection (very rare), 2) acute rejection encountered in about 70% of patients over the first 3 months, and 3) late rejection, which can lead to the vanishing bile duct syndrome (VBDS). Diagnosis of rejection is made by liver biopsy. Prophylactic immunosuppression includes cyclosporin, methylprednisolone and azathioprine. Cyclosporin toxicity and drug interactions are reviewed. Treatment of acute rejection episodes comprises an initial bolus of high doses of corticoid drugs; if there is no response, antilymphocyte globulin or monoclonal antibodies may have to be used. Infection is the main cause of death following OLT. Early infections, mostly intra-abdominal and pulmonary, are bacterial or fungal. Vital (especially CMV) and other opportunistic infections occur generally after the second week. Retransplantation, carried out in 10 to 25% of patients, may be urgent in case of primary graft failure, or hepatic artery thrombosis associated with graft failure, or hepatic artery thrombosis associated with graft failure. Other indications are early graft rejection with severe hepatic dysfunction, chronic rejection with severe VBDS, and recurrence of the initial disease.
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PMID:[Liver transplantation in adults: postoperative management and development during the first months]. 262 46

Bacterial infection is a serious and often fatal complication of patients with liver disease and can prove fatal either directly or by precipitation of gastrointestinal bleeding, renal failure, or hepatic encephalopathy. At greatest risk are patients with alcoholic cirrhosis or decompensated chronic liver disease, or cases of acute liver disease who progress to fulminant hepatic failure or subacute hepatic necrosis. Infection appears to be unusual in patients with primary biliary cirrhosis. The site and type of infection is unrelated to the aetiology of the liver disease. Bacteraemia, pneumonia, urinary tract infection and spontaneous bacterial peritonitis are most common but infective endocarditis and meningitis, especially with pneumococci, are easily overlooked. Clinical suspicion of infection must be high as the only indication may be a general deterioration in the patients' clinical state, increasing encephalopathy or renal impairment. In the case of patients with fulminant hepatic failure, infection may precipitate the initial or recurrent encephalopathy and contributes to death in 10% of fatal cases. Spontaneous bacterial peritonitis is now recognized to occur in the absence of clinical features of peritonitis. The PMN content of the ascitic fluid may provide the only indication of infection and is the most readily available screening test. The most common types of organism responsible for all types of infection are Gram-negative enteric and streptococci, especially pneumococci, while infection with anaerobes is rare. Risk factors for infection include decompensated alcoholic liver disease, fulminant hepatic failure, gastrointestinal bleeding, invasive practical procedures and impaired host defence mechanisms against infection. Of the host defence mechanisms, impaired function of the reticuloendothelial system, complement, and PMNs represent the most common and serious defects. Defects of humoral immunity are present in ascitic fluid from patients with cirrhosis and are probably a major reason for development of spontaneous bacterial peritonitis. Diuresis improves these functions and reduces the risk of peritonitis. Treatment of infections even with the appropriate antibiotic is still associated with a high mortality but the use of adjuvant gut sterilization is promising, particularly in cases infected with Gram-negative enteric organisms. Infusions of fresh frozen plasma, blood and cryoprecipitate improve some systemic host defences and may be beneficial in the treatment and reduction of risk of infection.
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PMID:Bacterial infections complicating liver disease. 265 49

Bone marrow transplantation is the treatment of choice of many haematological disorders but its success is limited by two major complications, graft-versus-host disease (GVHD) and pulmonary disorders. Of the first 31 patients transplanted at St. James's Hospital (1984-1986) 16 (52%) had a successful outcome. Of the 15 patients who died, two died of GVHD and one of recurrent leukaemia. All others had severe pulmonary disease either causing death directly (9 cases) or contributing to death from toxic encephalopathy, carditis or recurrent leukaemia (1 case each). The principal forms of pulmonary disease were cytomegalovirus pneumonitis (4 cases), acute haemorrhagic pulmonary oedema (4 cases) and pneumocystis carinii pneumonia (2 cases). There were single cases of staphylococcal pneumonia and idiopathic pulmonary fibrosis. Aspergillus was a second pathogen in two cases. Pulmonary damage due to conditioning chemoradiotherapy and to GVHD probably underlies this high incidence of pulmonary disease. T-cell depletion to limit the incidence of GVHD together with increased prophylaxis against CMV and pneumocystis carinii will probably substantially reduce these complications in the near future.
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PMID:Pulmonary disease following allogeneic bone marrow transplantation. 266 67

115 cases of immunocompromised patients complicated with fungal pneumonia treated during the period from April 1968 to December 1986 were retrospectively studied. 96 were male and 19 female. Their age ranged from 6 to 84. The incidence increased significantly in recent years especially after 1983. Severe liver disease was the underlying disease in 102 (88.7%) patients. 108 (93.9%) had received antibiotics and 55 (47.9%) corticosteroids. Fungi species isolated were candida in 107 (54.9%), aspergillus in 82 (36.9%), penicillium in 7 (3.6%), mucormycetes in 6 (3%) and reotrichum in 3 (1.5%). Fever, cough, expectoration, moist rales diminished breath sounds and increase of W. B. C. and neutrophils were the important clinical features. The roentgenologic findings vary with the nature and extent of the pathologic process. Disseminated mycoses were found in 9 of the 18 autopsied cases. The characteristic pathologic findings were inflammation, abscess formation, vasculitis, infarction and hemorrhage. Extrapulmonary features such as enteritis, purulent nephritis, abnormal EKG, encephalopathy and rash were present. 93 cases received antifungal therapy including garlicin, clotrimazole, amphotericin B, nystatine, miconazole, 5-fluctosine and ketoconazole. Because these drug combinations were so complex, it is difficult to evaluate their efficiency. However the survival rate was somewhat elevated in recent years. The mortality rate of this series was 80.9%.
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PMID:[A retrospective study of 115 cases of fungal pneumonia]. 273 37

We have retrospectively evaluated 24 sepsis episodes caused by viridans streptococci in 23 neutropenic children during a 21 months period at the Pediatric Hematology Unit of St. Louis Hospital. The underlying malignancies included acute lymphoblastic leukemia, acute non lymphoblastic leukemia, aplastic anemia and solid tumor. In 17 children neutropenia, defined as a neutrophil count of less than 500 per cubic millimeter, was caused by cytotoxic chemotherapy. For 6 other children neutropenia was consequential to pretransplant treatment regimen for autologous bone marrow transplantation including cytotoxic chemotherapy and total body irradiation. All patients had a silicone rubber atrial catheter. In 9 patients sepsis was associated only with fever for less than 48 hours. In 5 other children fever was prolonged more than 72 hours in spite of specific antimicrobial therapy. No other organism was isolated. In 10 patients, however, the infectious syndrome was severe and the features included cardiac failure (7 patients), pneumonia (7 patients) resembling adult respiratory distress syndrome, encephalopathy (3 patients) without meningitis and proteinuria, 7 of these patients needed a management in a pediatric intensive care unit and 2 died in spite of adapted antibiotics. Streptococci were isolated in blood cultures in 23 children.
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PMID:[Frequency and severity of systemic infections caused by Streptococcus mitis and sanguis II in neutropenic children]. 278 Jan 2

The histochemical demonstration of iron and the iron content was examined in the brain of a case of the special type of hepatocerebral encephalopathy (HCE). The patient had suffered from a liver disease since 36 years old. At 44 years old, she experienced the first attack of twilight state with flapping tremor. She had predilection for eating beans. Her personality gradually became euphoric with the recurrent episodes of unconsciousness. At 54 years old, she died of the complication of melena, renal insufficiency and pneumonia. The liver showed cirrhotic changes and iron content of liver was 0 or 1 after MacDonald's criterion scale. The histopathological findings of the brain showed the characteristic changes of HCE, which were incomplete softening and spongy state pseudolaminarilly extending in the deep layer of the cerebral cortex, the proliferation of the severely changed Alzheimer 2 type glia with or without intranuclear carmine positive substance. The deparaffinized sections, 20 mu in thickness, which were not fastened on slides were used for the histochemical study of iron, because iron deposits displaced inside of the brain tissues when the paraffin sections were fastened on slide glasses in the constant-temperature bath. The iron deposition was found in the central gyrus, superior temporal gyrus, medial and lateral occipito-temporal gyrus and middle temporal gyrus of occipital lobe. The iron accumulated in the ground substance, glia cell bodies, glia nuclei and unknown bodies in the 3-6 layers of cerebral cortex of these gyri. The iron accumulation demonstrated histochemically in other parts of the brain were group 1, 2 by Spatz, mammillary body, glia cell bodies in cerebellar white matter and pons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Iron deposition in the brain of a case of the special type of hepatocerebral encephalopathy]. 280 22


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