Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of malignant neuroleptic syndrome in a 55 years old male diagnosed 3 years ago of alcoholic paranoid psychosis who was chronically treated with haloperidol, clothiapine, and phenobarbital. Twenty one days after neuroleptic drug withdrawal the patient was admitted to the recovery room because of hyperthermia (40.2 degrees C), left basal pneumonia, acute respiratory insufficiency, extrapyramidal rigidity, mutism, dysarthria, deep coma, hypotension, and tachycardia. Two days after he presented massive rhabdomyolysis, atrial flutter with hemodynamic deterioration which reverted to sinus rhythm and acute anterolateral and inferior myocardial infarction documented by enzyme rise and electrocardiographic alterations. Rhabdomyolysis and myocardial infarction were the precipitating factors of the renal insufficiency. A malignant neuroleptic syndrome was suspected and intravenous treatment with dantrolene sodium 1.5 mg/kg every 24 hours was initiated. Bromocriptine was not administered. The patient died 14 days after in the course of a sepsis and cardiogenic shock.
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PMID:[Malignant neuroleptic syndrome associated with myocardial infarction, acute renal insufficiency and rhabdomyolysis]. 168 57

Griseofulvin administration was associated with the development of absolute neutropenia in six of seven (86%) cats with feline immunodeficiency virus (FIV) infection. The neutropenia was severe (less than 400 neutrophils/microliter) in four of the six affected cats, and one cat died from sepsis. Neutrophil counts returned to baseline values within 15 days after drug withdrawal in all surviving cats. No symptoms or hematologic abnormalities were observed in four normal (FIV-seronegative) cats treated with the same lot of griseofulvin at equivalent doses. Neutropenia recurred in two of two FIV-seropositive cats upon griseofulvin rechallenge. Cats with FIV infections appear to be at increased risk for griseofulvin-associated neutropenia. This phenomenon may be analogous to the increased frequency of antibiotic-induced neutropenias observed in humans infected with the human immunodeficiency virus.
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PMID:Severe neutropenia associated with griseofulvin therapy in cats with feline immunodeficiency virus infection. 207 57

Authors have studied 45 babies born during past five years to drug-addicted mothers. Increase in number han been remarkable: from 0.095 per thousand live births in 1980 to 1.57 in 1984. There was and 16.3% incidence for preterm infants, 34.8% for low birth weight and 18.6% were small for gestational age. One third (30.2%) suffered infections, mostly sepsis. Morbidity was high in these babies, caused mainly by prematurity. Drug withdrawal syndrome appeared in 26 babies (60.4%) at an age of 13 +/- 10 hours. Fifteen of these babies (57.6%) required pharmacological treatment during 10 +/- 7.3 days, with a good response, and only two cases needed treatment for more than a month. There were no deaths in the neonatal period. In our experience children of heroin addicted mothers form a group difficult to study because their parents give not reliable data, they have high morbidity and true problems begin when they leave hospital.
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PMID:[Newborn infants of mothers addicted to heroin. Study of 45 cases]. 334 60

This review shows that hyponatremia is the most common cause of burn seizures in children, followed by a history of epilepsy, hypoxia, sepsis with high fever, unknown aetiology and drug toxicity or sudden drug withdrawal. This study also shows that burn seizure is most common in younger children and is related to size and degree of burn. We recommend close monitoring of metabolism, haemodynamics, arterial blood gases, wound and blood cultures, and levels of abnormalities in serum, electrolytes, glucose, Ca, P and Mg. Prompt corrections of any problems in these areas can be vital. Invasive procedures for the diagnosis of seizures, including lumbar puncture and EEG, should be reserved for infrequent non-responding cases.
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PMID:Seizure disorders in burned children: a retrospective review. 878 29

A healthy 70-year-old woman who took nimesulide for 5 days, presented 2 weeks later with jaundice for which no other cause was found. Laboratory evidence of coagulopathy, hypoalbuminaemia and hypoglycaemia were present on admission, and liver biopsy showed massive necrosis of hepatocytes and severe inflammatory infiltrate. Despite supportive and corticosteroid treatment, her jaundice deepened and progressive acute renal failure developed, characterized by a 'prerenal' profile changing into irreversible acute tubular necrosis pattern, coma, occult Gram-negative sepsis and death. Although rare, nimesulide-associated hepatotoxicity and nephrotoxicity may occur and should be recognized as early as possible, to ensure immediate drug withdrawal and treatment.
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PMID:Fatal hepatitis and renal failure during treatment with nimesulide. 1094 99

Understanding the consequences of drug withdrawal on immune function and host defense to infection is important. We, and others, previously demonstrated that morphine withdrawal results in immunosuppression and sensitizes to lipopolysaccharide-induced septic shock. In the present study, the effect of morphine withdrawal on spontaneous sepsis and on oral infection with Salmonella enterica serovar Typhimurium was examined. Mice were chronically exposed to morphine for 96 h by implantation of a slow-release morphine pellet. Abrupt withdrawal was induced by removal of the pellet. In the sepsis model, bacterial colonization was examined and bacterial species were identified by necropsy of various tissues. It was found that at 48 h postwithdrawal, morphine-treated mice had enteric bacteria that were detected in the Peyer's patches (4/5), mesenteric lymph nodes (4/5), spleens (4/10), livers (6/10), and peritoneal cavities (8/10). In placebo pellet-withdrawn mice, only 2/40 cultures were positive. The most frequently detected organisms in tissues of morphine-withdrawn mice were Enterococcus faecium followed by Klebsiella pneumoniae. Both organisms are part of the normal gastrointestinal flora. In the infection model, mice were orally inoculated with S. enterica 24 h post-initiation of abrupt withdrawal from morphine. Withdrawal significantly decreased the mean survival time and significantly increased the Salmonella burden in various tissues of infected mice compared to placebo-withdrawn animals. Elevated levels of the proinflammatory cytokines were observed in spleens of morphine-withdrawn mice, compared to placebo-withdrawn mice. These findings demonstrate that morphine withdrawal sensitizes to oral infection with a bacterial pathogen and predisposes mice to bacterial sepsis.
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PMID:Morphine withdrawal lowers host defense to enteric bacteria: spontaneous sepsis and increased sensitivity to oral Salmonella enterica serovar Typhimurium infection. 1692 15

Review of the robust literature using acute drug injection paradigms points clearly to the conclusion that morphine is immunosuppressive. In contrast, studies of the effect of subacute or chronic administration of morphine on immune function is limited, with variable results. In some cases tolerance to the immunosuppressive effects of the drug is clearly demonstrated, but in other cases, selected immune parameters do not demonstrate tolerance. Discrepancies in findings may result from differences in species or route and manner of drug administration. Even fewer studies (total of 10) have been published on the effects of withdrawal on immune function. Most immune parameters tested are suppressed following drug withdrawal. Recovery time to baseline response levels varies in the studies. In the single report of withdrawal in humans, immune function was suppressed for up to 3 years. It is clearly established that withdrawal suppresses capacity of murine spleen cells to make an ex vivo antibody response, which contrasts with evidence of polarization of the lymphocytes towards a Th2 phenotype. Several laboratories have shown that subacute and chronic exposure to morphine, as well as drug withdrawal, sensitize to the lethal effects of bacterial lipopolysaccharide. Underlying sepsis, combined with morphine-induced hypofunction of the hypothalamic-pituitary-adrenal (HPA) axis, may be occult variables modulating immune responses during opioid administration and withdrawal. As episodes of withdrawal are common among drug abusers, more intensive investigation is warranted on the effects of withdrawal on immune function, on mechanisms of immune modulation, and on sensitization to infection.
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PMID:Effects of opioid tolerance and withdrawal on the immune system. 1804 Aug 1

Drug-induced hypersensitivity syndrome (DIHS), also called drug rash with eosinophilia and systemic symptoms (DRESS), is a severe reaction usually characterized by fever, rash, and multiorgan failure, occurring 1-8 weeks after drug introduction. It is an immune-mediated reaction involving macrophage and T-lymphocyte activation and cytokine release, although no consensus has been reached as to its etiology. The skin, hematopoietic system, and liver are frequently involved. DIHS can mimic severe sepsis, viral infection, adult-onset Still disease (AOSD), or lymphoproliferation.We describe 24 consecutive patients with DIHS who were hospitalized between September 2004 and March 2008. Criteria for inclusion in this observational study were suspected drug reaction, eosinophilia >or=500/microL and/or atypical lymphocytes, involvement of at least 2 organs (skin being 1 of them), with suggestive chronology and exclusion of other diagnoses. Our cohort of 12 women and 12 men had a median age of 49 years (range, 22-82 yr), and 11 had skin phototype V or VI. Patients with mild or no rash were immunocompromised (7/24)- defined as treatment with prednisone (>or=10 mg/d) and another immunosuppressant drug, or human immunodeficiency virus infection. All patients were febrile (>38 degrees C), 14 had localized or generalized edema, 7 had pharyngitis, 8 had lymphadenopathy, 22 had hepatitis, 4 had nephritis, 2 had noninfectious and nonlithiasic angiocholitis or cholecystitis. Ten patients were hypotensive, 5 of whom had associated laboratory signs and/or imaging findings suggestive of acute myocardial dysfunction. Half of the patients had hemogram abnormalities, including eosinophilia. Nine DIHS patients fulfilled the Fautrel criteria for AOSD diagnosis, including glycosylated ferritin <20% in 4/11, with or without laboratory characteristics of hemophagocytosis. Twenty DIHS episodes occurred during the less sunny months of October to March.We determined 25-hydroxyvitamin D3 (25[OH]D3) levels in 18 patients and found that 9 patients had vitamin D deficiency (<25 nmol/L or <10 microg/L) and 5 had vitamin D insufficiency (25-50 nmol/L). Moreover, 25(OH)D3 levels were inversely correlated with ferritin values. After culprit-drug withdrawal, outcomes were favorable for all patients, including those with cardiac abnormalities under slow tapering of glucocorticoids.We recommend looking for the frequent but underdiagnosed hypersensitivity myocarditis with noninvasive diagnostic tools, such as N-terminal probrain natriuretic peptide, and promptly withdrawing the culprit drug and starting glucocorticoids. Vitamin D deficiency might be a DIHS risk or severity factor, especially for patients with high skin phototype and during the winter. Because DIHS clinical and laboratory patterns share similarities with AOSD and hemophagocytosis, DIHS should be included in their differential diagnoses.
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PMID:Drug-induced hypersensitivity syndrome: clinical and biologic disease patterns in 24 patients. 1944 Jan 16

Hypersensitivity to azathioprine can manifest with a wide clinical spectrum. Azathioprine-induced Sweet's syndrome (SS) is rare and usually overlooked because it can mimic disease exacerbation and sepsis. This study aims to characterize the clinical findings of azathioprine-induced SS. A retrospective analysis of the records of three patients diagnosed with azathioprine-induced SS and a review of the relevant English-language published work was performed. Twelve (71%) of the 17 patients were male, ranging 9-89 years in age (mean, 47.2). The time of onset after starting azathioprine was 5-28 days (mean, 13.3). The most common associated disease was inflammatory bowel disease including ulcerative colitis and Crohn's disease (76%). The clinical features typically consisted of fever and classic rash of SS with pustules and vesicles. The lesions occurred most commonly on the face and trunk. Systemic involvement was rare and no hypotension or shock was reported as seen in azathioprine hypersensitivity syndrome. Thiopurine methyltransferase activity is not predictive of this type of adverse effect. Most patients dramatically responded to systemic corticosteroids. Azathioprine-induced SS may be underdiagnosed because it can be easily misinterpreted as inflammatory bowel disease-associated skin eruption. Patients with inflammatory bowel disease may be at higher risk of this condition. Early recognition and drug withdrawal can decrease morbidity of the patients.
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PMID:Azathioprine-induced Sweet's syndrome and published work review. 2329 21

Diencephalic storms or paroxysmal sympathetic storms are characterized by episodic hyperhidrosis, hypertension, tachypnea, tachycardia, and abnormal posturing. These have been reported to occur in patients with hydrocephalus, intracranial tumors, and hypoxic, ischemic, or traumatic brain injury. They can be easily misdiagnosed as seizures, uncontrolled pheochromocytoma, drug withdrawal, thyroid storm, hypertensive crises, and sepsis or anxiety attacks. The most effective treatment to control these symptoms is yet to be identified. We present 2 individuals exhibiting these sympathetic surges; one whose symptoms were controlled with phenobarbital and the other with clonidine and oxycodone. Palliative medicine physicians should be made aware of this unusual complication.
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PMID:Diencephalic storms from leptomeningeal metastases and leukoencephalopathy: a rare and clinically important complication. 2329 74


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