Cases reported "Acute Disease"

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1/32. Olanzapine-induced acute pancreatitis.

    OBJECTIVE: To report the first published case of olanzapine-induced acute pancreatitis. CASE SUMMARY: A 72-year-old white woman was admitted to the intensive care unit (ICU) with acute hemorrhagic pancreatitis and unintentional verapamil overdose. The patient did not consume alcohol and had undergone a cholecystectomy in the past; other medical causes of pancreatitis had been ruled out. She was taking several medications chronically, but olanzapine was started six days prior to the onset of acute abdominal symptoms. According to the Naranjo probability scale, olanzapine was considered the probable cause of acute pancreatitis in this patient. Following a 12-day stay in the ICU, the patient was transferred to the ward where she died a few days later of unrelenting peritonitis secondary to acute pancreatitis. DISCUSSION: A literature search (1966-July 2000) and contact with the manufacturer failed to detect any published reports of acute pancreatitis associated with olanzapine. The contribution of concomitant medications taken prior to ICU admission in initiating or worsening the pancreatitis was deemed unlikely. More common causes of acute pancreatitis, such as ethanol consumption and gallstones, were also ruled out in this patient. Therefore, olanzapine was rated as a probable cause for acute pancreatitis in our patient. The mechanism of this adverse reaction is unknown. CONCLUSIONS: This is believed to be the first published report suspecting olanzapine, an atypical antipsychotic agent, to have caused acute hemorrhagic pancreatitis in a patient, leading to admission to the ICU and, eventually, death secondary to unrelenting peritonitis.
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2/32. Shwachman-diamond syndrome in a Mexican family.

    Shwachman-diamond Syndrome (SDS) is an inherited condition with multisystemic abnormalities including pancreatic exocrine dysfunction, neutropenia, short stature, and skeletal abnormalities. In this report, we describe the case of a 14-year-old female with a history of neutropenia, pancreatic exocrine insufficiency and pancreatic endocrine sufficiency, pancreatic lipomatosis (10), and the development of myeloid leukemia. Postmortem examination revealed a high probability of SDS. We also describe the clinical findings in the patient's six siblings, suggesting this as a familial form of SDS. Because the gene(s) responsible for this syndrome have not yet been identified, genetic confirmation is not yet possible. This is the first report in the literature of a Mexican family with probable SDS.
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3/32. hepatitis b vaccine related-myelitis?

    We present four incidental cases that developed partial myelitis following the administration of hepatitis b vaccine in 1998. The first two cases, a 33-year-old man and a 42-year-old woman developed progressive sensory symptoms without motor involvement within 4 weeks following the vaccination. Their magnetic resonance imaging (MRI) disclosed similar lesions consistent with myelitis at their cervical spinal cord. A comparable inflammatory lesion was seen at the T9-T10 levels of the spinal cord in the third case, who was a 40-year-old woman presenting with numbness in her legs and urinary retention following the vaccination. The fourth case who was a 42-year-old woman, presented with sensory symptoms in her left extremities, which developed 3 months after the vaccination. Her MRI showed a hyperintense lesion at C6. She also had two tiny lesions in her cranial MRI. In all cases, there was no history of preceding infections and no clinical evidence suggestive of any other disorders that may cause myelopathy. All patients recovered completely within 3 months with the exception of the third patient who developed new neurological symptoms after 12 months. Similar clinical and imaging presentation of myelitis following hepatitis b vaccination within a 1 year period with no other demonstrable clinical and laboratory evidence for any other disorder raise the probability of a causal link between these two events.
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4/32. bupropion-induced acute dystonia.

    OBJECTIVE: To report a case of acute dystonia consisting of neck stiffness, trismus, and unilateral temporomandibular joint (TMJ) pain and subluxation secondary to an increase in sustained-release (SR) bupropion. CASE SUMMARY: A 44-year-old white man with a history of chronic low-back pain and tension headaches, taking no other medications, was started on bupropion SR 150 mg once a day for depression. The dosage was increased to 150 mg SR twice a day and eventually augmented with buspirone 15 mg 3 times a day. He developed bilateral trismus, inability to rotate his head laterally, and spontaneous left TMJ subluxation. Symptoms recessed with discontinuation of both medications and failed to reappear with a trial of buspirone 15 mg 3 times a day alone. A retrial of bupropion alone evidenced no adverse effects at a dosage of 150 mg SR once a day. However, when the dosage was increased to 150 mg SR twice a day, the patient reexperienced initial signs of neck stiffness, jaw muscle tightness, and left TMJ subluxation within 24-48 hours. Reduction of the bupropion dosage to 150 mg SR once daily stopped the symptoms; the patient has continued at this dosage without adverse effects for > 1 year. DISCUSSION: Medication-induced focal dystonias usually present with dramatic head (most frequently oral-buccal) and neck muscle spasm with occasional jaw clenching, bruxism, and TMJ syndrome. In this case, the rapid onset of neck and jaw symptoms within 24-48 hours of an increase of bupropion SR from 150 mg once a day to 150 mg twice a day suggest that the patient may have been sensitized by an initial trial of bupropion and buspirone, or by the increased dose of bupropion alone. Both agents are reported to interact with both the dopaminergic and serotonergic systems. Although buspirone has been implicated in inducing acute dystonia, it did not do so in this case when used alone at a dose of 45 mg a day. During a second trial of bupropion SR 150 mg a day, neck and jaw symptoms recurred within 24-48 hours of increasing the dose to 150 mg SR twice a day. The symptoms receded when the bupropion dose was returned to 150 mg SR once a day, suggesting a dose-response relationship. The Naranjo probability scale indicated that this untoward reaction was probable. CONCLUSIONS: This case suggests that selected patients may experience dose-related acute dystonic adverse reactions to bupropion with or without buspirone augmentation. Dystonias, which usually follow administration of antipsychotics, have been linked to acute dopamine depletion and basal ganglion-derived gamma synchronization dysfunction. Acute dystonia symptoms may begin within hours of starting or changing antipsychotic drug dosage; however, 90% of symptoms are observed during the first 3-5 days of starting or increasing dosage. To the best of our knowledge, there have been no reports of bupropion-induced dystonia.
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5/32. Rofecoxib: a possible cause of acute colitis.

    Nonsteroidal antiinflammatory agents may cause relevant small bowel and colonic side effects, apart from gastroduodenal lesions. The synthesis of selective cyclooxygenase-2 (COX-2) inhibitors has been an important breakthrough in antiinflammatory therapy by decreasing the incidence of upper gastrointestinal lesions. However, there is little information available concerning their effects on gut mucosa distally to the duodenum. A case history is described of a 52-year-old woman with a temporary colostomy after resection of a sigmoid tumor and who presented with bloody diarrhea 5 days after beginning therapy with rofecoxib. The hemorrhage had its origin in the transverse colon, and the endoscopic appearance was that of actively bleeding acute hemorrhagic colitis. No other colonic lesions were detected, nor was there any evidence of related infection, bleeding diathesis, or other systemic diseases. On discontinuing rofecoxib and instituting parenteral rehydration, the bleeding and diarrhea stopped. Endoscopic follow-up revealed regenerating mucosa in the transverse colon. The time relation, the absence of other causes of hemorrhage, and the clinical evolution all strongly support the probability of a causal relation between rofecoxib and hemorrhagic colitis. This case may raise awareness concerning the possibility of colonic lesions related to the new COX-2 inhibitors, similar to what is known about nonselective antiinflammatory agents.
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6/32. Congenital leukaemia: the Dutch experience and review of the literature.

    We reviewed Dutch patients and those described in the literature with congenital leukaemia in the past 25 years, with the intention to obtain an overview of the characteristics of this rare disease. Among the 117 patients reviewed, acute myeloid leukaemia (AML) was more frequent (64%) than acute lymphoblastic leukaemia (ALL, 21%). Most patients had a high leukaemic cell load with hepatosplenomegaly, leukaemia cutis and hyperleucocytosis. Cytogenetic abnormalities were found in the majority of the patients tested (72%); 11q23 abnormalities were found in less than half of them (42%). The probability of overall survival at 24 months was only 23%. When congenital AML and ALL were compared, clinical characteristics and overall survival were not significantly different. However, in patients at risk, the probability of event-free survival (EFS) and disease-free survival (DFS) were significantly higher in AML than in ALL, 43% versus 13% and 68% versus 0% respectively. Among the congenital AML cases, six spontaneous remissions have been described. In conclusion, the clinical characteristics of congenital leukaemia differ from those of leukaemia in older children and prognosis is generally poor. Once complete remission is achieved, patients with AML fare better than those with ALL. Chemotherapy for congenital leukaemia needs improvement to increase the sustained remission rate.
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7/32. Acute cholestatic hepatitis associated with celecoxib.

    OBJECTIVE: To report a case of acute cholestatic hepatitis associated with the selective cyclooxygenase-2 inhibitor celecoxib. CASE SUMMARY: A 41-year-old white man was hospitalized for jaundice after 2 doses of celecoxib 200 mg for pain associated with right-knee trauma. Laboratory workup showed hyperbilirubinemia, mildly elevated serum transaminase concentrations, and cholestasis. Abdominal imaging showed no dilation of the biliary tree. histology showed cholestasis, with bile plugs in dilated bile canaliculi and a mild portal infiltrate that are highly suggestive of drug-induced cholestasis. DISCUSSION: This is the fourth report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient. CONCLUSIONS: Cholestatic hepatitis is a well-recognized adverse effect of several drugs. Although celecoxib is considered to have a very low potential for hepatic toxicity, well-documented reports of adverse reactions can contribute significantly to the definition of more accurate safety profiles for new drugs introduced into clinical practice.
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8/32. patients with acute pulmonary embolism should have an echocardiogram to guide treatment decisions.

    A 62-year-old man with a past medical history notable for hypertension, osteoarthritis, and calf deep vein thrombosis at age 55 following a total hip arthroplasty presents to the emergency department with acute-onset dyspnea and right-sided pleuritic chest pains. His medications consist of a calcium channel blocker and a COX-2 inhibitor. Pretest clinical suspicion for pulmonary embolism (PE) is high. ventilation and perfusion lung scintigraphy are interpreted as being high-probability for PE. The nurse asks if a stat transthoracic echocardiogram should be ordered.
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9/32. Acute interstitial nephritis due to pantoprazole.

    OBJECTIVE: To describe what is believed, as of November 4, 2003, to be the first case published in the literature of acute interstitial nephritis (AIN) due to pantoprazole. CASE SUMMARY: A 77-year-old white woman presented to the hospital with elevated serum creatinine, oliguria for the past 24 hours, arthralgia, fatigue, fever, and bilateral flank pain. The patient had initiated treatment with oral pantoprazole 40 mg/d for gastroesophageal reflux 2 months prior to admission. After 5 weeks of therapy, she stopped taking pantoprazole due to general malaise. Upon admission, all home medications, including pantoprazole, were reinitiated based on the patient's medication list. serum creatinine increased to 6.1 mg/dL on day 4 of admission from a baseline of 1.0 mg/dL. Pantoprazole therapy was promptly discontinued, and prednisone 40 mg/d was initiated. urinalysis revealed eosinophils, and a subsequent renal biopsy confirmed a diagnosis of AIN. The serum creatinine level gradually declined over 2 weeks, and the patient was discharged home with a serum creatinine level of 1.6 mg/dL. The Naranjo probability scale suggests a highly probable relationship between AIN and pantoprazole therapy in this patient. DISCUSSION: drug hypersensitivity reactions are the most common cause of AIN. There have been several reported cases of omeprazole-induced AIN. Although there are very few prospective data on the efficacy of treatment of drug-induced AIN, corticosteroids may have a role in recovery of renal function. prednisone doses of 1 mg/kg/d have been suggested. CONCLUSIONS: physicians should be aware that drug-induced AIN can be associated with proton-pump inhibitors. Early detection of this rare adverse reaction may prevent acute renal insufficiency.
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10/32. Acute delirium associated with combined diphenhydramine and linezolid use.

    OBJECTIVE: To report a case of delirium with hallucinations presumably caused by the combination of diphenhydramine and linezolid. CASE SUMMARY: A 56-year-old white man was receiving diphenhydramine 300 mg/d for 2 days to treat pruritus caused by a bullous rash possibly induced by vancomycin. He subsequently developed visual and auditory hallucinations, with erratic, aggressive behavior persisting for 3 days. Central anticholinergic syndrome was first suspected, but the long duration and exaggerated response by a patient not prone to anticholinergic toxicity suggest that a second agent may have enhanced the reaction. DISCUSSION: The pharmacodynamic properties of linezolid make this drug a likely contributor to the marked, prolonged effects experienced by this patient. The Naranjo probability scale suggests a possible relationship between the reaction and the combination of diphenhydramine and linezolid. CONCLUSIONS: Drug-induced delirium can occur with several drugs, including diphenhydramine. Linezolid has dopaminergic properties that may enhance the central nervous system effects of anticholinergics. Precautionary monitoring of mental status should be advised when concomitantly administering linezolid with drugs in this class.
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