1/19. Lamotrigine overdose presenting as anticonvulsant hypersensitivity syndrome.OBJECTIVE: To describe the laboratory and physical manifestations of lamotrigine toxicity presenting as anticonvulsant hypersensitivity syndrome. CASE SUMMARY: A 49-year-old white man presented to our institution with a two-day history of low-grade fever, erythema, and edema involving the periorbital area. Five days earlier, he had been placed on lamotrigine treatment for bipolar disorder. He inadvertently received four daily doses of lamotrigine 2700 mg each. physical examination was significant for periorbital edema and discrete and confluent blanching red macules and papules involving the face, trunk, and extremities. Laboratory tests revealed leukocytosis, hepatitis, and acute renal failure. With normalization of the laboratory results, the eruptions and edema gradually resolved. DISCUSSION: Lamotrigine toxicity can lead to periorbital edema, rash, and multiorgan system abnormalities. This presentation has clinical and laboratory similarities with anticonvulsant hypersensitivity syndrome, which suggests that at some threshold concentration the amount of lamotrigine may overwhelm the body's ability to metabolize the drug, leading to a similar hypersensitivity reaction. Lamotrigine is a relatively new agent, and this report may provide useful insights on evaluating the clinical toxicology of this agent. CONCLUSIONS: Healthcare providers should be aware that lamotrigine overdose may present with multiorgan involvement, similar to anticonvulsant hypersensitivity syndrome.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
2/19. Hepatic calcification by sequelae of chronic schistosomiasis japonica: report of four cases.Due to the elimination of intermediate hosts and the improvement of clinical care, most parasitic infections have been effectively controlled in developing countries. Recently, the increase of the worldwide tourism, especially to Mainland china, and the migration of overseas workers from endemic countries have led to more parasitic infections that should not be overlooked by physicians. Assessment of diffuse liver disease with physical examination and laboratory findings is notoriously inaccurate. Thus, physicians use liver biopsy for accurate diagnoses. We present 4 patients with hepatic schistosomiasis japonica which were diagnosed using imaging before liver biopsy. Hepatic schistosomiais japonica has a tendency to cause dystrophic calcification and fibrosis in the liver. According to the results, a combination of ultrasonography and computed tomography (CT), used to recognize characteristic calcification patterns, seem useful to physicians for accurate diagnoses. Thus, unnecessary biopsy procedures can be avoided.- - - - - - - - - - ranking = 11.440434693241keywords = physical examination, physical (Clic here for more details about this article) |
3/19. The challenge of diagnosing the cause of jaundice.The patient presenting with jaundice may have a variety of hepatobiliary or hematologic conditions. Understanding the causes of jaundice and the history and physical examination hallmarks provide the basis for choosing the most efficacious laboratory and diagnostic studies. A case report illustrating the reasoning involved in distinguishing between the different causes of jaundice is presented.- - - - - - - - - - ranking = 11.440434693241keywords = physical examination, physical (Clic here for more details about this article) |
4/19. portal vein thrombosis and liver disease.portal vein thrombosis can occur secondary to infection, surgical intervention, or as a result of liver dysfunction. Its development can precipitate the need for emergency interventions including endoscopy, transjugular intrahepatic portosystemic stents (TIPS), portacaval shunts, or even liver transplantation. portal vein thrombosis occurs slowly and silently. portal vein thrombosis is not discovered until gastrointestinal hemorrhage develops in the patient unless the thrombosis is diagnosed on routine surveillance diagnostic testing. portal vein thrombosis can be diagnosed by Doppler ultrasonography, computed tomography scan, or magnetic resonance imaging. Late identification of portal vein thrombosis can lead to increased morbidity and mortality of the patient population. patients with portal vein thrombosis can be successfully managed with early identification and collaboration between the patient and the health care team for ongoing monitoring and treatment. Patient education involves assisting the patient in the understanding of esophageal varices, the various treatment modalities, their physical limitations, and the need for monitoring and management of the portal hypertension.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
5/19. mulibrey nanism: review of 23 cases of a new autosomal recessive syndrome.Mulibrey (muscle, liver, brain, eye) nanism is probably an autosomal recessive condition characterized by progressive growth failure of prenatal onset, triangular face with hydrocephaloid skull, general thinness and muscular hypotonicity, peculiar voice, venous congestion caused by pericardial constriction, and pigment dispersion and yellowish dots in ocular fundi. Two thirds of the patients had cutaneous nevi flammei and one third cystic fibrous dysplasia of the tibia. Probably a substantial portion of the affected are lost by early abortion and others by infantile death. The physical capacity and life expectancy seem to vary depending on the degree of the cardiac affection.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
6/19. Cases from the Osler Medical Service at Johns Hopkins University.A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen.On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. urinalysis revealed an elevated specific gravity and numerous muddy granular casts. hepatitis a, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm.What is the diagnosis?- - - - - - - - - - ranking = 11.440434693241keywords = physical examination, physical (Clic here for more details about this article) |
7/19. Liver glycogenosis as early manifestation in type 1 diabetes mellitus.Clinical symptoms and biochemical findings related to liver dysfunction are not generally reported among the presentation features of Type 1 diabetes mellitus (T1DM) in infancy and childhood. To our knowledge this is the first paper reporting two children with a clinical and biochemical picture of hepatic glycogenosis at the presentation of T1DM. In both cases at beginning of insulin therapy liver function and dimensions were absolutely normal, even though glycometabolic status had been severely altered for many days at T1DM onset. Both hepatomegaly and aminotransferase abnormalities were first found only some days after the institution of treatment with supraphysiological insulin doses. In both patients the improvement of glycometabolic control under insulin therapy was followed within some weeks by a complete physical and biochemical recovery, as typically reported in hepatic glycogenosis. These case reports demonstrate that hepatic glycogenosis can occur at any stage of T1DM and may even be one of its earliest manifestations, together with those classically reported at the onset of T1DM. Since long-standing hyperglycaemia and overinsulinisation are metabolic pre-requisites for hepatic glycogen storage, liver glycogenosis should be expected to be not uncommon during the first phases of T1DM, especially in the cases who are initially treated with supraphysiological insulin doses.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
8/19. safety of liver biopsy in acute sickle hepatic crisis.Hepatic dysfunction is a commonly recognized complication of sickle cell crisis. The cause of hepatic compromise is usually made evident from physical examination, clinical history, laboratory testing, and noninvasive imaging. There are occasions when liver biopsy is required to define the etiology of the hepatic dysfunction. Liver biopsy during acute sickle hepatic crisis can result in hemorrhage and death. Careful consideration of alternatives must be explored prior to performing liver biopsy on a patient with acute sickle hepatic crisis. If biopsy cannot be delayed, close hemodynamic monitoring of the patient postbiopsy is essential.- - - - - - - - - - ranking = 11.440434693241keywords = physical examination, physical (Clic here for more details about this article) |
9/19. Strenuous exercise simulating hepatic injury during vaccine trials.Three healthy young men participating in phase 1 clinical vaccine trials had unexplained increases in their serum transaminase levels. Retrospective analysis indicated that these volunteers had participated in strenuous physical training 2-5 days prior to the noted elevations. The pattern of serum enzyme elevations, initially thought to be consistent with hepatic injury, were associated with parallel increases in creatine phosphokinase. One individual consented to repeat his exercise regimen. This was followed by a recurrence of the same pattern of increases in serum enzymes, including creatine phosphokinase. Thus, in trials where serum enzymes will be measured, it may be prudent to encourage subjects to refrain from increasing their activity above that which they normally perform.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
10/19. autopsy case of Dubin-Johnson syndrome with pneumonia and abetalipoproteinemia-like lipid profile.We report the autopsy of a 79-year-old Japanese woman with Dubin-Johnson syndrome accompanied by pneumonia, an abetalipoproteinemia-like lipid profile and acanthocytosis. On admission, physical examination of the patient revealed malnutrition. blood tests revealed marked inflammatory changes and mild liver dysfunction. Chest X-ray indicated bilateral pneumonia. Total cholesterol, low-density lipoprotein (LDL) cholesterol and triglyceride levels were 89 mg/dL, 5 mg/dL and 6 mg/dL, respectively. Peripheral blood smears revealed numerous acanthocytes. Despite the administration of antibiotics and nutritional support, the patient died. autopsy revealed a black liver, atrophy of fat tissue on the mesentery, and pneumonia with bilateral pleural effusion. We believe that the abetalipoproteinemia-like lipid profiles in this case were caused by malnutrition and the inflammatory changes rather than the direct effects of Dubin-Johnson syndrome. We base this conclusion on the following three findings: 1) the patient's lipid profile before hospitalization was in the normal range, 2) her serum LDL cholesterol and triglyceride levels gradually increased after nutritional support began, and 3) blood tests revealed marked inflammatory changes (c-reactive protein 9.0 mg/dL; interleukin-6 16.4 pg/mL). This case provides important information that enhances our understanding of lipid metabolism under conditions of malnutrition and inflammation.- - - - - - - - - - ranking = 11.440434693241keywords = physical examination, physical (Clic here for more details about this article) |
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