Cases from the Osler Medical Service at Johns Hopkins University. Zieve syndrome

Presenting features

A 47-year-old African American man was admitted to the Osler Medical Service with a chief complaint of light-headedness. He was a heavy drinker and consumed 2 pints of fortified wine every day. On the day of admission, he had been at home consuming alcohol when he stood up, became lightheaded, and immediately had to sit down. He denied any loss of consciousness, dyspnea, hematemesis, coffee-ground emesis, lower abdominal pain, bright red blood per rectum, or melena, but he recalled a burning epigastric discomfort. The patient's medical history was notable only for a 20-year history of hypertension and recently diagnosed type 2 diabetes mellitus. He was not taking any medications. He had a normal hematocrit of 43% 6 months prior to admission.Physical examination showed a supine heart rate of 115 beats per minute and blood pressure of 165/90 mm Hg, without orthostatic changes. There was scleral icterus and a jaundiced palate, but no other stigmata of end-stage liver disease. His abdominal examination was unremarkable; there were no masses, tenderness, or hepatosplenomegaly. Rectal examination revealed guaiac-negative stool. The chest radiograph and electrocardiogram were unremarkable.On admission, the laboratory examination was notable for the following values: hematocrit, 22.8% with a mean corpuscular volume of 86.7 fL and a red cell distribution width of 25.7%; absolute reticulocyte count, 177,500/mm³; total bilirubin, 4.2 mg/dL; direct bilirubin, 2.3 mg/dL; albumin, 3.3 g/dL; lactate dehydrogenase, 481 U/L; aspartate aminotransferase, 106 U/L; and alanine aminotransferase, 44 U/L. The prothrombin and activated partial prothrombin times were normal. There was no evidence of iron, vitamin B₁₂, or folate deficiency. The patient's haptoglobin level was severely depressed (<6 mg/dL) with a negative direct Coomb test and normal glucose-6-phosphate dehydrogenase activity. A peripheral blood smear was compatible with hemolysis and demonstrated normocytic, normochromic erythrocytes with moderate poikilocytosis, as well as rare spherocytes and target cells Figure 1).On the second day of hospitalization, a lipid panel revealed hypercholesterolemia with a total cholesterol level of 300 mg/dL. Due to the patient's complaint of burning epigastric pain and long history of alcohol consumption, esophagogastroduodenoscopy was performed and revealed grade 1 nonbleeding esophageal varices.What is the diagnosis?     

Cases from the Osler Medical Service at Johns Hopkins University. Pseudoachalasia due to esophageal adenocarcinoma

Presenting features

A 69-year-old man presented with nausea and vomiting. He was in good health until 2 years before presentation, when he first noted occasional difficulty eating solid foods. He could chew food without difficulty, but sometimes he had the sensation that the food was lodged in his chest. This sensation would persist for several hours; occasionally, he would need to induce emesis for relief.These episodes of chest discomfort became more frequent over time. Two weeks before presentation, he had to induce emesis after every meal and began having difficulty ingesting both liquids and solids. On the day of his presentation, he awoke at 3:00 am feeling hungry. He drank some juice, after which he had emesis and chest pain, which led him to believe that he was having a myocardial infarction.His past medical history included hypercholesterolemia and gastroesophageal reflux disease attributed to a hiatal hernia. His only medication was simvastatin, which he stopped taking 1 month before presentation because he thought that it was con-tributing to his difficulty in swallowing. He had not smoked for more than 30 years. He previously drank one beer a day but recently stopped drinking as well. A review of systems was notable for an unintentional weight loss of 20 lbs during the past 6 months.On admission, his vital signs were normal. His chest, cardiac, and abdominal examinations were unremarkable. His electrocardiogram and laboratory tests were normal. A barium swallow (Figure 1 and Figure 2) demonstrated tapering of the distal esophagus.What is the diagnosis?     

Cases from the Osler Medical Service at Johns Hopkins University

Presenting features

A 66-year-old man with a history of alcohol-induced cirrhosis was admitted to the Johns Hopkins Hospital with the chief complaints of jaundice and lower extremity swelling. Three weeks before admission, he first noticed gradually worsening jaundice and leg swelling, as well as abdominal distension, fatigue, and anorexia. He denied nausea, vomiting, fevers, night sweats, diarrhea, abdominal pain, hematemesis, hematochezia, and melena.His past medical history was remarkable only for the diagnosis of cirrhosis 8 years before admission, when he had presented with a bleeding esophageal varix. At that time, he decided to abstain from alcohol permanently but to continue smoking cigarettes. His medications at the time of the current admission included spironolactone, megestrol acetate, furosemide, propranolol, pantoprazole, and metoclopramide.On physical examination, he appeared markedly jaundiced and fatigued. He had both scleral and sublingual icterus as well as multiple facial telangiectasias and a right epicanthal xanthoma. His heart and lung examinations were unremarkable. His abdomen was distended but soft and nontender with no organomegaly. He had a palpable fluid wave, shifting dullness, and caput medusae, but no spider angiomata or gynecomastia. His lower extremities showed 2+ pitting edema extending to the lower abdomen. There was no palmar erythema, asterixis, or evidence of hepatic encephalopathy.Initial laboratory studies revealed the following: serum sodium, 130 mEq/L; chloride, 93 mEq/L; ammonia, 97.1 μg/dL; aspartate aminotransferase, 250 U/L; alanine aminotransferase, 102 U/L; alkaline phosphatase, 672 U/L; albumin, 2.8 g/dL; and total bilirubin, 23.6 mg/dL, with a direct fraction of 17.2 mg/dL. The hematocrit was 36.4% with a normal mean corpuscular volume and normal coagulation times. Paracentesis revealed transudative fluid with 303 white blood cells (67% neutrophils), a lactate dehydrogenase level of 93 U/L, a total protein level of 1.4 g/dL, and an albumin level of 0.7 g/dL (serum ascites to albumin gradient, 2.1 g/dL). Hepatitis serologies were negative and the serum alfa-fetoprotein level was 52 ng/mL.A right upper quadrant ultrasound showed ascites around a shrunken, nodular liver with a coarse, heterogeneous echo texture, as well as echogenic material in the region of the portal vein with no portal blood flow. A computed tomographic (CT) scan of the abdomen with three-dimensional reconstruction following the administration of intravenous contrast material (Figures 1 and 2) revealed innumerable indeterminate hypodense lesions measuring 1 cm or less scattered diffusely throughout the liver. In addition, the portal vein was markedly dilated with evidence of thrombus extending both intrahepatically and extrahepatically to the portal confluence.What is the diagnosis?     

Cases from the Osler Medical Service at Johns Hopkins University. Diffuse colonic angiodysplasia with chronic iron deficiency anemia

Presenting features

A 53-year-old African American woman with a past medical history of menorrhagia was admitted to The Johns Hopkins Hospital for dyspnea that had worsened over the past several months. During this time, she noticed increasing breathlessness with activity, as well as occasional dark stools and a craving for ice chips. Initially, she had dyspnea with ambulation, but in the weeks leading up to admission she began to struggle with activities of daily living, including dressing herself and brushing her hair. By the day of admission, she complained of shortness of breath at rest. She denied fever, chest discomfort, orthopnea, paroxysmal nocturnal dyspnea, presyncope, syncope, hematemesis, or bright red blood per rectum.On physical examination, the patient appeared dyspneic and fatigued. She was tachycardic with a wide pulse pressure and bounding peripheral pulses. She was not orthostatic. There was prominent conjunctival pallor. Her precordium was hyperdynamic. The lungs were clear to auscultation without rales or fine inspiratory crackles. Her nail beds were normal, but palmar creases were not seen on her hands. She had 2+ bilateral lower extremity pitting edema up to her thighs. Rectal examination revealed guaiac-negative stool.Laboratory analysis revealed the following: hemoglobin, 2.7 g/dL; hematocrit, 11%; mean corpuscular volume, 62.3 fL; red cell distribution width, 24.8%; absolute reticulocyte count, 37.6 K/mm³; and albumin, 3.0 g/dL. The patient's serum iron level was 14 μg/dL and her saturation iron was 3%, consistent with iron deficiency anemia. A peripheral blood smear showed microcytosis, anisocytosis, and hypochromia. Serum levels of aminotransferases, thyroid-stimulating hormone, vitamin B₁₂, folate, haptoglobin, lactate dehydrogenase, and antiendomysial antibody were normal, as were CD59 expression and a thalassemia screen. A chest radiograph revealed clear lung fields without infiltrates, and an electrocardiogram showed normal sinus rhythm without low voltage. Echocardiography revealed a hyperdynamic left ventricle with an ejection fraction of 75%, consistent with high output.What is the diagnosis?     

Virus-associated hemophagocytic syndrome and hemorrhagic jejunal ulcer caused by cytomegalovirus infection in a non-compromised host; a case report of unusual entity

A 76-year-old man was admitted to our hospital with abdominal pain, nausea, and vomiting. The patient was diagnosed as ileus by abdominal radiography, which showed an enlarged bowel and an air-fluid level. Computed tomography of the abdomen showed a thickened intestinal wall. His general status suddenly worsened, and he was placed on a respirator and catecholamines to prevent acute respiratory distress syndrome, septic shock, and disseminated intravascular coagulation. He had continuous fresh anal bleeding. Total colonoscopy showed bloody stool originating from the ileum. Emergency operation was performed for hemorrhagic shock under general anesthesia. Intraoperative jejunal endoscopy revealed deep linear ulcers with bleeding in the jejunum, and 30 cm of the jejunum was resected. Histopathologic examination revealed cytomegalic cells with intranuclear inclusion bodies in the tissues surrounding the ulcers, and it was diagnosed as cytomegaloviral enterocolitis with hemophagocytic syndrome in a non-compromised adult.     

Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation.The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status.During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.     

Can pancreatitis be associated with amiodarone hepatotoxicity?

We report a patient with classical features of amiodarone hepatotoxicity who died of progressive liver failure. Throughout the course of his illness, he had epigastric pain, nausea, vomiting, and persistent mild to moderate elevation of amylase and lipase in his serum and peritoneal fluid. Pancreatitis due to amiodarone has not been reported. We raise the question of whether or not the pancreas is yet another organ subject to amiodarone toxicity and speculate as to possible pathogenesis. We suggest that patients on amiodarone who develop abnormal liver enzymes, nausea, vomiting, or abdominal pain be evaluated not only for hepatotoxicity, but for pancreatitis as well.     

Churg-Strauss syndrome (allergic granulomatous antiitis) with multiple perforating ulcers of the small intestine,multiple ulcers of the colon,and mononeuritis multiplex

A case of Churg-Strauss syndrome with multiple perforations of the small intestine is described. A 31-year-old woman was admitted with a complaint of epigastric pain. She had a history of bronchial asthma. One week before admission, white blood cell count was 20 800/mm³ with 59% eosinophils. Neurological examination on admission disclosed mononeuritis multiplex with paresthesia in both the lower and upper extremities. At colonoscopy, there were scattered aphthous ulcers in the colon. Ophthalmological examination revealed allergic conjunctivitis. After admission, hypereosinophilia increased to as high as 36 000/mm³. Oral administration of prednisolone (60 mg/day) was begun. On the 3rd day of the treatment, the eosinophil count decreased dramatically, to 400/mm³, while severe abdominal pain developed. Since abdominal X-ray film revealed free air in the abdominal cavity, emergency laparotomy was performed and multiple intestinal ulcers with perforations were found. Partial ileectomy was performed. Pathological findings of the resected specimen were interpreted as a necrotizing angiitis with extravascular granuloma. Since the operation, the patient has been asymptomatic, except for neurological symptoms. Hypereosinophilia has decreased without treatment to counts averaging 270/mm³, within 3 months. On the basis of the clinical features and histopathological findings, a diagnosis of Churg-Strauss syndrome was established.     

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?     

Cases from the Osler Medical Service at Johns Hopkins University

Presenting features

A healthy 44-year-old man presented to the Johns Hopkins Hospital after two episodes of nonpurulent hemoptysis, each consisting of approximately one-half cup of blood. The episodes were painless and were preceded by minimal coughing. The blood was bright red and without clots. He denied a recent history of upper respiratory tract infection, chest trauma, chest pain, or nasal/sinus disease. He had a chronic nonproductive “smoker’s cough.” He denied a recent history of fevers, chills, night sweats, hematuria, joint pains, epistaxis, or weight loss, and had no allergies. His past medical history was notable for neurogenic diabetes insipidus and diet-controlled diabetes mellitus. His only medication was intranasal desmopressin acetate. He smoked two packs of cigarettes daily for more than 20 years and rarely drank alcohol.On physical examination, he was afebrile, with normal heart rate and blood pressure. His oxygen saturation was 94% on room air, and his respiratory rate was 16 beats per minute. His lungs were clear to auscultation bilaterally, without evidence of crackles or wheezes. He had bilateral digital clubbing. His white blood cell count was 10,770/mm³, with a normal differential. His hematocrit was 46%, and his platelet count was normal. Blood chemistries and urinanalysis were normal. A posteroanterior and lateral chest radiograph obtained on admission demonstrated moderate diffuse interstitial fibrosis involving the upper and lower lung (Figure 1A and 1B ). What is the diagnosis?     

Acute pancreatitis caused by an ectopic mediastinal parathyroid adenoma

A 22-year-old man was admitted to our hospital because of epigastric pain. Blood tests showed leukocytosis (8940?cells/mm³) and increased serum amylase levels (787?IU/L); an abdominal computed tomography (CT) scan revealed an enlarged pancreas and peripancreatic fluid collection. On the basis of these findings, he was diagnosed with acute pancreatitis. Hypercalcemia (13.5?mg/dL) and increased levels of parathormone (>3200?pg/dL) were also detected using a high-sensitivity assay; we therefore considered hypercalcemia and primary hyperparathyroidism to be the possible causes of the acute pancreatitis. A ^99mTc-sestamibi scan showed accumulation of parathyroid tissue in the left mediastinum, and a tumor was noted on the left side of the aortic arch on a thoracic CT scan. Our final diagnosis was acute pancreatitis due to hypercalcemia induced by an ectopic mediastinal parathyroid adenoma. Ectopic parathyroid tumors can thus cause acute pancreatitis, and ^99mTc-sestamibi and CT scans are useful for their diagnosis and localization.     

A case of acute phlegmonous gastritis causing gastroparesis and cured with medical treatment alone

Acute phlegmonous gastritis is an uncommon disease, often fatal condition characterized by suppurative bacterial infection of the gastric wall. It has a high mortality rate mainly because the diagnosis is usually made late. Until recently, gastrectomy in combination with antibiotics was recommended. We had experienced a case of 66-year-old man presented with epigastric pain, nausea, vomiting, and hematemesis, followed by aspiration pneumonia. At upper gastrointestinal endoscopy, the gastric lumen was narrow, and the mucosa was severely inflamed, which was erythematous, swelled, and showed necrotic areas covered with purulent exudate. Klebsiella oxytoca and Acinetobacter lwoffii were isolated in the gastric tissue culture. Contrast-enhanced computerized tomography scan of abdomen demonstrated diffuse gastric wall thickening and an intramural abscess in the gastric antral wall. Although delayed gastric emptying by gastroparesis prolonged the in-hospital period, the only medical treatment with antibiotics alone successfully cured the patient without gastrectomy.     

Coinfection with Giardia lamblia and Clostridium difficile after use of ranitidine

A 49-year-old man presented with a 3-week history of vomiting and diarrhea. He reported foamy stools but no blood or melena and had crampy epigastric pain. He denied usage of antibiotics. He had been taking ranitidine for intermittent epigastric pain for the last few months and noted an 11-pound weight loss during the 3 weeks before admission. Stool was positive for Clostridium difficile toxin and Giardia lamblia antigen. Cultures and occult blood tests were negative. Oral metronidazole, 500 mg 3 times a day, was administered, and the patient was hydrated. The diarrhea resolved, and patient was discharged on the fourth hospital day. Prior antibiotic therapy is the most common risk factor for C difficile colitis. This patient developed concomitant infection with C difficile and G lamblia while he used ranitidine. He had no other risk factors for these infections. Hence, we propose that ranitidine-induced hypochlorhydria predisposed this patient to the enteric infections.     

Gastrointestinal bleeding: dyspeptic symptoms and clinical course in relation to use of non-steroidal antiinflammatory drugs

To study the symptoms of NSAID-associated gastroduodenal bleeding, 94 patients (median age 71 years, range 19-90), were included in a prospective, clinical trial where hematemesis or melena from gastroduodenal ulceration or haemorrhagic/erosive gastritis were the inclusion criteria. NSAID use within one month was studied in relation to subjective symptoms prior to admission and to clinical course of the episode. Significantly fewer of the NSAID users (n = 54) than the non-users (n = 40) had experienced prior peptic ulceration or dyspeptic symptoms. Otherwise, no differences were seen between users and non-users, as regards pre-admission epigastric pain, heartburn or nausea. Also, the clinical course was similar in the two groups. We also found sporadic and regular NSAID use to be similar in this respect. These data do not support the alleged masking of ulcer symptoms by NSAIDs in bleeding ulcers.     

Hepatic fasciolasis diagnosed in state phase

INTRODUCTION: Hepatic fasciolosis is a zoonosis that accidentally can invade the human. REPORT OF A CASE: 62 years old male, farmer, lives in a rural community in Tehuacan, Puebla, Mexico. His living space is not provided with running water nor drainage. He has contact with sheep and bovines. Started presenting symptoms two years before. Suffered from myalgia, joint pain, fever of 38 degrees C and epigastric pain that radiated the hypocondrium and the right shoulder. He had diarrhea five times in 24 hours as well as lack of appetite that lead to a weight loss of 20 kilograms in two years. He was hospitalized and the physical examination revealed diminished muscular mass, right hypocondrium pain and hepatomegaly of 3 cm below costal margin. He said he ate watercress (Nasturium officinalis) two or three times a week. Blood test revealed erythrocytes of 3.6 x 105 mm3; hemoglobin of 11.9 g/dL; hematocrit of 30%; leukocytes 8950 mm3; neutrophils 65%; lymphocytes of 30%; eosinophils of 3%; monocytes of 1% and basophiles of 1%. Globular sedimentation was 83 mm and hemoglobin concentration was 33. Liver test results were normal and mycobacterium in fecal samples was negative, but stool detection tests revealed eggs of Fasciola hepatica. The diagnosis was hepatic fasciolosis in its biliar stage. Dehidrohemetine (1.5 mg/kg) was administered during 10 days. Symptoms disappeared within 48 hours. CONCLUSION: The lack of knowledge about fasciolosis makes it hard to diagnose it. The publication of case reports must help to facilitate its diagnosis.     

Gastrointestinal symptoms associated with enteric-coated sulfasalazine (Azulfidine EN tablets)

Abstract

To investigate both the incidence and the dosage used to treat gastrointestinal (GI) symptoms associated with enteric-coated sulfasalazine (Azulfidine EN, AZL) in patients with rheumatoid arthritis (RA), we studied the clinical history of 153 RA patients, and any available data on GI symptoms that might have been associated with AZL. GI symptoms appeared in 64 (42.5%) of the 153 cases. There were 19 events of nausea, vomiting, or dyspepsia, 14 events each of epigastric discomfort and reduction or loss of appetite, 10 events of epigastric, stomach, or abdominal pain, 9 events of heartburn, 8 events of mouth ulcer, 3 events each of loss of taste and abdominal bloating or borborygmus, 2 events each of diarrhea or loose stools, hematemesis or melanemia, and gastric or esophageal ulcer, and 1 event of stomatitis. These results indicate that GI symptoms associated with AZL are usually mild and treatment can continue, with almost all cases responding to a reduction in dose or drug cessation. In some cases, a histamine receptor-2 blocker or proton pump inhibitor is also required.     

Cases from the Osler Medical Service at Johns Hopkins University

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?     

ASCARIASIS AS A CAUSE OF RECURRENT ABDOMINAL PAIN

Ascariasis is the most common helminthic infection in developing countries. It may cause chronic abdominal pain, tenderness and bloating. Our aim is to report a case of acute episodic abdominal pain and pancreatitis associated with ascariasis. We report a 59‐year‐old female patient who was admitted for acute abdominal pain, having had several previous similar events before one of them was diagnosed as acute idiopathic pancreatitis. On admission, her physical exam was normal. Laboratory results showed hemoglobin 12.2 g/dL, white blood cell count 11 900 cells/mm³, eosinophils 420 cells/mm³, serum amylase 84 IU/mL, lipase 22 IU/mL and normal liver function tests. Abdominal ultrasound and a plain abdominal X‐ray were also normal. An upper endoscopy showed round white worms in the duodenum and the stomach, some of them with bile in their intestines. The intestinal parasites were diagnosed as Ascaris lumbricoides, and the patient was started on albendazole, with full recovery within a week. We believe that ascariasis should be considered in patients with recurrent abdominal pain and idiopathic pancreatitis.     

Cannabinoid hyperemesis syndrome： Clinical diagnosis of an underrecognised manifestation of chronic cannabis abuse

Cannabis is a common drug of abuse that is associated with various long-term and short-term adverse effects.The nature of its association with vomiting after chronic abuse is obscure and is underrecognised by clinicians. In some patients this vomiting can take on a pattern similar to cyclic vomiting syndrome with a peculiar compulsive hot bathing pattern, which relieves intense feelings of nausea and accompanying symptoms. In this case report, we describe a twentytwo year-old-male with a history of chronic cannabis abuse presenting with recurrent vomiting, intense nausea and abdominal pain. In addition, the patient reported that the hot baths improved his symptoms during these episodes. Abstinence from cannabis led to resolution of the vomiting symptoms and abdominal pain. We conclude that in the setting of chronic cannabis abuse, patients presenting with chronic severe nausea and vomiting that can sometimes be accompanied by abdominal pain and compulsive hot bathing behaviour, in the absence of other obvious causes, a diagnosis of cannabinoid hyperemesis syndrome should be considered.     

Gastrointestinal symptoms associated with enteric-coated sulfasalazine (Azulfidine EN tablets)

 To investigate both the incidence and the dosage used to treat gastrointestinal (GI) symptoms associated with enteric-coated sulfasalazine (Azulfidine EN, AZL) in patients with rheumatoid arthritis (RA), we studied the clinical history of 153 RA patients, and any available data on GI symptoms that might have been associated with AZL. GI symptoms appeared in 64 (42.5%) of the 153 cases. There were 19 events of nausea, vomiting, or dyspepsia, 14 events each of epigastric discomfort and reduction or loss of appetite, 10 events of epigastric, stomach, or abdominal pain, 9 events of heartburn, 8 events of mouth ulcer, 3 events each of loss of taste and abdominal bloating or borborygmus, 2 events each of diarrhea or loose stools, hematemesis or melanemia, and gastric or esophageal ulcer, and 1 event of stomatitis. These results indicate that GI symptoms associated with AZL are usually mild and treatment can continue, with almost all cases responding to a reduction in dose or drug cessation. In some cases, a histamine receptor-2 blocker or proton pump inhibitor is also required. Received: October 11, 2001 / Accepted: March 29, 2002 Correspondence to: S. Okubo