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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the past 40 years primary hyperparathyroidism (PHP) has changed from a rare, severe disease of the bones and kidneys to a common disease with hypertension, peptic ulcer, pancreatitis, easy fatigue and proximal muscle weakness. We have during these 40 years examined one of the greatest group of patients with PHP. PHP had its maximum incidence in women over the age of 40. The disease is four times frequent in women as in man. The incidence of hypertension and peptic ulcer between patients with PHP is higher as compared with the incidence of these diseases in general populations. The severity of bone changes in individual patients with PHP does not result from the direct action of a single hormone only. Parathyroid hormone (PTH) have hypotensive and vasodilator effects on various vascular beds. The resting blood flow in the limbs of our patients with PHP is increased in comparison with control subjects. PTH increases plasma renin activity in normotensive controls. This effect is partly blocked by beta adrenergic blockers.
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PMID:[Primary hyperparathyroidism]. 871 83

Pancreas divisum is a rare congenital anomaly of the pancreatic ducts that has been implicated in pancreatitis. In addition, the finding of a Santorinicele, which is a cystic dilatation of the dorsal duct, suggests that there is an obstruction associated with a congenital or acquired weakness of the mucosa. We used an endoscopic technique to treat a child with recurrent pancreatitis who was found to have pancreas divisum and a large Santorinicele.
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PMID:Recurrent pancreatitis in a child with pancreas divisum. Endoscopic therapy of a Santorinicele. 1052 45

In this article, we report the case of a 16-month-old German boy who was admitted to the Children's Hospital of Stuttgart with a 4-week history of intermittent fever, decreased appetite, weakness, fatigue, and difficulty sleeping. He was healthy at birth and remained so for the first 15 months of his life. On admission, physical examination showed enlarged cervical, axillary, and inguinal lymph nodes, as well as hepatosplenomegaly. Laboratory data revealed pancytopenia, elevated liver function tests, and hypergammaglobulinemia. Blood, stool, and urine culture results were negative. Viral infections and rheumatologic and autoimmune disorders were ruled out, but a positive titer for Leishmania antibodies was noted. In a liver and bone marrow biopsy, the amastigote form of the parasite could not be seen in cells. The promastigote form of Leishmania was found and the diagnosis of visceral leishmaniasis was made by combining the cultures of both the liver and the bone marrow biopsy material in 5 mL 0.9% saline on brain heart infusion agar, supplemented with defibrinated rabbit blood and incubated at 25 to 26 degrees C for 5 days. The parasite was identified by Southern blot analysis as Leishmania infantum. Specific therapy with the antimonial compound sodium stibogluconate with a dose of 20 mg/kg body weight was begun immediately. Within 4 days, the patient became afebrile. The side effects of treatment, including erosive gastritis, cholelithiasis, worsening hepatosplenomegaly, elevation of liver enzymes, pancreatitis, and electrocardiogram abnormalities, necessitated the discontinuation of treatment after 17 days. On discharge 4 weeks later, the patient was stabilized and afebrile with a normal spleen, normal complete blood count, normal gammaglobulins, and decreasing antibody titers to Leishmania. During the next 24 months, the patient experienced intermittent episodes of abdominal pain, decreased appetite, recurrent arthralgia, and myalgia. But at his last examination in January 1998, he was well; all symptoms mentioned above had disappeared. Because the child had never left Germany, nonvector transmission was suspected and household contacts were examined. His mother was the only one who had a positive antibody titer against Leishmania donovani complex. She had traveled several times to endemic Mediterranean areas (Portugal, Malta, and Corse) before giving birth to the boy. But she had never been symptomatic for visceral leishmaniasis. Her bone marrow, spleen, and liver biopsy results were within normal limits. Culture results and polymerase chain reaction of this material were negative. A Montenegro skin test result was positive, indicating a previous infection with Leishmania. Western blot analysis showed specific recognition by maternal antibodies of antigens of Leishmania cultured from the boy's tissue. Visceral leishmaniasis is endemic to several tropical and subtropical countries, but also to the Mediterranean region. It is transmitted by the sand fly (Phlebotomus, Lutzomyia). Occasional nonvector transmissions also have been reported through blood transfusions, sexual intercourse, organ transplants, excrements of dogs, and sporadically outside endemic areas. Only 8 cases of congenital acquired disease have been described before 1995, when our case occurred. In our patient, additional evaluation showed that the asymptomatic mother must have had a subclinical infection with Leishmania that was reactivated by pregnancy, and then congenitally transmitted to the child. Visceral leishmaniasis has to be considered in children with fever, pancytopenia, and splenomegaly, even if the child has not been to an endemic area and even if there is no evidence of the disease in his environment, because leishmaniasis can be transmitted congenitally from an asymptomatic mother to her child.
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PMID:Congenital transmission of visceral leishmaniasis (Kala Azar) from an asymptomatic mother to her child. 1054 91

In 16 dogs, the diagnosis of canine leishmaniasis could be detected by direct microscopic identification, by determination of the antibody titre or by PCR method (peripheral blood/bone marrow). On the basis of the clinical and laboratory diagnostic results 9 cases of the cutaneous type and 7 dogs of the combined cutaneous-visceral type (+ mono- or polyarthritis, hepatopathy and/or renal insufficiency as well as occular manifestation) have been classified. Therapy was: GLUCANTIME in 6 dogs, allopurinol in 3 dogs as single agent, combination-therapy GLUCANTIME and allopurinol in 7 dogs. During GLUCANTIME-treatment the following adverse reactions could be observed: general weakness, reduced food intake up to anorexia, vomiting and diarrhoea. Laboratory parameters showed sporadically leucopenia or pancreatitis. Adverse reactions during allopurinol therapy were: vomitus/diarrhoea or urine concrements. One dog with GLUCANTIME therapy, 2 dogs with allopurinol as well as 2 dogs with combination therapy are clinically symptom-free at the moment (peripheral blood and bone marrow: PCR negative). The remaining 11 patients showed a good to very good improvement of the clinical symptoms. However, since the peripheral blood respectively the bone marrow continue to be PCR positive, relapses have to be expected in these dogs.
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PMID:Clinical follow-up examination after treatment of canine leishmaniasis. 1062 23

Hereditary tyrosinemia results from an inborn error in the final step of tyrosine metabolism. Neurological manifestations have been reported in nearly half of patients during illness to have characteristics of altered consciousness, weakness, anorexia, vomiting, and pain in the extremities and abdomen. His physical findings and laboratory results pointed out acute pancreatitis. There have been some reports of acute and chronic pancreatitis in patients with metabolic diseases; however, this is the first case with tyrosinemia type I who exhibited clinical and biochemical findings of acute pancreatitis during neurological crisis. The presented case suggests the possibility that the pancreas is affected in neurological crisis. The determination of amylase concentration both in serum and urine samples of further cases will clarity the association between pancreatitis and neurological crisis.
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PMID:Neurological crisis mimicking acute pancreatitis in tyrosinemia type I. 1077 Jan 19

The first girl of an unrelated couple was noted to have failure to thrive since age 3 months, generalized hypotonia and weakness, hepatomegaly, hypoglycemia, and lactic acidosis at 4 months. She was found to have severe mitochondrial DNA (mtDNA) depletion and respiratory chain complex IV deficiency in both skeletal muscle and liver but without other common mtDNA mutations. Her younger brother developed vomiting at age 3 weeks and was diagnosed as having pyloric stenosis. His skeletal muscle and liver also showed severe mtDNA depletion. He developed generalized weakness and hypotonia, hepatomegaly, and lactic acidosis at age 3 months. Both siblings died of hepatic failure and hemorrhagic complication before 6 months of age. The brother also had chemical pancreatitis, which had not been reported before in mtDNA depletion in children. Severe mtDNA depletion may present with nonspecific symptoms such as vomiting, failure to thrive, and developmental delay; multiorgan involvement such as hepatomegaly, pancreatitis, and myopathy occurs later. Mitochondrial DNA depletion should be considered in the differential diagnosis in children with developmental delay or failure to thrive of unknown etiology.
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PMID:Mitochondrial DNA depletion in children. 1119 1

Brucella infection is a systemic disease, but the microorganism rarely causes infections in the gastrointestinal system such as hepatitis, cholecystitis, colitis and pancreatitis. Spontaneous bacterial peritonitis due to Brucella is extremely rare. Herein, we report a case of cirrhosis complicated with nongranulomatous hepatitis and peritonitis, both due to Brucella. A 63 year-old man with diabetes mellitus was admitted to hospital with complaints of weakness, backache, abdominal pain and abdominal swelling. On the basis of physical examination and laboratory findings, cryptogenic cirrhosis and spontaneous bacterial peritonitis were diagnosed. Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture. Liver biopsy findings revealed cirrhosis and a nongranulomatous hepatitis which was thought might be due to Brucella infection. Doxycycline and rifampicin, in addition to diuretics were administered for spontaneous ascites infection due to Brucella. A week later, the patient's condition improved and he became afebrile. After two months of therapy, the ascites had almost disappeared.
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PMID:Spontaneous bacterial peritonitis due to Brucella infection. 1461 44

Our objective is to present a case of symptomatic lead toxicity (plumbism) with abdominal colic and hemolytic anemia following a gunshot wound. It is a retrospective case report and the setting is in a teaching hospital in south central Los Angeles. The case report is that of a patient who presented with abdominal pain, generalized weakness, and hypertension following multiple gunshot wounds, 15 years previously. Other causes of abdominal pain and weakness--such as diabetes mellitus, alcohol abuse, pancreatitis, and substance abuse--were ruled out. Interventions included treatment with the newer oral chelating agent, Succimer (2, 3-dimercaptosuccinic acid), and subsequent surgery. The main outcome was the initial reduction in blood lead levels with improvement of symptoms. Because of a recurrent rise in the blood lead levels, the patient was again treated with Succimer and underwent surgery to remove two bullet fragments from the face. We conclude that lead toxicity should be ruled out in patients presenting with abdominal cramps and a history of a gunshot wound. Prompt therapy--including environmental intervention and chelation therapy--is mandatory, and surgical intervention may be necessary.
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PMID:Gunshot-induced plumbism in an adult male. 1462 Jul 13

Aneurysms of the portal venous system are increasingly reported in the past five years. Congenital weakness of the venous wall, trauma, pancreatitis and portal hypertension are possible etiologies. Surgical intervention is indicated in case of symptomatic aneurysms with or without progressive expansion of the aneurysm diameter. The treatment of asymptomatic splenic vein aneurysms remains debated. We report the case of an asymptomatic and uncomplicated splenic vein aneurysm for which a conservative approach was advocated with regular follow-up by means of Doppler ultrasonography. After six years of follow-up the aneurysm diameter has not changed and no complications were observed.
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PMID:Aneurysm of the splenic vein. 1528 46

Mitochondrial toxicity has been implicated in the development of a variety of nucleoside reverse transcriptase inhibitor-associated syndromes. Mitochondrial damage and decreases in mitochondrial DNA levels have been demonstrated in various tissues of patients treated with NRTIs, especially in conjunction with exposure to stavudine. Clinical syndromes that may be mediated by mitochondrial toxicity include hyperlactatemia and lactic acidosis, hepatic steatosis, lipoatrophy, peripheral neuropathy, HIV-associated neuromuscular weakness syndrome, pancreatitis, skeletal myopathies, and cardiomyopathy. Early recognition of these syndromes in their mild forms involves close monitoring and a high index of suspicion. This may allow prompt discontinuation of the causative agent(s) and initiation of appropriate therapeutic measures, thereby increasing the chances of reversibility of the syndrome.
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PMID:Mitochondrial dysfunction: patient monitoring and toxicity management. 1531 67


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