Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Besides the well-known adverse effects of clozapine, such as granulocytopenia, tiredness and hypersalivation, acute pancreatitis is known to be a very rare complication of the drug. In the literature a total of five case reports have been published so far. We report a case of asymptomatic pancreatitis subsequent to clozapine treatment at therapeutic doses in a 38-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient was rehospitalized after an acute exacerbation of the psychosis subsequent to an attempt to change medication on an outpatient basis. Treatment with clozapine was initiated again. During phases of progressively increasing the clozapine dose, serum levels of amylase and lipase were increased; after maintaining daily doses of clozapine of 300 mg and/or 600 mg the pancreatic enzymes normalized quickly within a few days. The patient did not report any pancreas-related complaints, nor did specific diagnostic studies produce any indicative result, only a minor thickening of the head and body of the pancreas in the ultrasound. It is assumed that the phenomenon of subclinical, asymptomatic pancreatitis during increasing dosage of clozapine occurs more often than previously supposed. The monitoring of serum amylase levels during slow increase in clozapine is recommended; if leukocytosis or eosinophilia is present, the possibility of even a subclinical and asymptomatic pancreatitis should be considered.
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PMID:Asymptomatic pancreatitis associated with clozapine. 1033 68

A 22-year-old woman began to have the symptoms of anorexia, high fever, cough and general fatigue from June of 1997. She was admitted in our hospital on Aug. 8th, 1997 for the further detail examination because of pancytopenia and positive antinuclear antibody (ANA). Her laboratory findings and clinical symptoms were compatible with systemic lupus erythematosus (SLE) such as leukopenia, proteinuria, hypocomplementemia, positive ANA, elevated titer of autoantibodies including anti-DNA, anti-Sm, anti-RNP antibodies, polyarthralgia and photosensitivity. The administration of oral prednisolone (40 mg/day) was started on Aug. 15th, 1997 under the diagnosis of SLE. However, she had severe abdominal pain in epigastrium with elevated serum amylase, ascites and dull shape of pancreas tail by CT scan compatible with acute pancreatitis. On Aug. 18th, her general condition was worsening with fever, epigastralgia, abdominal distension, anemia, weak palpation of radial artery, hypotension, tachycardia, shallow breathing and cold sensation on both extremities as shock. In spite of steroid pulse therapy with nafamostat mesilate intraarterial infusion, her condition was not improved. The dose of 50 mg/day of cyclophosphamide was added to the regimen on Aug. 22nd. Then, gradually her condition started to be restored. Anemia, leukopenia, hypocomplementemia continued. Second steroid pulse therapy was done on Sep. 5th. After then, she became better in her clinical symptoms and laboratory data. The dose of PSL was tapered to 15 mg/day and 7.5 mg/day update of Oct. 1998 without the pseudcysts found after pancreatitis. She is a rare case who recovered from severe acute pancreatitis due to SLE itself.
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PMID:[A case of systemic lupus erythematosus associated with severe acute pancreatitis]. 1043 57

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

Despite being banned in many countries and having its use severely restricted in others, pentachlorophenol (PCP) remains an important pesticide from a toxicological perspective. It is a stable and persistent compound. In humans it is readily absorbed by ingestion and inhalation but is less well absorbed dermally. Its distribution is limited, its metabolism extensive and it is eliminated only slowly. Assessment of the toxicity of PCP is confounded by the presence of contaminants known to cause effects identical to those attributed to PCP. However, severe exposure by any route may result in an acute and occasionally fatal illness that bears all the hallmarks of being mediated by uncoupling of oxidative phosphorylation. Tachycardia, tachypnoea, sweating, altered consciousness, hyperthermia, convulsions and early onset of marked rigor (if death occurs) are the most notable features. Pulmonary oedema, intravascular haemolysis, pancreatitis, jaundice and acute renal failure have been reported. There is no antidote and no adequate data to support the use of repeat-dose oral cholestyramine, forced diuresis or urine alkalinisation as effective methods of enhancing PCP elimination in poisoned humans. Supportive care and vigorous management of hyperthermia should produce a satisfactory outcome. Chronic occupational exposure to PCP may produce a syndrome similar to acute systemic poisoning, together with conjunctivitis and irritation of the upper respiratory and oral mucosae. Long-term exposure has also been reported to result in chronic fatigue or neuropsychiatric features in combination with skin infections (including chloracne), chronic respiratory symptoms, neuralgic pains in the legs, and impaired fertility and hypothyroidism secondary to endocrine disruption. PCP is a weak mutagen but the available data for humans are insufficient to classify it more strongly than as a probable carcinogen.
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PMID:Pentachlorophenol poisoning. 1457 43

Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). MCPs usually show a chronic, slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. Although several proteins with signalling, assembling, transport, enzymatic function can be impaired in MCP, most frequently the activity of the respiratory chain (RC) protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. MCPs represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in MCP are the peripheral nervous system (myopathy, polyneuropathy, lactacidosis), brain (leucencephalopathy, calcifications, stroke-like episodes, atrophy with dementia, epilepsy, upper motor neuron signs, ataxia, extrapyramidal manifestations, fatigue), endocrinium (short stature, hyperhidrosis, diabetes, hyperlipidaemia, hypogonadism, amenorrhoea, delayed puberty), heart (impulse generation or conduction defects, cardiomyopathy, left ventricular non-compaction heart failure), eyes (cataract, glaucoma, pigmentary retinopathy, optic atrophy), ears (deafness, tinnitus, peripheral vertigo), guts (dysphagia, vomiting, diarrhoea, hepatopathy, pseudo-obstruction, pancreatitis, pancreas insufficiency), kidney (renal failure, cysts) and bone marrow (sideroblastic anaemia). Apart from well-recognized syndromes, MCP should be considered in any patient with unexplained progressive multisystem disorder. Although there is actually no specific therapy and cure for MCP, many secondary problems require specific treatment. The rapidly increasing understanding of the pathophysiological background of MCPs may further facilitate the diagnostic approach and open perspectives to future, possibly causative therapies.
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PMID:Mitochondriopathies. 1500 63

Several paraneoplastic inflammatory conditions, particularly autoimmune diseases, have been described in association with myelodysplastic syndromes (MDS). However, to date, recurrent acute pancreatitis has never been described in association with MDS. A 44-year-old man presented with prolonged fever and fatigue. Aortitis and pericarditis were diagnosed simultaneously with MDS, refractory anemia with excess blast type 2. His erythrocyte sedimentation rate and c-reactive protein were markedly elevated. The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed. Pain and pancreatic enzymes, however, improved rapidly with escalation of corticosteroid dosage. Multiple attempts at discontinuing the drug resulted in symptomatic flare-ups. Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied. Induction chemotherapy and high-dose corticosteroids, however, controlled both conditions. A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML. All etiologies for recurrent acute pancreatitis were ruled out. The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of acute pancreatitis and MDS/AML suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.
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PMID:Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. 1562 95

We present case report of primary hyperparathyroidism treated surgically as well as a review of literature concerning this subject. The disease of not well known etiology presents with elevated parathormon levels and hypercalcemia. Primary hyperparathyroidism which states 85% percent of all kinds of hyperparathyroidism is usually parathyroid adenoma, in 11-15% glandular hyperplasia and in 1-4% parathyroid cancer. Clinical symptoms are muscle weakness and fatigue, nephrolithiasis, occasionally peptic ulcers, pancreatitis, hypertension. Laboratory test reveal increased level of PTH, hypercalcemia, elevated alkaline phosphatase levels and decreased phosphorus levels. Diagnostic imaging techniques such as ultrasonography, MRI or CT have sensitivity about 52-75%. Highest sensitivity in localization of ectopic parathyroid adenoma has sestamibi scintigraphy with technetium-99. Skeleton x-rays show typical changes in distal parts of bones and osteopenia. Treatment of choice is surgical excision of adenoma. Normalization of PTH and calcium levels after surgery and improvement of renal, musculoskeletal and circulatory system function could be achieved in 95%. Most common complications are recurrent laryngeal nerve injury, hypo- or hyperparathyroidism, bleeding or stridor.
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PMID:[Primary hyperparathyroidism--case report and review of the literature]. 1682 51

A hiccup is involuntary, paroxysmal inspiratory movements of the chest wall associated with diaphragm and accessory respiratory muscle contractions, with the synchronized closure of glottis. The mechanism underlying this common primitive reflex plays an important role in protecting airways against esophageal aspiration. The hiccup reflex mechanism is based on the afferent pathway (vagus and phrenic nerve and sympathetic fibers innervating chest organs, the abdomen, the ear, the nose and the throat stimulation, and the stimulation of hiccup center in the central nervous system, mainly reflecting psychogenic or metabolic disorders) and the efferent pathway (phrenic nerves). An incidental hiccup is a common problem, usually resolves spontaneously and does not present a clinical issue. The clinical issue arises in the case of pathologic persistent hiccups or symptomatic secondary hiccups which may lead to significant fatigue, insomnia or depression. Generally, pathologic hiccups are associated with considerable discomfort concerning both the "stigmatized" person and his or her personal surroundings in which it evokes different emotions, from amusement through impatience to uneasiness and the suggestion of a medical visit as an expression of concern for a given person. The most common causes of pathologic symptomatic hiccups are nervous system diseases, either the central nervous system (proliferative, angiogenic, inflammatory disorders), or the peripheral nervous system: the irritation of the phrenic nerve (proliferative disorders, goitre) and the vagus nerve (otolaryngologic diseases, meningitis, esophageal, stomach and duodenal diseases, hepatitis, pancreatitis, enteritis). The vagus nerve irritation with subsequent hiccups may be caused by chest disorders (injury, surgery) and heart diseases (myocardial infarction). In the present paper we describe the case of a 62-year-old male with recurrent hiccups associated with exertion as a secondary symptom of myocardial ischemia.
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PMID:Hiccups as a myocardial ischemia symptom. 1847 62

Sorafenib is a novel oral multikinase inhibitor that targets Raf serine/threonine and receptor tyrosine kinases, and inhibits tumor cell proliferation and angiogenesis. We have conducted a phase I study of sorafenib to determine the safety, tolerability, pharmacokinetics, and potential efficacy of this agent in 31 Japanese patients with advanced refractory solid tumors. Sorafenib (100-600 mg) was given as a single dose followed by a 7-day wash-out period, and then administrated twice daily (bid). The most frequent drug-related adverse events were rash/desquamation (61%), hand-foot skin reactions (39%), diarrhea (36%), and elevations of serum lipase (36%) and amylase (26%) levels. Dose-limiting toxicities (DLTs) were grade 3 diarrhea at 200 mg bid and grade 3 fatigue at 600 mg bid. Grade 3 and 4 pancreatic enzyme elevations were observed at 200-600 mg bid, but they were not deemed dose-limiting because they were asymptomatic and were not associated with pancreatitis or chronic damage to the pancreas. The AUC and C(max) of sorafenib increased linearly with dose up to 400 mg bid. Partial responses were observed in one of 10 patients with non-small cell lung cancer and one of three patients with renal cell carcinoma. In conclusion, sorafenib 400 mg bid was well tolerated in Japanese patients with advanced refractory solid tumors. The recommended dose for future clinical trials is 400 mg bid.
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PMID:Phase I and pharmacokinetic study of sorafenib, an oral multikinase inhibitor, in Japanese patients with advanced refractory solid tumors. 1847 34

Drugs used for treating inflammatory bowel disease are known to have a number of gastrointestinal and liver adverse effects. 5-ASA products are relatively safe and have few adverse events. In contrast sulfasalazine has side effects in 11-40% of treated patients including fatigue, nausea, abdominal pain and diarrhoea. Glucocorticoids can induce or propagate peptic ulcers and upper GI bleeding especially in combination with NSAIDs. Thioguanins may have severe gastrointestinal side effects including gastrointestinal complaints (in up to 12%), hepatotoxicity (up to 4%) and pancreatitis (1%). Nodular regenerative hyperplasia (NRH) is an important potential side effect of thiopurine therapy especially in men with Crohn's disease after ileocecal resection. NRH may ultimately lead to portal hypertension. A major concern of methotrexate therapy in IBD besides myelosuppression and pulmonary fibrosis is hepatotoxicity. 5mg of folic acid substitution per week potentially decreases gastrointestinal side effects by 80% without interfering with the efficacy of methotrexate. Besides renal dysfunction, tremor, hirsutism, hypertension and gum hyperplasia cyclosporine is known to have a number of gastrointestinal side effects that occur with less frequency such as diarrhoea (up to 8%) nausea and vomiting (up to 10%) and hepatotoxicity in 1-4%. Rare gastrointestinal adverse events are gastritis and peptic ulcers. Paying attention to these potential deleterious side effects is mandatory for physicians treating IBD patients.
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PMID:Gastrointestinal and liver adverse effects of drugs used for treating IBD. 2022 29


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