Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It's well known that patients was acquired immunodeficiency syndrome (AIDS) can develop various kinds of hepatobiliopancreatic diseases, for causes related to AIDS and for causes not related to HIV infection. The authors describe a case to their attention due to a suspected acute pancreatitis. The patient presented with abdominal pain, increased serum alkaline phosphatase and amylase levels. Serological test and stool concentration didn't show any opportunistic infection (Cytomegalovirus, Cryptosporidium). Abdominal ultrasonography showed enlargement of the head of the pancreas, gallbladder with biliary sludge, and a little dilatation of the biliary tree. The patient didn't feel better despite the medical treatment, so considering the probability of the migration of calculus, the patient underwent cholecystectomy. After the operation the patient felt better quickly. This case confirms the presence in HIV patients of pancreatitis for causes unrelated to AIDS like cholelithiasis as we showed, alcoholism, hypercalcemia, and the importance of an opportune surgical treatment that was resolutive.
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PMID:[Acute pancreatitis and AIDS]. 932 71

The results of treatment of 319 patients with acute pancreatitis are analyzed, 48 from them (15.1%)--with pancreanecrosis. Etiologic factors in destructive pancreatitis were alcohol addiction (41.67%), cholelithiasis (37.5%), hyperlipidemia (10.41%), hypercalcemia (4.17%), postoperative (4.17%). Location of the necrosis in parapancreatic fat cellular tissue was detected in 6 patients, in pancreatic head--in 8 and both in pancreatic head and corpus--in 11, in corpus and in tail--in 10; total pancreo-necrosis was observed in 5 patients. Therapeutic measures were conservative and only in cholelithiasis cholecystectomy was performed as well as drainage of the choledochus and abdominal cavity. Intensive care was aimed at blocking pancreatic and gastric secretion, inhibition of pancreatic enzymes ferments and suppressing mediators of inflammation, immunocorrection, prophylaxis of infection in the necrotic tissues. Desintoxication was carried out by combination of infusion therapy with forced diuresis, usage of extracorporeal methods and laparoscopic sanation of the abdominal cavity with subsequent lavage. Surgical interventions were carried out in far-off period only for complications of pancreanecrosis. Mortality rate in pancreanecrosis made up 20.85% and in total number of patients with acute pancreatitis--3.13%.
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PMID:[The clinical picture and treatment of destructive pancreatitis]. 968 Aug 11

Acute pancreatitis has many causes, the most common being biliary tract disease and alcoholism. Other etiologic categories are abdominal trauma; postoperative, including endoscopic retrograde cholangiopancreatography; metabolic, including hypercalcemia and hypertriglyceridemia; Infectious; idiopathic; and drug-induced. The drugs most strongly associated with pancreatitis are sulfonamides, thiazides, furosemide, estrogens, and tetracycline. Approximately 100 cases of pancreatitis induced by angiotensin-converting enzyme inhibitor have been reported to the US Food and Drug Administration, of which about 20 involved lisinopril. We report a case of pancreatitis occurring only 3 hours after intake of lisinopril by a man without other risk factors for the illness. The patient had experienced a similar but less severe reaction to this medication 3 months earlier. This case probably represents the first time a patient was rechallenged with lisinopril and had a more significant adverse reaction.
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PMID:Acute pancreatitis following lisinopril rechallenge. 972 73

Diseases of the parathyroid gland are uncommon in women of childbearing age. However, total serum calcium is lower in normal pregnancy, but ionized serum calcium remains within normal limits. Serum parathyroid levels are slightly decreased in the second half of pregnancy. Primary hyperparathyroidism, if unrecognized, may increase maternal and fetal morbidity, which is related to the level of serum calcium. The most common cause is a single parathyroid adenoma, accounting for about 80% of cases. Maternal complications include acute pancreatitis, hypercalcemia crisis, and toxemia. An increased incidence of prematurity and neonatal hypocalcemia has been reported when maternal hypercalcemia is significantly elevated. Other causes of hypercalcemia are rare in pregnancy. Hypoparathyroidism is seldom seen in pregnancy; the most common cause is after surgical throidectomy. The doses of vitamin D and calcium do not change during pregnancy; however, hypercalcemia may develop in the postpartum period. Serum calcium should be determined at every trimester of pregnancy and at regular intervals after delivery, and in a significant number of patients, the dose of vitamin D should be reduced. Osteoporosis has been recognized most frequently in the last few years. It appears that those patients with a family history of osteoporosis and those on heparin therapy have a tendency to develop symptoms of the disease in pregnancy. Finally, lactation is not contraindicated in women with osteoporosis; although there is a slight decrease in bone density in the few months after delivery, this is a transient event and bone densitometry returns to prepregnancy levels in most women. Recent studies indicate that there is no need for calcium therapy during lactation with few exceptions, such as lactating adolescents, mothers nursing more than one child, and mothers with closely-spaced pregnancies.
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PMID:Parathyroid disorders of pregnancy. 988 Jan 18

Hyperparathyroidism and hypercalcaemia are considered to be a rare cause of acute pancreatitis. The relationship between hyperparathyroidism and pancreatic inflammatory disease remains controversial, but it may be related to the translation from inactive to active trypsinogen by hypercalcaemia. Surgical correction of parathyroid disease and normalization of serum calcium levels may ameliorate the acute pancreatitis. Also the mechanism of pathologic zymogen activation during acute pancreatitis remain unknown; probably the pancreatic "autodigestion" is the result of anomalous intracellular transport of secretory proteins activated by lysosomal hydrolases. A case of acute pancreatitis and hyperparathyroidism due to solitary parathyroid adenoma occurred in a 66-years-old woman is reported. After the excision of parathyroid adenoma the serum calcium levels and the function of the pancreas returned to normal. This suggests a cause and effect relationship between hyperparathyroidism and acute pancreatitis.
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PMID:[Primary hyperparathyroidism and acute pancreatitis. A rare clinical association]. 1047 68

In healthy subjects, the 3 known pancreatic trypsinogens, which are endopeptidases belonging to the chymotrypsin superfamily, are activated by enterokinase and partial autoactivation in the duodenum. The premature activation of trypsinogen in the pancreatic interstitium, with the subsequent activation of other pancreatic zymogens, is believed to lead to the autodigestion of the gland, this being the first event in acute pancreatitis. The mechanisms that lead to trypsinogen, activation in acute pancreatitis are largely unknown. However, ischemia, hypercalcemia and the activation of cathepsin B (by cholecystokinin) are thought to be of importance. The easiest and most reliable way to assess trypsinogen activation is the measurement of the activation peptide, TAP, in urine, plasma, pancreatic tissue or ascitic fluid. In the animal model of acute pancreatitis, TAP in ascites and pancreatic tissue has been shown to correlate with the presence and extent of necroses. It has proven to be a good marker for the severity of pancreatitis and is a useful marker in examining the pathophysiology and possible treatment modalities in the animal model of acute pancreatitis. Studies on TAP in human acute pancreatitis were most commonly focused on urinary TAP. Within a 48-hour time frame after the onset of the disease, TAP was a good predictor of the severity of acute pancreatitis. The main advantage over other markers, such as CRP, is that TAP is the earliest marker of necrosis to be increased. Also, increased levels of TAP in ascitic fluid were shown to correlate well with pancreatic necroses. In our experience, plasma TAP was found to have a "diagnostic window" within the first 3 days predicting pancreatic necroses. Positive TAP gave a very good positive prediction and a high specificity towards the development of pancreatic necroses, but did not differ between necrotizing pancreatitis with systemic complications or uncomplicated necrotizing pancreatitis. We therefore think that plasma TAP is a very good marker for local complication in acute pancreatitis and its routine measurements may help to identify patients at a high risk within the first days of the disease.
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PMID:Mechanism and role of trypsinogen activation in acute pancreatitis. 1057 41

We present a rare case of acute pancreatitis associated with temporal lobectomy due to intractable seizure in a 23-year-old man. The patient underwent elective right temporal lobectomy and hippocampectomy. Severe upper abdominal pain occurred just 10 hours after surgery. The diagnosis of acute pancreatitis was based on the elevation of serum amylase and lipase levels, and the findings of abdominal computerized tomography. Other possible causative factors of acute pancreatitis including alcohol, biliary tract stone, hypertriglyceridemia, hypercalcemia, hyperparathyroidism, biliary dysmotility and autoimmune disease were excluded by a series of examinations. The possibility of drug-induced pancreatitis was very low in this patient. The patient was discharged after supportive treatment. No recurrence of seizure or abdominal pain was noted in the three months after discharge. Acute abdominal pain after brain surgery deserves clinical evaluation for acute pancreatitis.
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PMID:Acute pancreatitis associated with temporal lobectomy and intractable seizure. 1074 19

The plasma soluble melanins (PSM) form spontaneously in vitro and in vivo and their formation involves oxidative polymerization and copolymerization of dopa, catecholamines, homogentisic acid, 3-hydroxyanthranilic acid, p-aminophenol, p-phenylenediamine, and other end(ex)ogenous ortho and para polyhydroxy-, (poly)hydroxy(poly)amino- and polyamino-phenyl compounds. The build up of PSM is visible within 2-3 h after the start of incubation at 37 degrees C with 1 mg/ml of plasma. PSM also form similarly in blood and these processes cause hemolysis. The mean quantity of PSM in normal human plasma is 1.61+/-0.1 (S.D.) mg/ml (n = 20) and in normal human urine is 1.1+/-1.2 g/24 h collection (n = 8). They contribute to the yellow color of plasma and urine. Antioxidants delay the formation of PSM. The deposited melanins also form from these precursors. Reactive oxygen side products (ROSP) are generated during and after melanogenesis. Melanins in vivo are generally associated with proteins or with proteins and lipids. The PSM-protein-lipid complexes are called plasma soluble lipofuscins (PSL), because they have histochemical and fluorescence properties similar to those of solid lipofuscins. The soluble and deposited melanins (SDM) and their intermediates have similar toxic chemical reactivities. The oxidizing quinoid (they can produce partially and completely substituted conjugates) and the semiquinoid free radical intermediates are also moieties in most human melanin structures. Soluble melanins formed from dopa, or dopamine, or norepinephrine in weak alkaline solution have been shown to be toxic to human CD4+ lymphoblastic cells (MT-2) at higher than 10 microg/ml concentrations. Alkaptonuria with high levels of homogentisic acid in the plasma is a potentially fatal disease, exhibiting the toxic effects of the homogentisic acid melanin (soluble and deposited), its intermediates and the ROSP. Patients with alkaptonuria develop arthritis and often suffer from other diseases too, including cardiovascular disease (frequent cause of death) and kidney disease. Pheochromocytoma, with high levels of catecholamines in the plasma is another potentially fatal disease. The catecholamine PSM of pheochromocytoma have very light yellow or practically no colors, due to the concentrations and chemical structures. Pheochromocytomas can cause hypertension, cardiovascular disease (frequent cause of death), kidney disease, stroke, cancer, amyloid formation and can mimic many other diseases, including acute pancreatitis, carcinoid, neuroblastoma, psychiatric illness, hypercalcemia, retinal vascular lesions, and diabetes mellitus. Pheochromocytoma is potentially fatal even in patients without hypertension. Following trauma and surgery, heavily pigmented eyes are apt to experience greater inflammation than lightly pigmented eyes. In Parkinson's disease those neurons are lost first in the substantia nigra and locus ceruleus which contain the greatest amounts of neuromelanins. The antihypertensive alphamethyldopa causes Parkinson's syndrome. It forms PSM in a short time in vitro. The side effects of L-dopa (immobility episodes alternate with normal or involuntary movements; psychotic abnormalities) suggest that the SDM, their intermediates and the ROSP present naturally in vivo are involved in the cause of Parkinson's disease and Alzheimer's disease. There is a large overlap between these two diseases. (ABSTRACT TRUNCATED)
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PMID:The probable involvement of soluble and deposited melanins, their intermediates and the reactive oxygen side-products in human diseases and aging. 1124 35

Induction of acute pancreatitis follows a uniform mechanism independent of the different etiologic factors such as gallstones, alcohol, ischemia, hyperlipidemia, hypercalcemia, hereditary and others. Each cause seems to affect primarily the acinar cell, resulting in premature intracellular activation of trypsinogen and other digestive enzymes. Activated enzymes and oxygen free radicals injure the acinar cell and cause a release of cytokines and vasoactive mediators, attract inflammatory cells and activate the vascular endothelium as well as the expression of adhesion molecules. The disturbance of the pancreatic microcirculation induces a progression from edematous to necrotizing pancreatitis independent of the early intracellular events, including protease activation. Specific therapy must be directed towards microperfusion failure as a secondary pathogenetic step, since the initial enzyme activation and cytokine release is irreversible by the time of clinical presentation. In experimental designs comparable to the clinical situation the following therapeutic principles have proven beneficial: increase of blood fluidity by dextran, inhibition of leukocyte-endothelium interaction by ICAM-1 antibodies, and blockade of local vasoconstriction by endothelin-receptor antagonists.
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PMID:[New pathophysiologic knowledge about acute pancreatitis]. 1078 41

The authors present the case of a 78-year-old female patient who was admitted on account of acute pancreatitis complicated by acute myocardial infarction. The authors detected in the patient a serum repeatedly high calcium levels and high levels of intact parathormone. Scintigraphic examination revealed marked foci in the middle of the neck at the level of the inferior pole of the thyroid gland. These examinations confirmed the diagnosis of primary hyperparathyroidism. In view of the patient a serious condition, conservative treatment of hypercalcaemia and acute pancreatitis and myocardial infarction was started. The patient was released into domiciliary care after 40 days in hospital in a state of cardiopulmonary compensation, with cystic transformation of the pancreas and without signs of acute pancreatitis.
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PMID:[Acute pancreatitis as the road to diagnosis of primary hyperparathyroidism]. 1134 34


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