Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The essence of the problem, as previously reported, indicated that few complications of acute appendicitis occur as long as the infection is contained within the appendix, but once the invading bacteria have penetrated the peritoneal appendicular surface or have invaded the regional circulation, any one or more of a series of serious complications can develop. Thus, rightfully, emphasis has been placed upon early removal of the inflamed appendix before penetration has occurred as the best method of preventing complications. We have shown that early appendectomy is predicated on early diagnosis and that diagnostic delay is not limited to extremes of age. The diagnosis may be obscured by an accurate, although misleading, history of prior acute attacks, by precident acute disease, such as viral gastroenteritis and by unimpressive symptoms blunted by intercurrent chronic illness, such as diabetes mellitus. If the elements of periumbilical pain, anorexia, nausea or vomiting and the migration of pain to the right lower abdominal quadrant are contained within the clinical history, one must suspect transmural progression of acute appendicitis; frequent inpatient examinations will allow earliest diagnosis and, thereby, fewest perforations and their attendant serious complications. Misdiagnosis is common. Any patient observed for an ostensibly nonsurgical acute condition of the abdomen who fails to improve markedly during a brief course of appropriate specific or supportive therapy must be thoroughly re-evaluated as a potential surgical candidate. Despite the proliferation of accessible laboratory tests and imaging procedures, the early diagnosis of appendicitis rests upon the clinical skills of the physician. A high index of suspicion is crucial. As Doctor Warfield M. Firor, former senior surgeon commented: "Pain and tenderness at any point where the appendix can lie must raise the diagnostic possibility of appendicitis."
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PMID:Reasons for delay of the diagnosis of acute appendicitis. 670 39

Four patients who developed anorexia nervosa after the onset of diabetes mellitus are described. It is postulated that the co-occurrence of the two conditions was not coincidental, but that each contributed to the development of the other. The nature and treatment of diabetes offer numerous opportunities for the anorexic patient to lose weight by a variety of dangerous maneuvers, including adjustment of the insulin dose, failure to inject insulin, secret vomiting, and failure to provide urine samples. Treatment of patients with both conditions is a therapeutic challenge to the psychiatrist and diabetologist. A behavior management program combined with psychotherapy is most often effective.
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PMID:Anorexia nervosa and diabetes mellitus. 683 99

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

Ten patients with diabetic gastroparesis were selected for a randomized, double-blind, controlled trial of metoclopramide. Each patient had longstanding insulin-requiring diabetes mellitus and symptoms of gastric stasis. The patients were evaluated for the symptoms of gastric stasis and radionucleotide gastric emptying was measured before the patients entered the study and after they were given either metoclopramide or placebo treatment. Metoclopramide, 10 mg orally, stimulated an increase in the rate of gastric emptying (56.8% +/- 7.4%) in contrast to the response to placebo (37.6% +/- 7.7%) (p less than 0.01). The overall symptoms and symptoms of vomiting were markedly reduced during metoclopramide treatment in contrast to those during placebo treatment. Before the study five patients were constipated (less than three bowel movements per week); during metoclopramide treatment the patients' bowel habits were improved. There was a poor correlation between improved gastric emptying and decreased symptoms. Metoclopramide may improve symptoms of diabetic gastric stasis through two mechanisms: its peripheral effect on gastric smooth muscle, which increases gastric emptying; and its central effects on the chemoreceptor vomiting zone, which decrease nausea.
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PMID:Metoclopramide to treat gastroparesis due to diabetes mellitus: a double-blind, controlled trial. 706 59

The case of a 26 year old woman who had been taking tranexamic acid to prevent uterine bleeding due to an IUD and who died from thrombosis of the left internal carotid artery is reported. The patient's father had died at age 54 of myocardial infarction. Otherwise the family history was entirely negative for thromboembolic disease. The patient was a mild smoker. She had been previously healthy and in particular, she was not affected with hypertension, diabetes, or dyslipidemia. She had carried to term 2 uncomplicated pregnancies. 40 days prior to hospital admission her gynecologist had inserted an IUD. The insertion of the IUD was followed by persistent uterine bleeding, and for this reason she began treatment with tranexamic acid (1.5 g/daily). Uterine bleeding persisted despite this treatment, and the IUD was removed. Because of persistence of a mild uterine bleeding, tranexamic acid was continued. 2 hours before admission the patient suddenly presented a left sided hemiparesis with disarthria and vomiting. On admission she was stuporous. The left side of her face drooped and the strength of the left arm and leg was markedly decreased. Both arm and leg reflexes were symmetrical. Her blood pressure was 110/70. An electroencephalogram on arrival confirmed a right sided cerebral lesion. Subsequently the patient's condition deteriorated rapidly. She developed a full left hemiplegia and became deeply comatose. A CAT scan performed 4 hours after admission showed no abnormalities. A CAT scan performed 3 days after admission showed a large cerebral infarction involving nearly the whole right cerebral hemisphere. The patient's condition remained essentially unchanged until she died 6 days after admission. Permission for autopsy was refused. Antifibrinolytic drugs competitively inhibit plasminogen activators and noncompetitively plasmin. Thromboembolic complications after the administration of antifibrinolytic drugs have long been recognized. The use of IUDs is often associated with troublesome uterine bleeding and particularly excessive menstrual bleeding. To avoid these complaints, antifibrinolytic drugs are increasingly used.
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PMID:Tranexamic acid, intrauterine contraceptive devices and fatal cerebral arterial thrombosis. Case report. 710 62

Clinical and laboratory features and risk factors for diabetic gastroparesis (DGP) were investigated in 226 diabetics on chronic dialysis; 106 subjects (43%) had DGP diagnosed by persistent vomiting improved with the use of prokinetic agents and 120 (control group) had no clinical DGP. Type 1 diabetics had DGP more frequently than type 2 diabetics (70 vs. 37%). The DGP group had longer duration of diabetes (21 +/- 8 vs. 13 +/- 6 years), higher frequency of diabetic orthostatic hypotension (95 vs. 33%), enteropathy (49 vs. 5%), blindness (52 vs. 23%), myocardial infarction (86 vs. 42%), extremity gangrene (54 vs. 27%) and cerebrovascular accidents (43 vs. 25%), lower serum albumin 32.3 +/- 3.9 vs. 35.4 +/- 3.8 g/l), urea (24.0 +/- 5.5 vs. 25.5 +/- 5.5 mmol/l) and creatinine (710 +/- 210 vs. 820 +/- 220 mumol/l), and higher serum TCO2 (20.9 +/- 3.1 vs. 19.8 +/- 2.7 mmol/l) than the control group (all differences significant at p +/- 0.004). Glycemic control was adequate in 24% of the DGP group subjects and 83% of the control subjects (p < 0.001). Annual hospitalization rate was 49 +/- 48 days/patient in the DGP group and 16 +/- 27 days/patient in the control group (p < 0.001). Median patient survival was 24 +/- 2 months in the DGP group and 61 +/- 9 months in the control group (p < 0.0001). Logistic regression identified long duration of diabetes and poor glycemic control as risk factors for DGP. In diabetics on dialysis, DGP is associated with high frequency of other diabetic complications, low serum albumin and creatinine, and high morbidity and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastroparesis in diabetics on chronic dialysis: clinical and laboratory associations and predictive features. 747 16

About one-half of patients with insulin- or non-insulin-dependent diabetes have delayed gastric emptying (diabetic gastroparesis). Some of them complain of epigastric pain, nausea, vomiting or postprandial fullness (diabetic dyspepsia), although only a minority are severely symptomatic. Diabetic gastroparesis is clinically relevant not only by virtue of the symptoms induced but also because it may contribute to inadequate glycaemic control and impaired absorption of orally administered drugs. Recent data suggest that abnormal blood glucose control, not only autonomic neuropathy, contribute to the pathogenesis of disordered gastric motility. In most cases diabetic gastroparesis is diagnosed clinically in the absence of demonstrable lesions of the upper gastrointestinal tract. To evaluate gastric emptying, scintigraphy is the 'gold standard'. Gastrokinetic drugs are of help in the treatment of gastroparesis: erythromycin is the first choice in acute presentations and cisapride for chronic symptoms. New macrolides with prokinetic action and devoid of antibacterial properties are very promising and should add another pharmacologic approach to control dyspepsia and gastroparesis in diabetic patients in the future.
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PMID:Gastroparesis and dyspepsia in patients with diabetes mellitus. 749 57

Zygomycosis is an uncommon, but frequently fatal, fungal infection caused by members of the class Zygomycetes. The risk factors include diabetes mellitus, uremia, leukemia and use of deferoxamine as an iron-chelating agent; healthy persons also are occasionally infected. Those fungi, spread by their ubiquitous spores, most frequently involve the respiratory system. Rhinocerebral zygomycosis occurs predominantly in patients with uncontrolled diabetic ketoacidosis. Pulmonary zygomycosis most frequently is observed in granulocytopenic and corticosteroid-treated patients. Other clinical manifestations are gastrointestinal, cutaneous, disseminated and miscellaneous. This report concerns a previously robust farmer who suffered from left upper lung abscess caused by Rhizopus spp.-one member of the order Mucorales. Initially, it was intended to administer amphotericin B to a total dose of 2,000 mg; however, the patient could not tolerate such side effects as nausea, vomiting and refused further management when the cumulative dose was 948 mg. However, he did recover without further fever and cough. Chest X-ray, followed every three months, disclosed satisfactory improvement.
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PMID:Zygomycotic lung abscess: a case report. 755 21

Clinical features of cerebellar infarction in the territory of the superior cerebellar artery (SCA) were investigated in six male patients, ranging in age from 50 to 69 years. In all patients, there were MR images of infarction located in the area supplied by the SCA. The lesion was on the left-side in 2, right-side in 3 and bilateral (recurrent) in 1 patient. The onset of disease occurred with nausea, vomiting and floating sensation, with no overt brain stem signs other than symptoms of unilateral cerebellar ataxia and dysarthria. Five of the 6 patients had heart disease and cerebral angiography without definite evidence of SCA occlusion, strongly suggesting occlusion of the artery at its periphery due to cardiogenic embolism. A comparison of these 6 patients with those reported previously in Japan suggests that patients with SCA occlusion may be divided into two distinct subgroups: one manifesting diffuse brain stem signs in addition to cerebellar signs, and the other showing cerebellar signs as the only neurologic manifestation. In the former group, comprising the vast majority of patients, SCA occlusion occurred at the origin of the vessel due to a thrombus under a state of hypertension, diabetes mellitus or malignancy, producing signs of brain stem involvement, such as dissociating sensory disturbance and Horner's sign. While in the latter group, which included these 6 patients, paucity of brain stem signs, absence of definite cerebral angiographic evidence of SCA occlusion, and the presence of heart disease were distinguishing clinical features. Cardiogenic cerebral embolism was probably the underlying pathology in many of the cases and the functional prognosis was favorable.
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PMID:[Cerebellar infarction in the territory of the superior cerebellar artery, presenting a predominant cerebellar symptom--with special reference to its pathophysiology]. 761 47

Some diabetic patients--particularly those with nausea and vomiting--frequently have evidence of delayed gastric emptying while other diabetic patients may in fact exhibit accelerated gastric emptying. Whether the presence or absence of symptoms of upper gastrointestinal dysfunction correlated with objective measures of gastric emptying in insulin dependent diabetic subjects was investigated. Twenty one insulin dependent diabetic patients underwent a solid phase gastric emptying scintiscan using in vivo labelled chicken liver. Thirteen patients had symptoms suggestive of gastrointestinal dysfunction (nausea, vomiting, early satiety, or constipation), while eight patients had no gastrointestinal symptoms. Eleven patients had orthostatic hypotension. All patients had been diabetic since childhood or adolescence. As a group, the diabetic patients showed a half time (T50) of gastric emptying (mean (SD) 150.0 min (163.7) that was not significantly different from that of 12 healthy control subjects (148.1 min (62.4)). Those diabetic patients without gastrointestinal symptoms and without orthostatic hypotension, however, showed a gastric emptying half time (70.1 min (41.6)) that was significantly faster than that of the control subjects. Conversely, those diabetic patients with nausea, vomiting, and early satiety (or early satiety alone) showed T50 values that were significantly greater than those of the diabetic patients without these symptoms. No correlation was found between the T50 value and the duration of diabetes, the fasting blood glucose at the time of study, or the respiratory variation in heart rate (E:I ratio). These observations indicate that highly variable rates of gastric emptying occur in insulin dependent diabetic patients, and that accelerated gastric emptying may occur in diabetic patients who have no symptoms of gastrointestinal dysfunction.
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PMID:Highly variable gastric emptying in patients with insulin dependent diabetes mellitus. 856 52


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