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

Beagle dogs were allocated to 4 groups, each consisting of 3 males and 3 females, which received 0.055, 0.165 or 0.495 mg paraquat (PQ)/kg/day sc for 4 w to investigate subacute toxicity. Recovery 4 and 8 w postadministration was studied. In the early stage there was vomiting, decreased activity and undernourishment. Induration and ulcers at the injection sites were seen. The group receiving 0.495 mg PQ/kg had reduced food ingestion and occasional decreases in water consumption until the end of the 4-w injection period. Three animals in the 0.495 mg PQ/kg group were sacrificed in the moribund stage with marked decreases in body weight. Ophthalmologic examination at 4 w of recovery detected hemorrhage around the nasalis vein of the left fundus in 1 animal that received 0.495 mg PQ/kg. No abnormal changes in electrocardiography (ECG) were noted throughout the experimental period. Slightly increased urinary protein, reticulocyte counts, and fibrinogen were observed in a few animals in each group. A few animals that received 0.165 or 0.495 mg PQ/kg had increased phospholipid, blood urea nitrogen, and creatine phosphokinase. The lungs of the moribundly sacrificed animals had moderate atelectasis, localized atelectasis, moderate thickening of alveolar wall and pleura, proliferation of fibroblast-like cells, and abundant fibers in interstitium and alveoli. In the liver there was slight hemorrhage along the gallbladder. On electron microscopy of the lung, proliferation of fibroblasts, myofibroblasts and type II alveolar cells, and some mast cells were observed in thickened alveolar walls. Abundant collagen fibers, destroyed cell debris and mitotic figures of spindle-shaped fibroblasts were also observed in the dilated interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Subacute toxicity of paraquat in beagle dogs: clinicopathology and pathologic examinations. 162 56

Health practitioners use many methods and agents to bring on cervical ripening in early pregnancy, such as intracervical tents and pharmacological techniques, to induce a therapeutic abortion. Prostaglandins alter myometrial and cervical tissue and are the most often used pharmacological technique. Reduced collagen concentration, an increase in water volume, an increase in prostaglandins (PGE2, PGI2, and PGF2 alpha), and a change in the glycosaminoglycan (GAG) content coincide with cervical ripening, yet the mechanism responsible for these changes is obscure. Prostaglandins appear to cause the breakdown of collagen or change the GAG/proteoglycan content. Research shows that prostaglandins can initiate cervical ripening at any stage of pregnancy. Estradiol stimulates prostaglandin production thereby al so inducing cervical dilation. Relaxin also demonstrates an ability to ripen the cervix. In addition, mifepristone (RU-486) is gaining acceptance as a cervical ripening agent. In fact, RU-486 and gemeprost have at least 95% success rate compared to 92% for gemeprost alone or 85% with RU-486 alone. The only effective and acceptable prostaglandins to use at gestation of 0-8 weeks are sulprostone, gemeprost, and 9-methylene-PGE2. At t his gestational age, pharmacological modulation is all that is needed. Even though they are effective (abortion rate 90%), side effects are expected to occur (pain, nausea, and vomiting). Similarly, prostaglandin analogues are preferable for cervical ripening in women at 8-12 weeks gestation. Suction curettage or other surgical techniques then are used to remove the conceptus. At 12-16 weeks gestation, many physicians prefer the same protocol as that of 8-12 weeks gestation. Other choose to infuse PGE2 and saline into the amniotic fluid to stimulate uterine contractions. Another procedure at 12-16 weeks involves 1mg vaginal pessaries of gemeprost every 3 hours to ripen the cervix and stimulate contractions. After 16 weeks, the methods for 12-16 weeks still apply.
 ...
PMID:Pharmacological modulation of cervical compliance in the first and second trimesters of pregnancy. 187 72

A case of polyarteritis nodosa (PN) in childhood involving various organs such as the gastrointestinal tract, skin, CNS, kidneys and liver with hypogammaglobulinemia is reported. This 6 month old girl was admitted to our hospital with vomiting, diarrhea, bloody stools with mucous and weight loss. For the past 5 months she had these abdominal symptoms. She was diagnosed as having PN of the Kussmaul-Maier variety on the grounds of the biopsy of skin lesion where a necrotizing vasculitis was found. Prednisolone and methylprednisolone pulse treatment were not effective in suppressing the progress of the disease. At the age of 1 year 7 month a combination therapy of prednisolone and immunosuppressants (cyclophosphamide) was started and this was found to be effective. She was discharged when she was 2 year and 2 month. The dosage of prednisolone was tapered as the activity of the PN decreased and she did well with a maintainance dosage of 9.5 mg/day. At 3 year 6 month of age she suddenly developed hypertension (the plasma renin activity was found to be 16.6 ng/m/hr. and the aldosterone 220 ng/dl). CNS involvement such as spinal cord dysfunction, left sided convulsions, cerebral hemorrhage developed 5 months later. Methylprednisolone pulse therapy was performed 3 times and 2 mg/kg/day of prednisolone was administered. In spite of this therapy she passed away with a massive cerebral hemorrhage at the age of 4 year 8 month. Unfortunately an autopsy was not performed. Results of the immunological tests proved that the hypogammaglobulinemia was a common variable immunodeficiency (CVI). It has been reported that primary immuno-deficiency syndrome is often associated with collagen disease and auto-immune disease. This lack of the defense mechanism against the virus or extra antigen could be related to the onset of collagen and auto-immune disease. As the correlation between CVI and PN has not been clarified this case is of interest as concerns the cause of PN.
 ...
PMID:[A case of hypogammaglobulinemia associated with polyarteritis nodosa presenting a variety of symptoms in childhood]. 197 16

Angioedema is characterized by a well-demarcated swelling on the skin, oropharyngolaryngeal tissue, or the gastrointestinal wall. Underlying mechanisms may include IgE-mediated reactions, complement activation, inhibition of the cyclo-oxygenase pathway of arachidonic acid metabolism, direct release of mediators from mast cells, and activation of the kinin-forming system. Foods, drugs, inhalants, insect bites, blood transfusion, collagen vascular disease, infections, physical factors, neoplasms, and hereditary factors can cause angioedema through one or more of these mechanisms. Chronic angioedema lasts more than 6 weeks or recurs during this period. Acute angioedema is a self-limited disorder and resolves spontaneously, or with simple therapy, in several days; the patient rarely requires a complete work-up. Chronic angioedema may necessitate a detailed history, physical examination, and limited clinical or laboratory tests to exclude serious underlying illnesses. The H1 antihistamines are used for the treatment of both acute and chronic angioedema. An H2 antihistamine, a second H1 antihistamine, or rarely even a low dose of corticosteroid may be added to the regimen if H1 antihistamine alone fails to control chronic angioedema. Hereditary angioedema is an autosomal dominant disease that is caused by C1INH deficiency. In patients with this disorder, swelling of the lip, pharynx, and extremities may follow trauma to soft tissue. Other clinical manifestations include abdominal pain, nausea, vomiting, and suffocation because of laryngeal swelling. Diagnosis can be confirmed by the finding of low levels of C4 and C2 and the absence of nonfunction of C1INH. Androgens reverse the biochemical defects.
 ...
PMID:Angioedema. 286 18

Reye's syndrome (RS) is generally considered a childhood disease. We report our experience with RS in adults in the metropolitan Milwaukee area. Reye's syndrome was diagnosed in seven 18- to 46-year-old adults. The diagnostic criteria were as follows: viral prodrome followed by vomiting and encephalopathy without focal neurological signs, normal cerebrospinal fluid values, increased levels of serum aminotransferases (transaminase), prolonged prothrombin time, elevated blood ammonia levels, and characteristic microvesicular fatty liver and mitochondrial changes. None of the patients was hypoglycemic. The diagnosis of RS was entertained in 22 but confirmed in only seven patients. In cases of non-Reye's encephalopathy, drug ingestion presented as one of the most difficult differential diagnostic problems, which also included alcohol abuse, collagen vascular disease, and hepatitis B surface antigenemia. Clinical jaundice, distinctly uncommon in RS, was present in only one patient who presented to us in stage V coma. In adults, RS is more difficult to diagnose and should be suspected more frequently in patients with unexplained altered behavior following a viral illness and vomiting. Liver biopsy can be performed safely and is usually mandatory in adults. Patients with RS diagnosed during stage I or II coma and treated experienced an uneventful recovery.
 ...
PMID:Reye's syndrome in adults. Diagnostic considerations. 380 May 31

We report the case of a 56-year-old woman with a history of episodes of vomiting and coma. Hyperammoniemia , hypouremia , hypercitrullinemia and the decreased arginino -succinic synthetase activity on skin fibroblast cultures permitted us to diagnose citrullinemia. We think that the skin changes, i.e. atrophy of the epidermis, thin and short collagen bundles, dystrophic elastic fibers, increased fundamental matrix, were due to the undernutrition state and were not specific. The dosage of the amino acids of the total skin showed a decreased hydroxylation of lysine in the insoluble fraction, and the presence of proline and hypdroxyproline in the soluble fraction. These metabolic changes were not specific and evidenced the disorganization and the lysis of the connective tissue due to the under-nutritional state. The nail changes, i.e. clubbed fingers and 'half-and-half nail' syndrome, were not specific either. The hair changes mentioned by other authors in newborns and young children, i.e. sparse and brittle blond hair, presence of transverse opaque bands ('irregularly banded hair'), were not present in our case. We only found changes in the cuticle and some trichorrhexis which were not specific of the disease either.
 ...
PMID:Skin, hair and nail changes in a case of citrullinemia with late manifestation. 672 76

An extremely rare case of ruptured cerebral aneurysm associated with a fenestrated vertebral artery in osteogenesis imperfecta (OI) is presented. A 33-year-old female suffering from OI was admitted to our hospital with severe headache and vomiting. A CT scan revealed subarachnoid hemorrhage. Cerebral angiography with four vessel study showed a fenestration in the V3 portion of the left vertebral artery and a dilatation in its V4 portion, but no cerebral aneurysm was detected. After conservative treatment for three weeks, repeated angiography demonstrated an aneurysm of the anterior communicating artery. A neck clipping of the aneurysm was performed successfully. The patient was discharged with no neurological deficits. OI is a hereditary connective tissue disease characterized by bone fragility. From her family history and clinical findings, the patient was suspected to have OI type I of Sillence's classification. Among the connective tissue diseases, OI does not have complications in the cerebrovascular system as frequently as other connective tissue diseases do, for example, Marfan's syndrome, Ehlers-Danlos syndrome, or pseudoxanthoma elasticum. Carotid-cavernous fistula and moyamoya disease have been the only complications reported in OI. However, dilatation of the aortic root and increased vascular fragility have been reported recently in OI. Although this is the first reported case of a ruptured aneurysm accompanied by a fenestration and a dilatation of the vertebral artery associated with OI, it was suggested that vascular fragility caused by collagen abnormality might affect the cerebral vasculature.
 ...
PMID:[A case of ruptured cerebral aneurysm associated with fenestrated vertebral artery in osteogenesis imperfecta]. 775 27

Unexplained fractures are characteristic of both osteogenesis imperfecta (OI) and non-accidental injury (NAI) but in most cases the diagnosis is straightforward. However, in a few OI patients an initial diagnosis of NAI is made. Factors contributing to such difficulties include failure to recognise that OI can occur without a family history, without blue sclerae, without osteopenia, without an excess of Wormian bones, or with metaphyseal fractures. In addition we report on 39 patients with an unusual history in that fractures only occurred in the first year of life. Rib fractures, metaphyseal abnormalities and periosteal reactions were common. The initial diagnosis was usually OI if the fractures occurred in hospital, but NAI if they appeared to have been sustained at home. Additional findings such as anaemia, vomiting, hepatomegaly, and apnoeic attacks were often found in these patients. The disorder has some similarities to the syndrome of infantile copper deficiency. Like the latter it is particularly common in preterm infants and in twins. Therefore, we are attempting to examine the incidence of significant hypocupraemia in unselected preterm infants. We suggest that the likely cause of this "temporary brittle bone disease" is a temporary deficiency of an enzyme, perhaps a metalloenzyme, involved in the post-translational processing of collagen.
 ...
PMID:Osteogenesis imperfecta: the distinction from child abuse and the recognition of a variant form. 817 41

A 33-year-old woman had an undifferentiated tumor originating in the cerebral dysgenetic lesion resembling fibrous cartilage. She had a headache, vomiting, late-onset epilepsy and left hemiparesis. The lesion was located in the right temporal lobe on computed tomographic (CT) scan. It was totally resected and only local irradiation was performed postoperatively. Normal cortical architectures were lost in the resected specimens. Straight or curved fasciculi composed of fine collagen fibers were distributed in parallel and perpendicular to the cortical surface in the mildly eosinophilic hyaline matrix. Hypertrophic astrocytes were scattered with low cellularity in these abnormal cortices. Clusters of tumor cells were observed in a few areas. The tumor cells, having oval and relatively vesicular nuclei with a few prominent nucleoli and basophilic well-circumscribed narrow cytoplasm, had proliferated diffusely with a cobblestone appearance. Immunohistochemical and electron microscopic investigations demonstrated no evidence of specific differentiation, either. There were 14.5 mitotic figures/high power field on average and most nuclei of the tumor cells were strongly positive for proliferating cell nuclear antigen (PCNA). Moreover, subarachnoid dissemination of the tumor cells were apparent in a few areas. Nevertheless the patient returned to work and no recurrence was observed for 10 years postoperatively. We concluded that neoplastic transformation occurred de novo in the dysgenetic cortex.
 ...
PMID:Undifferentiated tumor originating in the cerebral dysgenetic lesion resembling fibrous cartilage: case report. 895 22

We describe a case of sudden death caused by a rare complication of Crohn's disease. A 29-year-old man with Crohn's disease who had not taken medications regularly complained of nausea, vomiting, and abdominal pain for 2 days, and then died suddenly. Autopsy revealed protruding intestinal loops filled with gas, internal fistulas between fused loops of the terminal ileum, and complete obstruction of the fistulous tract. The histologic findings of transmural inflammation consisting of lymphocytic infiltration, accumulation of partially hyalinized collagen, and fibrosis in the skip areas from the ileum to the cecum were compatible with Crohn's disease. Furthermore, marked emaciation, atrophic change of the heart muscle, and diffuse fatty change of the liver were found. Although the patient died of obstructive ileus caused by a stricture produced by progression of Crohn's disease, he was severely affected by malnutrition which may have been fatal. This case not only illustrates that Crohn's disease can cause obstructive ileus and sudden death, but also makes the forensic pathologist realize the importance of suspecting the presence of an active inflammatory bowel disease in a patient with internal fistulas or malnutrition.
 ...
PMID:Sudden death of a patient with Crohn's disease. 978 Jun 67


1 2 3 4 Next >>