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)

We studied 50 patients (28 male and 22 female) with the hyper-IgD and periodic fever syndrome. Most patients originated from Europe, namely The Netherlands (28 cases; 56%), France (10 cases, 20%), and Italy (3 cases, 6%), but 1 patient was from Japan. A hereditary component is suggested by 18 patients coming from 8 families. The syndrome is typified by a very early age at onset (median, 0.5 years) and life-long persistence of periodic fever. Characteristically, attacks occur every 4-8 weeks and continue for 3-7 days, but the individual variation is large. Attacks feature high spiking fever, preceded by chills in 76% of patients. Lymphadenopathy is commonly present (94% of patients). During attacks, 72% of patients complained of abdominal pains, 56% of vomiting, 82% of diarrhea, and 52% of headache. Joint involvement is common in the hyper-IgD syndrome with poly-arthralgia in 80% and a non-destructive arthritis, mainly of the large joints (knee and ankle), in 68% of patients. Eighty-two percent of patients reported skin lesions with some attacks; these demonstrated vasculitis histologically. Serositis has been seen in only 3 patients (6%), while amyloidosis has not been recorded in any of the patients with this syndrome. Immunizations precipitated attacks in 54% of patients. All patients had a persistently elevated serum IgD level (> 100 U/mL), and in 82% of cases the serum IgA was likewise elevated. During attacks there is an acute-phase response adjudged by leukocytosis, neutrophilia, and increased ESR. The etiology remains to be elucidated, and treatment is supportive. The hyper-IgD syndrome is distinct from other periodic fever syndromes like systemic-onset juvenile rheumatoid arthritis, adult-onset Still disease, and familial Mediterranean fever.
 ...
PMID:Hyperimmunoglobulinemia D and periodic fever syndrome. The clinical spectrum in a series of 50 patients. International Hyper-IgD Study Group. 819 36

We report three cases of histologically verified systemic amyloidosis with polyneuropathy. Common to them were early onset progressive peripheral sensorimotor disturbance starting in the legs and prominent autonomic dysfunctions such as postural hypotension, anhidrosis, and loss of pupillary light reflexes. Other characteristic features included vomiting, alternating diarrhea and constipation, opacities of the vitreous bodies, and congestive heart failure. All these clinical manifestations resemble type I familial amyloid polyneuropathy described by Andrade in 1952 from Portugal. Sural nerve biopsy stained with Congo red showed typical green birefringence under polarized light microscope. Histologically verified familial cases of this form of amyloid polyneuropathy have not been reported from Taiwan before.
 ...
PMID:Type I familial amyloid polyneuropathy--report of a family in Taiwan. 822 Dec 94

Amyloid deposits in leptomeningeal vessels, subarachnoid, subpial, and subependymal cerebrospinal regions, spinal ganglia, peripheral nerves, and some internal organs (predominantly heart and kidney) characterize a dominantly inherited disease in a Hungarian family. We found four definitely and three probably affected members in this family of 56 persons in four generations. Clinical features in all definitely diseased patients include disturbance of memory, psychomotor deceleration, ataxia, and hearing loss. In most patients there was temporary disorientation, migraine-like headache with vomiting, and tremor. Some patients had nystagmus, pyramidal signs with spastic paraparesis, hallucinations, urinary retention, and obstipation. Single patients had facial tics and sleep disorders. Progressive visual disturbance and clinically manifest polyneuropathy were absent. CSF protein was markedly elevated in all patients. CT showed characteristic symmetric calcification along the sylvian fissure; MRI after contrast administration showed prominent enhancement at the surface of the sylvian fissures, brainstem, and cerebellum. Autopsy data was available in three definitely affected patients and in one unaffected family member. Immunohistochemistry identified the amyloid deposits as of the AF (transthyretin, TTR) type; DNA studies revealed a novel TTR missense mutation at codon 18 (TTR Asp18Gly). According to clinical features, pathologic alterations, and molecular studies, this disease is a novel type of systemic familial amyloidosis with disease manifestation clinically restricted to the CNS. It is similar to the oculoleptomeningeal amyloidoses but can be clinically diagnosed by characteristic CTs and the absence of progressive visual impairment.
 ...
PMID:Familial meningocerebrovascular amyloidosis, Hungarian type, with mutant transthyretin (TTR Asp18Gly) 896 Jul 46

Three members of a Taiwanese kindred developed severe, systemic, early onset (< age 25 years), biopsy-proven amyloidosis. Clinical features included upper and lower extremity sensorimotor neuropathy, abdominal pain, vomiting, corneal ulcerations, cardiomyopathy, and syncope. Immunohistochemical analysis indicated that the deposits consisted of transthyretin. Molecular genetic studies revealed a heterozygous codon 55 point mutation, resulting in a proline for leucine-substitution, a mutation previously associated with aggressive familial amyloidosis in a US kindred of Dutch and German descent. The clinical courses and echocardiographic findings are typical for many types of amyloidosis; the pathologic data and genetic studies were necessary to establish a precise diagnosis.
 ...
PMID:Familial amyloidosis in one Chinese family: clinical, immunological, and molecular genetic analysis. 915 4

A 63-year-old woman who started to have polyarthralgia in December 1993 has been diagnosed as rheumatoid arthritis (RA) and treated with muscular injection of gold sodium thiomalate. She began to have nausea, vomiting, anorexia and watery diarrhea in October 1995. A year later, she had to receive intravenous infusion on admission since more frequent watery diarrhea occurred more than ten times within a day. On admission in our hospital in December 1996, she had proteinuria in addition to gastrointestinal symptoms. The biopsy specimen from stomach, duodenum and kidney proved systemic amyloidosis associated with RA. In spite of steroid-pulse, dimethyl sulfoxide (DMSO) and colchicine therapy, profound proteinuria in nephrotic syndrome was continued in association with hypoproteinemia, anasarca and renal failure. She was treated on hemodialysis and intravenous hyperalimentation (IVH) until November 1997 when A-V shunt operation on left forearm was performed. However, the shunt was not available for HD and she suffered from septicemia and died on December 1997. This patient was a rare case of secondary systemic amyloidosis associated with RA in early clinical course.
 ...
PMID:[A case of secondary systemic amyloidosis associated with rheumatoid arthritis after 3-year disease duration]. 1033 14

A 60-year-old woman presented to our hospital with repeated vomiting. Upper gastrointestinal endoscopy revealed a 1 cm diameter ulcer with clean base on the roof of the gastric antrum. Histological examination of gastric biopsies revealed abundant amorphous eosinophilic deposits in the submucosa. Congo red stain for amyloid was positive. A barium follow-through study revealed a mass in the jejunum causing incomplete obstruction. Urine for Bence Jones protein was negative. Serum protein electrophoresis did not reveal any abnormal band and serum immunoelectrophoresis did not detect any monoclonal immunoglobulin. Bone marrow examination, however, revealed an increased proportion of plasma cells. Subsequent immunohistochemical staining demonstrated monoclonal lambda light chains in the marrow plasma cells, thereby confirming a plasma cell dyscrasia. Amyloidosis involving the gastrointestinal tract can produce a wide variety of non-specific symptoms and signs. A high index of suspicion is necessary to arrive at an early diagnosis. Management consists of supportive therapy for the gastrointestinal tract as well as treatment of the underlying condition.
 ...
PMID:Intestinal obstruction and gastrointestinal bleeding due to systemic amyloidosis in a woman with occult plasma cell dyscrasia. 1041 43

Gastritis, vomition and weight loss are common in captive cheetahs (Acinonyx jubatus). Gastric spiral bacteria (Helicobacter spp.) and the very small, viviparous nematode Ollulanus tricuspis, a stomach worm of cats, are believed to be important causes. Three sibling cheetahs at Wellington Zoo, New Zealand, developed chronic vomiting, diarrhoea and debility. Their parents were both South African-born. Response to antibacterial treatment was poor. Endoscopic examinations revealed chronic lymphoplasmacytic gastritis and Ollulanus infection. Treatment with oxfendazole and pyrantel embonate resulted in clinical improvement; however, 1 cheetah, which died 7 months later as a result of a ruptured liver due to hepatic amyloidosis, still had Ollulanus worms present in her stomach. Ollulanus tricuspis is a significant cause of gastritis and vomiting in captive cheetahs, lions and tigers, as well as wild cougars and tigers. The parasite has not yet been found in sub-Saharan Africa. Because of the unusual characteristics of this parasite, the literature on its life history and techniques for diagnosis is reviewed.
 ...
PMID:Gastric Ollulanus tricuspis infection identified in captive cheetahs (Acinonyx jubatus) with chronic vomiting. 1121 40

Renal involvement in amyloidosis leads to chronic renal failure. Prognosis is poor. Although amyloid deposits are frequent in adrenal glands, symptomatic adrenal dysfunction is uncommon. We report the case of a 63-year-old man with chronic renal failure (serum creatinine: 202 micromol/L) subsequent to amyloidosis who was referred to our unit for vomiting, dehydration despite a persistent nephrotic syndrome, acidosis, hyponatremia (121 mmol/l) and hyperkaliemia (7.1 mmol/l). A synacthen test was performed and disclosed adrenal insufficiency. Despite the initiation of substitution therapy, the patient died one month later from Addisonian crisis. Features of adrenal insufficiency may be masked by those of chronic renal failure, emphasizing the importance of adrenal explorations in patients with chronic renal failure due to amyloidosis.
 ...
PMID:[Adrenocortical insufficiency in renal amyloidosis]. 1124 Apr 1

Amyloidosis of the gastrointestinal tract is often asymptomatic. We report a 65-year-old man who presented with anorexia, dyspepsia and vomiting. Endoscopy showed nodular duodenal mucosa, which on histology showed amyloidosis. The patient died two weeks later.
 ...
PMID:Duodenal amyloidosis. 1238 46

DMSO is an amphipathic molecule with a highly polar domain and two apolar methyl groups, making it soluble in both aqueous and organic media. It is one of the most common solvents for the in vivo administration of several water-insoluble substances. Despite being frequently used as a solvent in biological studies and as a vehicle for drug therapy, the side-effects of DMSO (undesirable for these purposes) are apparent from its utilization in the laboratory (both in vivo and in vitro) and in clinical settings. DMSO is a hydrogen-bound disrupter, cell-differentiating agent, hydroxyl radical scavenger, intercellular electrical uncoupler, intracellular low-density lipoprotein-derived cholesterol mobilizing agent, cryoprotectant, solubilizing agent used in sample preparation for electron microscopy, antidote to the extravasation of vesicant anticancer agents, and topical analgesic. Additionally, it is used in the treatment of brain edema, amyloidosis, interstitial cystitis, and schizophrenia. Several systemic side-effects from the use of DMSO have been reported, namely nausea, vomiting, diarrhea, hemolysis, rashes, renal failure, hypertension, bradycardia, heart block, pulmonary edema, cardiac arrest, and bronchospasm. Looking at the multitude of effects of DMSO brought to light by these studies, it is easily understood how many researchers working with DMSO (or studying one of its specific effects) might not be fully aware of the experiences of other groups who are working with it but in a different context.
 ...
PMID:Multidisciplinary utilization of dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. 1266 39


<< Previous 1 2 3 4 5 Next >>