Gene/Protein Disease Symptom Drug Enzyme Compound
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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Snake bites caused by viperid snakes of Atheris genus are extremely rare, envenoming of a bite of related viper Proatheris superciliaris was described only once in the literature. The present case study depicts the envenoming of a 57 years old Czech man, a private herpetologist, who was bitten to his finger. He developed painful local reaction, nausea, hematuria, hypertension, chest and lumbar pain. Coagulopathy and thrombocytopenia subsequently developed as well as acute renal failure, hepatic and lung lesion. Intensive care therapy was purely symptomatic and supportive as no antisera exists. Treatment included haemodialysis, substitution of fresh frozen plasma and platelets. Patient completely recovered during 1 month.
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PMID:Envenoming by the viperid snake Proatheris superciliaris: a case report. 1861 80

The range of diseases in which intravenous immunoglobulin (IVIG) is effective has expanded significantly since its initial use in primary antibody deficiency. This biological medicine must comply with three conditions: therapeutic efficacy, clinical tolerance and viral safety. Factors relevant to the viral safety of IVIG include: effective use of donor exclusion criteria, screening of donations in order to exclude potentially infectious donations, testing of plasma pools for evidence of viral infection, validated steps for removal and/or inactivation of potentially present infectious agents, equipment cleaning, traceability of lots, and post-marketing follow-up of patients. Variables potentially affecting the risk and intensity of adverse events associated with administration of IVIG include: patient age, underlying condition, dose, concentration, IgA content, stabilizing agent and rate of infusion. Mild adverse reactions (headache, flushing, low backache, nausea) are often associated with a fast infusion rate, and respond rapidly on slowing the infusion. Very rare serious and potentially fatal side effects include: anaphylactic reactions, aseptic meningitis, acute renal failure, and thrombotic complications. Many of these serious adverse reactions have occurred in patients who had significant risk factors or underlying disease states. Clinicians should pay close attention to patient selection and consider the potential risk/benefit ratio versus alternate therapies.
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PMID:Adverse reactions and pathogen safety of intravenous immunoglobulin. 1869 Sep 45

OBJECTIVES: 5-Fluorouracil (5-FU) is an integral part of treatment of GI malignancies. While normal DPD enzyme activity is rate limiting in 5-FU catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. METHODOLOGY: Twenty-three patients were tested for DPD deficiency after excessive toxicities from 5-FU and/or capecitabine. DPD activity was evaluated by Peripheral Blood Mononuclear Cell (PBMC) radioassay, genotyping of DPYD gene by Denaturing High Performance Liquid Chromatography (DHPLC), or 2-(13)C uracil breath test (UraBT). RESULTS: Of 23 patients with excessive toxicities from 5-FU and/or capecitabine, 7 (30%) were DPD deficient with a median age of 66 years, M:F ratio = 1.3:1 and ethnicities included Caucasian (71%), African-American (14%) and South-Asian (14%). DPD activity ranged from 0.064 - 0.18nmol/min/mg. Three patients were treated with bolus 5-FU/LV, two with capecitabine, and two with high dose bolus 5-FU with 2', 3', 5'-tri-O-acetyluridine. Toxicities included mucositis (71%), diarrhea (43%), skin rash (43%), memory loss/altered mental status (43%), cytopenias (43%), nausea (29%), hypotension (14%), respiratory distress (14%) and acute renal failure (14%) Re-challenge with capecitabine in one patient after the Mayo regimen caused grade 3 hand-foot syndrome. Genotypic analysis of the DPYD gene in one patient with severe leucopenia demonstrated a heterozygous mutation (IVS14+1 G>A, DPYD). The UraBT in two patients of 112.8; PDR of 49.4%) and borderline normal values revealed 1 to be DPD-deficient (DOB(50) of 130.9; PDR of 52.5%) in a second patient. There were 2 toxicity-related deaths among (DOB(50) DPD-deficient patients (28%). CONCLUSIONS: DPD deficiency was observed in several ethnicities. Akin to 5-FU, capecitabine can also lead to severe toxicities in DPD-deficient patients. Screening patients for DPD deficiency prior to administration of 5-FU or capecitabine using UraBT could potentially lower risk of toxicity. Future studies should validate this technique.
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PMID:DIHYDROPYRIMIDINE DEHYDROGENASE DEFICIENCY (DPD) IN GI MALIGNANCIES: EXPERIENCE OF 4-YEARS. 1884 42

A 45-year-old female with a background of poorly differentiated ovarian adenocarcinoma treated with bilateral salpingo-oophorectomy presented with one week history of nausea, vomiting and decreased urine output. On examination, she was mildly dehydrated but haemodynamically stable. Abdominal examination revealed tender swelling in upper abdomen. Biochemistry revealed that she had acute renal failure and interestingly the acute renal failure was out of proportion to the degree of dehydration. Abdominal ultrasound showed marked distension of the stomach without any evidence of renal tract obstruction. She was aggressively treated with volume replacement and careful monitoring of input and output. She responded very well to fluid replacement and her renal failure resolved within four days of treatment. This case illustrates a case of acute renal failure secondary to gastroparesis which resolved after treatment of renal failure. Patients with chronic renal failure are prone to develop gastroparesis but it is extremely rare to have gastric stasis following acute renal failure. This case also illustrates the importance of aggressive treatment of a reversible but potentially fatal medical condition which could have been easily overlooked in view of patient's poorly differentiated ovarian cancer.
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PMID:A case report of gastroparesis secondary to acute renal failure. 1902 8

Familial renal hypouricemia is a hereditary disease characterized by extraordinary high renal uric acid clearance and is associated with acute renal failure (ARF). An 18-year-old sumo wrestler developed ARF after anaerobic exercise. Several hours after the exercise, he had a pain in the loins with oliguria, headache, and nausea. On admission, his serum uric acid was decreased despite the elevation of serum creatinine (9.5 mg/dL). The level of creatine kinase was normal and there was no myoglobinuria or urolithiasis. Magnetic resonance imaging showed no significant abnormality. Renal function improved completely within 2 weeks of hydration treatment. After remission, hypouricemia became obvious (1.0 mg/dL) from the initial level of uric acid (6.1 mg/dL) and fractional excretion of uric acid was 49%. Polymerase chain reaction of a urate anion exchanger known to regulate blood urate level (SLC22A12 gene: URAT1) demonstrated that homozygous mutations in exon 4 (W258X). Both parents showed heterozygous mutation of the URAT1 gene, but both siblings showed no mutation. Thus, we describe a Japanese sumo wrestler of familial renal hypouricemia complicated with anaerobic exercise-induced ARF, with definite demonstration of genetic abnormality in the responsible gene, URAT1.
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PMID:Acute renal failure after exercise in a Japanese sumo wrestler with renal hypouricemia. 1909 27

Selenium (Se) is an essential trace element in human and animal nutrition. It is also widely utilized in industrial processes. Reports of acute selenium toxicity in humans are rare. We report a case of a 23-year-old female who consumed about 100 mL of liquid selenite broth and presented with severe nausea, vomiting, abdominal pain, hematemesis and acute renal failure (ARF). The serum selenium level was significantly increased. Gastro-duodenoscopy revealed severe corrosive gastritis. Renal biopsy showed features of acute tubular necrosis (ATN), affecting primarily the proximal tubules. The patient was managed with gastric lavage, blood transfusions, infusion of fresh frozen plasma (FFP) and platelet concentrates and hemo-dialysis. The patient was discharged five weeks after admission and her renal functions recovered completely by eight weeks after admission. She continues to be on regular follow-up for any possible sequelae of mucosal corrosive damage. This case highlights a case of selenium intoxication from selenite broth resulting in ARF and corrosive gastritis. The recovery was complete.
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PMID:Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis. 1911 27

Hypertension is the most common cardiovascular condition in the United States. It can lead to end organ damage and increased mortality risk if it is not properly controlled. In most situations where blood pressure has to be brought down quickly, an intravenous agent with a quick onset of action is often used. Clevidipine is the first third-generation IV dihydropyridine calcium channel blocker that has a high degree of vascular selectivity and an ultra-fast onset and offset of blood pressure lowering effect. In various clinical trials, clevidipine has shown to be safe and effective in controlling acute blood pressure elevations in patients with hypertensive emergencies, preoperative hypertension, and postoperative hypertension. The most common adverse events noted are atrial fibrillation, nausea, headache, and acute renal failure. Overall, clevidipine is a useful addition to available intravenous agents in reducing blood pressure during acute situations. The acceptance of this agent to hospital formularies may ultimately depend on its perceived ease of administration, clinically relevant benefits over other available agents, and acquisition costs.
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PMID:Clevidipine: a novel ultra-short-acting calcium antagonist. 1938 89

A patient with mantle cell non-Hodgkin's lymphoma presented herself with fever, nausea, right upper quadrant pain on the 7th day of R-CHOP chemotherapy. After hospitalization with the suspicion of acute cholecystitis, she received antibiotherapy with G-CSF because of emerging neutropenia at the 10th day of chemotherapy. Abdominal computed tomography revealed small infarcts in the spleen and kidneys. The ecchymotic lesion which developed on her right lateral malleolus, became bullous in the following days and treated as ecthyma gangrenosum. Although the patient was afebrile with a normal neutrophil count on the third day of antibiotherapy, she developed acute renal failure and deteriorated rapidly. The patient underwent hemodialysis but expired on the 10th day of hospitalization. Post mortem autopsy findings showed ischemic infarction and necrosis of parenchyma due to mycotic thrombosis of arteries and veins of many organs (heart, lung, diaphragm, kidneys, spleen, gut mucosa) as well as invasion of vessel walls and parenchyma by mucor. We reviewed mucormycosis in the light of this case.
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PMID:Fatal disseminated mucormycosis in a patient with mantle cell non-Hodgkin's lymphoma: an autopsy case. 2019 Dec 5

We report the case of an 87-year-old white woman with myasthenia gravis who presented with nausea, shortness of breath, azotemia, and hyperkalemia shortly after completing a course of intravenous immunoglobulin (IVIG). She had been receiving monthly transfusions of IVIG, but this time had received daily infusions for 5 days rather than 1 day. She had received this same dose in the past without incident. Her history was significant for coronary artery disease, atrial fibrillation, deep venous thrombosis, pulmonary embolism, chronic steroid use, and recurrent urinary tract infection. On examination, she was slightly confused, mildly dehydrated, had a grade II systolic ejection murmur along the upper left sternal border, had bilateral and symmetric mild weakness of the upper and lower extremities, and exhibited mild edema of the lower extremities. Before transfer from the emergency room, she was found to have an elevated serum urea nitrogen and creatinine of 55 and 5.8 mg/dL (19.6 mmol/L and 512.7 micromol/L, respectively). Creatinine 8 days earlier was 0.9 mg/dL (79.6 micromol/L). The hospital course of the acute renal failure is presented with a review of the literature on cases of acute renal failure after IVIG.
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PMID:Case report: acute renal failure after administering intravenous immunoglobulin. 2020 65

Solar burn reactivation, a rare and idiosyncratic drug reaction, has been reported with the use of a variety of drugs. This reaction is believed to be the result of exposure to ultraviolet light during the subsiding phase of an acute inflammatory reaction. It affects areas of the body that have been previously sunburned. We describe a 16-year-old girl who was receiving treatment for acute lymphoblastic leukemia and experienced a second-degree solar burn reactivation reaction to methotrexate. The patient had a mild sunburn on her face and shoulders the day she went to the oncology clinic for her interim maintenance chemotherapy with vincristine 1.5 mg/m(2)/dose and methotrexate 100 mg/m(2)/dose. Three days later, she returned to the clinic with a 2-day history of fever (<or= 100.2 degrees F), nausea, vomiting, and malaise; the sunburn on her face and shoulders also had become severe, without further sun exposure. Laboratory results revealed elevated blood urea nitrogen and serum creatinine concentrations, and her methotrexate level was elevated at 0.9 mM. The patient was diagnosed with acute renal failure, dehydration, methotrexate toxicity, and second-degree solar burn reactivation reaction. She was admitted to the children's hospital and treated with sodium bicarbonate, acetaminophen with codeine, ondansetron, and silvadene cream. On hospital day 3, the patient's methotrexate level decreased to less than 0.1 mM. The sunburn continued to heal, and after a 14-day hospital stay, complicated by a streptococcal infection, grade 3 mucositis, bacteremia, and mild gastritis and duodenitis, the patient recovered and was discharged. Use of the Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 6) between the patient's solar burn reactivation and methotrexate. Although methotrexate-induced solar burn reactivation is rare, clinicians should be aware of this potential adverse reaction and consider delaying administration of methotrexate by 5-7 days if a patient reports ultraviolet-related erythema in the past 2-4 days or presents with a notable sunburn.
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PMID:Solar burn reactivation induced by methotrexate. 2033 62


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