Vidarabine
Vidarabine Phosphate
Acyclovir
Stomatitis, Herpetic
Cystitis
Encephalitis
Herpes Simplex
Antiviral Agents
Foscarnet
Phosphonoacetic Acid
Polyomavirus Infections
Herpes Zoster
Ophthalmic Solutions
Hypoxanthines
Iontophoresis
Injections, Intramuscular
Simplexvirus
Herpetic keratitis. Proctor Lecture. (1/867)
Although much needs to be learned about the serious clinical problem of herpes infection of the cornea, we have come a long way. We now have effective topical antiviral drugs. We have animal models which, with a high degree of reliability, clearly predict the effect to be expected clinically in man, as well as the toxicity. We have systemically active drugs and the potential of getting highly active, potent, completely selective drugs, with the possibility that perhaps the source of viral reinfection can be eradicated. The biology of recurrent herpes and stromal disease is gradually being understood, and this understanding may result in new and better therapy of this devastating clinical disease. (+info)Fludarabine, cyclophosphamide, and dexamethasone (FluCyD) combination is effective in pretreated low-grade non-Hodgkin's lymphoma. (2/867)
PURPOSE: Fludarabine phosphate is effective as a single agent in low-grade non-Hodgkin's lymphoma (NHL). Combined with other antineoplastic agents it enhances the antitumor effect. Our aim was to define the therapeutic efficacy and toxicity of a combination of fludarabine, cyclophosphamide and dexamethasone (FluCyD) in patients with advanced low-grade lymphoma. PATIENTS AND METHODS: Twenty-five adults with pretreated advanced-stage low-grade NHL were treated with three-day courses of fludarabine 25 mg/m2/day, cyclophosphamide 350 mg/m2/day, and dexamethasone 20 mg/day, every four weeks for a maximum of six courses. RESULTS: Of the 25 patients, 18 (72%) responded, 8 (32%) achieving CR and 10 (40%) PR. Seven were failures. The median follow-up was 21 months (5-26). Eight CR patients remain in CR after 5-21 months. Of 10 PR patients, 3 are in continuous PR without further treatment after 12, 17 and 18 months. Myelosuppression was the most prevalent toxic effect. Although severe granulocytopenia (granulocyte count nadir < 500/microliter) and thrombocytopenia (platelet count nadir < 50,000/microliter) occurred in only 10% and 16% of courses, respectively, slow granulocyte or platelet count recovery caused delay of 40% of the courses. Nine patients (36%) required discontinuation of therapy because of persistent granulocytopenia and/or thrombocytopenia: three after one course, three after 2-4 courses, and three after five courses. Thirteen infectious episodes in 11 patients complicated 11% of courses. Two of 10 patients monitored for the circulating EBV load showed increased viral load. One of these developed aggressive lymphoma. CD4+ lymphocytes declined from a pre-therapy median value of 425/microliter to 141/microliter post-treatment (P = 0.001). Non-hematologic toxicities were rare and mild. CONCLUSIONS: The combination of fludarabine with cyclophosphamide and dexamethasone is effective in pretreated advanced-stage low-grade NHL. It may broaden the range of therapeutic options in the salvage treatment of these patients. The main toxicity of this combination is prolonged myelosuppression that may cause treatment delay or withdrawal. The benefit of adding granulocyte colony-stimulating factor, particularly in patients with poor marrow reserve, needs to be investigated. (+info)Autologous transplantation of chemotherapy-purged PBSC collections from high-risk leukemia patients: a pilot study. (3/867)
We have recently demonstrated that the combination of the alkylating agent nitrogen mustard (NM) and etoposide (VP-16) is capable of eliminating, ex vivo, leukemic cells contaminating PBSC collections and this is associated with a significant recovery of primitive and committed hematopoietic progenitor cells. Based on these data a pilot study on autologous transplantation of NM/VP-16 purged PBSC for high-risk leukemic patients was recently initiated. Twelve patients (seven females and five males) with a median age of 46 years (range 18-57) have been treated. Two patients had acute myeloblastic leukemia (AML) resistant to conventional induction treatment, four patients had secondary AML in I complete remission (CR), one patient was in II CR after failing a previous autologous BM transplantation, while two additional AML individuals were in I CR achieved after three or more cycles of induction treatment. Two patients with high-risk acute lymphoblastic leukemia (ALL) in I CR and one patient with mantle cell lymphoma and leukemic dissemination were also included. Eight patients showed karyotypic abnormalities associated with a poor clinical outcome. The mobilizing regimens included cytosine arabinoside and mitoxantrone with (n = 6) or without fludarabine (n = 3) followed by subcutaneous administration of G-CSF (5 microg/kg/day until the completion of PBSC collection) and G-CSF alone (n = 3) (15 microg/kg/day). A median of two aphereses (range 1-3) allowed the collection of 7.2 x 10(8) TNC/kg (range 3.4-11.5), 5 x 10(6) CD34+ cells/kg (range 2.1-15.3) and 9.2 x 10(4) CFU-GM/kg (0.3-236). PBSC were treated with a constant dose of 20 microg of VP-16/ml and a median individual-adjusted dose (survival < or = 5% of steady-state BM CFU-GM) of NM of 0.7 microg/ml (range 0.25-1.25). Eleven patients were reinfused after busulfan (16 mg/kg) and Cy (120 mg/kg) conditioning with a median residual dose of 0.3 x 10(4) CFU-GM/kg (0-11.5). The median time to neutrophil engraftment (>0.5 x 10(9)/l) for evaluable patients was 25 days (range 12-59); the median time to platelet transfusion independence (>20 and >50 x 10(9)/l) was 40 days (18-95) and 69 days (29-235), respectively. Hospital discharge occurred at a median of 25 days (18-58) after stem cell reinfusion. Four individuals are alive in CR (n = 3) or with residual nodal disease (n = 1 lymphoma patient) with a follow-up of 32, 26, 3 and 14 months, respectively. Seven patients died due to disease progression or relapse (n = 5) or extrahematological transplant toxicity (n = 2). Our data suggest that pharmacological purging of leukapheresis collections of leukemic patients at high-risk of relapse is feasible and ex vivo treated cells reconstitute autologous hematopoiesis. (+info)Effect of 9-beta-D-arabinofuranosyladenine 5'-monophosphate and 9-beta-D-arabinofuranosylhypoxanthine 5'-monophosphate on experimental herpes simplex keratitis. (4/867)
Treatment of established experimental keratitis caused by herpes simplex virus with 9-beta-d-arabinofuranosyladenine 5'-monophosphate (Ara-AMP) or 9-beta-d-arabinofuranosylhypoxanthine 5'-monophosphate (Ara-HxMP) showed that the Ara-AMP, in a concentration of 2 or 20%, had a significant effect on the keratitis but that 0.4% Ara-HxMP showed only minimal activity. Ara-AMP was also effective in the treatment of idoxuridine-resistant keratitis. No local toxicity with a high concentration (20%) of Ara-AMP was seen, but the duration of therapy was brief. (+info)Fludarabine and epirubicin in the treatment of chronic lymphocytic leukaemia: a German multicenter phase II study. (5/867)
PURPOSE: Fludarabine has been reported to be the most effective single-agent in previously treated chronic lymphocytic leukaemia (CLL). Based on the in vitro synergism of fludarabine with anthracyclines and on results showing a higher efficacy of CHOP against COP we attempted to improve treatment results with a combination of fludarabine and an anthracycline. PATIENTS AND METHODS: The aim of the multicenter study was to evaluate the rate and duration of remissions and investigate the toxic and immunosuppressive effects of fludarabine and epirubicin in the treatment of CLL in Binet stages B and C as first-line therapy or in first relapse. Thirty-eight patients were treated with fludarabine 25 mg/m2 on days 1-5 and epirubicin 25 mg/m2 on days 4 and 5. RESULTS: The overall response rate (OR) was 82% (95% confidence interval (95% CI): 66%-92%) with a CR rate of 32% (95% CI: 18%-49%). For the 25 previously untreated patients the OR was 92% (95% CI: 74%-99%) including 40% CRs (95% CI: 21%-61%). Granulocytopenia grade 3 occurred in 23% of all evaluable cycles, and grade 4 in 17%. The median remission duration was 19 months (range 6-37 months). CONCLUSION: The results show that the combination of fludarabine and epirubicin is tolerable and highly effective in the treatment of CLL. With the addition of epirubicin to fludarabine, it appears possible to achieve a higher response rate and a more rapid response, especially of nodal manifestations. This regimen can be administered in an outpatient facility except for the first cycle because of the risk of a tumour lysis. The possible benefit of the combination presented here in the treatment of CLL in comparison to single-agent fludarabine treatment is presently under study in a prospective randomized multicenter study. (+info)Fludarabine treatment in B-cell chronic lymphocytic leukemia: response, toxicity and survival analysis in 47 cases. (6/867)
BACKGROUND AND OBJECTIVE: Fludarabine monophosphate (FAMP) is a purine analog with specific therapeutic activity in B-cell chronic lymphocytic leukemia (CLL). Its current use as front-line therapy of CLL is still a matter of debate both because of the controversial results of the clinical trials so far reported and because of the toxicity profile of the drug. In order to contribute to clarifying the possible role of FAMP, we report a retrospective analysis of the results obtained with the purine analog in CLL patients in different phases of the disease. DESIGN AND METHODS: Forty-seven patients affected by advanced CLL, 36% untreated, 31.9% relapsed and 31.9% resistant, were treated with FAMP 25 mg/m2/day, either for 4 days every 3 weeks in 29 cases, or for 5 days every 4 weeks in 18. The median number of FAMP cycles was 6 (range 2-11). Response was defined according to total tumor mass (TTM) score reduction and toxicity was expressed according to WHO grading criteria. The median follow-up of the series was 13 months from the beginning of FAMP therapy. RESULTS: Out of 47 evaluable patients the response rate was 74.4%, with 34% complete response (CR). The overall response rate was 94%, 80% and 46.6% in untreated, relapsed and resistant cases, respectively; a significantly higher number of responses was associated with no previous treatment and number of FAMP cycles. Fifty-three percent of all cases and 58.8% of untreated ones did not experience any toxicity. Treatment-related side effects were mainly autoimmune phenomena in untreated patients and infectious complications in treated ones. One heavily pre-treated patient died because of neurologic complications. Median time to re-treatment was18 months (range 1-30) and was influenced by age and previous treatment. The overall median survival was 35.7 months with a significantly higher proportion of surviving cases among RAI 0-II stages, responders and patients receiving more than 5 FAMP cycles. INTERPRETATION AND CONCLUSIONS: The present report confirms the high efficacy of FAMP in previously pre-treated cases with acceptable toxicity and encourages its use as front-line treatment provided that the results of randomized trials demonstrate its superiority over conventional chemotherapy. The possible development of autoimmune phenomena should, however, be considered seriously. (+info)Randomized phase II study of fludarabine + cytosine arabinoside + idarubicin +/- all-trans retinoic acid +/- granulocyte colony-stimulating factor in poor prognosis newly diagnosed acute myeloid leukemia and myelodysplastic syndrome. (7/867)
Preclinical data suggest that retinoids, eg, all-trans retinoic acid (ATRA), lower concentrations of antiapoptotic proteins such as bcl-2, possibly thereby improving the outcome of anti-acute myeloid leukemia (AML) chemotherapy. Granulocyte colony-stimulating factor (G-CSF) has been considered to be potentially synergistic with ATRA in this regard. Accordingly, we randomized 215 patients with newly diagnosed AML (153 patients) or high-risk myelodysplastic syndrome (MDS) (refractory anemia with excess blasts [RAEB] or RAEB-t, 62 patients) to receive fludarabine + ara-C + idarubicin (FAI) alone, FAI + ATRA, FAI + G-CSF, or FAI + ATRA + G-CSF. Eligibility required one of the following: age over 71 years, a history of abnormal blood counts before M.D. Anderson (MDA) presentation, secondary AML/MDS, failure to respond to one prior course of chemotherapy given outside MDA, or abnormal renal or hepatic function. For the two treatment arms containing ATRA, ATRA was given 2 days (day-2) before beginning and continued for 3 days after completion of FAI. For the two treatment arms including G-CSF, G-CSF began on day-1 and continued until neutrophil recovery. Patients with white blood cell (WBC) counts >50,000/microL began ATRA on day 1 and G-CSF on day 2. Events (death, failure to achieve complete remission [CR], or relapse from CR) have occurred in 77% of the 215 patients. Reflecting the poor prognosis of the patients entered, the CR rate was only 51%, median event-free survival (EFS) time once in CR was 36 weeks, and median survival time was 28 weeks. A Cox regression analysis indicated that, after accounting for patient prognostic variables, none of the three adjuvant treatment combinations (FAI + ATRA, FAI + G, FAI + ATRA + G) affected survival, EFS, or EFS once in CR compared with FAI. Similarly, there were no significant effects of either ATRA ignoring G-CSF, or of G-CSF ignoring ATRA. As previously found, a diagnosis of RAEB or RAEB-t rather than AML was insignificant. There were no indications that the effect of ATRA differed according to cytogenetic group, diagnosis (AML or MDS), or treatment schedule. Logistic regression analysis indicated that, after accounting for prognosis, addition of G-CSF +/- ATRA to FAI improved CR rate versus either FAI or FAI + ATRA, but G-CSF had no effect on the other outcomes. We conclude that addition of ATRA +/- G-CSF to FAI had no effect on CR rate, survival, EFS, or EFS in CR in poor prognosis, newly diagnosed AML or high-risk MDS. (+info)Fludarabine-based non-myeloablative chemotherapy followed by infusion of HLA-identical stem cells for relapsed leukaemia and lymphoma. (8/867)
Many patients have not been offered potentially curative allogeneic marrow transplants because of the toxicity of myeloablative regimens in the setting of advanced age or organ dysfunction. We treated five patients, ineligible for myeloablative chemotherapy due to one of these criteria, with fludarabine-based non-myeloablative chemotherapy followed by reinfusion of G-CSF-mobilised allogeneic peripheral blood progenitor cells (PBPC). Two patients died early of multi-organ failure. Another patient with massive splenomegaly was infused with a suboptimal number of PBPC; no engraftment was documented. The remaining two patients demonstrated mixed chimerism early post-transplant, but by 3 and 6 months respectively, engraftment was almost entirely of donor origin. One of these patients, transplanted with relapsed AML, remains in remission with extensive chronic GVHD at 17 months. The other patient, transplanted with chemorefractory mantle cell lymphoma, progressed early post-transplant but entered remission coincident with the onset of severe GVHD following cessation of cyclosporin A, suggesting a powerful graft-versus-mantle cell lymphoma effect. These preliminary observations suggest this approach results in engraftment and GVHD/graft-versus-tumour effects similar to myeloablative regimens and may provide an alternative in patients ineligible for conventional conditioning regimens. (+info)Vidarabine is an antiviral medication used to treat herpes simplex infections, particularly severe cases such as herpes encephalitis (inflammation of the brain caused by the herpes simplex virus). It works by interfering with the DNA replication of the virus.
In medical terms, vidarabine is a nucleoside analogue that is phosphorylated intracellularly to the active form, vidarabine triphosphate. This compound inhibits viral DNA polymerase and incorporates into viral DNA, causing termination of viral DNA synthesis.
Vidarabine was previously used as an injectable medication but has largely been replaced by more modern antiviral drugs such as acyclovir due to its greater efficacy and lower toxicity.
Vidarabine phosphate is a antiviral medication used to treat herpes simplex encephalitis, a severe form of brain infection caused by the herpes simplex virus. It works by inhibiting the replication of the virus in human cells. Vidarabine phosphate is the salt of vidarabine, which is a nucleoside analogue that gets incorporated into viral DNA during replication, leading to termination of the DNA chain and preventing further viral reproduction. It is administered through intravenous (IV) infusion in a hospital setting.
Arabinonucleotides are nucleotides that contain arabinose sugar instead of the more common ribose or deoxyribose. Nucleotides are organic molecules consisting of a nitrogenous base, a pentose sugar, and at least one phosphate group. They serve as the monomeric units of nucleic acids, which are essential biopolymers involved in genetic storage, transmission, and expression.
Arabinonucleotides have arabinose, a five-carbon sugar with a slightly different structure than ribose or deoxyribose, as their pentose component. Arabinose is a monosaccharide that can be found in various plants and microorganisms but is not typically a part of nucleic acids in higher organisms.
Arabinonucleotides may have potential applications in biochemistry, molecular biology, and medicine; however, their use and significance are not as widespread or well-studied as those of the more common ribonucleotides and deoxyribonucleotides.
Acyclovir is an antiviral medication used for the treatment of infections caused by herpes simplex viruses (HSV) including genital herpes, cold sores, and shingles (varicella-zoster virus). It works by interfering with the replication of the virus's DNA, thereby preventing the virus from multiplying further. Acyclovir is available in various forms such as oral tablets, capsules, creams, and intravenous solutions.
The medical definition of 'Acyclovir' is:
Acyclovir (brand name Zovirax) is a synthetic nucleoside analogue that functions as an antiviral agent, specifically against herpes simplex viruses (HSV) types 1 and 2, varicella-zoster virus (VZV), and Epstein-Barr virus (EBV). Acyclovir is converted to its active form, acyclovir triphosphate, by viral thymidine kinase. This activated form then inhibits viral DNA polymerase, preventing further replication of the virus's DNA.
Acyclovir has a relatively low toxicity profile and is generally well-tolerated, although side effects such as nausea, vomiting, diarrhea, and headache can occur. In rare cases, more serious side effects such as kidney damage, seizures, or neurological problems may occur. It is important to take acyclovir exactly as directed by a healthcare provider and to report any unusual symptoms promptly.
Herpetic stomatitis is a medical condition characterized by inflammation and sores or lesions in the mouth and mucous membranes caused by the herpes simplex virus (HSV). It is typically caused by HSV-1, which is highly contagious and can be spread through direct contact with an infected person, such as through kissing or sharing utensils.
The symptoms of herpetic stomatitis may include small, painful blisters or ulcers in the mouth, gums, tongue, or roof of the mouth; difficulty swallowing; fever; and swollen lymph nodes. The condition can be painful and make it difficult to eat, drink, or talk.
Herpetic stomatitis is usually self-limiting and will resolve on its own within 1-2 weeks. However, antiviral medications may be prescribed to help reduce the severity and duration of symptoms. It's important to practice good oral hygiene during an outbreak to prevent secondary infections.
It's worth noting that herpes simplex virus can also cause cold sores or fever blisters on the lips and around the mouth, which are similar to the lesions seen in herpetic stomatitis but occur outside of the mouth.
Cystitis is a medical term that refers to inflammation of the bladder, usually caused by a bacterial infection. The infection can occur when bacteria from the digestive tract or skin enter the urinary tract through the urethra and travel up to the bladder. This condition is more common in women than men due to their shorter urethras, which makes it easier for bacteria to reach the bladder.
Symptoms of cystitis may include a strong, frequent, or urgent need to urinate, pain or burning during urination, cloudy or strong-smelling urine, and discomfort in the lower abdomen or back. In some cases, there may be blood in the urine, fever, chills, or nausea and vomiting.
Cystitis can usually be treated with antibiotics to kill the bacteria causing the infection. Drinking plenty of water to flush out the bacteria and alleviating symptoms with over-the-counter pain medications may also help. Preventive measures include practicing good hygiene, wiping from front to back after using the toilet, urinating after sexual activity, and avoiding using douches or perfumes in the genital area.
Encephalitis is defined as inflammation of the brain parenchyma, which is often caused by viral infections but can also be due to bacterial, fungal, or parasitic infections, autoimmune disorders, or exposure to toxins. The infection or inflammation can cause various symptoms such as headache, fever, confusion, seizures, and altered consciousness, ranging from mild symptoms to severe cases that can lead to brain damage, long-term disabilities, or even death.
The diagnosis of encephalitis typically involves a combination of clinical evaluation, imaging studies (such as MRI or CT scans), and laboratory tests (such as cerebrospinal fluid analysis). Treatment may include antiviral medications, corticosteroids, immunoglobulins, and supportive care to manage symptoms and prevent complications.
Herpes Simplex is a viral infection caused by the Herpes Simplex Virus (HSV). There are two types of HSV: HSV-1 and HSV-2. Both types can cause sores or blisters on the skin or mucous membranes, but HSV-1 is typically associated with oral herpes (cold sores) and HSV-2 is usually linked to genital herpes. However, either type can infect any area of the body. The virus remains in the body for life and can reactivate periodically, causing recurrent outbreaks of lesions or blisters. It is transmitted through direct contact with infected skin or mucous membranes, such as during kissing or sexual activity.
Antiviral agents are a class of medications that are designed to treat infections caused by viruses. Unlike antibiotics, which target bacteria, antiviral agents interfere with the replication and infection mechanisms of viruses, either by inhibiting their ability to replicate or by modulating the host's immune response to the virus.
Antiviral agents are used to treat a variety of viral infections, including influenza, herpes simplex virus (HSV) infections, human immunodeficiency virus (HIV) infection, hepatitis B and C, and respiratory syncytial virus (RSV) infections.
These medications can be administered orally, intravenously, or topically, depending on the type of viral infection being treated. Some antiviral agents are also used for prophylaxis, or prevention, of certain viral infections.
It is important to note that antiviral agents are not effective against all types of viruses and may have significant side effects. Therefore, it is essential to consult with a healthcare professional before starting any antiviral therapy.
Foscarnet is an antiviral medication used to treat infections caused by viruses, particularly herpes simplex virus (HSV) and varicella-zoster virus (VZV). It is a pyrophosphate analog that inhibits viral DNA polymerase, preventing the replication of viral DNA.
Foscarnet is indicated for the treatment of severe HSV infections, such as mucocutaneous HSV in immunocompromised patients, and acyclovir-resistant HSV infections. It is also used to treat VZV infections, including shingles and varicella zoster virus (VZV) infection in immunocompromised patients.
Foscarnet is administered intravenously and its use requires careful monitoring of renal function and electrolyte levels due to the potential for nephrotoxicity and electrolyte imbalances. Common side effects include nausea, vomiting, diarrhea, and headache.
Phosphonoacetic acid (PAA) is not a naturally occurring substance, but rather a synthetic compound that is used in medical and scientific research. It is a colorless, crystalline solid that is soluble in water.
In a medical context, PAA is an inhibitor of certain enzymes that are involved in the replication of viruses, including HIV. It works by binding to the active site of these enzymes and preventing them from carrying out their normal functions. As a result, PAA has been studied as a potential antiviral agent, although it is not currently used as a medication.
It's important to note that while PAA has shown promise in laboratory studies, its safety and efficacy have not been established in clinical trials, and it is not approved for use as a drug by regulatory agencies such as the U.S. Food and Drug Administration (FDA).
Polyomavirus infections refer to the infectious diseases caused by polyomaviruses, a type of small, non-enveloped DNA viruses that are capable of infecting humans and animals. There are several different types of polyomaviruses that can cause infection, including JC virus (JCV), BK virus (BKV), KI virus (KIV), WU virus (WUV), and Merkel cell polyomavirus (MCPyV).
Infection with these viruses typically occurs during childhood and is usually asymptomatic or associated with mild respiratory illness. However, in immunocompromised individuals, such as those with HIV/AIDS or organ transplant recipients, polyomavirus infections can lead to more serious complications, including nephropathy (BKV), progressive multifocal leukoencephalopathy (JCV), and Merkel cell carcinoma (MCPyV).
Diagnosis of polyomavirus infections typically involves the detection of viral DNA or antigens in clinical samples, such as blood, urine, or tissue biopsies. Treatment is generally supportive and aimed at managing symptoms, although antiviral therapy may be used in some cases. Prevention strategies include good hygiene practices and avoiding close contact with individuals who are known to be infected.
Herpes zoster, also known as shingles, is a viral infection that causes a painful rash. It's caused by the varicella-zoster virus, which also causes chickenpox. After you recover from chickenpox, the virus lies dormant in your nerve cells and can reactivate later in life as herpes zoster.
The hallmark symptom of herpes zoster is a unilateral, vesicular rash that occurs in a dermatomal distribution, which means it follows the path of a specific nerve. The rash usually affects one side of the body and can wrap around either the left or right side of your torso.
Before the rash appears, you may experience symptoms such as pain, tingling, or itching in the area where the rash will develop. Other possible symptoms include fever, headache, fatigue, and muscle weakness. The rash typically scabs over and heals within two to four weeks, but some people may continue to experience pain in the affected area for months or even years after the rash has healed. This is known as postherpetic neuralgia (PHN).
Herpes zoster is most common in older adults and people with weakened immune systems, although anyone who has had chickenpox can develop the condition. It's important to seek medical attention if you suspect you have herpes zoster, as early treatment with antiviral medications can help reduce the severity and duration of the rash and lower your risk of developing complications such as PHN.
Ophthalmic solutions are sterile, single-use or multi-dose preparations in a liquid form that are intended for topical administration to the eye. These solutions can contain various types of medications, such as antibiotics, anti-inflammatory agents, antihistamines, or lubricants, which are used to treat or prevent ocular diseases and conditions.
The pH and osmolarity of ophthalmic solutions are carefully controlled to match the physiological environment of the eye and minimize any potential discomfort or irritation. The solutions may be packaged in various forms, including drops, sprays, or irrigations, depending on the intended use and administration route.
It is important to follow the instructions for use provided by a healthcare professional when administering ophthalmic solutions, as improper use can lead to eye injury or reduced effectiveness of the medication.
Hypoxanthine is not a medical condition but a purine base that is a component of many organic compounds, including nucleotides and nucleic acids, which are the building blocks of DNA and RNA. In the body, hypoxanthine is produced as a byproduct of normal cellular metabolism and is converted to xanthine and then uric acid, which is excreted in the urine.
However, abnormally high levels of hypoxanthine in the body can indicate tissue damage or disease. For example, during intense exercise or hypoxia (low oxygen levels), cells may break down ATP (adenosine triphosphate) rapidly, releasing large amounts of hypoxanthine. Similarly, in some genetic disorders such as Lesch-Nyhan syndrome, there is an accumulation of hypoxanthine due to a deficiency of the enzyme that converts it to xanthine. High levels of hypoxanthine can lead to the formation of kidney stones and other complications.
Iontophoresis is a medical technique in which a mild electrical current is used to deliver medications through the skin. This process enhances the absorption of medication into the body, allowing it to reach deeper tissues that may not be accessible through topical applications alone. Iontophoresis is often used for local treatment of conditions such as inflammation, pain, or spasms, and is particularly useful in treating conditions affecting the hands and feet, like hyperhidrosis (excessive sweating). The medications used in iontophoresis are typically anti-inflammatory drugs, anesthetics, or corticosteroids.
"Intramuscular injections" refer to a medical procedure where a medication or vaccine is administered directly into the muscle tissue. This is typically done using a hypodermic needle and syringe, and the injection is usually given into one of the large muscles in the body, such as the deltoid (shoulder), vastus lateralis (thigh), or ventrogluteal (buttock) muscles.
Intramuscular injections are used for a variety of reasons, including to deliver medications that need to be absorbed slowly over time, to bypass stomach acid and improve absorption, or to ensure that the medication reaches the bloodstream quickly and directly. Common examples of medications delivered via intramuscular injection include certain vaccines, antibiotics, and pain relievers.
It is important to follow proper technique when administering intramuscular injections to minimize pain and reduce the risk of complications such as infection or injury to surrounding tissues. Proper site selection, needle length and gauge, and injection technique are all critical factors in ensuring a safe and effective intramuscular injection.
Simplexvirus is a genus of viruses in the family Herpesviridae, subfamily Alphaherpesvirinae. This genus contains two species: Human alphaherpesvirus 1 (also known as HSV-1 or herpes simplex virus type 1) and Human alphaherpesvirus 2 (also known as HSV-2 or herpes simplex virus type 2). These viruses are responsible for causing various medical conditions, most commonly oral and genital herpes. They are characterized by their ability to establish lifelong latency in the nervous system and reactivate periodically to cause recurrent symptoms.
Intravenous injections are a type of medical procedure where medication or fluids are administered directly into a vein using a needle and syringe. This route of administration is also known as an IV injection. The solution injected enters the patient's bloodstream immediately, allowing for rapid absorption and onset of action. Intravenous injections are commonly used to provide quick relief from symptoms, deliver medications that are not easily absorbed by other routes, or administer fluids and electrolytes in cases of dehydration or severe illness. It is important that intravenous injections are performed using aseptic technique to minimize the risk of infection.
Microbial drug resistance is a significant medical issue that refers to the ability of microorganisms (such as bacteria, viruses, fungi, or parasites) to withstand or survive exposure to drugs or medications designed to kill them or limit their growth. This phenomenon has become a major global health concern, particularly in the context of bacterial infections, where it is also known as antibiotic resistance.
Drug resistance arises due to genetic changes in microorganisms that enable them to modify or bypass the effects of antimicrobial agents. These genetic alterations can be caused by mutations or the acquisition of resistance genes through horizontal gene transfer. The resistant microbes then replicate and multiply, forming populations that are increasingly difficult to eradicate with conventional treatments.
The consequences of drug-resistant infections include increased morbidity, mortality, healthcare costs, and the potential for widespread outbreaks. Factors contributing to the emergence and spread of microbial drug resistance include the overuse or misuse of antimicrobials, poor infection control practices, and inadequate surveillance systems.
To address this challenge, it is crucial to promote prudent antibiotic use, strengthen infection prevention and control measures, develop new antimicrobial agents, and invest in research to better understand the mechanisms underlying drug resistance.
Vidarabine
Vidarabine phosphate
Tectitethya crypta
Herpes simplex
Thymidine kinase from herpesvirus
DnaG
Herpes simplex keratitis
Arabinosyl nucleosides
Neonatal meningitis
ATC code S01
ATC code J05
C10H14N5O7P
C10H13N5O4
Allopurinol
Nucleoside analogue
List of drugs: Vf-Vz
Varicella zoster virus
List of MeSH codes (D13)
Trifluridine
Vidarabine - Wikipedia
Successful vidarabine therapy for adenovirus type 11-associated acute hemorrhagic cystitis after allogeneic bone marrow...
Comparison of acyclovir and vidarabine in immunocompromised children with varicella-zoster virus infection - PubMed
A case of acyclovir-resistant herpes simplex encephalitis improved dramatically by vidarabine (Ara-A)<...
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Acyclovir IV Infusion: Package Insert - Drugs.com
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Table 1 - Eastern Equine Encephalitis in Children, Massachusetts and New Hampshire,USA, 1970-2010 - Volume 19, Number 2...
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Betaxolol Hydrochloride|N0000004400
DeCS 2013 - December 17, 2013 version
Acyclovir1
- Vidarabine is more toxic and less metabolically stable than many of the other current antivirals such as acyclovir and ganciclovir. (wikipedia.org)
Cytarabine2
- These compounds led to the synthesis of a new generation, sugar modified nucleoside analog vidarabine, and the related compound cytarabine. (wikipedia.org)
- For recognizing a strong inhibitor, we have accomplished docking studies on the major virus protease with 4 natural product species as anti COVID-19 (SARS-CoV-2), namely "Vidarabine", "Cytarabine", "Gemcitabine" and "Matrine" which have been extracted from Gillan's leaves plants. (techscience.com)
Antiviral5
- Vidarabine or 9-β-D-arabinofuranosyladenine (ara-A) is an antiviral drug which is active against herpes simplex and varicella zoster viruses. (wikipedia.org)
- This metabolite still possesses antiviral activity, but is 10-fold less potent than vidarabine. (wikipedia.org)
- In addition to the potential anticancer properties antiviral activity of Vidarabine was also demonstrated in 1965. (wikipedia.org)
- Antiviral drugs used include vidarabine or interferon alpha-2b. (medscape.com)
- Fludarabine Phosphate Injection, USP contains fludarabine phosphate, a fluorinated nucleotide analog of the antiviral agent vidarabine, 9-ß-D-arabinofuranosyladenine (ara-A) that is relatively resistant to deamination by adenosine deaminase. (guidelinecentral.com)
Reverse transcript1
- Vidarabine Monophosphate for Injection a reverse transcriptase inhibitors medicine used to treat herpes virus stomatitis, dermatitis, viral herpes zoster, etc. (inopha.net)
Polymerase2
- This is the active form of vidarabine and is both an inhibitor and a substrate of viral DNA polymerase. (wikipedia.org)
- Viral strains resistant to vidarabine show changes in DNA polymerase. (wikipedia.org)
Injection2
- We are China supplier of Vidarabine Monophosphate for Injection. (inopha.net)
- Contact us to get Vidarabine Monophosphate for Injection price online if plan to buy it from China GMP manufacturers. (inopha.net)
Whitley2
- It was University of Alabama at Birmingham researcher and physician Richard J. Whitley in 1976 where the clinical effectiveness of vidarabine was first realized, and vidarabine was used in the treatment of many viral diseases. (wikipedia.org)
- In 1977, the world's first effective treatment for a viral disease occurred at University Hospital when Richard Whitley, M.D., and Charles Alford developed vidarabine. (uab.edu)
Synthesis2
- The Mechanism of action of vidarabine Vidarabine works by interfering with the synthesis of viral DNA. (wikipedia.org)
- citation needed] Chemical synthesis of Vidarabine was first attained in 1960, as a part of studies on developing potential anticancer agents by B. R. Baker et al. (wikipedia.org)
Agent1
- Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolys. (invivogen.com)
Effective1
- Vidarabine seemed to be equally effective in this respect. (umn.edu)
Trifluridine1
- Other drugs that have been used to treat the oculars signs associated with FHV-1 are vidarabine, trifluridine, and idoxuridine. (wedgewoodpharmacy.com)
Acyclovir and vidarabine5
- Intravenous acyclovir and vidarabine were compared in the treatment of varicella-zoster virus (VZV) infection in 25 immunocompromised children--13 with acute lymphocytic leukemia, three with other types of cancer, two with immunodeficiency and in seven undergoing prednisolone treatment. (nih.gov)
- While acyclovir and vidarabine were equally effective for VZV infection, in herpes zoster acyclovir was more effective. (nih.gov)
- A comparison of acyclovir and vidarabine. (nih.gov)
- Comparative trial of acyclovir and vidarabine in disseminated varicella-zoster virus infections in immunocompromised patients. (nih.gov)
- Pharmacotherapy for HSE consists of acyclovir and vidarabine. (medscape.com)
Idoxuridine1
- used for epithelial keratitis that has not responded to idoxuridine or vidarabine. (pdr.net)
Varicella Zoste1
- Structural modifications of vidarabine have proven partially effective at blocking deamination, such as replacement of the amine with a methoxy group (ara-M). This results in about a 10-fold greater selectivity against Varicella Zoster Virus than ara-A, however analog of vidarabine is inactive against other viruses due to it not being able to be phosphorylated. (wikipedia.org)
PMID1
- 11483782) , and the other comparing vidarabine with acyclovir (PMID: 1988829) . (nih.gov)
Nucleoside1
- These compounds led to the synthesis of a new generation, sugar modified nucleoside analog vidarabine, and the related compound cytarabine. (wikipedia.org)
Ganciclovir1
- Vidarabine is more toxic and less metabolically stable than many of the other current antivirals such as acyclovir and ganciclovir. (wikipedia.org)
Herpes3
- Vidarabine was given intravenously to eight patients with varicella and to eight with herpes zoster at a dose of 10 mg/kg/day. (nih.gov)
- Dive into the research topics of 'A case of acyclovir-resistant herpes simplex encephalitis improved dramatically by vidarabine (Ara-A)'. Together they form a unique fingerprint. (elsevierpure.com)
- A case of acyclovir-resistant herpes simplex encephalitis improved dramatically by vidarabine (Ara-A) . Japanese Journal of National Medical Services , 44 (7), 728-732. (elsevierpure.com)
Nucleosides1
- This earlier work gave impetus to further synthetic studies on the nucleosides with the β-D-arabinofuranosyl moiety including Vidarabine, and the isolation of Vidarabine from the fermentation culture broth of Streptomyces antibioticus. (wikipedia.org)
Anticancer1
- citation needed] Chemical synthesis of Vidarabine was first attained in 1960, as a part of studies on developing potential anticancer agents by B. R. Baker et al. (wikipedia.org)
Inhibitor2
- This is the active form of vidarabine and is both an inhibitor and a substrate of viral DNA polymerase. (wikipedia.org)
- The use of an inhibitor of adenosine deaminase to increase the half-life of vidarabine has also been tried, and drugs such as dCF and EHNA have been used with a small amount of success. (wikipedia.org)
Adenosine1
- Vidarabine is an analog of adenosine with the D-ribose replaced with D-arabinose. (wikipedia.org)
Therapeutic agents1
- Within the body it can be treated by a number of drugs and therapeutic agents including aciclovir, zoster-immune globulin(ZIG), and vidarabine. (creativebiomart.net)
Viral3
- The anti-viral activity of vidarabine was first described by M. Privat de Garilhe and J. De Rudder in 1964. (wikipedia.org)
- It was University of Alabama at Birmingham researcher and physician Richard J. Whitley in 1976 where the clinical effectiveness of vidarabine was first realized, and vidarabine was used in the treatment of many viral diseases. (wikipedia.org)
- Viral strains resistant to vidarabine show changes in DNA polymerase. (wikipedia.org)
Infection2
- Vidarabine may be one therapeutic option in life-threatening adenovirus infection. (nih.gov)
- Cytomegalovirus infection can choose erbiumphosphate, propoxy-1 guanosine, or vidarabine. (funtoy.com)
Ocular1
- Systemic absorption is unlikely following ocular administration even when nasolacrimal secretions are swallowed, since vidarabine is rapidly deaminated in the gastrointestinal tract. (pharmacycode.com)
Drugs1
- Tell your doctor of all over-the-counter and prescription medications you may use including: zidovudine, barbiturates (e.g., phenobarbital), theophylline, vidarabine, other drugs which depress the immune system (e.g., anti-cancer type). (patientassistance.com)
Treatment2
- Sequential vidarabine infusion in the treatment of polyoma virus-associated acute haemorrhagic cystitis late after allogeneic bone marrow transplantation. (nih.gov)
- In varicella, vidarabine significantly shortened the time from the start of treatment to cessation of new lesion formation compared with acyclovir. (nih.gov)
Therapy2
Active1
- After obtaining informed consent, vidarabine, which has been shown to be active against adenovirus in vitro, was started. (nih.gov)