Persius/hicric huggingface dataset:
Valacyclovir warnings and precautions

# Warnings And Precautions

### Thrombotic Thrombocytopenic Purpura/Hemolytic Uremic Syndrome (TTP/HUS)
TTP/HUS, in some cases resulting in death, has occurred in patients with advanced HIV1 disease and also in allogeneic bone marrow transplant and renal transplant recipients participating in clinical trials of VALTREX at doses of 8 grams per day. Treatment with VALTREX should be stopped immediately if clinical signs, symptoms, and laboratory abnormalities consistent with TTP/HUS occur.

### Acute Renal Failure
Cases of acute renal failure have been reported in:
- Elderly patients with or without reduced renal function. Caution should be exercised when administering VALTREX to geriatric patients, and dosage reduction is recommended for those with impaired renal function .
- Patients with underlying renal disease who received higher-than-recommended doses of VALTREX for their level of renal function. Dosage reduction is recommended when administering VALTREX to patients with renal impairment .
- Patients receiving other nephrotoxic drugs. Caution should be exercised when administering VALTREX to patients receiving potentially nephrotoxic drugs.
- Patients without adequate hydration. Precipitation of acyclovir in renal tubules may occur when the solubility (2.5 mg/mL) is exceeded in the intratubular fluid. Adequate hydration should be maintained for all patients.
In the event of acute renal failure and anuria, the patient may benefit from hemodialysis until renal function is restored .

### Central Nervous System Effects
Central nervous system adverse reactions, including agitation, hallucinations, confusion, delirium, seizures, and encephalopathy, have been reported in both adult and pediatric patients with or without reduced renal function and in patients with underlying renal disease who received higher-than-recommended doses of VALTREX for their level of renal function. Elderly patients are more likely to have central nervous system adverse reactions. VALTREX should be discontinued if central nervous system adverse reactions occur .
Vesicle-associated membrane protein 8
Vesicle-associated membrane protein 8 is a protein that in humans is encoded by the VAMP8 gene.
Synaptobrevins/VAMPs, syntaxins, and the 25-kD synaptosomal-associated protein SNAP25 are the main components of a protein complex involved in the docking and/or fusion of synaptic vesicles with the presynaptic membrane. The protein encoded by this gene is a member of the vesicle-associated membrane protein (VAMP)/synaptobrevin family. It is associated with the perinuclear vesicular structures of the early endocytic compartment. It has been found that VAMP8 interacts specifically with the soluble NSF-attachment protein (alpha-SNAP), most likely through an VAMP8-containing SNARE complex. Phosphorylation of VAMP8 inside the conserved SNARE-domain can suppress vesicle fusion.

# Interactions
Vesicle-associated membrane protein 8 has been shown to interact with STX4, SNAP23, STX1A, STX8 and STX7.
Yale-Brown obsessive compulsive scale

# Overview
Yale-Brown Obsessive Compulsive Scale  sometimes referred to as Y-BOCS  is a test to rate the severity of obsessive-compulsive disorder (OCD) symptoms.
The Yale-Brown Obsessive Compulsive Scale was designed newly from the ground up by Dr. Wayne Goodman and colleagues.  It is used extensively in research and clinical practice to both determine severity of OCD and to monitor improvement during treatment. This scale, which measures obsessions separately from compulsions, specifically measures the severity of symptoms of obsessive-compulsive disorder without being biased towards the type of obsessions or compulsions present.
The scale is a clinician-rated, 10-item scale, each item rated from 0 (no symptoms) to 40 (extreme symptoms). The results can be interpreted as follows:
- 0-7 Subclinical
- 8-15 Mild
- 16-23 Moderate
- 24-31 Severe
- 32-40 Extreme
Patients scoring in the mild range or higher should consider professional help in alleviating obsessive-compulsive symptoms.
2017 ACC/AHA Hypertension Guidelines

# 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults

# Guidelines for Lifestyle modification:

## Nonpharmacological Interventions

## Strategies to Promote Lifestyle Modification

## Structured, Team-Based Care Interventions for Hypertension Control

## Electronic Health Record (EHR) and Patient Registries

## Telehealth Interventions to Improve Hypertension Control

## Quality Improvement Strategies

## Quality Improvement Strategies

## The Plan of Care for Hypertension

# Guidelines for Medical therapy:

## General Principles of Drug Therapy

## Treatment Threshold and the Use of Cardiovascular Disease (CVD) Risk Estimation to Guide Drug Treatment of Hypertension

## Blood Pressure (BP) Goal for Patients With Hypertension

## Choice of Initial Medication

## Choice of Initial Monotherapy Versus Initial Combination Drug Therapy

## Follow-Up After Initiating Antihypertensive Drug Therapy

## Monitoring Strategies to Improve Control of Blood Pressure (BP) in Patients on Drug Therapy for High BP

## Stable Ischemic Heart Disease (SIHD)

## Heart Failure

## Heart Failure With Reduced Ejection Fraction

## Heart Failure With Preserved Ejection Fraction

## Chronic Kidney Disease (CKD)

## Recommendations for Treatment of Hypertension in Patients With CKD

## Hypertension After Renal Transplantation

## Recommendations for Treatment of Hypertension After Renal Transplantation

## Acute Intracerebral Haemorrhage (ICH)

## Acute Ischemic Stroke

## Secondary Stroke Prevention

## Peripheral Arterial Disease (PAD)

## Diabetes Mellitus

## Atrial Fibrillation (AF)

## Valvular Heart Disease (VHD)

## Aortic Disease

## Racial and Ethnic Differences in Treatment

## Pregnancy

## Older Persons

## Hypertensive CrisesEmergencies and Urgencies

## Cognitive Decline and Dementia

## Patients Undergoing Surgical Procedures

## Antihypertensive Medication Adherence Strategies
3-hydroxy-3-methylglutaryl-CoA lyase
3-hydroxy-3-methylglutaryl-CoA lyase (or HMG-CoA lyase) is an enzyme that in human is encoded by the HMGCL gene located on chromosome 1. It is a key enzyme in ketogenesis (ketone body formation). It is a ketongenic enzyme in the liver that catalyzes the formation of acetoacetate from HMG-CoA within the mitochondria. It also plays a prominent role in the catabolism of the amino acid leucine.

# Structure
The HMGCL gene encodes a 34.5-kDa protein that is localized to the mitochondrion and peroxisome. Multible isoforms of the proteins are known due to alternative splicing. The major isoform (isoform 1) is most highly expressed in the liver whereas isoform 2 is found in energy-demanding tissues including the brain, heart, and skeletal muscle.
Structure of the HMGCL protein has been resolved by X-ray crystallography at 2.1-A resolution, and reveals that the protein may function as a dimer. Substrate access to the active site of the HMGCL enzyme involves substrate binding across a cavity located at the C-terminal end of a beta barrel structure. In addition, the lysine 48 residue which is mutated in patients with 3-hydroxy-3-methylglutaryl-CoA lyase deficiency is also found to be necessary for substrate binding.

# Function
The HMGCL protein plays an essential role in breaking down dietary proteins and fats for energy.  It catalyzes the reaction:
(S)-3-hydroxy-3-methylglutaryl-CoA = acetyl-CoA + acetoacetate.
and requires a divalent metal ion as co-factor.
The enzyme is required for ketogenesis in the liver, and is also responsible for processing the amino acid leucine inside the mitochondrion
Deficiency 
HMG-CoA lyase deficiency causes hypoketotic hypoglycemia similar to that is caused by HMGCS2 mutations but also leads to organic acid accumulation and metabolic acidosis due to altered leucine metabolism. This disorder can be mistaken for Reye syndrome because of the symptoms of vomiting, lethargy, and convulsions.

# Clinical significance
Mutations in the HMGCL gene cause 3-hydroxy-3-methylglutaryl-CoA lyase deficiency (HMGCLD), a rare autosomal recessive inborn error of metabolism characterized by disruption of ketogenesis and L-leucine catabolism. To-date more than 30 different mutations including missense mutations of different residues have been associated with patients with HMGCLD in diverse families and ethnicities. HMGCLD typically presents in the first year of the patient's life after a fasting period. Clinical acute symptoms include vomiting, seizures, metabolic acidosis, hypoketotic hypoglycemia, and lethargy.

# Interactions
HMGCL interacts with itself to form homodimers and homotetramers. It is also shown in yeast two-hybrid experiments to interact with DNAJA1.
ACG guidelines classification scheme

# Overview
The GRADE system of quality of evidence and strength of recommendation gives insight into the confidence of the American College of Gastroenterology in the recommendation and the likelihood that further research would change said recommendation.

# Classification of Recommendation

## GRADE system of quality of evidence and strength of recommendation:
Quality of Evidence
Strength of Recommendation
The strength of recommendation is determined based on a benefit vs. cost/risk to patient.
Albright's hereditary osteodystrophy

# Overview
Albright hereditary osteodystrophy (or Martin-Albright syndrome) is an autosomal dominant form of osteodystrophy, and is otherwise known as Pseudohypoparathyroidism type 1a.  The syndrome bears the name of Fuller Albright, who was also responsible for characterizing Albright syndrome as well as a number of other bone disorders.
The disorder is characterized by a lack of renal responsiveness to parathyroid hormone, resulting in low serum calcium, high serum phosphate, and appropriately high serum parathyroid hormone.  Patients with Albright hereditary osteodystrophy have short stature, characteristically shortened fourth and fifth metacarpals, and rounded faces.
Albright hereditary osteodystrophy is commonly known as Pseudohypoparathyroidism because the kidney responds as if parathyroid hormone were absent.  In fact, blood levels of parathyroid hormone are elevated in Pseudohypoparathyroidism due to the continued hypocalcemia.
ATPase, Na+/K+ transporting, alpha 1
Sodium/potassium-transporting ATPase subunit alpha-1 is an enzyme that in humans is encoded by the ATP1A1 gene.
The protein encoded by this gene belongs to the family of P-type cation transport ATPases, and to the subfamily of Na+/K+-ATPases. Na+/K+-ATPase is an integral membrane protein responsible for establishing and maintaining the electrochemical gradients of Na and K ions across the plasma membrane. These gradients are essential for osmoregulation, for sodium-coupled transport of a variety of organic and inorganic molecules, and for electrical excitability of nerve and muscle. This enzyme is composed of two subunits, a large catalytic subunit (alpha) and a smaller glycoprotein subunit (beta). The catalytic subunit of Na+/K+-ATPase is encoded by multiple genes. This gene encodes an alpha 1 subunit. Alternatively spliced transcript variants encoding different isoforms have been identified.
In melanocytic cells ATP1A1 gene expression may be regulated by MITF.

# Clinical relevance
Mutations in this gene have been associated with aldosterone-producing adenomas and secondary hypertension.
Acrodermatitis (patient information)
For the WikiDoc page for this topic, click here

# Overview
Acrodermatitis is a childhood skin condition that may be accompanied by mild symptoms of fever and malaise. It may also be associated with hepatitis B and other viral infections.

# What are the symptoms of Acrodermatitis?
- Rash or patch on skin
- Brownish-red or copper-colored patch that is firm and flat on top
- String of bumps may appear in a line
- Generally not itchy
- Rash looks the same on both sides of the body
- Rash may appear on the palms and soles -- it does not occur on the back, chest, or belly area (this is one of the ways it is identified -- by the absence of the rash from the trunk of the body)
Other symptoms that may appear include:
- Swollen abdomen
- Swollen lymph nodes
- Tender lymph nodes

# What causes Acrodermatitis?
The cause of acrodermatitis is poorly understood, but its link with other infections is well- documented.
In Italian children, acrodermatitis is seen frequently with hepatitis B, but this link is rarely seen in the United States. Epstein-Barr virus (EBV, mononucleosis) is the virus most often associated with acrodermatitis. Other associated viruses inclcude, cytomegalovirus, coxsackie viruses, parainfluenza virus, respiratory syncytial virus (RSV), and some live virus vaccines.
A rare, genetic form of acrodermatitis is acrodermatitis enteropathica. In this disorder, zinc is poorly absorbed from the diet. Adding zinc supplements to the diet improves the condition. This form of the disorder can be associated with other abnormalities and development delays.

# Diagnosis
Your doctor can diagnosed this condition by simply looking at the skin and rash. The liver, spleen, and lymph nodes may be swollen.
The following tests may be done to confirm the diagnosis or rule out other conditions:
- Bilirubin level
- Hepatitis virus serology or hepatitis B surface antigen
- Liver enzymes (liver function tests)
- Screening for EBV antibodies
- Serum zinc level may be tested in acrodermatitis enteropathica
- Skin biopsy

# When to seek urgent medical care?
Call your health care provider if your child has signs of this condition.

# Treatment options
Acrodermatitis by itself is not treated. Infections associated with this condition, such as hepatitis B and Epstein-Barr, should be treated appropriately.
Acrodermatitis enteropathica improves when zinc levels are returned to normal.

# Where to find medical care for Acrodermatitis?
Directions to Hospitals Treating Acrodermatitis

# What to expect (Outlook/Prognosis)?
Acrodermatitis usually disappears on its own without treatment or complication. However, the associated conditions must be watched carefully.

# Possible complications
Complications occur as a result of associated conditions, rather than as a result of acrodermatitis.

# Sources
Acute rheumatic fever case study one

# Clinical Summary
A 21-year-old male with sickle cell anemia had recurrent attacks of acute rheumatic fever beginning at age 14.
Mitral insufficiency and stenosis were present by age 16.
On prophylactic antibiotics, the patient had no evidence of recurrence until three weeks before his final admission, when an upper respiratory infection developed. A few weeks later he developed acute migratory polyarthritis. This was associated with rapid deterioration of cardiac function and death.

## Autopsy Findings
At autopsy, the heart was enlarged (weighing 675 grams) especially the left atrium. Both the aortic and mitral valves showed fibrosis as well as the fresh, tiny verrucae characteristic of acute rheumatic fever.

## Images
Image courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- This is a gross photograph of mitral valve demonstrating marked thickening and fibrosis of the valve leaflet. There are also numerous foci of fibrinoid necrosis within the cusps and friable vegetations (verrucae) along the lines of closure (arrows). These irregular, warty projections are found at sites of erosion on the inflamed endocardial surface. The verrucae probably result from the precipitation of fibrin where the leaflets impinge on each other.
- This is a low-power photomicrograph of heart tissue. Little can be seen at this magnification, except that the tissue looks relatively normal.
- This is a higher-power photomicrograph of myocardium showing cellular accumulations--Aschoff bodies (arrows)--within the interstitium of the myocardium. These are found especially around blood vessels.
- This is a higher-power photomicrograph of myocardium containing Aschoff bodies (arrows) within the interstitium.
- This high-power photomicrograph of myocardium shows the cellular detail of an Aschoff body. Aschoff bodies are foci of fibrinoid necrosis surrounded by lymphocytes, macrophages, an occasional plasma cell, and plump activated histiocytes called Anitschkow cells or Aschoff cells (arrows). These distinctive cells have abundant amphophilic cytoplasm and central round-to-ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon resembling a caterpillar (hence the designation caterpillar cells).
- This high-power photomicrograph of myocardium shows the cellular detail of another Aschoff body. In this case there appears to be a multinucleated Aschoff giant cell (arrow).
Addenbrooke's Charitable Trust (ACT)
Addenbrooke's Charitable Trust (ACT) (established 1987) is the official independent registered charity for Addenbrooke's Hospital, Cambridge, UK.
ACT's objective is to support and promote the work of Addenbrooke's for the benefit of patients and staff, by raising extra funds to enhance services, facilities and research.
Many hospitals across the UK rely on fundraising activities to supplement publicly funded services. Donations received by ACT make a real difference to patients and staff at Addenbrookes. Monies raised play a critical role in keeping Addenbrookes at the forefront of medical diagnosis, treatment and research, by enabling the purchase of sophisticated equipment not affordable through NHS budgets, funding specialist staff and providing financial support for environmental enhancements.
Charitable donations have contributed to funds in most departments around the hospital. ACT manages the charitable funds in an effective way and aims to invest and disburse money successfully, ensuring that funds are used for the purposes for which they are raised.
Addenbrooke's Charitable Trust (ACT) registered charity number: 1048868
American College of Chest Physicians

# Overview
The American College of Chest Physicians (ACCP) is a medical organization consisting of physicians and non-physician specialists in the field of chest medicine, which includes pulmonology, thoracic surgery, and critical care medicine.
"Fellow of the College of Chest Physicians" (FCCP) is a title given to a doctor who specializes in pulmonology, thoracic surgery, and critical care medicine.  FCCP is used as a post-nominal title, such as John Citizen, MD, FCCP. To be eligible for the Fellowship, a physician in the United States of America or Canada must be board certified in both a primary board and an applicable subspecialty board, have at least 18 months experience in the field, and be sponsored by two Fellows of the College.  Non-physicians who do active work in chest medicine  including those with a Ph.D., Pharm.D., D.Sc., or a doctorally-prepared nurse  are also eligible for the fellowship. Physicians outside of the United States and Canada are also eligible for the Fellowship.  International Fellows (also given the designation FCCP) must have three years' experience in their field after the completion of training.
Chest is a medical journal published by the ACCP.

# Classes of Recommendations
- Class I: Evidence and/or general agreement that a given diagnostic procedure or treatment is beneficial, useful, and effective.
- Class II: Conflicting evidence and/or a divergence of opinion about the usefulness or efficacy of the treatment or procedure.
- Class IIa: Weight of evidence or opinion is in favour of usefulness or efficacy.
- Class IIb: Usefulness or efficacy is less well established by evidence or opinion.
- Class III: Evidence or general agreement that the treatment or procedure is not useful or effective and, in some cases, may be harmful.

# Level of Evidence
- Level of Evidence: A Data derived from multiple randomized clinical trials or meta-analyses.
- Level of Evidence: B Data derived from a single randomized clinical trial or large non-randomized studies.
- Level of Evidence: C Consensus of opinion of the experts and/or small studies, retrospective studies, and registries.
Amphotericin B clinical pharmacology

# Clinical Pharmacology

## Pharmacokinetics
The assay used to measure amphotericin B in the blood after the administration of ABELCET does not distinguish amphotericin B that is complexed with the phospholipids of ABELCET from amphotericin B that is uncomplexed.
The pharmacokinetics of amphotericin B after the administration of ABELCET are nonlinear. Volume of distribution and clearance from blood increase with increasing dose of ABELCET, resulting in less than proportional increases in blood concentrations of amphotericin B over a dose range of 0.6-5 mg/kg/day. The pharmacokinetics of amphotericin B in whole blood after the administration of ABELCET and amphotericin B desoxycholate are:
The large volume of distribution and high clearance from blood of amphotericin B after the admistration of ABELCET probably reflect uptake by tissues. The long terminal elimination half-life probably reflects a slow redistribution from tissues. Although amphotericin B is excreted slowly, there is little accumulation in the blood after repeated dosing. AUC of amphotericin B increased approximately 34% from day 1 after the administration of ABELCET 5 mg/kg/day for 7 days. The effect of gender or ethnicity on the pharmacokinetics of ABELCET has not been studied.
Tissue concentrations of amphotericin B have been obtained at autopsy from one heart transplant patient who received three doses of ABELCET at 5.3 mg/kg/day:
This pattern of distribution is consistent with that observed in preclinical studies in dogs in which greatest concentrations of amphotericin B after ABELCET administration were observed in the liver, spleen, and lung; however, the relationship of tissue concentrations of amphotericin B to its biological activity when administered as ABELCET is unknown.

## Special Populations
- Hepatic Impairment:
The effect of hepatic impairment on the disposition of ABELCET is not known.
- Renal Impairment:
The effect of renal impairment on the disposition of ABELCET is not known. The effect of dialysis on the elimination of ABELCET has not been studied; however, amphotericin B is not removed by hemodialysis when administered as amphotericin B desoxycholate.
- Pediatric and Elderly Patients:
The pharmacokinetics and pharmacodynamics of pediatric patients (16 years of age) and elderly patients (65 years of age) have not been studied.