Persius/hicric huggingface dataset:
Famciclovir drug interactions

# Drug Interactions

## Potential for FAMVIR to Affect Other Drugs
The steady-state pharmacokinetics of digoxin were not altered by concomitant administration of multiple doses of famciclovir (500 mg three times daily). No clinically significant effect on the pharmacokinetics of zidovudine, its metabolite zidovudine glucuronide, or emtricitabine was observed following a single oral dose of 500 mg famciclovir coadministered with zidovudine or emtricitabine.
An in vitro study using human liver microsomes suggests that famciclovir is not an inhibitor of CYP3A4 enzymes.

## Potential for Other Drugs to Affect penciclovir
No clinically significant alterations in penciclovir pharmacokinetics were observed following single-dose administration of 500 mg famciclovir after pretreatment with multiple doses of allopurinol, cimetidine, theophylline, zidovudine, promethazine, when given shortly after an antacid (magnesium and aluminum hydroxide), or concomitantly with emtricitabine. No clinically significant effect on penciclovir pharmacokinetics was observed following multiple-dose (three times daily) administration of famciclovir (500 mg) with multiple doses of digoxin.
Concurrent use with probenecid or other drugs significantly eliminated by active renal tubular secretion may result in increased plasma concentrations of penciclovir.
The conversion of 6-deoxy penciclovir to penciclovir is catalyzed by aldehyde oxidase. Interactions with other drugs metabolized by this enzyme and/or inhibiting this enzyme could potentially occur. Clinical interaction studies of famciclovir with cimetidine and promethazine, in vitro inhibitors of aldehyde oxidase, did not show relevant effects on the formation of penciclovir. raloxifene, a potent aldehyde oxidase inhibitor in vitro, could decrease the formation of penciclovir. However, a clinical drug-drug interaction study to determine the magnitude of interaction between penciclovir and raloxifene has not been conducted.
Fidaxomicin adverse reactions

# Adverse Reactions

## Clinical Trials Experience
Because clinical trials are conducted under widely varying conditions, adverse event rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of any other drug and may not reflect the rates observed in practice.
The safety of DIFICID 200 mg tablets taken twice a day for 10 days was evaluated in 564 patients with CDAD in two active-comparator controlled trials with 86.7% of patients receiving a full course of treatment.
Thirty-three patients receiving DIFICID (5.9%) withdrew from trials as a result of adverse reactions (AR). The types of AR resulting in withdrawal from the study varied considerably. Vomiting was the primary adverse reaction leading to discontinuation of dosing; this occurred at an incidence of 0.5% in both the fidaxomicin and vancomycin patients in Phase 3 studies.
The following adverse reactions were reported in <2% of patients taking DIFICID tablets in controlled trials:

### Gastrointestinal Disorders
Abdominal distension, Abdominal tenderness, Dyspepsia, Dysphagia, flatulence, Intestinal obstruction, Megacolon

### Investigations
Increased blood alkaline phosphatase, Decreased blood bicarbonate, Increased hepatic enzymes, Decreased platelet count

### Metabolism and Nutrition Disorders
Hyperglycemia, Metabolic Acidosis

### Skin and Subcutaneous Tissue Disorders
Drug eruption, Pruritus, Rash

## Post Marketing Experience
Adverse reactions reported in the post marketing setting arise from a population of unknown size and are voluntary in nature. As such, reliability in estimating their frequency or in establishing a causal relationship to drug exposure is not always possible.
Hypersensitivity reactions (dyspnea, angioedema, rash, and pruritus) have been reported.
Fitzsimmons-Guilbert syndrome
Fitzsimmons-Guilbert syndrome is an extremely rare genetic disease characterized by a slowly progressive spastic paraplegia, skeletal anomalies of the hands and feet with brachydactyly type E, cone-shaped epiphyses, abnormal metaphysealphalangeal pattern profile, sternal anomaly (pectus carinatum or excavatum), dysarthria, and mild intellectual deficit.

# History
Fitzsimmons and Guilbert first described male uniovular twins, aged 20 years, who had had slowly progressive spastic paraplegia from early in life. Both had skeletal abnormalities of the hands and feet: brachydactyly, cone-shaped epiphyses, and an abnormal metaphyseal-phalangeal pattern profile. In addition, they had nonspecific dysarthria and low-normal intellectual capacity.
Since the original report, three more cases have been described, including two (Lacassie et al) with a more severe mental retardation and a different metacarpal-phalangeal pattern profile, though these cases may represent a new disease entity.

# Pathophysiology
With so few described cases, establishing the basic pathophysiological mechanisms or genetic abnormalities has not been possible.
Flexor hallucis longus muscle

# Overview
The Flexor hallucis longus muscle (FHL) is a muscle of the leg.
It is one of the deep muscles of the posterior compartment of the leg.  the other deep muscles of the leg are flexor digitorum longus and tibialis posterior.  FHL is the largest and most powerful of these deep muscles.
The Flexor hallucis longus is situated on the fibular side of the leg. It arises from the inferior two-thirds of the posterior surface of the body of the fibula, with the exception of 2.5 cm. at its lowest part; from the lower part of the interosseous membrane; from an intermuscular septum between it and the Peroni, laterally, and from the fascia covering the Tibialis posterior, medially.
The fibers pass obliquely downward and backward, and end in a tendon which occupies nearly the whole length of the posterior surface of the muscle.
This tendon lies in a groove which crosses the posterior surface of the lower end of the tibia, the posterior surface of the talus, and the under surface of the sustentaculum tali of the calcaneus; in the sole of the foot it runs forward between the two heads of the Flexor hallucis brevis, and is inserted into the base of the last phalanx of the great toe. The grooves on the talus and calcaneus, which contain the tendon of the muscle, are converted by tendinous fibers into distinct canals, lined by a mucous sheath.
As the tendon passes forward in the sole of the foot, it is situated above, and crosses from the lateral to the medial side of the tendon of the Flexor digitorum longus, to which it is connected by a fibrous slip.

# Variations
Usually a slip runs to the Flexor digitorum and frequently an additional slip runs from the Flexor digitorum to the Flexor hallucis. Peroneocalcaneus internus, rare, origin below or outside the Flexor hallucis from the back of the fibula, passes over the sustentaculum tali with the Flexor hallucis and is inserted into the calcaneum.

# Additional images
- Bones of the right leg. Posterior surface.
- Left calcaneus, inferior surface.
- Bones of the right foot. Plantar surface.
- Coronal section through right talocrural and talocalcaneal joints.
- Muscles of the back of the leg. Deep layer.
- Muscles of the sole of the foot. Second layer.
- The popliteal, posterior tibial, and peroneal arteries.
- Circumpatellar anastomosis.
- Nerves of the right lower extremity Posterior view.
- The plantar nerves.
Flexor hallucis brevis muscle

# Overview
The Flexor hallucis brevis arises, by a pointed tendinous process, from the medial part of the under surface of the cuboid bone, from the contiguous portion of the third cuneiform, and from the prolongation of the tendon of the Tibialis posterior which is attached to that bone.
It divides in front into two portions, which are inserted into the medial and lateral sides of the base of the first phalanx of the great toe, a sesamoid bone being present in each tendon at its insertion.
The medial portion is blended with the Abductor hallucis previous to its insertion; the lateral portion with the Adductor hallucis; the tendon of the Flexor hallucis longus lies in a groove between them; the lateral portion is sometimes described as the first Interosseous plantaris.

# Variations
Origin subject to considerable variation; it often receives fibers from the calcaneus or long plantar ligament. Attachment to the cuboid sometimes wanting. Slip to first phalanx of the second toe.

# Additional images
- Bones of the right foot. Plantar surface.
Kinase insert domain receptor
Kinase insert domain receptor (KDR, a type III receptor tyrosine kinase) also known as vascular endothelial growth factor receptor 2 (VEGFR-2) is a VEGF receptor. KDR is the human gene encoding it. KDR has also been designated as CD309 (cluster of differentiation 309). KDR is also known as Flk1 (Fetal Liver Kinase 1).
The Q472H germline KDR genetic variant affects VEGFR-2 phosphorylation and has been found to associate with microvessel density in NSCLC.

# Interactions
Kinase insert domain receptor has been shown to interact with SHC2, Annexin A5 and SHC1.
Fluconazole contraindications

# Contraindications
- DIFLUCAN (fluconazole) is contraindicated in patients who have shown hypersensitivity to fluconazole or to any of its excipients.
- There is no information regarding cross-hypersensitivity between fluconazole and other azole antifungal agents.
- Caution should be used in prescribing DIFLUCAN to patients with hypersensitivity to other azoles.
- Coadministration of terfenadine is contraindicated in patients receiving DIFLUCAN (fluconazole) at multiple doses of 400 mg or higher based upon results of a multiple dose interaction study.
- Coadministration of other drugs known to prolong the QT interval and which are metabolized via the enzyme CYP3A4 such as cisapride, astemizole, erythromycin, pimozide, and quinidine are contraindicated in patients receiving fluconazole.
Flucytosine adverse reactions

# Adverse Reactions
The adverse reactions which have occurred during treatment with Ancobon are grouped according to organ system affected.
- Cardiovascular: Cardiac arrest, myocardial toxicity, ventricular dysfunction.
- Respiratory: Respiratory arrest, chest pain, dyspnea.
- Dermatologic: Rash, pruritus, urticaria, photosensitivity.
- Gastrointestinal: Nausea, emesis, abdominal pain, diarrhea, anorexia, dry mouth, duodenal ulcer, gastrointestinal hemorrhage, acute hepatic injury including hepatic necrosis with possible fatal outcome in debilitated patients, hepatic dysfunction, jaundice, ulcerative colitis, enterocolitis, bilirubin elevation, increased hepatic enzymes.
- Genitourinary: Azotemia, creatinine and BUN elevation, crystalluria, renal failure.
- Hematologic: Anemia, agranulocytosis, aplastic anemia, eosinophilia, leukopenia, pancytopenia, thrombocytopenia, and fatal cases of bone marrow aplasia.
- Neurologic: Ataxia, hearing loss, headache, paresthesia, parkinsonism, peripheral neuropathy, pyrexia, vertigo, sedation, convulsions.
- Psychiatric: Confusion, hallucinations, psychosis.
- Miscellaneous: Fatigue, hypoglycemia, hypokalemia, weakness, allergic reactions, Lyells syndrome.
Pharyngeal pouch (embryology)
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# Overview
In the development of vertebrate animals, Pharyngeal or branchial pouches form on the endodermal side between the branchial arches, and pharyngeal grooves (or clefts) form the lateral ectodermal surface of the neck region to separate the arches. The pouches line up with the clefts, and these thin segments become gills in fish.

# The pouches

## First pouch
This is the only pouch in which the endoderm and ectoderm remain close together, as the tympanic membrane.  There is minimal mesoderm in the tympanic membrane.
- The endoderm lines the future auditory tube, middle ear, mastoid antrum, and inner layer of the tympanic membrane.
- The ectoderm lines the future external acoustic meatus and outer layer of the tympanic membrane.
- Mesoderm  remains as the middle portion of the tympanic membrane, where the endoderm of the first pharyngeal pouch and the ectoderm of the first pharyngeal cleft have met.
Other mesoderm derivatives include:  Meckel's cartilage (mandible, malleus, incus, sphenomandibular ligament), muscles (temporalis, masseter, later and medial pterygoids, mylohyoid, anterior belly digastric, tensor tympani, tensor veli palatini, anterior 2/3 tongue), and nerves (CN V2, CN V3).

## Second pouch
- Contributes to the middle ear, tonsils, supplied by the facial nerve.

## Third pouch
- The third pouch possesses Dorsal and Ventral wings. Derivatives of Dorsal include the inferior parathyroid glands, while the ventral wings fuse to form the cytoreticular cells of the thymus. The main nerve supply to the derivatives of this pouch is Cranial Nerve IX, glossopharyngeal nerve.

## Fourth pouch
- Derivatives include the superior parathyroid gland and parafollicular C-Cells of the thyroid gland.

## Fifth pouch
- Rudimentary structure, becomes part of the fourth pouch contributing to thyroid C-cells.
Gallbladder volvulus overview

# Overview
Volvulus is twisting of a non solid organ around its mesentric axis. Gallbladder volvulus is twisting or rotation of the gallbladder along the axis of the cystic duct and vascular pedicle (cystic artery).

# Historical Perspective
It was first described by Wendal in 1898.

# Pathophysiology
Torsion of gall bladder leads to occlusion of the cystic duct and the cystic artery. This torsion can be complete (180o - 360o) or incomplete (< 180o). Incomplete torsion causes obstruction of the bile duct and vascular supply may be spared. In complete obstruction both are compromised. This occlusion leads to an increased amount of bile in the lumen and a decreased flow of blood to the organ. Increased pressure in the lumen with ischemia leads to acute inflammation causing a surgical emergency.

# Diagnosis

## History and Symptoms
Presentation of gallbladder volvulus is very non -specific. It is tough to diagnose based upon just the history and symptoms because patients present with acute abdominal pain with or without vomiting. At times there may be a tender mobile mass palpated suggestive of a floating gallbladder.
Gamma glutamyl transpeptidase
Gamma glutamyl transferase (GGT or GGTP, or Gamma-GT) (EC 2.3.2.2) is primarily a liver enzyme.

# Function
It is involved in the transfer of amino acids across the cellular membrane. It is also involved in glutathione metabolism by transfering the glutamyl moiety to a varitey of acceptor molecules including water, certain L-amino acids and peptides. Leaving the cystein product to preserve intracellular homeostasis of oxidative stress. 

# Location
GGT is found on the cell surface on all cells, with particularly high concentrations in the liver, bile ducts and kidney.
The enzyme is also present in other tissues, such as the epididymis.

# Clinical significance
Its level in the blood may be tested for, as an elevated level may indicate an abnormality in the liver, though this can be caused by a number of conditions including:
- congestive heart failure
- cholestasis (congestion of the bile ducts)
- cirrhosis of the liver
- Restricted blood flow to the liver
- restricted venous outflow from liver like Budd-Chiari syndrome
- Necrosis of the liver
- Liver tumors
- hepatitis
- hepatotoxic drugs
Its levels are increased in chronic and acute alcohol abuse.
Ganciclovir adverse reactions

# Adverse Reactions
During clinical trials, the most frequent adverse events seen in patients treated with the Vitrasert Implant involved the eye.
During the first two months following implantation, visual acuity loss of 3 lines or more, vitreous hemorrhage, and retinal detachments occurred in approximately 10-20% of patients. Cataract formation/lens opacities, macular abnormalities, intraocular pressure spikes, optic disk/nerve changes,hyphemas and uveitis occurred in approximately 1-5%.
Adverse events with an incidence of less than 1% were: retinopathy, anterior chamber cell and flare, synechia, hemorrhage (other than vitreous), cotton wool spots, keratopathy, astigmatism, endophthalmitis, microangiopathy, sclerosis, choroiditis, chemosis,phthisis bulbi, angle closure glaucoma with anterior chamber shallowing, vitreous detachment, vitreous traction, hypotony, severe post-operative inflammation, retinal tear, retinal hole, corneal dellen, choroidal folds, pellet extrusion from scleral wound, and gliosis.
Hahnemann University Hospital
Hahnemann University Hospital established in 1885 is a hospital in Center City, Philadelphia. It is affiliated with Drexel University College of Medicine, and serves as its Center City Hahnemann campus.

# History
In 1993 Hahnemann University Hospital was bought by Allegheny General. In 1994 the Woman's Medical College of Pennsylvania and the Medical College of Pennsylvania merged to form the MCP Hahnemann School of Medicine, a part of the Allegheny University of the Health Sciences. In 1998 the parent company of the Allegheny University of the Health Sciences, Allegheny Health Education and Research Foundation, declared bankruptcy. Tenet Healthcare Corporation then acquired the bankrupt Allegheny University, its holdings which included Hahnemann University Hospital, and some of the other regional hospitals. Roxborough Memorial Hospital, St. Christophers Hospital for Children and Warminster Hospital were included in the additional holdings.

# Drexel
When Tenet acquired the holdings of the Allegheny University it created MCP Hahnemann University and arranged for Drexel University to assume its operation. In 2002 Tenet Healthcare agreed for MCP Hahnemann University to be merged into Drexel for a period of 20 years, Tenet also agreed to an affiliation between the Drexel University College of Medicine and Tenet's teaching hospitals in the Philadelphia area, with Hahnemann University Hospital being one of those.
Hemetsberger indole synthesis
The Hemetsberger indole synthesis (also called the Hemetsberger-Knittel synthesis) is a chemical reaction that thermally decomposes a 3-aryl-2-azido-propenoic ester into an indole-2-carboxylic ester.
Yields are typically above 70%.  However, this is not a popular reaction, due to the lack of stability and difficulty in synthesizing the starting material.

# Reaction mechanism
The mechanism is unknown.  However, aziridine intermediates have been isolated.  The mechanism is postulated to proceed via a nitrene intermediate.
Obliterative portal venopathy
Synonyms and keywords: Hepatoportal sclerosis

# Overview
Hepatoportal sclerosis (HPS) is a rare disorder characterized by sclerosis of the intrahepatic portal veins.

# Pathophysiology

## Pathology
Histopathologic findings are
- Periportal fibrosis
- Occlusion of small portal veins
- Sclerosis of the portal venous system
- Proliferation of small vascular channels within/around portal tracts

# Causes
- Exposure to toxic substances (arsenic or vinyl chloride)
- Drugs (vitamin A, 6-mercaptopurine
- Autoimmune and connective tissue diseases
- Systemic or intra abdominal infections
- Clotting factor abnormalities

# Differentiating from other Diseases
Differential diagnosis from liver cirrhosis is crucial and may be difficult. A large liver biopsy specimen, together with expertise and awareness of the examiner, are requested for optimal diagnosis.

# Epidemiology and Demographics
The prevalence of this disease is unknown, and the distribution is worldwide, with many cases reported in Asia.

## Age
The disease can occur at any age.

## Gender
Both males and females are equally affected.

# Natural History, Complications and Prognosis

## Complications
- Liver failure
- Ascites
- Encephalopathy

## Prognosis
Current overall prognosis is good (80% survival at ten years after the diagnosis).  Male patients and patients with disease onset before 40 years of age show a poorer prognosis.

# Diagnosis

## Symptoms
Lethargy and in advanced stages symptoms of liver failure

## Physical Examination

### Eye
- Jaundice

### Abdomen
- Ascites
- Spleenomegaly
- Signs of portal hypertension

### Neurologic
- Confusion
- Encephalopathy

## Laboratory Findings

### Blood and Biomarker Studies
- Pancytopenia
- Elevated liver enzymes
- Liver function tests

### Endoscopy
- Esophageal varices

### Biopsy
- Evidence of sclerosis of portal tract
- Delineates the portal system and helps in the identification of lesions.

# Treatment
Variceal bleeding is the main cause for morbidity and mortality.  Treatment of active bleeding and its prophylaxis can follow the recommendations for patients with cirrhosis.  In considering spleenectomy, the high risk of thrombosis in the portal venous system should be taken into account
Herpetic keratoconjunctivitis
Herpetic keratoconjunctivitis is a form of keratitis and conjunctivitis associated with herpes simplex virus.:370
It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea. Primary infection typically presents as swelling of the conjunctiva and eye-lids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.  The effect of the lesions varies, from minor damage to the epithelium (superficial punctate keratitis), to formation of dendritic ulcers. Infection is unilateral, affecting one eye at a time.  Additional symptoms include dull pain deep inside the eye, mild to acute dryness, and sinusitis. Most primary infections resolve spontaneously in a few weeks.  Healing can be aided by the use of oral and topical antivirals.
Subsequent recurrences may be more severe, with infected epithelial cells showing larger dendritic ulceration, and lesions forming white plaques. The epithelial layer is sloughed off as the dendritic ulcer grows, and mild inflammation (iritis) may occur in the underlying stroma of iris. Sensation loss occurs in lesional areas, producing generalised corneal anaesthesia with repeated recurrences. Recurrence can be accompanied by chronic dry eye, low grade intermittent conjunctivitis, or chronic unexplained sinusitis. Following persistent infection  the concentration of viral DNA reaches a critical limit. Antibody responses against the viral antigen expression in the stroma can trigger a massive autoimmune response in the eye.  The response may result in the destruction of the corneal stroma, resulting in loss of vision due to opacification of the cornea. This is known as immune-mediated stromal keratitis.
Hibernation induction trigger
Hibernation induction trigger (hibernation inducement trigger or HIT) is a substance found in the blood of hibernating animals. If blood is taken from a hibernating squirrel in the winter and injected into another squirrel in the spring, the normally active squirrel goes into hibernation. HIT can also be found in the blood of hibernating bears.
Researchers were able to prolong the life of an isolated pig's heart with HIT. This may have potentially important implications for organ transplant, as it could allow organs to survive for up to 18 or more hours, outside the human body. This would be a great improvement from the current 6 hours.
NASA is co-funding research into HIT, with an eye to long-duration space travel for humans.
Chemically, HIT is an opioid-like substance.