Side effects
In myelofibrosis, the most common side effects include thrombocytopenia (low blood platelet counts), anaemia (low red blood cell counts), neutropenia (low levels of neutrophils), urinary tract infections (infection of the structures that carry urine), bleeding, bruising, weight gain, hypercholesterolaemia (high blood cholesterol levels), dizziness, headache and raised liver enzyme levels.In polycythaemia vera, the most common side effects include anemia (low red blood cell counts) and thrombocytopenia (low blood platelet count), bleeding, bruising,  hypercholesterolaemia (high blood cholesterol levels), hypertriglyceridemia (high blood fat levels), dizziness, raised liver enzyme levels and high blood pressure.In acute graft-versus-host disease, the most common hematologic adverse reactions include anemia, thrombocytopenia, and neutropenia. The most common nonhematologic adverse reactions include infections and edema.Immunologic side effects have included herpes zoster (shingles) and case reports of opportunistic infections. Metabolic side effects have included weight gain. Laboratory abnormalities have included alanine transaminase (ALT) abnormalities, aspartate transaminase (AST) abnormalities, and mildly elevated cholesterol levels. Mechanism of action
Ruxolitinib is a janus kinase inhibitor (JAK inhibitor) with selectivity for subtypes JAK1 and JAK2. Ruxolitinib inhibits dysregulated JAK signaling associated with myelofibrosis. JAK1 and JAK2 recruit signal transducers and activators of transcription (STATs) to cytokine receptors leading to modulation of gene expression. History
In March 2012 the phase III Controlled Myelofibrosis Study with Oral JAK Inhibitor-I (COMFORT-I) and COMFORT-II trials showed significant benefits by reducing spleen size and relieving debilitating symptoms.In September 2021, ruxolitinib cream (sold under the brand name Opzelura) was approved for medical use in the United States for the treatment of mild to moderate atopic dermatitis (AD).
Camptodactyly is a medical condition that causes one or more fingers or toes to be permanently bent. It involves fixed flexion deformity of the proximal interphalangeal joints. Camptodactyly can be caused by a genetic disorder. In that case, it is an autosomal dominant trait that is known for its incomplete genetic expressivity. This means that when a person has the genes for it, the condition may appear in both hands, one, or neither. A linkage scan proposed that the chromosomal locus of camptodactyly was 3q11.2-q13.12. Causes
The specific cause of camptodactyly remains unknown, but there are a few deficiencies that lead to the condition. A deficient lumbrical muscle controlling the flexion of the fingers, and abnormalities of the flexor and extensor tendons.A number of congenital syndromes may also cause camptodactyly:

Jacobsen syndrome
Beals syndrome
Blau syndrome
Freeman–Sheldon syndrome
Cerebrohepatorenal syndrome
Weaver syndrome
Christian syndrome 1
Gordon syndrome
Jacobs arthropathy-camptodactyly syndrome
Lenz microphthalmia syndrome
Marshall–Smith–Weaver syndrome
Oculo-dento-digital syndrome
Tel Hashomer camptodactyly syndrome
Toriello–Carey syndrome
Trisomy 13
Stuve–Wiedemann syndrome
Loeys–Dietz syndrome
Fetal alcohol syndrome
Fryns syndrome
Marfan syndrome
Carnio-carpo-tarsal dysthropy

Genetics
The pattern of inheritance is determined by the phenotypic expression of a gene—which is called expressivity. Camptodactyly can be passed on through generations in various levels of phenotypic expression, which include both or only one hand. This means that the genetic expressivity is incomplete. It can be inherited from either parent. In most of its cases, camptodactyly occurs sporadically, but it has been found in several studies that it is inherited as an autosomal dominant condition. Treatment
If a contracture is less than 30 degrees, it may not interfere with normal functioning. The common treatment is splinting and occupational therapy.