Dactylitis – see Psoriatic arthritis (PsA).

Deficiency of phagocytosis Inefficient function of professional phagocytes expressed predominantly as an increased susceptibility to infectious diseases. It is divided into a primary deficiency that is caused by abnormal or missing relevant genes and secondary deficiency that can be induced physiologically (infants and elderly) through poor nutrition, harmful factors of the external environment, various disorders or the toxic effect of xenobiotics, including drugs. The most important of the primary defects of phagocytosis include: chronic granulomatous disease, leukocyte adhesion deficiency (LAD syndrome), Job’s syndrome, Chédiak-Higashi syndrome, the deficiency of specific granules, myeloperoxidase deficiency, glucose-6-phosphate dehydrogenase deficiency and tuftsin deficiency.

Deficiency of vitamin D It is accompanied by increased secretion of the parathyroid hormone, which mostly keeps calcaemia within normal range. Risk groups are exclusively breastfed infants with no vitamin D supplementation; in winter months also populations living north of the 40th degree of latitude due to deficiency of UV light, in particular individuals with dark complexion; and people covering their skin, for example, for religious reasons (Muslims). The level of vitamin D saturation in the body is determined by plasma concentration of calcidiol (25-hydroxycholecalcipherol). 75 nmol/L is considered an optimum value. It is estimated that 30–50 % of the population in the USA and Europe may have decreased vitamin D saturation in the body during a calendar year. Since vitamin D is a steroid hormone affecting the expression of more than 900 genes, some think that its deficiency may be connected with the increased incidence of autoimmune, oncologic and cardiovascular diseases. A significant long-term vitamin D deficiency leads to the development of deficiency rickets with impaired mineralization of osteoid tissue, subsequent range of pathologic manifestations on the skeleton and typical X-ray findings of long-bone metaphysis. These findings, together with increased plasma alkaline phosphatase activity concentration, are decisive for the establishment of the diagnosis. Severe untreated rachitis leads to hypocalcaemia and hypophosphataemia with all clinical consequences. Rarely, autosomal recessive hereditary forms of rickets with kidney alpha-hydroxylase deficiency (vitamin D-dependent type I rachitis) or dysfunction of vitamin D receptors with peripheral calcitriol resistance occur.

Deformities These are often the result of rheumatic inflammatory and degenerative disorders. In rheumatoid arthritis, there may be deformities of the hand and fingers – swan neck deformity, boutonniere deformity, mallet finger deformity, Z deformation of the thumb, flexion and subluxation deformities or ulnar deviation in the metacarpophalangeal (MCP) joints, bayonet position in the wrist, volar subluxation or luxation of the radiocarpal joint (drop hand).

Dendrites Thin branched projections arising from the body of the nerve cell. They serve as an input region for stimuli and transmission of electrical impulses to the cell body.

Denosumab (Prolia®) Fully human antibody against RANKL (see RANKL) intended for the treatment of postmenopausal osteoporosis in order to reduce the incidence of vertebral and non-vertebral fractures and fractures of the hip. Denosumab (Prolia®) is also indicated for the treatment of reduced bone mineral density in men treated with hormonal ablation due to prostatic carcinoma; in these patients, denosumab reduces the risk of vertebral fractures. Denosumab therapy is applied in the form of a subcutaneous injection at the dose of 60 mg every 6 months. Patients must have sufficient calcium and vitamin D intake.

Dermatomyositis – see Idiopathic inflammatory myopathies (IIM), Noninflammatory myopathies and Juvenile dermatomyositis (JDM).

DEXA – see DXA

Diabetes mellitus A metabolic disorder of glucose, lipids and proteins that occurs as a consequence of a relative or absolute lack of insulin, or its insufficient effect. In 1990, the WHO accepted a new classification, according to which diabetes has two basic types. Type I has two subtypes either immunologically conditioned or idiopathic. Insulin resistance or deficit prevails in type II. The other specific types of diabetes are genetic disturbance of β-cell function, genetic disturbances of the effect of insulin, disorders of the endocrine pancreas, endocrinopathies, diabetes induced by drugs and chemical agents and rare forms of immunologically conditioned diabetes.