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At least 685 records · Page 38Linked to original sources
PubMed1992

[Congenital cutaneous Langerhans histiocytosis. Apropos of 7 cases].

Seven cases of congenital Langerhans' cell histiocytosis (LH) are reported, with emphasis on clinical and immunohistochemical features. This is a polymorphic disease at birth. In 4/7 cases, the diffuse, generalized rash could be classified as cutaneous Letterer-Siwe disease (LSD); 3/4 remained purely cutaneous and healed in less than 3 months; whereas the fourth-one persisted, pulmonary lesions appeared, and the infant died on his 40th day. In 3/7 cases, the clinical diagnosis at birth was either a Blueberry Muffin Baby (BMB) or Hashimoto-Pritzker type LH (HPLH); the lesions healed rapidly, although one cas was contradictory: typical BMB at birth, histology mimicking a monoblastic cutaneous leukemia, no T.O.R.C.H. syndrome, normal bone marrow, immunophenotyping of LH, auto-involution; 2/3 were MZ twins, both with few lesions. We would like to stress the fact that the clinical spectrum of LH should include BMB, which, however, in most cases must be considered a differential diagnosis. Regarding cutaneous congenital LH, an eponymic classification (LSD, HPLH) is difficult to follow strictly, because overlapping pictures are observed. There is a wide spectrum of cutaneous congenital LH. The main problem at birth is the lack of prognostic criteria. Neither the presence of the rash at birth, nor its type and extension, is necessarily evidence of risk of systemic disease. Cases of HPLH involute, as also do cases of cutaneous LSD, and the "Blueberry Muffin" type of LH; overlapping clinical aspects exist. Histopathological data, electron microscopy or immunohistochemistry, define LH, but they do not enable the outcome to be predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis, Differential↗
PubMed1992

Characterization of the original Christmas disease mutation (cysteine 206----serine): from clinical recognition to molecular pathogenesis.

Christmas disease was first reported as a distinct clinical entity in two manuscripts published in 1952. The eponym associated with this disorder, is the surname of the first patient examined in detail and reported by Biggs and colleagues in a paper describing the clinical and laboratory features of seven affected individuals. This patient has severe factor IX coagulant deficiency (less than 0.01 units/ml) and no detectable circulating factor IX antigen (less than 0.01 units/ml). Coding sequence and splice junctions of the factor IX gene from this patient have been amplified in vitro through the polymerase chain reaction (PCR). One nucleotide substitution was identified at nucleotide 30,070 where a guanine was replaced by a cytosine. This mutation alters the amino acid encoded at position 206 in the factor IX protein from cysteine to serine. The non conservative nature of this substitution, the absence of this change in more than 200 previously sequenced factor IX genes and the fact that the remainder of the coding region of this gene was normal, all provide strong circumstantial evidence in favour of this change being the causative mutation in this patient. The molecular characterization of this novel mutation in the index case of Christmas disease, contributes to the rapidly expanding body of knowledge pertaining to Christmas disease pathogenesis.

Amino Acid Sequence↗
PubMed2005

Takayasu's disease presenting with pain chest, prolonged pyrexia and pleural effusion.

Takayasu's disease (TD) is a diffuse arteriopathy recognised by various names viz. Takayasu Arteritis, Takayasu's Disease, Takayasu Syndrome, Pulseless Disease, Non-specific Aortoarteritis, Reversed Coarctation, Aortic Arch Syndrome, Aortitis Syndrome, Young Female Arteritis, Idiopathic Arteritis and Martorell Syndrome. Though described about a century ago and with many eponyms, TD yet remains a challenging problem regarding etiopathogenesis, clinical presentation and management. We present a case of TD with pyrexia of unknown origin (PUO), angina and left sided pleural effusion.

Adult↗
PubMed2006

Airway management: a patient with Madelung disease.

This case study describes a 51-year-old, ASA physical status II Hispanic man who underwent liposuction to the anterior neck and resection of adipose tissue of the posterior neck. The patient was diagnosed with multiple symmetric lipomatosis, better known by its eponym, Madelung disease. This disease is characterized by abnormal adipose tissue growth primarily in the neck and shoulder regions. As a result of this pathology, a complete airway assessment was challenging. The patient's Mallampati classification was class III with visualization of the soft palate only. Other elements of a full assessment such as thyromental distance, sternomental distance, and tracheal orientation were impossible to evaluate because of the extreme circumferential girth of the adipose tissue in the neck. In addition, flexion and extension of the neck was limited by a minimum of 20 degrees because of the pathology. The patient was deemed as having a difficult airway, and an awake fiberoptic intubation was planned and used successfully. The subsequent surgical procedure progressed without incident, and the patient was transferred to a stepdown unit for monitoring of his airway postoperatively.

Airway Obstruction↗
PubMed2006

Unexplained somatic symptoms--diagnostic window for mental disorders.

Prevalence of common mental diseases eg, anxiety disorders and depression in primary care, general practice and specialists clinics is high but theirdiagnosis in these settings are poor, main reason being the absence of psychological complaints by patients. Such patients commonly present with physical symptoms suggestive of systemic diseases but examination and investigations often fail to substantiate organic basis of these so-called unexplained somatic symptoms (USSs). Several studies have shown that patients with USSs suffer from anxiety and depression. But these USSs are mostly misinterpreted or ignored by clinicians resulting in poor rates of diagnosis. The study objective was to devise algorithm for better and early diagnosis of. mental diseases in a specialist clinic practice setting. Common USSs were interpreted as regards their symptom-correlates both physical and mental and documented while taking detailed history, physical examination and needed investigations to diagnose systemic diseases. The study was in phases during three years and included 1297 patients in four cohorts which included one group of 154 patients with common USSs, treated with long term antidepressants. Data of all patients were recorded in microsoft excel spread-sheets for analysis. Commonest presenting USSs were so-called "gas", "acidity" and "dysentery" expressed in vernacular terms. On elucidation these were found to mean wide varieties of physical symptoms-complexes that were not typical of specific systemic diseases; 85% in one group and 73% in another with these USSs and their symptom-correlates when positively screened for symptoms of neurotic diseases (ICD-10) after detailed history taking were found to have anxiety and depression. Psychiatric comorbidity with systemic diseases was found in various percentages in three different cohorts when these USSs were properly evaluated. By patients' own assessments, 84.4%, 88% and 90% of those presenting with USSs of so-called "gas", "acidity" and "dysentery" (with their symptom-correlates) and who were put on three different low dose antidepressant treatment groups had satisfactory to good results so long as they were being taken regularly. These common USSs and the underlying physical symptoms-correlates were eponyms of anxiety disorders and non-major depression. General practitioners and specialists eg, gastroenterologists, cardiologists, neurologists, etc, should heed the USSs as the starting point for early diagnosis and treatment of comorbid mental disorders along with the systemic diseases for better treatment compliance and outcome and quality of life. Training of physicians and medical students in the diagnosis and management of patients with USSs should be emphasised in clinical teaching programmes. An algorithm for early diagnosis and management of common mental disorders in general and clinic practice is suggested.

Abdominal Pain↗
PubMed1990

Kaposi's varicelliform eruption. Absence of ocular involvement.

The eponym Kaposi's varicelliform eruption (KVE) describes a characteristic syndrome of disseminated vesicopustules that occasionally complicates a number of dermatoses. Among these, the most common is atopic dermatitis, and the inciting agent is most often herpes simplex virus (HSV). Very few reports of ocular herpetic disease exist among the many cases of KVE reported in the literature, despite extensive cutaneous involvement with herpetic lesions. We describe 10 patients with KVE, none of whom have developed evidence of herpetic ocular disease despite widespread facial involvement in all patients. All random conjunctival swab cultures performed in 3 patients were positive for growth of viable HSV. Although ocular exposure to HSV may commonly occur in KVE, ocular pathology due to this virus does not appear to be a common sequela.

Acyclovir↗
PubMed1990

Ulcerative colitis associated chronic uveitis. Parasitization of intraocular leucocytes by mollicute-like organisms.

Uveitis is inflammation of the ocular vascular coats. Most uveitis is chronic, idiopathic, and considered to have an endogenous, possibly autoimmune pathogenesis. Chronic idiopathic uveitis occurs in isolation or with various systemic diseases including inflammatory bowel diseases. Using a transmission electron microscope vitreous leucocyte parasitizing and destroying mollicute-like organisms (MLO) are often found to cause chronic uveitis. Mollicutes are cell wall deficient bacteria. Mollicutes have a characteristic ultrastructural appearance. Extracellular mollicutes are fastidious, lipid-rich, and contain various potent cytotoxins. They cause human and animal diseases with autoimmune features. Morphologically similar organisms are intracellular non-cultivable pathogens that bear the eponym MLO. MLO are cytopathogenic, and cause host cell proliferation, destruction, and dysfunction. Uveitis producing MLO are detectable within parasitised vitreous lymphocytes, monocytes, and polymorphonuclear leucocytes. They appear as intracytoskeletal 0.005-0.01 micron diameter filaments and undulating pleomorphic trilaminar membrane bound 0.01-1.0 micron tubulo-spherical bodies. Cell wall deposition to form distinctive 'spore-like' cocci may also be seen. Inoculation of human uveitis MLO into mouse eyelids produces chronic uveitis. MLO also disseminate to produce chronic inflammatory disease in all organs including the gut. MLO are detectable in all the diseased organs. This report describes MLO parasitised vitreous and aqueous leucocytes in five ulcerative colitis patients with chronic uveitis. No microorganisms were cultivated using a wide variety of cultural techniques. The results indicate that MLO caused the uveitis of these patients. The possible role of this pathogen in human gut disease and Rifampin treatment of MLO disease are discussed.

Adult↗
PubMed1987

Acquired idiopathic sensory neuropathy. Report of three cases with a prolonged follow-up.

We have followed for more than ten years three women suffering from a S.N. which appeared in their fourth decade. In these patients no malignancy or other known toxic and infectious aetiologies could be found. According to the authors the clinical symptomatology as far as the C.S.F. and the neurophysiological findings justify the separation of S.N. from G.B.S., being the first disorder characterized by an elective damage of the neurones of the ganglia of the posterior roots. Therefore the eponym of "ganglio-neuronopathy" seems appropriate.

Adult↗
PubMed1988

Castleman's disease and related disorders.

Three disorders that bear the eponym of Castleman's disease (CD) are discussed. The localized CD of hyaline-vascular (HV) type features an architecturally abnormal, hypervascular lymphoid tissue with burned-out germinal centers, and presents as an asymptomatic, slowly growing mass. It may represent a lymphoid hyperplasia associated with excessive angiogenesis. The localized CD of plasma cell (PC) type, instead, features an architecturally recognizable lymph node with solid sheets of PCs and presents with systemic manifestations of inflammation and B cell hyperreactivity. It appears as a localized chronic reaction to unknown antigens. "Multicentric" CD indicates a clinicopathologic entity characterized by the histology of CD of "mixed" type, a predominantly lymphadenopathic presentation consistently involving peripheral nodes, manifestations of multisystem involvement, and an idiopathic nature. It is best considered as a systemic B cell lymphoproliferation, which probably arises in a setting of immunoregulatory deficit, and may result in the outgrowth of clonal B cell populations. An attempt is presented to place the latter two forms of CD in the larger perspective of idiopathic PC disorders, by taking into account both the nature of the diseases (hyperplastic, dysplastic, neoplastic) and the lymphocyte traffic system that is involved (bone marrow-bound, mucosa-associated or peripheral-node-bound). In such a scheme, localized CD, PC type, and multicentric CD appear as a hyperplastic and a dysplastic disorder, respectively, of peripheral-node-bound B cells, related to, and often associated with, primary nodal plasmacytoma and osteosclerotic myeloma (so-called POEMS, Takatsuki's or Crow-Fukase's syndrome).

Blood Vessels↗
PubMed1989

[Historical research on international medical terminology].

The history of medical terminology is part of the history of medicine. Historical study of medical terminology involves the following aims: 1. to investigate the role of Latin and Greek in medical terminology; 2. to study changes and trends in terminology, such as changes induced by better insight into certain phenomena, narrowing and broadening of the content of terms, development of models and of special means of word formation, fight against foreign elements in terminology, and the existence of synonyms and eponyms; 3. research into the origin and development of individual terms; 4. to establish the use of terms by individual authors; 5. to study trends towards unification of terminology; 6. to investigate theoretical views of physicians on medical terminology in the past. (Ref. 93.).

History, 16th Century↗
PubMed1986

Action myoclonus, Ramsay Hunt syndrome, and other cerebellar myoclonic syndromes.

Action myoclonus, reviewed in this chapter, is the term applied to arrhythmic muscular jerking induced by voluntary movement. It is made worse by attempts at precise or coordinated movement (intention myoclonus) and may also be provoked by certain sensory stimuli. The effective stimuli for action myoclonus is probably feedback from muscle afferents, although it may be initiated by corollary discharge from motor cortex to reticular formation before or at the onset of voluntary movement. The condition is usually associated with diffuse neuronal disease such as post-hypoxic encephalopathy, uremia, and the various forms of PME, although action myoclonus may be limited to one limb in some cases of focal cerebral damage. It is caused by hyperexcitability of the sensorimotor cortex (cortical reflex myoclonus) or reticular formation (reticular reflex myoclonus), or both. No consistent pathological change has been reported in autopsied cases of action myoclonus. The underlying disorder appears to be a loss of inhibitory mechanisms involving serotonin and possibly GABA as transmitter agents. The term PME is used for the association of myoclonus with degenerative changes in the nervous system which are commonly diffuse but may predominate in certain systems. There may or may not be associated tonic-clonic seizures, other manifestations of epilepsy, or dementia. Those cases of PME associated with Lafora inclusion bodies and cerebral storage diseases can be distinguished from the system degenerations. Systems which may be involved in the latter group include cerebellodentatorubral, pyramidal, extrapyramidal, optic, auditory, posterior columns and gracile and cuneate nuclei, spinocerebellar pathways, motor neurons of cranial nerves and anterior horns, and muscle fibers. Confronted with this diversity of pathological change, it seems unnecessary to make any clinical distinction between Ramsay Hunt syndrome and Unverricht-Lundborg syndrome (Baltic myoclonus) because cerebellar signs are found in patients described under both headings. Additional systems may be involved in individuals or families who are otherwise typical. All three names could well be joined in an eponymous title (Unverricht-Lundborg-Hunt disease) or the condition simply known as the systems degeneration type of PME, as Halliday (43) suggested. The cause of the condition (or spectrum of conditions) is at present unknown. Action myoclonus usually responds to sodium valproate or clonazepam, and some individuals, particularly those with posthypoxic myoclonus, improve with the administration of serotonin precursors.

Adolescent↗
PubMedDate not supplied

Gage's sign--revisited!

This article describes the use of the eponym "Gage's sign," one of the "at-risk" signs in Legg-Calvé-Perthes disease, described by Catterall in 1971. Catterall's description of this radiographic finding differs from the radiographic finding described by Gage in 1933. Thus, what we have come to call Gage's sign would be more appropriately called "Catterall's sign."

Femur↗
PubMed1988

Stargardt's disease: a review of the literature.

In 1909, Dr. Stargardt described seven patients who developed a juvenile onset macular degeneration with a striking presentation of yellowish flecks surrounding the macula. The eponym "Stargardt's disease" has since been used to describe this condition. However, there is some ambiguity in the literature concerning the characteristics which differentiate this condition from other hereditary retinal dystrophies. We have undertaken a review of the literature in an attempt to clarify the parameters of Stargardt's disease.

Color Perception↗
PubMed1988

[The wanderings of Jules Cloquet and Gustave Flaubert].

This is the story of a picaresque journey in France and in Corsica of Jules Cloquet (1790-1883), the French anatomist who described the well-known Cloquet's node and of Gustave Flaubert (1821-1880), the famous author of "Madame Bovary" and of many others novels. They were two vagabonds, Cloquet watching with slackness the young womanizering Flaubert. At 64 years of age, the lazy and meddlesome Cloquet stopped operating and writing. Surrounded by honors, he died at the age of 93, leaving his eponym to the Cloquet's node.

Anatomy↗
PubMed1987

Historical perspectives of Langerhans cell histiocytosis.

This brief review of the history of Langerhans cell histiocytosis brings us into touch with the history of medicine of the last 100 years and the opportunity to reflect on the progress in medicine in general. Hand, Christian, Schüller, Letterer, and Siwe represent far more than names to attach to eponyms. This historical overview takes us from the first descriptions of the disease in the literature through the modern efforts to take the X out of histiocytosis-X.

Diagnosis, Differential↗
PubMedDate not supplied

The enchanted herb: the work of early medical botanists in Australia.

The surgeons of the First Fleet sought not only adventure, but new herbal remedies that were awaiting discovery in the Australian bush. Within days of the foundation of the Colony at Sydney Cove in 1788, therapeutic experiments with wild currants, Eucalyptus kino (Botany Bay kino), and local "greens" were being undertaken. Scurvy and dysentery--part of the nation's foundation--prompted both a hunter-gatherer approach to new herbal remedies, and an empiricism which has continued to the present day. At least four of the 10 doctors of the First Fleet were keen botanists, and their endeavours established a precedent for medical "botanizing" which has become a living tradition over the ensuing 200 years. Before the onset of the 20th century, some 50 doctors who had studied botany in Australia had had their names appended to the native flora of the new continent. The eponyms that are preserved in the taxonomy of the country's flora comprise one record of the living history of Australia.

Australia↗
PubMed1987

Lumbar Scheuermann's. A clinical series and classification.

Scheuermann's disease of the thoracic spine is a well-defined entity, although its exact etiology is unknown. In the thoracolumbar or lumbar spine however, the criteria are much less strict for the application of this eponym. A retrospective review of all the cases of lumbar Scheuermann's disease seen at the Texas Scottish Rite Hospital revealed two distinct radiographic pictures. These consisted of a "classic" Scheuermann's and an "atypical" type characterized by vertebral end plate changes, disc space narrowing, and anterior Schmorl's nodes, but not otherwise fulfilling Sorenson's criteria. This group tended to occur in more athletic adolescents or those with a history of increased axial stress to the spine. A subgrouping of atypical Scheuermann's disease is proposed and includes acute traumatic intraosseous disc herniation. Based on these findings, a classification of lumbar Scheuermann's disease is proposed.

Adolescent↗
PubMed1987

Tin ear syndrome: rotational acceleration in pediatric head injuries.

An array of signs pathognomonic of child abuse is described for three young children. The eponym "tin ear syndrome" describes distinct unilateral ear bruising, radiographic evidence of ipisilateral cerebral edema with obliteration of the basilar cisterns, and hemorrhagic retinopathy. Rotational acceleration produced by blunt trauma to the ear is shown to be a necessary and sufficient cause for the production of this syndrome. An approximate value of 4,670 radians/s2 produced by a force of 309 to 347 N (70 to 80 lb) results in shear stress and tearing of the subdural veins, loss of cortical vasomotor tone, cerebral hyperemia, herniation, and death. Past history and environmental circumstances implicated child abuse in every case.

Battered Child Syndrome↗