Correlation Of Clinical Manifestations Research Articles

Correlation of clinical manifestations and condylar morphology of patients with temporomandibular degenerative joint diseases

ABSTRACT Objective To study the correlation between condylar morphology and clinical manifestations in patients with degenerative joint disease (DJD) of the temporomandibular joint (TMJ). Methods A total of 175 joints of 131 patients with DJD were included. Data on patients’ basic information and symptoms were collected and analyzed. Condylar morphology was evaluated using cone beam computed tomography (CBCT). The correlation between the condylar morphology and clinical manifestations was analyzed. Results The prevalence of joint noises, clicks, and crepitus was 93/175 (53%), 73/175 (42%), and 20/175 (11%), respectively. Condylar anteroposterior diameter and condylar height were correlated with pain. There was a correlation between the shape of the condyle in the sagittal plane and joint noise. Conclusion Condylar morphology and clinical features of DJD were correlated to some extent.

Case Report: Systemic lupus erythematous associated with thrombotic thrombocytopenic purpura, a diagnostic challenge

Thrombotic thrombocytopenic purpura (TTP) is an uncommon microangiopathic disease and often occurs as a complication of systemic lupus erythematous (SLE). However, this probable causal relationship has not been completely proven. The diagnostic differentiation of both diseases is difficult in the first instance because they share similar characteristics that may overlap. We present a case of a 32-year-old woman with antecedents of epilepsy since she was 12 years old. The patient was admitted to the emergency room with a clinical picture of headaches, fever, paleness in the skin and mucosa, confused state, paresthesia, and transient spasticity of the extremities. The laboratory results revealed Coombs negative direct autoimmune hemolytic anaemia, severe thrombocytopenia, significant elevation of the enzyme lactate dehydrogenase, and presence of schistocytes ++ in the peripheral film. In addition, positive antinuclear antibodies and positive anti-native DNA in titers of 1/320 and 1/160, respectively, were found. Renal function was conserved. We concluded that it was a case of TTP associated with SLE and indicated treatment with plasmapheresis and methylprednisolone pulses, obtaining a satisfactory response (normalization of biomarker levels, health condition) after the second session of plasmapheresis. Diagnosis of both SLE and TTP is often difficult to achieve; however, adequate correlation of clinical manifestations and laboratory tests, along with the help of partial therapeutic interventions, may lead to good clinical response.

Diagnosis of envenomation by Russell's and Echis carinatus viper: A clinical study at rural Maharashtra state of India.

Background:Envenoming by vipers Russell’s and Echis Carinatus are common accidents faced by farmers and labors. Both viper venom toxins alter coagulation mechanism in the victim. The dose of snake antivenin to neutralize the venom is empirical and varies. Though the clinical manifestations in both vipers bite envenoming are nearly similar but dose of antivenin required is more in Russell's viper. We studied in detail about the correlation of clinical manifestations and confirmed species of snake.Methods:Cases of vipers snake bites admitted for last two successive years were studied. Analysis by local manifestations, systemic involvement, 20 minute whole blood clotting test (20WBCT), identification of snake responsible for clinical effects are confirmed by the snake species brought by victims or bystanders, in case of where victim saw the snake bur failed to kill. The victims identified from pictures of big four poisonous snakes (Russell's viper, Echis carinatus, Cobra, and krait). Further confirmation from the species responsible is done by showing the hospital preserved specimen to identify the culprits.Findings:About 77 cases of viper bite studied of these 57 has clinical syndrome suggestive of Russell's viper (RV) bite, one has dry bite, 23 victims brought the killed specimen confirmed RV, of these 18 identified the specimen picture and 5 wrongly locate the species in pictures, 20 victims correctly identified the hospital preserved specimen while 3 failed to recognize. There were 28 patients who saw the snake while bitten but failed to kill, of these 20 patients identify correctly the species on picture while 8 failed to identify. Only 22 correctly identified the culprit by looking at the hospital preserved specimen and 6 were confused. One dry bite victim correctly identified the bitten snake species in picture and hospital preserved specimen.Interpretation:In viper bite poisoning clinical pictures and hospital specimen help to confirm the species are highly supportive for clinical diagnosis.

Correlation of Clinical Manifestations and C - reactive protein Level to Patients' Outcome in Acute Corrosive Poisoning

Caustic injury remains an important public health problem despite various regulatory efforts to reduce its occurrence. The aim of this study was to assess the correlation of initial clinical manifestations with patient outcomes and to evaluate the role of initial C-reactive protein (CRP) level as a prognostic marker in patients with acute corrosive poisoning. This prospective study was conducted on fifty-two patients with history of acute corrosives exposure in Tanta Toxicological Unit. Personal, toxicological data and vital signs were recorded, general and local examination (lips, tongue, palate and skin), routine laboratory investigation (arterial blood gases, liver & kidney function tests, C-reactive protein) and chest X-rays were performed to all patients on hospital admission. Patients were divided to either improved or complicated (chest complication or surgical interference). Most of the patients (53.8%) were in the age group (1-5 years), from rural regions and poisoning occurred accidentally (94.2%) by oral route (78.8%) with sodium hypochlorite (clor) (36.5%). The majority of patients suffered from gastrointestinal (GIT) symptoms. Higher number of patients who suffered from dysphagia and chest crepitation had significant complications. Statistically significant association was evident between patients’ outcome and each of modes of exposure, pre-hospitalization period, vomiting, respiratory manifestations, CRP level and X- ray finding. Additionally, the prediction of complication by a percentage of 72.2% may occur if CRP level increased more than 11.5 mg/dl. However, exclusion of complication in 80.5% of cases may occur when its level is less than 11.5 mg/dl. Hence, it may be useful as a prognostic marker for acute corrosive poisoning complications.

Childhood mastocytosis

Important advances have been achieved in recent years in adult mastocytosis. However, our knowledge about childhood mastocytosis is limited because invasive tests are not routinely performed in children. We ignore the frequency of systemic involvement in childhood mastocytosis, its outcome, and which are the main clinical and laboratory parameters associated with persistence into adult mastocytosis and its severity. Childhood mastocytosis is a clonal mast cell disease, with different activating mutations in the KIT gene discovered in most patients. Serum tryptase is the best marker for mast cell burden in children, and, at baseline, correlates well with the severity of symptoms in childhood mastocytosis. Systemic mastocytosis definitely may occur in children, but bone marrow studies to demonstrate a systemic involvement are not routinely performed nor recommended; it can be estimated that around 30% of children may have bone marrow involvement as demonstrated by showing aggregates of mast cells or by flow cytometry of mast cells expressing the aberrant CD25 marker. A new and improved classification of childhood mastocytosis is needed, and should be based on the correlation of clinical manifestations, morphology of mast cells in the skin, and the predicted outcome of the disease. The current classifications of childhood mastocytosis do not address any of these important issues.

Vasculitides of the gastrointestinal tract

Systemic vasculitis is often not considered as a possible diagnosis by clinicians because of its low prevalence compared with other more common diseases. Vasculitis can affect any end organ, and it is therefore often missed early on in disease progression. Gastrointestinal (GI) manifestations of vasculitis are considered rare and the presentation is often nonspecific. However, if there is significant involvement of the major vessels of the gastrointestinal system, life-threatening sequelae, including perforation and bowel ischemia, may occur. This makes early and immediate management crucial to improve long-term morbidity and mortality. Diagnosis of various GI vasculitides often relies on correlation of clinical manifestations with pathology and additional investigations. This paper reviews the various vasculitides that affect the GI tract, including systemic lupus erythematosus, mixed connective tissue disease, Henoch Schönlein purpura, polyarteritis nodosa, Churg-Strauss syndrome, Wegener's granulomatosis, microscopic polyangiitis, enterocolic lymphocytic phlebitis, and Behcet's disease. Segmental arterial mediolysis, mistakenly believed to be a vasculitis, is also discussed.

Delayed encephalopathy after carbon monoxide intoxication--long-term prognosis and correlation of clinical manifestations and neuroimages.

In order to understand the correlation between the clinical and neuroimaging manifestations and the long-term prognosis in delayed encephalopathy after carbon monoxide (CO) intoxication, we retrospectively reviewed 12 patients who had delayed encephalopathy from 89 patients with CO intoxication. There were 8 men and 4 women, with a mean age of 54.4 +/- 17.2 years (range: 11-79 years). All patients had prominent consciousness disturbance in the acute stage and received high flow of O2 or hyperbaric oxygen therapy. All of them regained consciousness within 1-7 days, but subsequently developed delayed encephalopathy. The delayed encephalopathy occurred from 14 to 45 days after recovery from the acute stage. The clinical manifestations included cognitive impairment, akinetic mutism, sphincter incontinence, gait ataxia and extrapyramidal syndromes such as chorea, dystonia, and parkinsonism. Brain MRI revealed multiple lesions in the subcortical white matter and basal ganglia, mostly in the globus pallidus, and to a lesser degree in the putamen, and caudate. In the follow-up period, sphincter incontinence first disappeared. The cognitive impairment improved greatly in the following few months, but the involuntary movements were improved only slightly. Some patients had persistent neurological sequelae, such as dystonia. Similary, the follow-up brain MRI showed a steady improvement. In conclusion, the delayed encephalopathy usually developed 2 weeks to 1.5 months after the acute phase of CO intoxication. Globus pallidus and subcortical white matter were commonly involved. The neurological manifestations improved and correlated roughly with the neuroimaging changes.

Subcutaneous Fat Necrosis in Pancreatic Disease A Review and Two New Case Reports

Subcutaneous fat necrosis is a rare and often overlooked sign of pancreatic disease. It is manifested in painful subcutaneous erythematous nodules, often found on the legs. The histopathological finding is pathognomic. Therefore, correlation of clinical manifestations with histopathological and laboratory findings may be helpful in recognizing some disorders of subcutaneous fat. Despite several studies, the cause of metastatic fat necrosis is unknown. I describe the syndrome, review the literature, and report two new cases.

Experimental stroke in gerbils: correlation of clinical, pathological and electroencephalographic findings and protein synthesis.

Cerebral ischemia was produced in gerbils by ligation of the right common carotid artery and the resulting clinical manifestations and pathological alterations, along with electroencephalographic findings, were followed from 30 minutes to 24 hours. Protein synthesis was evaluated with brain slices in vitro and subsequent cellular and subcellular fractionations. One group of animals developed clinical signs of cerebral ischemia and stroke very rapidly and often died within 12 hours. In these animals cerebral infarction was diffuse in the right side of brain within a few hours post-operatively and there was persistent suppression in the electroencephalographic recordings. Amino acid incorporation into protein of subcellular fractions was decreased to 50% of the opposite side at 30 minutes and further declined to less than 10% in 8 to 10 hours. Another group of animals survived to 24 hours in spite of severe neurological manifestations, and protein synthesis was about 15% of the control side at 24 hours. The suppression of protein synthesis was observed both in the neuronal and neurologlial fractions indicating similar vulnerability of these cellular elements toward cerebral ischemia as shown with cerebral anoxia in the past. It was emphasized that the correlation of clinical manifestations and biochemical data is very important to extract meaningful information from biochemical investigations in this model.